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Increasing awareness regarding CKD and self-care during COVID-19 pandemic has become the most important aspect for the nephrologists. Hence it is appropriate that the theme of the forthcoming World Kidney Day on 11 March 2021 should be "Strive for kidney health for everyone during COVID-19"

Implication for health policy/practice/research/medical education: Post-infectious glomerulonephritis (PIGN) can develop secondary to infections associated with bacterial, viral, fungal, protozoal, and helminthic parasites Recently, there is a serious concern regarding the occurrence of kidney dysfunctions and subsequent acute kidney injury (AKI) among COVID-19 patients The outcome data of COVID-19 in neonates and children demonstrated that the fatality rate is significantly higher in patients with AKI than in patients without AKI In the current COVID-19 pandemic, few instances of glomerulonephritis (GN) in patients affected by SARS-CoV-2 have been reported In this review, we investigated the PIGN concentrating on the COVID19-nephropathy, as well as its prevention and diagnosis strategies © 2021 The Author(s)

Coronavirus disease 2019 (COVID-19) is now a pandemic and its death toll is rocketing up. Patients with acute kidney injury (AKI) and chronic kidney disease (CKD) are at high risk of developing COVID-19 complications and COVID-19 infection can also lead to renal dysfunction. Considering the importance of kidney function in COVID-19 patients, the present review is aimed to dig into the available evidence about kidney and COVID-19. We summarize the mechanisms underlying the renal injury in COVID-19 patients, and treatment strategies in dialysis and kidney transplant patients. We conclude, it is imperative to highlight the early monitoring of patients with AKI and carefully control kidney function during severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) infection.

Background A case of homozygous familial lecithin:cholesterol acyltransferase (LCAT) deficiency with a novel homozygous LCAT missense mutation (replacement of methionine by arginine at position 293 in the amino acid sequence of the LCAT protein) is reported. Methods and Results The probable diagnosis was suggested by findings of marked high density lipoprotein (HDL) deficiency, corneal opacification, anemia, and renal insufficiency. The diagnosis was confirmed by two dimensional gel electrophoresis of HDL, the measurement of free and esterified cholesterol, and sequencing of the LCAT gene. Conclusions In our view the most important aspects of therapy to prevent the kidney disease that these patients develop is careful control of blood pressure and lifestyle measures to optimize non HDL lipoproteins. In the future replacement therapy by gene transfer or other methods may become available.

We sought to study new-onset microalbuminuria, its progression, and the decline of renal function in patients with type 1 diabetes. Using a cohort of 109 patients who developed new-onset microalbuminuria in the first 4 years following enrollment in the 1st Joslin Kidney Study, we simultaneously tracked the change in their renal function and urinary albumin excretion. Of these, 79 patients were followed for an average of 12 years after microalbuminuria onset, wherein their glomerular filtration rate was estimated by the Modification of Diet in Renal Disease Study formula and compared with their microalbuminuria and proteinuria. The concordance between these outcomes was weak. Only 12 of the 23 patients who progressed to advanced (stage 3–5) chronic kidney disease developed proteinuria, which, in general, did not precede but accompanied the progression to advanced chronic kidney disease. The remaining 11 patients who developed advanced disease had persistent microalbuminuria or returned to normal albuminuria. Thus, we found that one-third of patients with type 1 diabetes developed advanced chronic kidney disease relatively soon after the onset of microalbuminuria and this was not conditional on the presence of proteinuria. Contrary to the existing concept of early nephropathy in type 1 diabetes, less emphasis should be placed on the mechanisms of progression to proteinuria and more placed on mechanisms initiating and promoting the early decline of renal function that eventually progresses to advanced chronic kidney disease.

Albuminuria in individuals whose body mass index exceeds 40 kg/m(2) is associated with the presence of large glomeruli, thickened basement membrane and epithelial cellular (podocyte) distortion. Obstructive sleep apnea magnifies glomerular injury as well, probably through a vasoconstrictive mechanism. Insulin resistance from excess fatty acids is exacerbated by decreased secretion of high molecular weight adiponectin from adipose cells in the obese state. Adiponectin potentiates insulin in its post-receptor signaling resulting in glucose oxidation in mitochondria. Recent studies of podocyte physiology have concentrated on the structural and functional requirements that prevent glomerular albumin leakage. The architecture of the podocyte involves nephrin and podocin, proteins that cooperate to keep slit pores between foot processes competent to retain albumin. Insulin and adiponectin are necessary for high-energy phosphate generation. When fatty acids bind to albumin, the toxicity to proximal renal tubules is magnified. Albumin and fatty acids are elevated in urine of individuals with obesity related nephrotic syndrome. Fatty acid accumulation and resistin inhibit insulin and adiponectin. Study of cytokines produced by adipose tissue (adiponectin and leptin) and macrophages (resistin) has led to a better understanding of the relationship between weight and hypertension. Leptin, is presumably secreted after food intake to inhibit the midbrain/hypothalamic appetite centers. Resistance to leptin results in excess signaling to hypothalamic sympathetics leading to hypertension. Demonstration of the existence of a cerebral receptor mutation provide evidence for a role in hypertension of a central nervous reflex arc in humans. Further understanding of obesity-related renal dysfunction has been accomplished recently using experimental models. Rapid weight loss following bariatric surgery may reverse renal pathology of obesity with restoration of normal blood pressure.

Background and objectives: The aim of our study was to examine serum markers of the TNF and Fas pathways for association with cystatin-C based estimated glomerular filtration rate (cC-GFR) in subjects with type 1 diabetes (T1DM) and no proteinuria. Design, setting, participants, & measurements: The study group (the 2nd Joslin Kidney Study) comprised patients with T1DM and normoalbuminuria (NA) (n = 363) or microalbuminuria (MA) (n = 304). Impaired renal function (cC-GFR

Diabetes is the leading cause of end-stage renal disease (ESRD) in the USA [1]. The prevalence of diabetic kidney disease has increased steadily in proportion to the prevalence of diabetes [2]. Most patients with advanced diabetic kidney disease are overtly proteinuric. Still, clinicians are encountering diabetic patients without proteinuria, and at times even without microalbuminuria, who suffer from advanced chronic kidney disease (CKD) that seems out of proportion to nondiabetic patients with similar co-morbidities.

Patients with diabetes mellitus have a variety of platelet and coagulation system dysfunctions. At least theoretically, these can contribute to microvascular complications. Intensive glycemic control has been demonstrated to decrease microvascular complications in type 1 diabetics. We studied 16 patients with type 1 diabetes mellitus (11 men and five women; mean age, 39 years) with albuminuria greater than 0.1 g/d and/or proteinuria greater than 0.3 g/d and a creatinine clearance rate higher than 30 mL/min. They received a regimen including three to four injections of insulin per day with or without a weekly infusion of intravenous insulin, and were evaluated for 6 months. We compared the plasma level of von Willebrand factor, platelet aggregation responses to adenosine diphosphate (ADP), epinephrine, and collagen, and platelet adhesion at the beginning of the study and at follow-up intervals. Glycemic control improved significantly. There were no significant differences in the platelet aggregation responses to ADP (1.59 +/- 0.34 v 1.88 +/- 0.23 mmol/L, P = .3; normal, 4.6 +/- 0.2), epinephrine (0.50 +/- 0.20 v 1.11 +/- 0.31 mmol/L, P = .06; normal, 7.6 +/- 1.5), or collagen (92.4 +/- 6.61 v 82.60 +/- 3.78 seconds, P = .6; normal, 79.1 +/- 3.1) or in platelet adhesion (126.31 +/- 16.95 v 195.08 +/- 30.2 platelets, P = .34; normal, 68.6 +/- 1.4). Baseline von Willebrand factor increased, but not significantly (166.38% +/- 10.6% v 142.72% +/- 14.73%, P = .21; normal, 102.0% +/- 6.0%). In type 1 diabetic patients with established microvascular complications of nephropathy, a statistically significant improvement in glycemic control did not improve the in vitro platelet function abnormalities. Improved glycemic control delays the progression of microvascular disease through mechanisms not measured by tests of platelet function.

Renal transplant centers have evolved extensive cardiovascular evaluation protocols to screen potential candidates prior to initiation of dialysis. The risk of new cardiac events remains high even among patients initiating hemodialysis with no previous cardiac symptoms [1]. A key unanswered question remains whether prior thromboembolic events themselves have a role in prognosis for patients undergoing renal replacement therapy (RRT). We followed stable diabetic patients on RRT to determine whether a history of previous cardiovascular events (PCVE) could predict subsequent cardiovascular events (SCVE) and all cause mortality. After approval by Institutional Review Boards, clinically stable patients undergoing RRT in participating dialysis units were consecutively enrolled. PCVE included myocardial infarction, coronary artery intervention, peripheral bypass or amputation surgery, cerebrovascular accident, or carotid artery intervention and the occurrence of subsequent events until July 15, 2010. Subjects lost to follow up were censored at last documented clinic visit. For patients receiving a transplant during the study, follow up was concluded at surgery. Information retrieved from the Social Security Death Index was considered valid for end-point with cause of death “unknown.” Dialysis patients were considered under entry mode of treatment with either hemodialysis (HD) or peritoneal dialysis (PD) throughout the entire course of study. The Kaplan–Meier function was utilized to estimate years of event free interval (EFI); medians and 95% confidence limits are reported. Comparisons between function curves and medians were tested for significance using the log-rank test [2].

Historically, patients with type 1 diabetes and macroalbuminuria had high competing risks: cardiovascular death or renal failure. Here, we assessed these risks in patients receiving therapies implemented during the last 30 years. Between 1991 and 2004, we enrolled 423 white patients with type 1 diabetes who developed macroalbuminuria (albumin excretion rate, ≥300 μg/min). With follow-up for 98% through 2008, ESRD developed in 172 patients (incidence rate, 5.8/100 person-years), and 29 died without ESRD (mortality rate, 1/100 person-years). The majority of these outcomes occurred between ages 36 and 52 years with durations of diabetes of 21 to 37 years. The 15-year cumulative risks were 52% for ESRD and 11% for pre-ESRD death. During the 15 years of follow-up, the use of renoprotective treatment increased from 56 to 82%, and BP and lipid levels improved significantly; however, the risks for both ESRD and pre-ESRD death did not change over the years analyzed. There were 70 post-ESRD deaths, and the mortality rate was very similar during the 1990s and the 2000s (11/100 person-years versus 12/100 person-years, respectively). Mortality was low in patients who received a pre-emptive kidney transplant (1/100 person-years), although these patients did not differ from dialyzed patients with regard to predialysis eGFR, sex, age at onset of ESRD, or duration of diabetes. In conclusion, despite the widespread adoption of renoprotective treatment, patients with type 1 diabetes and macroalbuminuria remain at high risk for ESRD, suggesting that more effective therapies are desperately needed.

OBJECTIVE The purpose of this study was to examine prospectively whether renal hyperfiltration is associated with the development of microalbuminuria in patients with type 1 diabetes, after taking into account known risk factors. RESEARCH DESIGN AND METHODS The study group comprised 426 participants with normoalbuminuria from the First Joslin Kidney Study, followed for 15 years. Glomerular filtration rate was estimated by serum cystatin C, and hyperfiltration was defined as exceeding the 97.5th percentile of the sex-specific distribution of a similarly aged, nondiabetic population (134 and 149 ml/min per 1.73 m2 for men and women, respectively). The outcome was time to microalbuminuria development (multiple albumin excretion rate >30 μg/min). Hazard ratios (HRs) for microalbuminuria were calculated at 5, 10, and 15 years. RESULTS Renal hyperfiltration was present in 24% of the study group and did not increase the risk of developing microalbuminuria. The unadjusted HR for microalbuminuria comparing those with and without hyperfiltration at baseline was 0.8 (95% CI 0.4–1.7) during the first 5 years, 1.0 (0.6–1.7) during the first 10 years, and 0.8 (0.5–1.4) during 15 years of follow-up. The model adjusted for baseline known risk factors including A1C, age at diagnosis of diabetes, diabetes duration, and cigarette smoking resulted in similar HRs. In addition, incorporating changes in hyperfiltration status during follow-up had minimal impact on the HRs for microalbuminuria. CONCLUSIONS Renal hyperfiltration does not have an impact on the development of microalbuminuria in type 1 diabetes during 5, 10, or 15 years of follow-up.

Background and objectives: Early renal function decline begins before the onset of proteinuria in patients with type 1 diabetes. The association of elevated serum uric acid with advanced impaired renal function prompts an examination of its role in early renal function decline in patients before proteinuria develops. Design, setting, participants, & measurements: Patients with type 1 diabetes and normoalbuminuria or microalbuminuria were recruited to the Second Joslin Kidney Study. A medical history and measurements of BP, hemoglobin A1c, albumin excretion rate, and serum concentrations of uric acid and cystatin C were obtained. Estimated glomerular filtration rate was measured by a cystatin C–based formula. Results: We studied 364 patients with normoalbuminuria and 311 patients with microalbuminuria. Mean glomerular filtration rate in these groups was 119 and 99 ml/min, respectively. Mildly or moderately impaired renal function (

The results of recent outcome trials challenge hypotheses that tight control of both glycohemoglobin and blood pressure diminishes macrovascular events and survival among type 2 diabetic patients. Relevant questions exist regarding the adequacy of glycohemoglobin alone as a measure of diabetes control. Are we ignoring mechanisms of vasculotoxicity (profibrosis, altered angiogenesis, hypertrophy, hyperplasia, and endothelial injury) inherent in current antihyperglycemic medications? Is the polypharmacy for lowering cholesterol, triglyceride, glucose, and systolic blood pressure producing drug interactions that are too complex to be clini- cally identified? We review angiotensin-aldosterone mechanisms of tissue injury that magnify microvascular damage caused by hyperglycemia and hypertension. Many studies describe interruption of these mechanisms, without hemodynamic consequence, in the preservation of function in type 1 diabetes. Possible interactions between the renin-angiotensin-aldosterone system and physiologic glycemic control (through pulsatile insulin release) suggest opportuni- ties for further clinical investigation.

To determine whether the hypercoagulable state of patients with complications of diabetes can be reversed toward normal, a group of insulin-dependent individuals with proteinuria was treated with intensive insulin protocols. A statistically significant (P