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Background and Aims: Dehydration is a prevalent and costly healthcare concern, linked to heightened risks of acute kidney injury and in-hospital mortality. Despite its significance, limited evidence exists regarding its prevalence and correlation with renal function decline in apparently healthy individuals. This retrospective cohort study aimed to investigate the prevalence and association of dehydration with renal function decline and the development or progression of chronic kidney disease (CKD) in the general population. Methods: The medical records of subjects undergoing annual health check-ups from 2016 to 2019 at a single center in Taiwan were analyzed, and those with CKD stage V, insufficient data, or an increased estimated glomerular filtration rate (eGFR) were excluded. Serum osmolality, eGFR, and relevant parameters were measured. Logistic regression and Kaplan–Meier analyses were used to assess associations between osmolality and CKD-related outcomes. Results: Among the 4449 eligible subjects, those in the higher osmolality quartiles had an elevated risk of CKD or CKD progression. Multivariate analyses identified age, systolic blood pressure, serum osmolality, uric acid, proteinuria, and a history of diabetes as independent risk factors, with high-density lipoprotein being protective. Cumulative incidence curves demonstrated a significant increase in the risk of CKD with increasing osmolality levels. Restricted cubic spline analyses confirmed a nonlinear relationship between osmolality and CKD risk. Conclusions: Elevated serum osmolality independently predicted renal function decline and CKD development in apparently healthy individuals, and this effect persisted after adjusting for established risk factors. Our findings underscore the importance of addressing dehydration as a modifiable risk factor for CKD. [ABSTRACT FROM AUTHOR]

Objective: To assess the association between glycated haemoglobin (HbA1c) variability and risk of renal function decline in type 2 diabetes mellitus (T2DM). Research Design and Methods: A comprehensive search was carried out in PubMed, Embase, Web of Science and the Cochrane Library (until 12 March 2024). The Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) statement guidelines were followed for this meta‐analysis. HbA1c variability was presented as indices of the standard deviation (SD), coefficient of variation (CV), HbA1c variability score (HVS) and haemoglobin glycation index (HGI). This meta‐analysis was performed using random‐effect models. Results: Eighteen studies met the objectives of this meta‐analysis. The analyses showed positive associations between HbA1c variability and kidney function decline, with hazard ratio (HR) 1.26 (95% confidence interval [CI] 1.15–1.38) for high versus low SD groups, HR 1.47 (95% CI 1.30–1.65) for CV groups, HR 1.32 (95% CI 1.10–1.57) for HVS groups and HR 1.53 (95% CI 1.05–2.23) for HGI groups. In addition, each 1% increase in SD and CV was linked to kidney function decline, with HR 1.26 (95% CI 1.17–1.35), and 1.13 (95% CI 1.03–1.23), respectively. Also, each 1‐SD increase in SD of HbA1c was associated with deterioration in renal function, with HR 1.17 (95% CI 1.07–1.29). Conclusions: The four HbA1c variability indicators were all positively associated with renal function decline progression; therefore, HbA1c variability might play an important and promising role in guiding glycaemic control targets and predicting kidney function decline progression in T2DM. [ABSTRACT FROM AUTHOR]

The disorder of the "gut-kidney axis" exacerbates renal function decline in chronic kidney disease (CKD), and current CKD therapy is insufficient to address this issue. Hirudin has a palliative effect on the decline of renal function. However, whether hirudin can delay CKD by regulating the "intestinal renal axis" disorder remains unclear. Unilateral ureteral ligation (UUO) induced CKD rat model, and the rats were treated with bifidobacterium and hirudin for 36 days. After 14 and 36 days of modeling, kidney and colon tissues were collected for pathology, western blot (WB) assay, and quantitative real-time PCR (qPCR) detection. Serum samples were collected for renal function testing. Fecal samples were used for 16S rRNA sequencing and research on fecal bacterial transplantation. Lipopolysaccharide combine with adenosine 5'-triphosphate (LPS + ATP)-induced intestinal epithelial cell injury was treated with a nod-like receptor pyrin domain-associated protein 3 (NLRP3) inhibitor and hirudin. Protein expression was detected using WB and qPCR. The kidneys and colons of the CKD rats exhibited varying degrees of lesions. Creatinine (CRE), blood urea nitrogen (BUN), N-acetyl-β-D-glucosidase (NAG) enzyme, and serum uremic toxins were elevated. The expression of claudin-1 and occludin was decreased, NLRP3 inflammatory-related proteins were increased, and the gut microbiota was disrupted. These pathological changes were more pronounced after 36 days of modeling. Meanwhile, high-dose hirudin treatment significantly improved these lesions and restored the intestinal flora to homeostasis in CKD rats. In vitro, hirudin demonstrated comparable effects to NLRP3 inhibitors by upregulating claudin-1 and occludin expression, and downregulating NLRP3 inflammatory-related proteins expression. The dysbiosis of the gut microbiota and impaired intestinal epithelial barrier function in CKD are associated with renal dysfunction in CKD. Hirudin delays the progression of CKD by regulating the disorder of the "gut-kidney axis" and inhibiting the activation of the NLRP3-ASC-caspase-1 pathway. [ABSTRACT FROM AUTHOR]

Background: While extensive studies have elucidated the relationships between exposure to air pollution and chronic diseases, such as cardiovascular disorders and diabetes, the intricate effects on specific kidney diseases, notably primary glomerulonephritis (GN)—an immune-mediated kidney ailment—are less well understood. Considering the escalating incidence of GN and conspicuous lack of investigative focus on its association with air quality, investigation is dedicated to examining the long-term effects of air pollutants on renal function in individuals diagnosed with primary GN. Methods: This retrospective cohort analysis was conducted on 1394 primary GN patients who were diagnosed at Seoul National University Bundang Hospital and Seoul National University Hospital. Utilizing time-varying Cox regression and linear mixed models (LMM), we examined the effect of yearly average air pollution levels on renal function deterioration (RFD) and change in estimated glomerular filtration rate (eGFR). In this context, RFD is defined as sustained eGFR of less than 60 mL/min per 1.73 m2. Results: During a mean observation period of 5.1 years, 350 participants developed RFD. Significantly, elevated interquartile range (IQR) levels of air pollutants—including PM10 (particles ≤10 micrometers, HR 1.389, 95 % CI 1.2–1.606), PM2.5 (particles ≤2.5 micrometers, HR 1.353, 95 % CI 1.162–1.575), CO (carbon monoxide, HR 1.264, 95 % CI 1.102–1.451), and NO2 (nitrogen dioxide, HR 1.179, 95 % CI 1.021–1.361)—were significantly associated with an increased risk of RFD, after factoring in demographic and health variables. Moreover, exposure to PM10 and PM2.5 was associated with decreased eGFR. Conclusions: This study demonstrates a substantial link between air pollution exposure and renal function impairment in primary GN, accentuating the significance of environmental determinants in the pathology of immune-mediated kidney diseases.

Background Our goal was to create a simple risk‐prediction model for renal function decline after cardiac surgery to help focus renal follow‐up efforts on patients most likely to benefit. Methods and Results This single‐center retrospective cohort study enrolled 24 904 patients who underwent cardiac surgery from 2012 to 2019 at Fuwai Hospital, Beijing, China. An estimated glomerular filtration rate (eGFR) reduction of ≥30% 3 months after surgery was considered evidence of renal function decline. Relative to patients with eGFR 60 to 89 mL/min per 1.73 m2 (4.5% [531/11733]), those with eGFR ≥90 mL/min per 1.73 m2 (10.9% [1200/11042]) had a higher risk of renal function decline, whereas those with eGFR ≤59 mL/min per 1.73 m2 (5.8% [124/2129]) did not. Each eGFR stratum had a different strongest contributor to renal function decline: increased baseline eGFR levels for patients with eGFR ≥90 mL/min per 1.73 m2, transfusion of any blood type for patients with eGFR 60 to 89 mL/min per 1.73 m2, and no recovery of renal function at discharge for patients with eGFR ≤59 mL/min per 1.73 m2. Different nomograms were established for the different eGFR strata, which yielded a corrected C‐index value of 0.752 for eGFR ≥90 mL/min per 1.73 m2, 0.725 for eGFR 60–89 mL/min per 1.73 m2 and 0.791 for eGFR ≤59 mL/min per 1.73 m2. Conclusions Predictors of renal function decline over the follow‐up showed marked differences across the eGFR strata. The nomograms incorporated a small number of variables that are readily available in the routine cardiac surgical setting and can be used to predict renal function decline in patients stratified by baseline eGFR.

BackgroundPrevious studies have suggested that metabolic syndrome (MetS) components are associated with renal outcomes, defined as a decline in kidney function or reaching end-stage renal disease (ESRD). Elevated triglycerides (TGs) are a component of MetS that have been reported to be associated with renal outcomes. However, the association of TGs with renal outcomes in chronic kidney disease (CKD) patients independent of the other components of the MetS remains understudied.MethodsWe examined 1,657,387 patients with data on TGs and other components of MetS in 2004-2006 and followed up until 2014. Patients with ESRD on renal replacement therapy were excluded. We examined time to ESRD, estimated glomerular filtration rate (eGFR) slope (renal function decline), and time to incident CKD (eGFR

Abstract Objective The study’s purpose is to explore the link of serum albumin on renal progression in patients with chronic kidney disease (CKD). Methods This study was a secondary analysis of a prospective cohort study in which a total of 954 participants were non-selectively and consecutively collected from the research of CKD-ROUTE in Japan between November 2010 and December 2011. We evaluated the association between baseline ALB and renal prognosis (initiation of dialysis or 50% decline in eGFR from baseline) and renal function decline (annual eGFR decline) using the Cox proportional-hazards and linear regression models, respectively. We performed a number of sensitivity analyses to ensure the validity of the results. In addition, we performed subgroup analyses. Results The included patients had a mean age of (66.86 ± 13.41) years, and 522 (69.23%) were male. The mean baseline ALB and eGFR were (3.89 ± 0.59) g/dL and (33.43 ± 17.97) ml/min/1.73 m2. The annual decline in eGFR was 2.65 mL/min/1.73 m2/year. 218 (28.9%) individuals experienced renal prognosis during a median follow-up period of 36.0 months. The baseline ALB was inversely linked with renal prognosis (HR = 0.61, 95%CI: 0.45, 0.81) and renal function decline (β = -1.41, 95%CI: -2.11, -0.72) after controlling for covariates. The renal prognosis and ALB had a non-linear connection, with ALB’s inflection point occurring at 4.3 g/dL. Effect sizes (HR) were 0.42 (0.32, 0.56) and 6.11 (0.98, 38.22) on the left and right sides of the inflection point, respectively. There was also a non-linear relationship between ALB and renal function decline, and the inflection point of ALB was 4.1 g/dL. The effect sizes(β) on the left and right sides of the inflection point were -2.79(-3.62, -1.96) and 0.02 (-1.97, 1.84), respectively. Conclusion This study shows a negative and non-linear association between ALB and renal function decline as well as renal prognosis in Japanese CKD patients. When ALB is lower than 4.1 g/dL, ALB decline was closely related to poor renal prognosis and renal function decline. From a therapeutic point of view, reducing the decline in ALB makes sense for delaying CKD progression.

Abstract Background Tolvaptan was approved in the United States in 2018 for patients with autosomal dominant polycystic kidney disease (ADPKD) at risk of rapid progression as assessed in a 3-year phase 3 clinical trial (TEMPO 3:4). An extension study (TEMPO 4:4) showed continued delay in progression at 2 years, and a trial in patients with later-stage disease (REPRISE) provided confirmatory evidence of efficacy. Given the relatively shorter-term duration of the clinical trials, estimating the longer-term benefit associated with tolvaptan via extrapolation of the treatment effect is an important undertaking. Methods A model was developed to simulate a cohort of patients with ADPKD at risk of rapid progression and predict their long-term outcomes using an algorithm organized around the Mayo Risk Classification system, which has five subclasses (1A through 1E) based on estimated kidney growth rates. The model base-case population represents 1280 patients enrolled in TEMPO 3:4 beginning in chronic kidney disease (CKD) stages G1, G2, and G3 across Mayo subclasses 1C, 1D, and 1E. The algorithm was used to predict longer-term natural history health outcomes. The estimated treatment effect of tolvaptan from TEMPO 3:4 was applied to the natural history to predict the longer-term treatment benefit of tolvaptan. For the cohort, analyzed once reflecting natural history and once assuming treatment with tolvaptan, the model estimated lifetime progression through CKD stages, end-stage renal disease (ESRD), and death. Results When treated with tolvaptan, the model cohort was predicted to experience a 3.1-year delay of ESRD (95% confidence interval: 1.8 to 4.4), approximately a 23% improvement over the estimated 13.7 years for patients not receiving tolvaptan. Patients beginning tolvaptan treatment in CKD stages G1, G2, and G3 were predicted to experience estimated delays of ESRD, compared with patients not receiving tolvaptan, of 3.8 years (21% improvement), 3.0 years (24% improvement), and 2.1 years (28% improvement), respectively. Conclusions The model estimated that patients treated with tolvaptan versus no treatment spent more time in earlier CKD stages and had later onset of ESRD. Findings highlight the potential long-term value of early intervention with tolvaptan in patients at risk of rapid ADPKD progression.

Daiji Nagayama,1,2 Tomonori Sugiura,3 Su-Yeon Choi,4 Kohji Shirai5 1Department of Internal Medicine, Nagayama Clinic, Tochigi, Japan; 2Center of Diabetes, Endocrinology and Metabolism, Toho University, Sakura Medical Center, Chiba, Japan; 3Department of Cardiology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; 4Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Republic of Korea; 5Department of Internal Medicine, Mihama Hospital, Chiba, JapanCorrespondence: Daiji Nagayama, Nagayama Clinic, 2-12-22, Tenjin-Cho, Oyama-City, Tochigi, 323-0032, Japan, Tel/Fax +81-285-22-0219, Email deverlast96071@gmail.comAbstract: Obesity has been known to relate to various diseases and metabolic disorders. Since the implication of body shape has been mentioned, obesity can be divided into visceral obesity and subcutaneous obesity. The former is considered the upstream pathophysiology of metabolic syndrome (MetS), and has been emphasized worldwide for the prevention of cardiovascular diseases in the last quarter century. However, some prospective studies have shown that cardiovascular mortality and morbidity are not necessarily higher in patients with MetS compared to those without. Recently, cardio-ankle vascular index (CAVI) has been established as an indicator of arteriosclerosis. This parameter is independent of blood pressure at the measuring time, and reflects systemic arterial stiffness from the aortic origin to the ankle. However, since CAVI is not necessarily high in MetS patients, attempts have been made to clarify this unexpected phenomenon. In several studies, CAVI was found to correlate negatively with body mass index (BMI), and also with waist circumference (WC) which is a widely used representative visceral obesity index. On the other hand, a body shape index (ABSI) is also a visceral obesity index designed to be minimally associated with BMI, and is calculated by dividing WC by an allometric regression of weight and height. Replacing high WC with high ABSI in MetS diagnosis promoted the identification of MetS patients with increased CAVI in cross-sectional studies on Japanese and Korean populations. Additionally, the incidence of MetS diagnosed using high ABSI was associated with significant increase in CAVI after 1 year of observation. Enhanced predictive ability for renal function decline by replacing WC with ABSI in MetS diagnosis was also observed in a longitudinal study in Japanese urban residents. These findings suggest that MetS diagnosis using high ABSI instead of high WC as a visceral obesity index needs to be reconsidered. However, further research is desirable on Caucasian, whose body shape differs slightly from that of Asians.Keywords: CAVI, metabolic syndrome, waist circumference, a body shape index, renal function decline

Objective: The study's purpose is to explore the link of serum albumin on renal progression in patients with chronic kidney disease (CKD). Methods: This study was a secondary analysis of a prospective cohort study in which a total of 954 participants were non-selectively and consecutively collected from the research of CKD-ROUTE in Japan between November 2010 and December 2011. We evaluated the association between baseline ALB and renal prognosis (initiation of dialysis or 50% decline in eGFR from baseline) and renal function decline (annual eGFR decline) using the Cox proportional-hazards and linear regression models, respectively. We performed a number of sensitivity analyses to ensure the validity of the results. In addition, we performed subgroup analyses. Results: The included patients had a mean age of (66.86 ± 13.41) years, and 522 (69.23%) were male. The mean baseline ALB and eGFR were (3.89 ± 0.59) g/dL and (33.43 ± 17.97) ml/min/1.73 m2. The annual decline in eGFR was 2.65 mL/min/1.73 m2/year. 218 (28.9%) individuals experienced renal prognosis during a median follow-up period of 36.0 months. The baseline ALB was inversely linked with renal prognosis (HR = 0.61, 95%CI: 0.45, 0.81) and renal function decline (β = -1.41, 95%CI: -2.11, -0.72) after controlling for covariates. The renal prognosis and ALB had a non-linear connection, with ALB's inflection point occurring at 4.3 g/dL. Effect sizes (HR) were 0.42 (0.32, 0.56) and 6.11 (0.98, 38.22) on the left and right sides of the inflection point, respectively. There was also a non-linear relationship between ALB and renal function decline, and the inflection point of ALB was 4.1 g/dL. The effect sizes(β) on the left and right sides of the inflection point were -2.79(-3.62, -1.96) and 0.02 (-1.97, 1.84), respectively. Conclusion: This study shows a negative and non-linear association between ALB and renal function decline as well as renal prognosis in Japanese CKD patients. When ALB is lower than 4.1 g/dL, ALB decline was closely related to poor renal prognosis and renal function decline. From a therapeutic point of view, reducing the decline in ALB makes sense for delaying CKD progression. [ABSTRACT FROM AUTHOR]

Data regarding renal involvement in patients with hereditary transthyretin (ATTRv) amyloidosis are scarce and the natural course of chronic kidney disease (CKD) in this population remains unclear. This observational study, including adult patients diagnosed with ATTRv amyloidosis at the French Reference Centre for Cardiac Amyloidosis, investigated renal function outcome and its determinants. Multivariable logistic regression models identified factors associated with CKD at baseline. Determinants of the change in estimated glomerular filtration rate (eGFR) over 24 months of follow-up were assessed with a multivariable linear mixed-effects model. In total, 232 patients (78 women [34%], mean age: 64 years) with ATTRv amyloidosis were classified on the basis of their TTR variants: ATTRV122I (37%), ATTRV30M (29%), and other variants (34%). Median baseline eGFR was 78 ml/min/1.73 m2. Seventy-two patients (31%) had an eGFR below 60 ml/min/1.73m2 and 27/137 patients (20%) had significant proteinuria (urine protein/creatinine ratio ≥30 mg/mmol). Renal biopsy, performed in four cases, found typical Congo red-positive and TTR-labelled amyloid deposits in all cases. Older age (OR 1.07, p <.001) and a prior history of hypertension (OR 2.09, p =.04) were associated with a higher prevalence of CKD at baseline, whereas higher left ventricular global longitudinal strain (LVGLS) (OR 0.83, p <.001) was associated with a lower prevalence. The estimated change in eGFR was −7.12 [−9.61, −4.63] and −8.21 [−10.81, −5.60] ml/min/1.73 m2 after 12 and 24 months of follow-up, respectively. eGFR decline was independently associated with older age ((67–74], coefficient= −14.35 mL/min/1.73 m2, p <.01, >74, coefficient = −22.93 mL/min/1.73 m2, p <.001, versus <56), ATTRV122I (coefficient = −17.17 mL/min/1.73m2, p <.01, versus ATTRV30M) and LVGLS (coefficient = 1.22, p <.01). These data suggest that CKD is a common finding in patients with ATTRv amyloidosis, and that eGFR decline is rapid during the first year of evaluation. Older age, lower LVGLS and ATTRV122I were associated with a worse renal outcome. Further studies are now needed to evaluate effects of new targeted therapies on long term renal function. [ABSTRACT FROM AUTHOR]

Chronic kidney disease is a growing global health issue, contributing significantly to morbidity and mortality. The incidence of end-stage renal disease (ESRD) is approximately 100 per million population. Renal transplantation remains the cornerstone treatment for ESRD, with a projected 20-year survival rate of 60%. We aim to define the etiology of renal allograft dysfunction using the Banff 2019 classification by analyzing 200 renal allograft biopsies in correlation with creatinine levels across post-transplant time frames.200 renal allograft biopsies are analyzed using the recent Banff 2019 classification with creatinine levels and post-transplant duration correlation.The study included 150 (75%) male patients and 50 (25%) female patients, with the majority 78 (39%) representing the age group of 16-30 years. 36 (18%) biopsies were within 3-month post-transplant, while 92 (46%) were 2-year post-transplant. According to the Banff 2019 classification, 92 (46.0%) transplant rejection biopsies were identified, with most 54 (27%) exhibiting antibody-mediated rejection (Category 2), including 40 (20%) active acute antibody-mediated rejection (ABMR) and 14 (7.0%) chronic active ABMR. T-cell-mediated rejection (TCMR; Category 4) represented 12 (6%) biopsies, including 10 (5%) acute TCMR and 2 (1%) chronic active TCMR. Category 5, the miscellaneous group, represented 100 (50%) biopsies, out of which 32 (16%) exhibited calcineurin inhibitor (CNI) toxicity, 38 (19%) acute tubular necrosis, and 8 (4%) thrombotic microangiopathy. A notable variation in the dysfunction distribution across different post-transplant time frames indicated a temporal evolution in the underlying causes of allograft dysfunction. Specific Banff categories showed a robust association with renal dysfunction, potentially contributing to the elevation of creatinine levels and renal function deterioration.Our study highlights the intricate pathophysiology of renal allograft dysfunction. Most biopsies were attributed to ABMR whereas one-third of biopsies exhibited mixed lesions (ABMR and TCMR or ABMR and calcineurin inhibitor toxicity (CNIT)). Additionally, this study suggests that renal allograft rejection remains a significant contributor to graft dysfunction. A complex interplay between histological findings, Banff classification, and renal function is noted. A significant difference in the distribution of dysfunction across post-transplant time frames is noted suggesting a temporal evolution in the etiology of allograft dysfunction. Certain Banff categories demonstrate a stronger association with renal dysfunction that may influence creatinine level increase and renal function deterioration. In correspondence to the recent Banff 2019 guidelines for diagnosing ABMR, we emphasize the role of C4d staining on immunofluorescence or immunohistochemistry in allograft biopsies as imperative for timely diagnosis and immunosuppressant therapy adjustment, ultimately enhancing graft survival. Further research is needed to elucidate the underlying mechanisms driving renal dysfunction in different Banff categories, ultimately informing personalized management strategies for patients with renal allograft dysfunction. In line with the Banff 2019 guidelines for diagnosing ABMR, this study highlights the critical role of C4d staining through immunofluorescence or immunohistochemistry in allograft biopsies for early diagnosis and timely adjustment of immunosuppressive therapy, ultimately improving graft survival. [ABSTRACT FROM AUTHOR]

Research have shown that sleep is associated with renal function. However, the potential effects of sleep duration or quality on kidney function in middle-aged and older Chinese adults with normal kidney function has rarely been studied. Our study aimed to investigate the association of sleep and kidney function in middle-aged and older Chinese adults. Four thousand and eighty six participants with an eGFR ≥60 ml/min/1.73 m2 at baseline were enrolled between 2011 and 2015 from the China Health and Retirement Longitudinal Study. Survey questionnaire data were collected from conducted interviews in the 2011. The eGFR was estimated from serum creatinine and/or cystatin C using the Chronic Kidney Disease Epidemiology Collaboration equations (CKD-EPI). The primary outcome was defined as rapid kidney function decline. Secondary outcome was defined as rapid kidney function decline with clinical eGFR of 8 h of night time sleep after adjustments for demographic, clinical, or psychosocial covariates. Furthermore, daytime nap did not present significant risk in both rapid eGFR decline or CKD development. In conclusion, sleep quality was significantly associated with the development of CKD in middle-aged and older Chinese adults with normal kidney function.

Background The kidney has the highest level of selenium (Se) in the body, but the role of plasma Se in chronic kidney disease is uncertain. Objective We aimed to investigate the longitudinal association between baseline plasma Se and renal function decline in adults with hypertension and to explore possible effect modifiers. Methods This was a post hoc analysis of 935 men and women with hypertension aged 40 to 75 years from a folic-acid intervention trial (the China Stroke Primary Prevention Trial) in China. The baseline plasma Se was analyzed both as a continuous variable and as tertiles. The primary outcome was a rapid decline in renal function, defined as a mean decline in the estimated glomerular filtration rate of ≥ 5 mL/(min × 1.73 m2) per year. Results The median follow-up duration from baseline to outcome was 4.4 years. After multivariate adjustment, there was an inverse association between plasma Se and a rapid decline in renal function (per 10-unit increment; OR: 0.85; 95% CI: 0.73, 0.99). When the baseline plasma Se was assessed as tertiles, compared to the lowest tertile (<74.5 μg/L), a lower trend of the primary outcome was found in the second tertile (74.5 to < 89.4 μg/L; OR: 0.60; 95% CI: 0.34, 1.07) and the highest tertile (89.4 to <150 μg/L; OR: 0.42; 95% CI: 0.22, 0.80; P trend = 0.006). Furthermore, the Se-renal association was more pronounced among participants with folic acid treatment or with a higher baseline folate concentration (both P interaction values < 0.05). Conclusions In this sample of Chinese adults with hypertension, baseline plasma Se concentrations were inversely associated with the risk of renal function decline. The China Stroke Primary Prevention Trial was registered at clinicaltrials.gov as NCT00794885. [ABSTRACT FROM AUTHOR]

Background: Tolvaptan was approved in the United States in 2018 for patients with autosomal dominant polycystic kidney disease (ADPKD) at risk of rapid progression as assessed in a 3-year phase 3 clinical trial (TEMPO 3:4). An extension study (TEMPO 4:4) showed continued delay in progression at 2 years, and a trial in patients with later-stage disease (REPRISE) provided confirmatory evidence of efficacy. Given the relatively shorter-term duration of the clinical trials, estimating the longer-term benefit associated with tolvaptan via extrapolation of the treatment effect is an important undertaking.Methods: A model was developed to simulate a cohort of patients with ADPKD at risk of rapid progression and predict their long-term outcomes using an algorithm organized around the Mayo Risk Classification system, which has five subclasses (1A through 1E) based on estimated kidney growth rates. The model base-case population represents 1280 patients enrolled in TEMPO 3:4 beginning in chronic kidney disease (CKD) stages G1, G2, and G3 across Mayo subclasses 1C, 1D, and 1E. The algorithm was used to predict longer-term natural history health outcomes. The estimated treatment effect of tolvaptan from TEMPO 3:4 was applied to the natural history to predict the longer-term treatment benefit of tolvaptan. For the cohort, analyzed once reflecting natural history and once assuming treatment with tolvaptan, the model estimated lifetime progression through CKD stages, end-stage renal disease (ESRD), and death.Results: When treated with tolvaptan, the model cohort was predicted to experience a 3.1-year delay of ESRD (95% confidence interval: 1.8 to 4.4), approximately a 23% improvement over the estimated 13.7 years for patients not receiving tolvaptan. Patients beginning tolvaptan treatment in CKD stages G1, G2, and G3 were predicted to experience estimated delays of ESRD, compared with patients not receiving tolvaptan, of 3.8 years (21% improvement), 3.0 years (24% improvement), and 2.1 years (28% improvement), respectively.Conclusions: The model estimated that patients treated with tolvaptan versus no treatment spent more time in earlier CKD stages and had later onset of ESRD. Findings highlight the potential long-term value of early intervention with tolvaptan in patients at risk of rapid ADPKD progression. [ABSTRACT FROM AUTHOR]

Rationale & Objective: Females have a higher prevalence of chronic kidney disease (CKD) than males but are less likely to be treated with kidney replacement therapy (KRT). We studied the interaction between sex and the association of cardiometabolic risk factors for the decline in kidney function over time., Study Design: A population-based cohort study., Setting & Participants: 1,127,731 adults living in Wales, United Kingdom, within the Secure Anonymised Information Linkage Databank., Exposure: Sex and risk factors including age, estimated glomerular filtration rate (eGFR), cardiometabolic conditions, smoking, and socioeconomic deprivation. These risk factors were defined using primary care records., Outcome: The yearly declines in eGFR and the risk of incident kidney failure defined as long-term KRT and/or sustained eGFR<15mL/min/1.73m 2 ., Analytical Approach: Linear mixed effects models and Cox proportional hazards analysis., Results: The average decline in eGFR at age≤73 years was equal in males and females. After age 73 years, eGFR decline was faster in males than females, particularly for males with heart failure (males-1.22mL/min/1.73m 2 per year [95% CI, -1.25 to-1.20] vs females-0.87mL/min/1.73m 2 per year [95% CI, -0.89 to-0.85]) and current smokers (males-1.58mL/min/1.73m 2 per year [95% CI, -1.60 to-1.55] vs females-1.27mL/min/1.73m 2 per year [95% CI, -1.29 to-1.25]). Socioeconomic deprivation was one of the most impactful risk factors on eGFR decline among females aged>73 years, whereas cardiometabolic risk factors were more important among males. Older females at baseline were less likely to develop incident kidney failure than older males (P for age<0.001)., Limitations: Study of people who were almost exclusively White and who had blood laboratory test data. Reliance on creatinine-based eGFR. Albuminuria and body mass index data were incomplete., Conclusions: The eGFR decline was faster in males than in females, especially in the setting of heart failure and smoking. Socioeconomic deprivation was an important risk factor associated with eGFR decline, particularly for females. further work is required to explore less well-recognized risk factors, but these findings may inform clinical management strategies of CKD overall and within sex-specific groups., Plain-Language Summary: Kidney function is known to decline at a faster rate among males than females. This study incorporated blood laboratory test results from the routine care of 1.1 million adults living in the United Kingdom and found that the decline in kidney function associated with risk factors varied by sex. Before and at the age of 73 years, the decline in kidney function was similar between males and females. After age 73, cardiometabolic risk factors were associated with faster decline in kidney function among males than females, specifically heart failure and smoking. Socioeconomic deprivation was also associated with the decline in kidney function for both sexes, but it was a stronger risk factor among females. These findings may inform the management of kidney disease overall and within sex-specific groups., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Cardio-ankle vascular index (CAVI) was developed to reflect the stiffness of the arterial tree from the aortic origin to the ankle. This arterial stiffness parameter is useful for assessing the severity of cardiovascular disease (CVD) and its risk. However, compared to pulse wave velocity (PWV), the conventional gold standard of arterial stiffness parameter, there has been a concern regarding CAVI that there are fewer longitudinal studies for CVD. Furthermore, the accuracy of CAVI for atherosclerotic diseases compared to other parameters has not been well validated. This review article aims to summarize recent findings to clarify the predictive ability of CAVI in longitudinal studies. First, several large longitudinal studies have found that not only baseline CAVI but also CAVI changes during the observation period predict cardiovascular events. Second, CAVI may have superior discriminatory power for all-cause mortality and major adverse cardiovascular endpoints compared to PWV. Furthermore, one large longitudinal study found CAVI to be a stronger predictor for renal function decline compared to PWV as well as CAVI0, a variant of CAVI that mathematically excludes BP dependence. Additionally, CAVI shows the properties that allow the elucidation of specific hemodynamics in aortic valve disease or hypovolemia. In conclusion, CAVI may be a modifiable arterial stiffness parameter not only for predicting and preventing atherosclerotic diseases but also for elucidating specific hemodynamic pathophysiology. [ABSTRACT FROM AUTHOR]

A rapid decline in renal function can cause many complications, and therefore it is important to detect associated risk factors. Few studies have evaluated the associations among obesity-related indices and metabolic syndrome (MetS) with renal function decline. This longitudinal study aimed to explore these relationships in a large cohort of Taiwanese participants. The studied obesity-related indices were waist-to-height ratio (WHtR), A body shape index (ABSI), visceral adiposity index (VAI), lipid accumulation product (LAP), waist-to-hip ratio (WHR), body roundness index (BRI), conicity index (CI), body mass index (BMI), body adiposity index (BAI) and abdominal volume index (AVI). We included 122,068 participants in the baseline study, of whom 27,033 were followed for a median of four years. The baseline prevalence of MetS was 17.7%. Multivariable analysis showed that the participants with MetS and high VAI, WHtR, WHR, LAP, CI, BRI, BMI, BAI, AVI, and ABSI values were significantly associated with a high baseline estimated glomerular filtration rate (eGFR) (all p < 0.001). In addition, the participants with MetS (p < 0.001), high WHtR (p = 0.007), low LAP (p < 0.001), high BRI (p = 0.002), high CI (p = 0.002), high AVI (p = 0.001), high VAI (p = 0.017), and high ABSI (p = 0.013) were significantly associated with a low △eGFR, indicating a rapid decline in renal function. These results showed associations between MetS and high values of obesity-related indices except LAP with high baseline eGFR and rapid decline in kidney function. These findings suggest that screening for MetS and obesity may help to slow the decline in renal function in high-risk populations. [ABSTRACT FROM AUTHOR]

BackgroundThe nephrectomy for donation reduces the renal parenchyma and glomerular filtration rate (GFR). It is important to understand the clinical consequences of kidney donation by a living donor.MethodsIn this single-center, observational, retrospective study, we defined the renal and cardiovascular outcomes of living kidney donors. We analyzed data of 124 donors who donated at the Kidney Transplant Center (TC) of Bari between February 2002 and December 2018. Biometric data collected at visit 0, that is, at the time of the study of the donor candidate, and at visit 1, or rather at the last nephrological checkup (October-2018/August-2019) were compared.ResultsAn overall drop in GFR of 29 mL/min was observed over the analyzed period of 81+/-59 months. At visit 1, two donors developed chronic renal failure, including one in ESKD who underwent a kidney transplant. No relationship between age at donation and GFR drop was found. A trend toward an increase in obese people was reported; 28% of patients had compensated dyslipidemia and 35% were treated for hypertension. During the follow-up time, 3% had major cardiovascular events and 24% were lost to follow-up. One patient died.ConclusionThe age of the donor does not represent a basic element for reducing GFR or for the occurrence of major cardiovascular events. Furthermore, older donor candidates, in optimal health, should not be excluded from the donation. It is important to promote careful and timely follow-up of the donor, preventing the most common clinical consequences of nephrectomy, in consideration of the poor compliance of a large part of donors over the long-term post-donation period.

While extensive studies have elucidated the relationships between exposure to air pollution and chronic diseases, such as cardiovascular disorders and diabetes, the intricate effects on specific kidney diseases, notably primary glomerulonephritis (GN)—an immune-mediated kidney ailment—are less well understood. Considering the escalating incidence of GN and conspicuous lack of investigative focus on its association with air quality, investigation is dedicated to examining the long-term effects of air pollutants on renal function in individuals diagnosed with primary GN. This retrospective cohort analysis was conducted on 1394 primary GN patients who were diagnosed at Seoul National University Bundang Hospital and Seoul National University Hospital. Utilizing time-varying Cox regression and linear mixed models (LMM), we examined the effect of yearly average air pollution levels on renal function deterioration (RFD) and change in estimated glomerular filtration rate (eGFR). In this context, RFD is defined as sustained eGFR of less than 60 mL/min per 1.73 m2. During a mean observation period of 5.1 years, 350 participants developed RFD. Significantly, elevated interquartile range (IQR) levels of air pollutants—including PM 10 (particles ≤10 micrometers, HR 1.389, 95 % CI 1.2–1.606), PM 2.5 (particles ≤2.5 micrometers, HR 1.353, 95 % CI 1.162–1.575), CO (carbon monoxide, HR 1.264, 95 % CI 1.102–1.451), and NO 2 (nitrogen dioxide, HR 1.179, 95 % CI 1.021–1.361)—were significantly associated with an increased risk of RFD, after factoring in demographic and health variables. Moreover, exposure to PM 10 and PM 2.5 was associated with decreased eGFR. This study demonstrates a substantial link between air pollution exposure and renal function impairment in primary GN, accentuating the significance of environmental determinants in the pathology of immune-mediated kidney diseases. [Display omitted] • Air pollution impacts renal function in primary glomerulonephritis. • PM 10 , PM 2.5 , CO, NO 2 linked to higher renal function deterioration risk. • PM 10 , PM 2.5 , CO tied to lower estimated glomerular filtration rate. [ABSTRACT FROM AUTHOR]

In patients with ESRD, residual kidney function (RKF) contributes to achievement of adequate solute clearance. However, few studies have examined RKF in patients on hemodialysis. In a longitudinal cohort of 6538 patients who started maintenance hemodialysis over a 4-year period (January 2007 through December 2010) and had available renal urea clearance (CLurea) data at baseline and 1 year after hemodialysis initiation, we examined the association of annual change in renal CLurea rate with subsequent survival. The median (interquartile range) baseline value and mean±SD annual change of CLurea were 3.3 (1.9-5.0) and -1.1±2.8 ml/min per 1.73 m2, respectively. Greater CLurea rate 1 year after hemodialysis initiation associated with better survival. Furthermore, we found a gradient association between loss of RKF and all-cause mortality: changes in CLurea rate of -6.0 and +3.0 ml/min per 1.73 m2 per year associated with case mix-adjusted hazard ratios (95% confidence intervals) of 2.00 (1.55 to 2.59) and 0. 61 (0.50 to 0.74), respectively (reference: -1.5 ml/min per 1.73 m2 per year). These associations remained robust against adjustment for laboratory variables and ultrafiltration rate and were consistent across strata of baseline CLurea, age, sex, race, diabetes status, presence of congestive heart failure, and hemoglobin, serum albumin, and serum phosphorus levels. Sensitivity analyses using urine volume as another index of RKF yielded consistent associations. In conclusion, RKF decline during the first year of dialysis has a graded association with all-cause mortality among incident hemodialysis patients. The clinical benefits of RKF preservation strategies on mortality should be determined.

BackgroundIdentifying modifiable risk factors for chronic kidney disease (CKD) is essential for reducing its burden. Periodontal disease is common, modifiable and has been implicated as a novel potential CKD risk factor, but evidence of its association with kidney function decline over time is limited.MethodsIn a longitudinal retrospective cohort of 761 elderly men with preserved kidney function [estimated glomerular filtration rate > 60 mL/min/1.73 m(2) using a calibrated creatinine and cystatin C (eGFRcr-cys) equation] at baseline, we performed multivariable Poisson's regression to examine the association of severe periodontal disease with incident CKD, defined as incident eGFRcr-cys 5% annualized) eGFRcr-cys decline. Severe periodontal disease was defined in two ways: (i) ≥5 mm proximal attachment loss in 30% of teeth examined (European Workshop in Periodontology Group C, European Workshop); and (ii) 2+ interproximal sites with attachment loss ≥6 mm and 1+ interproximal sites with probing depth ≥5 mm (Centers for Disease Control/American Academy of Periodontology, CDC/AAP).ResultsAt baseline, the mean age was 73.4 (SD 4.8) years, the median eGFRcr-cys was 82.4 mL/min/1.73 m(2), and 35.5 and 25.4% of participants had severe periodontal disease by European Workshop and CDC/AAP criteria, respectively. After a mean follow-up of 4.9 years (SD 0.3), 56 (7.4%) participants had incident CKD. Severe periodontal disease was associated with a 2-fold greater rate of incident CKD [incidence rate ratio (IRR) 2.01 (1.21-3.44), P = 0.007] after adjusting for confounders compared with not severe periodontal disease by European Workshop criteria but did not reach statistical significance by CDC/AAP criteria [IRR 1.10 (0.63-1.91), P = 0.9].ConclusionsSevere periodontal disease may be associated with incident clinically significant kidney function decline among a cohort of elderly men.

BackgroundLeft ventricular hypertrophy is common and is associated with cardiovascular events and death among patients with known chronic kidney disease. However, the link between reduced glomerular filtration rate (GFR) and left ventricular mass index (LVMI) remains poorly explored among young and middle-aged adults with preserved kidney function. In this study, we examined the association of cystatin C-based estimated GFR (eGFRcys) and rapid decline in eGFR with subsequent LVMI.Study designObservational study.Setting & participantsWe included 2,410 participants from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort with eGFRcys > 60mL/min/1.73m(2) at year 15 and who had an echocardiogram obtained at year 25.PredictoreGFRcys at year 15 and rapid decline in eGFRcys (defined as >3% per year over 5 years from years 15 to 20).OutcomeLVMI measured at year 25.MeasurementsWe adjusted for age, sex, race, diabetes, body mass index, low- and high-density lipoprotein cholesterol levels, cumulative systolic blood pressure, and albuminuria.ResultsMean age was 40±4 (SD) years, 58% were women, and 43% were black. After 10 years of follow-up, mean LVMI was 39.6±13.4g/m(2.7). Compared with eGFRcys > 90mL/min/1.73m(2) (n = 2,228), eGFRcys of 60 to 75mL/min/1.73m(2) (n = 29) was associated with 5.63 (95% CI, 0.90-10.36) g/m(2.7) greater LVMI (P = 0.02), but there was no association of eGFRcys of 76 to 90mL/min/1.73m(2) (n = 153) with LVMI after adjustment for confounders. Rapid decline in eGFRcys was associated with higher LVMI compared with participants without a rapid eGFRcys decline (β coefficient, 1.48; 95% CI, 0.11-2.83; P = 0.03) after adjustment for confounders.LimitationsThere were a limited number of participants with eGFRcys of 60 to 90mL/min/1.73m(2).ConclusionsAmong young and middle-aged adults with preserved kidney function, eGFRcys of 60 to 75mL/min/1.73m(2) and rapid decline in eGFRcys were significantly associated with subsequently higher LVMI. Further studies are needed to understand the mechanisms that contribute to elevated LVMI in this range of eGFRcys.

We aimed to compare renal function changes in patients with atrial fibrillation (AF) prescribed different oral anticoagulants (OACs). We performed a retrospective analysis of Australian national primary care data. A total of 12,562 patients with AF and initiated OAC between 1 January 2013 and 31 December 2017 were included. Inverse probability of treatment weighting was used for balancing baseline characteristics and the risks of decline in estimated glomerular filtration rate (eGFR) in patients prescribed each OAC were compared. Compared with warfarin, prescribing of direct-acting oral anticoagulants (DOACs) was associated with a lower risk of renal function decline per 1000 person-years: hazard ratio (HR) 0.75, 95% confidence interval (CI) 0.68–0.81, p < 0.001 for ≥30% decline in eGFR; HR 0.28, 95% CI 0.20–0.41, p < 0.001 for eGFR decline to ≤30 mL/min/1.73 m2; and HR 0.45, 95% CI 0.35–0.58, p < 0.001 for serum creatinine doubling. Compared with dabigatran, rivaroxaban use had a significantly lowered risk of decline in eGFR to ≤30 mL/min/1.73 m2 (HR 0.29, 95% CI 0.13–0.66, p = 0.003) and risk of doubling of serum creatinine (HR 0.62, 95% CI 0.40–0.95, p = 0.030). The risk of renal function decline appeared to be lower in patients prescribed DOACs versus warfarin. [ABSTRACT FROM AUTHOR]

Background: Methylmalonic aciduria and homocystinuria, CblC type (OMIM #277400) is the most common disorder of cobalamin intracellular metabolism, an autosomal recessive disease, whose biochemical hallmarks are hyperhomocysteinemia, methylmalonic aciduria and low plasma methionine. Despite being a well-recognized disease for pediatricians, there is scarce awareness of its adult presentation. A thorough analysis and discussion of cobalamin C defect presentation in adult patients has never been extensively performed. This article reviews the published data and adds a new case of the latest onset of symptoms ever described for the disease.Results: We present the emblematic case of a 45-year-old male, describing the diagnostic odyssey he ventured through to get to the appropriate treatment and molecular diagnosis. Furthermore, available clinical, biochemical and molecular data from 22 reports on cases and case series were collected, resulting in 45 adult-onset CblC cases, including our own. We describe the onset of the disease in adulthood, encompassing neurological, psychiatric, renal, ophthalmic and thromboembolic symptoms. In all cases treatment with intramuscular hydroxycobalamin was effective in reversing symptoms. From a molecular point of view adult patients are usually compound heterozygous carriers of a truncating and a non-truncating variant in the MMACHC gene.Conclusion: Adult onset CblC disease is a rare disorder whose diagnosis can be delayed due to poor awareness regarding its presenting insidious symptoms and biochemical hallmarks. To avoid misdiagnosis, we suggest that adult onset CblC deficiency is acknowledged as a separate entity from pediatric late onset cases, and that the disease is considered in the differential diagnosis in adult patients with atypical hemolytic uremic syndromes and/or slow unexplained decline in renal function and/or idiopathic neuropathies, spinal cord degenerations, ataxias and/or recurrent thrombosis and/or visual field defects, maculopathy and optic disc atrophy. Plasma homocysteine measurement should be the first line for differential diagnosis when the disease is suspected. To further aid diagnosis, it is important that genes belonging to the intracellular cobalamin pathway are included within gene panels routinely tested for atypical hemolytic uremic syndrome and chronic kidney disorders. [ABSTRACT FROM AUTHOR]

Purpose: To externally validate the Palacios' equation estimating the new baseline glomerular filtration rate (NB-GFR) after partial or radical-nephrectomy (PN, RN) for Renal cancer carcinoma (RCC). Materials and methods: Our research group recently published two studies that investigated the association between renal function and cancer-specific survival in RCC. The first one included 3457 patients undergone RN or PN for a cT1-2 RCC coming from five high-volume centers; the second one considered 1767 patients undergone RN or PN for a cT1-4 RCC in a single high-volume center. From such datasets, available complete patients' data were used to calculate the predicted NB-GFR through the Palacios' equation: predicted NB-GFR = 35.03 + 0.65 ∙ preoperative GFR – 18.19 ∙ (if radical nephrectomy) – 0.25 ∙ age + 2.83 ∙ (if tumor size > 7 cm) – 2.09 ∙ (if diabetes). The observed NB-GFR was calculated by the CKD-EPI equation on serum creatinine at 3–12 months after surgery. Concordance between observed and predicted NB-GFR was evaluated by Lin's concordance correlation coefficient and Bland-Altman analysis. Results: 2419 patients were included (1210, cohort #1; 1219, cohort #2). The median observed NB-GFR value in cohorts #1 and #2 was 73.0 ml/min/1.73 m2 (IQR 56.1–90.1) and 64.2 ml/min/1.73 m2 (IQR 49.6–83); the median predicted NB-GFR was 71.1 ml/min/1.73 m2 (IQR 58–81.5) and 62.6 ml/min/1.73m2 (IQR 47.9–75.9). The concordance line showed a slope of 0.80 and 0.86, and an intercept at 11.02 and 5.41 ml/min/1.73 m2 in the cohort#1 and #2, respectively. The Palacio's equation moderately over-estimated and under-estimated NB-GFR, for values below and above the cut-off of 50 ml/min/1.73 m2 and 35 ml/min/1.73m2 in cohort#1 and #2. The Lin's concordance correlation coefficient was 0.79 (95% CI 0.77–0.81) and 0.83 (95% CI 0.82–0.85). Conclusions: We confirm the predictive performances of Palacios' equation, supporting its utilization in clinical practice. [ABSTRACT FROM AUTHOR]

Cardio-ankle vascular index (CAVI) was developed to reflect the stiffness of the arterial tree from the aortic origin to the ankle. This arterial stiffness parameter is useful for assessing the severity of cardiovascular disease (CVD) and its risk. However, compared to pulse wave velocity (PWV), the conventional gold standard of arterial stiffness parameter, there has been a concern regarding CAVI that there are fewer longitudinal studies for CVD. Furthermore, the accuracy of CAVI for atherosclerotic diseases compared to other parameters has not been well validated. This review article aims to summarize recent findings to clarify the predictive ability of CAVI in longitudinal studies. First, several large longitudinal studies have found that not only baseline CAVI but also CAVI changes during the observation period predict cardiovascular events. Second, CAVI may have superior discriminatory power for all-cause mortality and major adverse cardiovascular endpoints compared to PWV. Furthermore, one large longitudinal study found CAVI to be a stronger predictor for renal function decline compared to PWV as well as CAVI0, a variant of CAVI that mathematically excludes BP dependence. Additionally, CAVI shows the properties that allow the elucidation of specific hemodynamics in aortic valve disease or hypovolemia. In conclusion, CAVI may be a modifiable arterial stiffness parameter not only for predicting and preventing atherosclerotic diseases but also for elucidating specific hemodynamic pathophysiology. [ABSTRACT FROM AUTHOR]

Introduction: Several measures of blood pressure (BP) variability have been associated with kidney disease and cardiovascular events. Although BP is routinely measured during hospitalization in daily practice, the prognostic impact of in-hospital BP and its variability are uncertain. Methods: A total of 226 participants who underwent elective percutaneous coronary intervention (PCI) for stable coronary artery disease (CAD) were included. BP was measured by trained nurses during the 4-day hospitalization for PCI. BP variability was assessed by standard deviation (SD) and coefficient variation of systolic BP. Estimated glomerular filtration rate (eGFR) was calculated at baseline and follow-up (≥6 months). The cardiovascular end point was defined as a composite of cardiovascular death, acute coronary syndrome, stroke, heart failure hospitalization, and any coronary revascularization. Results: In-hospital BP was measured 9.5 ± 0.8 times. During a median follow-up period of 1.7 years, mean eGFR change was −1.7 mL/min/1.73 m2 per year, and 35 (15.5%) participants met the cardiovascular end point. Mean systolic BP and SD were negatively correlated with eGFR change. In the receiver operating characteristic curve analysis, SD of systolic BP predicted the cardiovascular end point (AUC 0.63, best cutoff value 14.2 mm Hg, p = 0.003). Kaplan-Meier analysis demonstrated a significantly higher incidence of the cardiovascular end point in patients with SD of systolic BP ≥14.2 mm Hg compared to their counterpart (p = 0.003). A multivariable analysis showed SD of systolic BP as an independent predictor for the cardiovascular end point. When assessed with coefficient variation, BP variability was similarly related to eGFR change and clinical outcomes. Conclusion: Greater in-hospital BP variability was associated with renal function decline and cardiovascular events in patients with stable CAD.

Abstract Background Hypertriglyceridemic waist (HTGW) phenotype has been suggested as a risk factor for chronic kidney disease (CKD). However, there is limited evidence on the relationship of triglyceride waist phenotypes with estimated glomerular filtration rate (eGFR) status and severity. Our aim was to explore the associations of triglyceride waist phenotypes with reduced eGFR and various decreased eGFR stages among Chinese adults. Methods A population-based, cross-sectional study was conducted among Chinese participants aged 20–74 years from June 2016 to December 2017 in Shanghai, China. An eGFR value below 60 mL/min/1.73 m2 was defined as decreased eGFR. HTGW phenotype was defined as triglyceride (TG) ≥1.7 mmol/L and a waist circumference (WC) of ≥90 cm for men and ≥ 80 cm for women. We examined the association of triglyceride waist phenotypes with decreased eGFR risk using the weighted logistic regression models. Results A total of 31,296 adults were included in this study. Compared with normal TG level/normal WC (NTNW) phenotype, normal TG level/enlarged WC (NTGW) and elevated TG level/enlarged WC (HTGW) phenotypes were associated with the increased risk of decreased eGFR. Multivariable-adjusted ORs (95% CI) associated with NTGW, elevated TG level/normal WC (HTNW), and HTGW phenotypes were 1.75 (1.41–2.18), 1.29 (0.99–1.68), and 1.99 (1.54–2.58), respectively. These associations between triglyceride waist phenotypes and decreased eGFR risk remained across almost all the subgroups, including sex, age, BMI, T2DM, and hypertension. HTGW phenotype was consistently positively associated with the risk of mildly and moderately decreased eGFR, but not with severely decreased eGFR risk. Conclusions HTGW was consistently associated with the increased risk of decreased eGFR and various decreased eGFR stages, except for severely decreased eGFR. Further prospective studies are warranted to confirm our findings and to investigate the underlying biological mechanisms.

BackgroundSepsis is known to cause renal function fluctuations during hospitalization, but whether these patients discharged from sepsis were still at greater risks of long-term renal adverse outcomes remains unknown.MethodsFrom 2011 to 2018, we included 1,12,628 patients with chronic kidney disease (CKD) aged ≥ 20 years. The patients with CKD were further divided into 11,661 sepsis group and 1,00,967 non-sepsis group. The following outcome of interest was included: all-cause mortality, readmission for acute kidney injury, estimated glomerular filtration rate decline ≥50% or doubling of serum creatinine, and end-stage renal disease.ResultsAfter propensity score matching, the sepsis group was at higher risks of all-cause mortality [hazard ratio (HR) 1.39, 95% CI, 1.31–1.47], readmission for acute kidney injury (HR 1.67, 95% CI 1.58–1.76), eGFR decline ≥ 50% or doubling of serum creatinine (HR 3.34, 95% CI 2.78–4.01), and end-stage renal disease (HR 1.43, 95% CI 1.34–1.53) than non-sepsis group.ConclusionsOur study found that patients with CKD discharged from hospitalization for sepsis have higher risks of subsequent renal adverse events.

Background: While extensive studies have elucidated the relationships between exposure to air pollution and chronic diseases, such as cardiovascular disorders and diabetes, the intricate effects on specific kidney diseases, notably primary glomerulonephritis (GN)-an immune-mediated kidney ailment-are less well understood. Considering the escalating incidence of GN and conspicuous lack of investigative focus on its association with air quality, investigation is dedicated to examining the long-term effects of air pollutants on renal function in individuals diagnosed with primary GN., Methods: This retrospective cohort analysis was conducted on 1394 primary GN patients who were diagnosed at Seoul National University Bundang Hospital and Seoul National University Hospital. Utilizing time-varying Cox regression and linear mixed models (LMM), we examined the effect of yearly average air pollution levels on renal function deterioration (RFD) and change in estimated glomerular filtration rate (eGFR). In this context, RFD is defined as sustained eGFR of less than 60 mL/min per 1.73 m 2 ., Results: During a mean observation period of 5.1 years, 350 participants developed RFD. Significantly, elevated interquartile range (IQR) levels of air pollutants-including PM 10 (particles ≤10 micrometers, HR 1.389, 95 % CI 1.2-1.606), PM 2.5 (particles ≤2.5 micrometers, HR 1.353, 95 % CI 1.162-1.575), CO (carbon monoxide, HR 1.264, 95 % CI 1.102-1.451), and NO 2 (nitrogen dioxide, HR 1.179, 95 % CI 1.021-1.361)-were significantly associated with an increased risk of RFD, after factoring in demographic and health variables. Moreover, exposure to PM 10 and PM 2.5 was associated with decreased eGFR., Conclusions: This study demonstrates a substantial link between air pollution exposure and renal function impairment in primary GN, accentuating the significance of environmental determinants in the pathology of immune-mediated kidney diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper, (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Evaluating the chronic course of chronic kidney disease (CKD) and identifying associated risk factors is essential for effective management. This study aims to identify risk factors and monitor the decline in renal function through prolonged follow-up of CKD patients. This retrospective cohort study included 410 CKD patients diagnosed between 2015 and 2022. Data collected included demographics, comorbidities, and repeated measurements of glomerular filtration rate (GFR) and proteinuria. Statistical analyses examined the association between GFR decline and risk factors such as age, diabetes, hypertension, and proteinuria during the follow-up period. The cohort showed a progressive decline in GFR over time. Significant associations were found between GFR decline and age, diabetes, hypertension, and higher proteinuria levels ( P < 0.001). Age was associated with a 0.32 ml/min decline in GFR per 1.73 m², while the coefficients for hypertension and diabetes were -2.98 and -4.21, respectively. A strong correlation was found between proteinuria and GFR decline (β = -6.78, P < 0.001). Early identification and management of risk factors are crucial for slowing CKD progression. These findings underscore the need for targeted interventions to preserve renal function and improve patient outcomes., Competing Interests: There are no conflicts of interest., (Copyright: © 2024 Journal of Pharmacy and Bioallied Sciences.)

Purpose: An increase in arterial stiffness is associated with rapid renal function decline (RFD) in patients with chronic kidney disease (CKD). The aim of this study was to investigate whether the radial augmentation index (rAI), a surrogate marker of arterial stiffness, affects RFD in individuals without CKD. Methods: A total of 3165 Chinese participants from an atherosclerosis cohort with estimated glomerular filtration rates (eGFR) of ≥ 60 mL/min/1.73 m2 were included in this study. The baseline rAI normalized to a heart rate of 75 beats/min (rAIp75) was obtained using an arterial applanation tonometry probe. The eGFRs at both baseline and follow-up were calculated using the equation derived from the Chronic Kidney Disease Epidemiology Collaboration. The association of the rAIp75 with RFD (defined as a drop in the eGFR category accompanied by a ≥ 25% drop in eGFR from baseline or a sustained decline in eGFR of > 5 mL/min/1.73 m2/year) was evaluated using the multivariate regression model. Results: During the 2.35-year follow-up, the incidence of RFD was 7.30%. The rAIp75 had no statistically independent association with RFD after adjustment for possible confounders (adjusted odds ratio = 1.12, 95% confidence interval: 0.99–1.27, p = 0.074). When stratified according to sex, the rAIp75 was significantly associated with RFD in women, but not in men (adjusted odds ratio and 95% confidence interval: 1.23[1.06–1.43], p = 0.007 for women, 0.94[0.76–1.16], p = 0.542 for men; p for interaction = 0.038). Conclusion: The rAI might help screen for those at high risk of early rapid RFD in women without CKD. [ABSTRACT FROM AUTHOR]

Background: Postoperative delirium significantly delays the recovery of patients. This study sought to explore the risk factors and to prevent postoperative delirium after orthopedic surgery. Materials and Methods: In the part of retrospective study, 456 cases over 70-year-old that underwent one of three types of orthopedic surgery were included and were defined as the retrospective group. The risk factors of postoperative delirium were analyzed by logistic regression. In the part of prospective study, 86 cases of the same age and the same surgery were included and were defined as the prospective group. Positive interventions were used by shortening the fasting time and increasing the perioperative rehydration. The differences of postoperative delirium incidence between the retrospective group and the prospective group were analyzed. Results: Compared with patients with normal postoperative electrolytes, postoperative creatinine <68.20 μmol/L, and fluid infusion during fasting >119.66 mL/h, postoperative electrolyte disorders (odds ratio [OR]: 2.864; 95% confidence interval [CI]: 1.374, 5.970), postoperative creatinine ≥68.20 μmol/L (OR: 2.660; 95% CI: 1.328, 5.328), and fluid infusion during fasting ≤119.66 mL/h (OR: 2.372; 95% CI: 1.197, 4.704) were the risk factors for postoperative delirium. After positive intervention, the postoperative delirium incidence of the prospective group was 5.8% (5/86), and it was lower than 18.4% (84/456) of the retrospective group (P < 0.05). Conclusions: Elevated postoperative creatinine, postoperative electrolyte disorders, and lower fluid infusion during fasting were three risk factors for postoperative delirium. By shortening the fasting time and increasing the perioperative rehydration, the incidence of postoperative delirium could be reduced. [ABSTRACT FROM AUTHOR]

Postoperative acute kidney injury (AKI) may complicate both open and endovascular aortic aneurysm repair (EVAR) and is associated with substantial morbidity, mortality, and health care expense. We aim to evaluate the incidence of postoperative AKI and factors associated with its occurrence and the effects of postoperative AKI on long-term renal function and mortality after open and EVAR in the Society for Vascular Surgery Vascular Quality Initiative registry. Elective aneurysm cases were identified including thoracic endovascular aortic aneurysm repair (TEVAR) and complex endovascular aortic aneurysm repair (cEVAR), infrarenal endovascular repair (EVAR) and infrarenal open repair (OAR) from 2003 to 2019. The preoperative estimated glomerular filtration rate (eGFR) was calculated using the Modification of Diet in Renal Disease formula and stratified based on chronic kidney disease (CKD) grades. Postoperative AKI was defined per the Vascular Quality Initiative definition as a creatinine increase of 0.5 mg/dL or if postoperative dialysis was required. Patients on preprocedural hemodialysis and those with previous renal transplant were excluded. Demographics and procedural factors were evaluated for predicting in-hospital postoperative AKI (all approaches) and at 9 to 21 months of long-term follow-up (EVAR only) using logistic regression modeling. We identified a total of 2813 cEVAR, 2995 TEVAR, 39,945 EVAR, and 8143 OAR patients. Of those, postoperative AKI occurred in 377 cEVAR (13.5%), 199 TEVAR (6.7%), 1099 EVAR (2.8%), and 1249 OAR (15.5%). Risk factors for postoperative AKI across all groups were worse preoperative eGFR, total number of blood transfusions, perioperative anemia, reinterventions, and postoperative respiratory complications. Additional procedure-specific risk factors of postoperative AKI were preoperative hemoglobin of less than 10 and contrast volume of 125 to 150 mL, hypertension, a low ejection fraction, and a history of percutaneous revascularization for EVAR; for both EVAR/cEVAR, renal artery coverage was a risk factor, whereas for OAR, male sex, non-White race, hypertension, suprarenal aortic cross-clamp, and increased renal ischemic time were risk factors. Among 8133 EVAR patients with long-term follow-up, a decrease in kidney function occurred in 56.7% of patients with postoperative AKI vs 19.9% without postoperative AKI (P <.001). The following risk factors were associated with a decrease in renal function at long-term follow-up: postoperative AKI, a preoperative eGFR of less than 90, and hypertension. A preoperative hemoglobin of greater than 12 was protective. Postoperative AKI was associated with significantly lower survival compared with no postoperative AKI across all procedures (log rank <0.001). Postoperative AKI occurs more often in patients with worse preoperative renal function, lower preoperative hemoglobin, and in open surgeries with inter-renal or suprarenal cross-clamping. Importantly, postoperative AKI is associated with increased mortality across all types of aortic repair. Given the long-term impact of postoperative AKI on outcomes for all aortic repairs and the limitations of current insensitive functional indices, there is a need to seek more sensitive indicators of decreases in early renal structural in this population. [ABSTRACT FROM AUTHOR]

Background Lower urinary excretion of the kidney tubule–specific biomarker epidermal growth factor (uEGF) is associated with increased risk of renal function [glomerular filtration rate (GFR)] loss in diabetes and in patients with established chronic kidney disease (CKD). We investigated whether uEGF is associated with rapid GFR decline or incident CKD in the general population. Methods Subjects without CKD or diabetes were recruited from the general population in Tromso, Norway [Renal Iohexol Clearance Survey (RENIS); N  = 1249] and Groningen, the Netherlands [Prevention of REnal and Vascular END-stage disease (PREVEND); N  = 4534], with a median follow-up of 5.6 and 7.4 years, respectively. GFR was measured by iohexol clearance in the RENIS and estimated using the CKD Epidemiology Collaboration creatinine–cystatin C equation in the PREVEND study. Rapid GFR decline was defined as an annual GFR loss >3.0 mL/min/1.73 m2 and in sensitivity analyses as subjects with the 10% steepest GFR slope within each cohort. Results Lower baseline uEGF excretion was associated with rapid GFR loss in both cohorts {RENIS, odds ratio [OR] per 1 μg/mmol lower uEGF 1.42 [95% confidence interval (CI) 1.06–1.91], P = 0.02; PREVEND, OR 1.29 [95% CI 1.10–1.53], P < 0.01}, adjusted for baseline GFR, albumin:creatinine ratio and conventional CKD risk factors. Similar results were obtained using the outcome of the 10% steepest GFR slope in each cohort. Lower uEGF levels were associated with incident CKD in the combined analysis of both cohorts. Conclusions Lower uEGF levels are associated with increased risk of rapid GFR loss and incident CKD in the general population. This finding, together with previous findings in CKD and high-risk populations, supports that uEGF may serve as a broadly applicable biomarker representing the tubular component of the current glomerulus-centric clinical risk assessment system. [ABSTRACT FROM AUTHOR]

Background: We aimed to evaluate serum bicarbonate as a risk factor for renal progression, cardiovascular events, and mortality in Korean CKD patients.Methods: We analyzed 1,808 participants from a Korean CKD cohort whose serum bicarbonate levels were measured at enrollment. Serum bicarbonate levels were categorized as low, lower normal, higher normal, and high (total carbon dioxide

Introduction Understanding the mechanisms underlying the differences in renal decline between men and women may improve sex-specific clinical monitoring and management. To this end, we aimed to compare the slope of renal function decline in older men and women in chronic kidney disease (CKD) Stages 4 and 5, taking into account informative censoring related to the sex-specific risks of mortality and dialysis initiation. Methods The European QUALity Study on treatment in advanced CKD (EQUAL) study is an observational prospective cohort study in Stages 4 and 5 CKD patients ≥65 years not on dialysis. Data on clinical and demographic patient characteristics were collected between April 2012 and December 2018. Estimated glomerular filtration rate (eGFR) was calculated using the CKD Epidemiology Collaboration equation. eGFR trajectory by sex was modelled using linear mixed models, and joint models were applied to deal with informative censoring. Results We included 7801 eGFR measurements in 1682 patients over a total of 2911 years of follow-up. Renal function declined by 14.0% [95% confidence interval (CI) 12.9–15.1%] on average each year. Renal function declined faster in men (16.2%/year, 95% CI 15.9–17.1%) compared with women (9.6%/year, 95% CI 6.3–12.1%), which remained largely unchanged after accounting for various mediators and for informative censoring due to mortality and dialysis initiation. Diabetes was identified as an important determinant of renal decline specifically in women. Conclusion In conclusion, renal function declines faster in men compared with women, which remained similar after adjustment for mediators and despite a higher risk of informative censoring in men. We demonstrate a disproportional negative impact of diabetes specifically in women. [ABSTRACT FROM AUTHOR]

Background: Diet modification, especially a decrease in salt intake, might be an important non-pharmacological strategy to improve chronic kidney disease (CKD) prognosis. Objectives: We conducted a prospective cohort study to investigate whether an intensive low-salt diet education program effectively attenuated the rate of renal function decline in hypertensive patients with CKD. Methods: This cohort study recruited 171 participants from a previous open-labelled, case-controlled, randomized clinical trial that originally consisted of 245 hypertensive CKD patients who were assigned to two groups, intensive low-salt diet or conventional education. We evaluated the renal outcomes, which included the rate of change in estimated glomerular filtration rate (eGFR) per year, the increase in serum creatinine ≥50%, the decrease in eGFR ≥30%, and the percent change in albuminuria throughout the entire study period. Results: The baseline characteristics of the cohort participants between the two groups were similar at the time of trial phase randomization. During the whole study period, the rate of renal function decline was significantly faster in the conventional group (0.11 ± 4.63 vs. –1.53 ± 3.04 mL/min/1.73 m2/year, p = 0.01). The percent of incremental change in serum creatinine ≥50% was 1.1% in the intensive group and 8.2% in the conventional group (p = 0.025), and the percent of decremental change in eGFR ≥30% was 3.3% in the intensive group and 11.1% in the conventional group (p= 0.048). With logistic regression analysis adjusted for related factors, we found that the conventional group showed a higher risk for deterioration in serum creatinine and eGFR during the entire study period. Especially, we found that the intensive education program preserved eGFR in participants with one, several, or all of the following characteristics at the time of randomization: older age, female, obese, had higher protein intake, higher amounts of albuminuria, higher salt intake. Conclusion: This cohort study demonstrated that an intensive low-salt diet education program attenuated the rate of renal function decline in hypertensive CKD patients independent of its effect on lowering salt intake or albuminuria during the 36 months of follow-up.

Background/Aims: Diabetic nephropathy (DN) is a leading cause of end-stage renal disease. Microalbuminuria (MA) is widely used to predict early progressive renal function decline (ERFD) of DN in type 2 diabetes mellitus (T2D) patients, but the sensitivity and specificity of MA have been questioned. Here, we determined the urine metabolites differences between T2D patients with MA who maintained stable renal function and those who progressed to ERFD in order to identify specific biomarkers of the progression of renal dysfunction. Methods: A total of 102 T2D patients with MA and normal renal function at baseline were followed up for 5–6 years. Of these, 52 patients were selected and classified into two groups according to the later renal function; 25 patients who experienced ERFD were regarded as the progressive group, while 27 patients who maintained stable renal function were considered as the stable group. In the pilot study, untargeted, broad-spectrum urine metabolomics was performed on the urine of 12 subjects from the progressive group (5 patients as “progressors”) and stable group (7 patients as “non-progressors”) to discover candidate markers. We then used a targeted metabolomics analysis to identify the selected markers in the urine of an additional 40 patients (20 from the progressive group as cases, and 20 from the stable group as controls) in the validation study. Results: A total of 318 known metabolites were detected in the pilot study and 6 metabolites with significant difference between progressors and non-progressors were identified. The levels of 4 metabolites, including azelaic acid, adipic acid, 5-hydroxyhexanoic acid, and L-tryptophan decreased significantly, while levels of L-pyroglutamic acid and D-norvaline increased observably in the progressors compared with non-progressors. Furthermore, in the validation study, 6 metabolites were confirmed by quantitative measurements and their concentrations were consistent with the changes in the pilot study. Concentrations of L-pyroglutamic acid and D-norvaline still increased in the cases, but were not statistically significant. Of the 4 metabolites with decreased concentrations among the cases, only 5-hydroxyhexanoic acid remained statistically significant while the other 3 metabolites did not differ between cases and controls. Conclusion: We have identified urine metabolites and shown that 5-hydroxyhexanoic acid can be used as a predictor of progression of ERFD in T2D patients with MA. This finding provides the new perspective that 5-hydroxyhexanoic acid may be useful to identify T2D patients with MA who are at risk of ERFD.

Abstract Background Keto-analogues administration plays an important role in clinical chronic kidney disease (CKD) adjunctive therapy, however previous studies on their reno-protective effect mainly focused on kidney pathological changes induced by nephrectomy. This study was designed to explore the currently understudied alternative mechanisms by which compound α-ketoacid tablets (KA) influenced ischemia–reperfusion (IR) induced murine renal injury, and to probe the current status of KA administration on staving CKD progression in Chinese CKD patients at different stages. Methods In animal experiment, IR surgery was performed to mimic progressive chronic kidney injury, while KA was administrated orally. For clinical research, a retrospective cohort study was conducted to delineate the usage and effects of KA on attenuating CKD exacerbation. End-point CKD event was defined as 50% reduction of initial estimated glomerular filtration rate (eGFR). Kaplan–Meier analysis and COX proportional hazard regression model were adopted to calculate the cumulative probability to reach the end-point and hazard ratio of renal function deterioration. Results In animal study, KA presented a protective effect on IR induced renal injury and fibrosis by attenuating inflammatory infiltration and apoptosis via inhibition of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. In clinical research, after adjusting basic demographic factors, patients at stages 4 and 5 in KA group presented a much delayed and slower incidence of eGFR decrease compared to those in No-KA group (hazard ratio (HR) = 0.115, 95% confidence interval (CI) 0.021–0.639, p = 0.0134), demonstrating a positive effect of KA on staving CKD progression. Conclusion KA improved IR induced chronic renal injury and fibrosis, and seemed to be a prospective protective factor in end stage renal disease.

Abstract Background The short-term efficacy of tolvaptan in patients with autosomal dominant polycystic kidney disease (ADPKD) has been demonstrated across several phase 3 trials, while the ADPKD Outcomes Model (ADPKD-OM) represents a validated approach to predict natural disease progression over a lifetime horizon. This study describes the implementation of a tolvaptan treatment effect within the ADPKD-OM and explores the potential long-term benefits of tolvaptan therapy in ADPKD. Methods The effect of tolvaptan on ADPKD progression was modelled by applying a constant treatment effect to the rate of renal function decline, consistent with that observed in the Tolvaptan Efficacy and Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Outcomes trial (TEMPO 3:4; ClinicalTrials.gov identifier NCT00428948). Predictions generated by the ADPKD-OM were compared against aggregated data from a subsequent extension trial (TEMPO 4:4; ClinicalTrials.gov identifier NCT01214421) and the Replicating Evidence of Preserved Renal Function an Investigation of Tolvaptan Safety Efficacy in ADPKD trial (REPRISE; ClinicalTrials.gov identifier NCT02160145). Following validation, an application of the ADPKD-OM sought to estimate the benefit of tolvaptan therapy on time to end-stage renal disease (ESRD), in a range of ADPKD populations. Results Model validation against TEMPO 4:4 and REPRISE demonstrated the accuracy and generalisability of the tolvaptan treatment effect applied within the ADPKD-OM. In simulated patients matched to the overall TEMPO 3:4 trial population at baseline, tolvaptan therapy was predicted to delay the mean age of ESRD onset by five years, compared to natural disease progression (57 years versus 52 years, respectively). In subgroup and sensitivity analyses, the estimated delay to ESRD was greatest among patients with CKD stage 1 at baseline (6.6 years), compared to CKD 2 and 3 subgroups (4.7 and 2.7 years, respectively); and ADPKD patients in Mayo subclasses 1C–1E. Conclusions This study demonstrated the potential for tolvaptan therapy to delay time to ESRD, particularly among patients with early-stage CKD and evidence of rapidly progressing disease. Data arising from this study highlight the value to be gained by early intervention and long-term treatment with tolvaptan, which may alleviate the economic and societal costs of providing care to patients who progress to ESRD.

A rapid decline in renal function can cause many complications, and therefore it is important to detect associated risk factors. Few studies have evaluated the associations among obesity-related indices and metabolic syndrome (MetS) with renal function decline. This longitudinal study aimed to explore these relationships in a large cohort of Taiwanese participants. The studied obesity-related indices were waist-to-height ratio (WHtR), A body shape index (ABSI), visceral adiposity index (VAI), lipid accumulation product (LAP), waist-to-hip ratio (WHR), body roundness index (BRI), conicity index (CI), body mass index (BMI), body adiposity index (BAI) and abdominal volume index (AVI). We included 122,068 participants in the baseline study, of whom 27,033 were followed for a median of four years. The baseline prevalence of MetS was 17.7%. Multivariable analysis showed that the participants with MetS and high VAI, WHtR, WHR, LAP, CI, BRI, BMI, BAI, AVI, and ABSI values were significantly associated with a high baseline estimated glomerular filtration rate (eGFR) (all p < 0.001). In addition, the participants with MetS (p < 0.001), high WHtR (p = 0.007), low LAP (p < 0.001), high BRI (p = 0.002), high CI (p = 0.002), high AVI (p = 0.001), high VAI (p = 0.017), and high ABSI (p = 0.013) were significantly associated with a low △eGFR, indicating a rapid decline in renal function. These results showed associations between MetS and high values of obesity-related indices except LAP with high baseline eGFR and rapid decline in kidney function. These findings suggest that screening for MetS and obesity may help to slow the decline in renal function in high-risk populations.

Introduction: The Oxford Classification score, which predicts renal outcomes for immunoglobulin A nephropathy (IgAN), is widely used in clinical practice. Nevertheless, the relationship between these markers and longitudinal changes in renal function are poorly understood. Methods: This was a population-based retrospective cohort study of 280 adults with biopsy-proven primary IgAN from 2011 to 2018. We used generalized additive mixed models to control for traditional kidney disease risk factors to analyze the associations between Oxford Classification MEST-C scores (mesangial hypercellularity, M; endocapillary hypercellularity, E; segmental glomerulosclerosis, S; tubular atrophy/interstitial fibrosis, T; crescents, C) and longitudinal changes in the estimated glomerular filtration rate (eGFR) after renal biopsy. Results: The median eGFR was 78.2 mL/min/1.73 m2 at baseline, and then it decreased on average by 1.3 mL/min/1.73 m2 per year in the entire cohort. In adjusted models, compared with patients without relative lesions, the presence of T > 50% (T2) (− 5.7; 95% confidence interval [CI], − 9.5 to − 2.0 mL/min/1.73m2 per year) was associated with the fastest eGFR decline. S present (S1) (− 2.9; 95% CI, − 4.6 to − 1.1 mL/min/1.73m2 per year) and C > 25% glomeruli (C2) (− 3.4; 95% CI, − 6.4 to − 0.5 mL/min/1.73m2 per year) also demonstrated steeper eGFR declines. However, we found no association between M > 0.5 (M1), E present (E1), T 26%– 50% (T1), and C present ≥ 1 glomerulus (C1), and progressive eGFR decline (p > 0.05). Conclusion: The Oxford Classification scores, S1, T2, and C2, were independently associated with the longitudinal decreases in renal function in patients with IgAN. These findings suggested therapies targeted at improving early damage to these lesions might be essential to delay renal progression. [ABSTRACT FROM AUTHOR]

Background: Our goal was to create a simple risk-prediction model for renal function decline after cardiac surgery to help focus renal follow-up efforts on patients most likely to benefit., Methods and Results: This single-center retrospective cohort study enrolled 24 904 patients who underwent cardiac surgery from 2012 to 2019 at Fuwai Hospital, Beijing, China. An estimated glomerular filtration rate (eGFR) reduction of ≥30% 3 months after surgery was considered evidence of renal function decline. Relative to patients with eGFR 60 to 89 mL/min per 1.73 m 2 (4.5% [531/11733]), those with eGFR ≥90 mL/min per 1.73 m 2 (10.9% [1200/11042]) had a higher risk of renal function decline, whereas those with eGFR ≤59 mL/min per 1.73 m 2 (5.8% [124/2129]) did not. Each eGFR stratum had a different strongest contributor to renal function decline: increased baseline eGFR levels for patients with eGFR ≥90 mL/min per 1.73 m 2 , transfusion of any blood type for patients with eGFR 60 to 89 mL/min per 1.73 m 2 , and no recovery of renal function at discharge for patients with eGFR ≤59 mL/min per 1.73 m 2 . Different nomograms were established for the different eGFR strata, which yielded a corrected C-index value of 0.752 for eGFR ≥90 mL/min per 1.73 m 2 , 0.725 for eGFR 60-89 mL/min per 1.73 m 2 and 0.791 for eGFR ≤59 mL/min per 1.73 m 2 ., Conclusions: Predictors of renal function decline over the follow-up showed marked differences across the eGFR strata. The nomograms incorporated a small number of variables that are readily available in the routine cardiac surgical setting and can be used to predict renal function decline in patients stratified by baseline eGFR.

Aims: Our aim was to investigate the effects of peripheral arterial stiffness on the risk of progression of renal disease in patients with type 2 diabetes (T2D).Methods: This was a single center, retrospective cohort study. Brachial-ankle pulse wave velocity (baPWV) tests were performed on T2D patients in 2015. Increased arterial stiffness was defined as baPWV of ≥ 1800 cm/s. We applied criteria for progression of renal disease according to EMPA-REG OUTCOME trial.Results: In total, 186 patients were enrolled in the final study. The mean age was 59.1 years and male:female ratio was 1.73:1. Thirteen (7%) patients progressed to renal disease during the average follow-up time of 35.3 months. In particular, the risk of progression to macroalbuminuria was significantly higher in the baPWV ≥ 1800 cm/s group (HR 6.216, p = 0.020). Individuals with a baPWV of ≥ 1800 cm/s (when comparisons were adjusted for age, sex, blood pressure, diabetes duration, eGFR, and use of renin-angiotensin system inhibitors) had a significantly higher risk of the progression of renal disease (HR = 8.480, p = 0.014).Conclusion: These results suggest that peripheral arterial stiffness (baPWV ≥ 1800 cm/s) may be a risk factor for the progression of renal disease in T2D patients.

Introduction: Using a discovery/validation approach we investigated associations between a panel of genes selected from a transcriptomic study and the estimated glomerular filtration rate (eGFR) decline across time in a cohort of type 1 diabetes (T1D) patients.Experimental: Urinary sediment transcriptomic was performed to select highly modulated genes in T1D patients with rapid eGFR decline (decliners) vs. patients with stable eGFR (non-decliners). The selected genes were validated in samples from a T1D cohort (n = 54, mean diabetes duration of 21 years, 61% women) followed longitudinally for a median of 12 years in a Diabetes Outpatient Clinic.Results: In the discovery phase, the transcriptomic study revealed 158 genes significantly different between decliners and non-decliners. Ten genes increasingly up or down-regulated according to renal function worsening were selected for validation by qRT-PCR; the genes CYP4F22, and PMP22 were confirmed as differentially expressed comparing decliners vs. non-decliners after adjustment for potential confounders. CYP4F22, LYPD3, PMP22, MAP1LC3C, HS3ST2, GPNMB, CDH6, and PKD2L1 significantly modified the slope of eGFR in T1D patients across time.Conclusions: Eight genes identified as differentially expressed in the urinary sediment of T1D patients presenting different eGFR decline rates significantly increased the accuracy of predicted renal function across time in the studied cohort. These genes may be a promising way of unveiling novel mechanisms associated with diabetic kidney disease progression.

Abstract Background Autosomal dominant polycystic kidney disease (ADPKD) is the leading inheritable cause of end-stage renal disease (ESRD); however, the natural course of disease progression is heterogeneous between patients. This study aimed to develop a natural history model of ADPKD that predicted progression rates and long-term outcomes in patients with differing baseline characteristics. Methods The ADPKD Outcomes Model (ADPKD-OM) was developed using available patient-level data from the placebo arm of the Tolvaptan Efficacy and Safety in Management of ADPKD and its Outcomes Study (TEMPO 3:4; ClinicalTrials.gov identifier NCT00428948). Multivariable regression equations estimating annual rates of ADPKD progression, in terms of total kidney volume (TKV) and estimated glomerular filtration rate, formed the basis of the lifetime patient-level simulation model. Outputs of the ADPKD-OM were compared against external data sources to validate model accuracy and generalisability to other ADPKD patient populations, then used to predict long-term outcomes in a cohort matched to the overall TEMPO 3:4 study population. Results A cohort with baseline patient characteristics consistent with TEMPO 3:4 was predicted to reach ESRD at a mean age of 52 years. Most patients (85%) were predicted to reach ESRD by the age of 65 years, with many progressing to ESRD earlier in life (18, 36 and 56% by the age of 45, 50 and 55 years, respectively). Consistent with previous research and clinical opinion, analyses supported the selection of baseline TKV as a prognostic factor for ADPKD progression, and demonstrated its value as a strong predictor of future ESRD risk. Validation exercises and illustrative analyses confirmed the ability of the ADPKD-OM to accurately predict disease progression towards ESRD across a range of clinically-relevant patient profiles. Conclusions The ADPKD-OM represents a robust tool to predict natural disease progression and long-term outcomes in ADPKD patients, based on readily available and/or measurable clinical characteristics. In conjunction with clinical judgement, it has the potential to support decision-making in research and clinical practice.

Introduction: Several measures of blood pressure (BP) variability have been associated with kidney disease and cardiovascular events. Although BP is routinely measured during hospitalization in daily practice, the prognostic impact of in-hospital BP and its variability are uncertain. Methods: A total of 226 participants who underwent elective percutaneous coronary intervention (PCI) for stable coronary artery disease (CAD) were included. BP was measured by trained nurses during the 4-day hospitalization for PCI. BP variability was assessed by standard deviation (SD) and coefficient variation of systolic BP. Estimated glomerular filtration rate (eGFR) was calculated at baseline and follow-up (≥6 months). The cardiovascular end point was defined as a composite of cardiovascular death, acute coronary syndrome, stroke, heart failure hospitalization, and any coronary revascularization. Results: In-hospital BP was measured 9.5 ± 0.8 times. During a median follow-up period of 1.7 years, mean eGFR change was −1.7 mL/min/1.73 m2 per year, and 35 (15.5%) participants met the cardiovascular end point. Mean systolic BP and SD were negatively correlated with eGFR change. In the receiver operating characteristic curve analysis, SD of systolic BP predicted the cardiovascular end point (AUC 0.63, best cutoff value 14.2 mm Hg, p = 0.003). Kaplan-Meier analysis demonstrated a significantly higher incidence of the cardiovascular end point in patients with SD of systolic BP ≥14.2 mm Hg compared to their counterpart (p = 0.003). A multivariable analysis showed SD of systolic BP as an independent predictor for the cardiovascular end point. When assessed with coefficient variation, BP variability was similarly related to eGFR change and clinical outcomes. Conclusion: Greater in-hospital BP variability was associated with renal function decline and cardiovascular events in patients with stable CAD. [ABSTRACT FROM AUTHOR]