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Background Acute kidney injury (AKI) survivors are at increased risk of major adverse kidney events (MAKEs), including chronic kidney disease (CKD), end-stage kidney disease (ESKD) and death. High-risk AKI patients may benefit from specialist follow-up, but factors associated with increased risk have not been reported. Methods We conducted a retrospective study of AKI patients admitted to a single centre between 2012 and 2016 who had a baseline estimated glomerular filtration rate (eGFR) >30 mL/min/1.73 m2 and were alive and independent of renal replacement therapy (RRT) at 30 days following discharge. AKI was identified using International Classification of Diseases, Tenth Revision codes and staged according to the Kidney Disease: Improving Global Outcomes criteria. Patients were excluded if they were kidney transplant recipients or if AKI was attributed to intrinsic kidney disease. We performed Cox regression models to examine MAKEs in the first year, defined as the composite of CKD (sustained 25% drop in eGFR), ESKD (requirement for chronic RRT or sustained eGFR <15 mL/min/1.73 m2) or death. We examined secondary outcomes (CKD, ESKD and death) using Cox and competing risk regression analyses. Results We studied 2101 patients (mean ± SD age 69 ± 15 years, baseline eGFR 72 ± 23 mL/min/1.73 m2). Of these, 767 patients (37%) developed at least one MAKE (429 patients developed CKD, 21 patients developed ESKD, 375 patients died). MAKEs occurred more frequently with older age [hazard ratio (HR) 1.16 per decade, 95% confidence interval (CI) 1.10–1.24], greater severity of AKI (Stage 2 HR 1.38, 95% CI 1.16–1.64; Stage 3 HR 1.62, 95% CI 1.31–2.01), higher serum creatinine at discharge (HR 1.04 per 10 µmol/L, 95% CI 1.03–1.06), chronic heart failure (HR 1.41, 95% CI 1.19–1.67), liver disease (HR 1.68, 95% CI 1.39–2.03) and malignancy (non-metastatic HR 1.44, 95% CI 1.14–1.82; metastatic HR 2.26, 95% CI 1.80–2.83). Traditional risk factors (e.g. diabetes and cardiovascular disease) had limited predictive value. Conclusions More than a third of AKI patients develop MAKEs within the first year. Clinical variables available at the time of discharge can help identify patients at increased risk of such events. [ABSTRACT FROM AUTHOR]

Background. The obective of this study was to perform a costeffectiveness analysis comparing intermittent with continuous renal replacement therapy (IRRT versus CRRT) as initial therapy for acute kidney injury (AKI) in the intensive care unit (ICU). Methods. Assuming some patients would potentially be eligible for either modality, we modeled life year gained, the quality-adjusted life years (QALYs) and healthcare costs for a cohort of 1000 IRRT patients and a cohort of 1000 CRRT patients. We used a 1-year, 5-year and a lifetime horizon. A Markov model with two health states for AKI survivors was designed: dialysis dependence and dialysis independence. We applied Weibull regression from published estimates to fit survival curves for CRRT and IRRT patients and to fit the proportion of dialysis dependence among CRRT and IRRT survivors. We then applied a risk ratio reported in a large retrospective cohort study to the fitted CRRT estimates in order to determine the proportion of dialysis dependence for IRRT survivors. We conducted sensitivity analyses based on a range of differences for daily implementation cost between CRRT and IRRT (base case: CRRT day $632 more expensive than IRRT day; range from $200 to $1000) and a range of risk ratios for dialysis dependence for CRRT as compared with IRRT (from 0.65 to 0.95; base case: 0.80). Results. Continuous renal replacement therapy was associated with a marginally greater gain in QALY as compared with IRRT (1.093 versus 1.078). Despite higher upfront costs for CRRT in the ICU ($4046 for CRRT versus $1423 for IRRT in average), the 5-year total cost including the cost of dialysis dependence was lower for CRRT ($37 780 for CRRT versus $39 448 for IRRT on average). The base case incremental costeffectiveness analysis showed that CRRT dominated IRRT. This dominance was confirmed by extensive sensitivity analysis. Conclusions. Initial CRRT is cost-effective compared with initial IRRT by reducing the rate of long-term dialysis dependence among critically ill AKI survivors. [ABSTRACT FROM AUTHOR]

Background To describe recent insights into glomerular haemodynamics in septic acute kidney injury (AKI). Methods We reviewed the literature with particular emphasis on recent findings in animal experiments and human studies in relation to renal macro- and micro-renal haemodynamics during septic AKI. Results The dominant paradigm is that septic AKI is due to decreased renal perfusion with ischaemic loss of glomerular filtration rate (GFR), ischaemic tubular cell injury and acute tubular necrosis (ATN). However, recent experimental and human studies challenge this view of the pathogenesis of septic AKI. In addition, rapid post-mortem and experimental histological studies do not support ATN as the histological substrate of septic AKI. Finally, more recent experimental evidence suggests that changes in the glomerular and peri-glomerular haemodynamics provide a more likely explanation for the loss of GFR seen in the early phases of septic AKI. Conclusions Despite a long-standing paradigm that septic AKI is due to renal hypo-perfusion and associated ATN, experimental and human studies increasingly suggest that changes in the state of the glomerular and peri-glomerular micro-vasculature are a more likely additional explanation for this condition. [ABSTRACT FROM AUTHOR]

Background. A blood urea nitrogen (BUN)/creatinine ratio (BCR) >20 (0.081 in international unit) is used to distinguish pre-renal azotemia (PRA) and acute tubular necrosis (ATN). However, there is little evidence that BCR can distinguish between these two conditions and/or is clinically useful. Methods. We conducted a retrospective study using a large hospital database. Patients were divided into three groups: ‘low BCR’ (if BCR when acute kidney injury (AKI) developed was ≤20), ‘high BCR’ (if BCR when AKI developed was >20) and ‘no AKI’ if patients did not satisfy any of the Risk, Injury, Failure, Loss and End-stage kidney disease criteria for AKI during hospitalization. Results. Among 20 126 study patients, 3641 (18.1%) had AKI. Among these patients, 1704 (46.8%) had a BCR <20 at AKI diagnosis (‘low BCR’) and 1937 (53.2%) had a BCR >20 (‘high BCR’). The average BCR for the two groups was 15.8 versus 26.1 (P < 0.001). Hospital mortality was significantly less in the ‘low-BCR’ group (18.4 versus 29.9%, P < 0.001). Multivariable logistic regression analysis for hospital mortality (‘no AKI’ as a reference) showed that the odds ratio of ‘high BCR’ (5.73) was higher than that of ‘low BCR’ (3.32). Conclusions. Approximately half of the patients with AKI have a BCR >20, the traditional threshold of diagnosing PRA. Unlike PRA patients who have a lower mortality than ATN patients, high BCR patients had higher hospital mortality compared with low BCR patients, which was confirmed with multivariable analysis. These findings do not support BCR as a marker of PRA. [ABSTRACT FROM PUBLISHER]

Background. Only a proportion of critically ill patients with severe [RIFLE (Risk, Injury, Failure, Loss, End-stage renal disease) criteria, class-F] acute kidney injury (AKI) appear to receive renal replacement therapy (RRT). The aim of this study was to study the characteristics and outcome of patients with severe (RIFLE-F) AKI who did not receive RRT. Methods. We identified all consecutive patients admitted to our institution that developed RIFLE-F AKI by creatinine criteria over a 3-year period and did not receive RRT, and compared their characteristics and outcomes with those of RIFLE-F RRT-treated patients. Results. Within the study period, 20 126 patients were admitted to our institution for >24 h. Among them, 2949 were admitted to the intensive care unit (ICU) and 195 developed RIFLE-F AKI. Of these, 90 received RRT (RRT patients) and 105 did not (no-RRT patients). Compared with RRT patients, no-RRT patients were similar in terms of age, gender and ward of origin. However, they had a shorter median ICU stay (2.7 versus 7.9 days; P < 0.001), required less mechanical ventilation (56.2 versus 70%; P < 0.05) and had a lower mean Acute Physiology and Chronic Health Evaluation III score (82.7 versus 86.7; P < 0.05). The two main reasons these patients did not receive RRT were limitations of medical therapy (LOMT) orders in 41 (39%) cases and expected renal functional improvement in 59 (56.2%). Mortality in no-RRT patients was 58.1% compared with 55.5% in the RRT group (P = 0.72). After exclusion of LOMT patients, the mortality of the no-RRT group, although lower than that of the RRT group, remained high (30.5 versus 55%; P < 0.001). Most of these deaths occurred after ICU discharge and appeared secondary to underlying chronic diseases or recurrence of the initial insult. Conclusions. After exclusion of LOMT patients, about a third of critically ill patients with severe (RIFLE-F) AKI did not receive RRT. A third of these patients died in hospital. The timing of the deaths and their underlying causes do not suggest that a broader application of RRT would have changed patient outcomes. [ABSTRACT FROM PUBLISHER]

Background. Acute kidney injury (AKI) is a common and serious complication of cardiopulmonary bypass (CPB) surgery. Hepcidin, a peptide hormone that regulates iron homeostasis, is a potential biomarker of AKI following CPB. Methods. We investigated the association between post-operative changes in serum and urinary hepcidin and AKI in 93 patients undergoing CPB. Results. Twenty-five patients developed AKI based on the Risk, Injury, Failure, Loss, End-stage kidney disease (RIFLE) criteria in the first 5 days. Serum hepcidin, urine hepcidin concentration, the urinary hepcidin:creatinine ratio and fractional excretion of hepcidin in urine rose significantly after surgery. However, urine hepcidin concentration and urinary hepcidin:creatinine ratio were significantly lower at 24 h in patients with RIFLE-Risk, Injury or Failure compared to those without AKI (P = 0.0009 and P < 0.0001, respectively). Receiver operator characteristic analysis showed that lower 24-h urine hepcidin concentration and urinary hepcidin:creatinine ratio were sensitive and specific predictors of AKI. The urinary hepcidin:creatinine ratio had an area under the curve for the diagnosis of RIFLE ≥ risk at 24 h of 0.77 and of 0.84 for RIFLE ≥ injury. Urinary hepcidin had similar predictive accuracy. Such predictive ability remained when patients with early creatinine increases were excluded. Conclusions. Urinary hepcidin and hepcidin:creatinine ratio are biomarkers of AKI after CPB, with an inverse association between its increase at 24 h and risk of AKI in the first five post-operative days. Measuring hepcidin in the urine on the first day following surgery may deliver earlier diagnosis and interventions. [ABSTRACT FROM AUTHOR]

Background. Sepsis is the most common trigger for acute kidney injury (AKI) in critically ill patients. We sought to determine whether there are unique patterns to urine sediment in septic compared with non-septic AKI. Methods. Prospective two center cohort study of adult critically ill patients with septic and non-septic AKI, defined by the RIFLE criteria. Eligible patients had clinical, physiologic and laboratory data extracted. Blood and urine were sampled for urine biochemistry, microscopy and neutrophil gelatinase-associated lipocalin (NGAL). A urine microscopy score (UMS) was derived based on the observed quantification of renal tubular cells and casts in the sediment. The UMS was compared between septic and non-septic AKI and correlated with NGAL, worsening AKI, renal replacement therapy (RRT) and hospital mortality. Results. Eighty-three patients were enrolled. Mean (SD) age was 64.3 (16.6) years, 60.2% were male, Charlson comorbidity score was 3.3 (2.8) and Acute Physiology and Chronic Health Evaluation II score was 21.4 (7.6). Septic AKI was present in 43 patients (51.8%). RIFLE class at enrollment was not different between groups (P = 0.43). Septic AKI was associated with higher UMS compared with non-septic AKI (P = 0.001). There was no correlation between UMS and fractional excretion of sodium (FeNa) or fractional excretion of urea (FeU). Elevated urine NGAL (uNGAL) correlated with higher UMS (P = 0.0003), while correlation with plasma NGAL was modest (P = 0.05). Worsening AKI occurred in 22.9% with no difference between septic and non-septic groups. A UMS score ≥3 was associated with increased odds of worsening AKI [adjusted odds ratio 8.0; 95% confidence intervals (CI), 1.03–62.5, P = 0.046]. For a UMS ≥3, sensitivity and specificity were 0.67 (95% CI, 0.39–0.86) and 0.95 (0.84–0.99) and positive and negative predictive values were 0.80 (0.49–0.94) and 0.91 (0.78–0.96) for detecting worsening AKI, respectively. While there were no differences between septic and non-septic AKI, higher UMS correlated with need for RRT (15.7%, P = 0.02) and in-hospital death (30.1%, P = 0.01); however, this did not persist in multivariable analysis. Conclusions. Septic AKI is associated with greater urine microscopy evidence of kidney injury compared with non-septic AKI, despite similar severity of AKI. A UMS ≥3 correlated with higher uNGAL and was predictive of worsening AKI. Urine microscopy may have a complementary role for discerning septic from non-septic AKI, discriminating severity and predicting worsening AKI in critically ill patients. [ABSTRACT FROM AUTHOR]

Background. Acute kidney injury (AKI) after cardiac surgery is a common and serious condition carrying significant costs. During cardiopulmonary bypass (CPB) surgery, modifiable factors may contribute to post-operative AKI. Their avoidance might be a potential target for nephroprotection. Methods. The objective of the present study was to identify and determine whether intraoperative hypotension, anaemia, or their combination, red blood cell transfusion or vasopressor use are independent risk factors for post-operative AKI defined by the RIFLE (renal Risk, Injury, Failure, Loss of renal function and End-stage renal disease) classification and other thresholds using a mixed logistic multivariate model. Results. We analysed 381 468 mean arterial pressure (MAP) measurements from 920 consecutive on-pump cardiac surgery patients. Overall, 19.5% developed AKI which was associated with an 8.2-fold increase in-hospital mortality. Haemoglobin concentration was an independent risk factor for AKI {odds ratio [OR] 1.16 per g/dL decrease [95% confidence interval (CI) 1.05–1.31]; P = 0.018} with systemic arterial oxygen saturation and pressure values not adding further strength to such an association. MAP alone or vasopressor administration was not independently associated with AKI but volume of red blood cell transfusion was, with its effect being apparent at a haemoglobin level of >8 g/dL (>5 mmol/L). In patients with severe anaemia (<25th percentile of lowest haemoglobin), the independent effect of hypotension (>75th percentile of area under the curve MAP <50 mmHg) on AKI was more pronounced [OR 3.36 (95% CI 1.34–8.41); P = 0.010]. Conclusion. Intraoperative avoidance of the extremes of anaemia, especially during severe hypotension and avoidance of transfusion in patients with haemoglobin levels >8 g/dL (>5 mmol/L) may help decrease AKI in patients undergoing cardiac surgery and represent targets for future controlled interventions. [ABSTRACT FROM PUBLISHER]

There is much symptomatic similarity between acute kidney disease and acute heart disease. Both may present with shortness of breath and chest discomfort, and thus it is not surprising that biomarkers of acute myocardial and renal disease often coexist in many physicians’ diagnostic work-up schedules. In this review we explore the similarities and differences between current and future tests of myocardial and renal injury and function, with particular emphasis on the diagnostic utility of currently available biomarkers to assist with the diagnosis of cardiorenal syndromes. Imaging studies have not traditionally been viewed as clinical biomarkers, but as tests of structure and function; they contribute to the diagnostic process, and we believe that they should be considered alongside more traditional biomarkers such as blood and urine measurements of circulating proteins and metabolites. We discuss the place of natriuretic peptides, novel tests of kidney damage as well as kidney function and conclude with a discussion of their place in guiding future research studies whose goals must include better characterization of the degree of dysfunction imposed on one organ system by failure of the other. [ABSTRACT FROM AUTHOR]

Background. A pre-morbid ‘baseline’ creatinine is required in order to diagnose and stage acute kidney injury (AKI) using the RIFLE classification. Estimation of baseline creatinine by solving the Modification of Diet in Renal Disease (MDRD) equation assuming a glomerular filtration rate of 75 ml/min/1.73 m2 has been widely used but never validated.Methods. We analysed four cohorts of intensive care unit (ICU) patients from three centres (two from Pittsburgh and one from Mayo and Austin). Three cohorts consisted of preselected patients without AKI (Pittsburgh 1 n = 1048, Mayo n = 737, Austin n = 333), and measured creatinine values in these cohorts were taken to represent baseline creatinine values. The last cohort (Pittsburgh 2 n = 468) consisted of unselected ICU patients with baseline creatinine values recorded within 1 year before ICU admission. Using the Pittsburgh 1 cohort, we derived an equation using the same anthropometric variables as the MDRD equation: baseline creatinine = 0.74 − 0.2 (if female) + 0.08 (if black) + 0.003 × age (in years). We then compared measured creatinine in the Mayo and Austin cohorts and recorded creatinine in the Pittsburgh 2 cohort to the estimated creatinine from: (i) the MDRD equation; (ii) our new equation; (iii) a gender-fixed creatinine of 0.8 mg/dl for females and 1.0 mg/dl for males.Results. Using any of the three methods, the median absolute error of the estimates was of the order of 0.1–0.2 mg/dl, and overall accuracy was similar. When the definition of AKI was limited to the severity grades of Injury and Failure, all three methods were able to generate 78–90% reliable results for preselected normal range cohorts, and 63–70% for the unselected cohort of ICU patients.Conclusions. Estimates of incidence of AKI in the critically ill using RIFLE classification can be affected by the bias and limited accuracy of methods to estimate baseline creatinine. Whenever possible, recorded creatinine values should be used as a reference of baseline. The use of the MDRD equation to estimate baseline creatinine when it is unknown may over- or underestimate some mild (Risk) AKI cases but is unlikely to misclassify patients in Injury and Failure. [ABSTRACT FROM AUTHOR]

Background.There are no suitably powered epidemiological studies of ‘transient azotaemia’ (TA). The objective of this study was to describe the epidemiology of TA and its independent association with hospital mortality. We hypothesized that TA would be associated with an independent increase in the risk of death. [ABSTRACT FROM PUBLISHER]

The article focuses on the prevention of acute kidney injury (AKI) components of cardio-renal syndromes (CRS). It states that type 1 acute cardio renal failure, which is characterized by an initial abrupt change in cardiovascular function, is prevented through blood pressure control, use of beta-adrenergic blockers (BB), and avoidance of non-steroidal anti-inflammatory agents. Furthermore, type 2 chronic CRS can be prevented through optimal intake of sodium and extracellular fluid volume.

Information about the Acute Dialysis Quality Initiative (ADQI) meeting, in Venice, Italy on September 3 to 6, 2008 is presented. During the event, participants identifies key questions, conducts systemic literature search and generate a bibliography of key subjects. After the discussion, definition and classification of cardio-renal syndromes are finalized.

The article offers information on the epidemiology of cardio-renal syndromes (CRS), presented during the 7th Acute Dialysis Quality Initiative (ADQI) meeting, in Venice, Italy on September 3 to 6, 2008. It mentions that the ailment is characterized as the worsening of heart function resulting to acute kidney injury (AKI) and development of acute CRS. Various types of research, clinical recommendations and illnesses associated with CRS are also discussed.

A consensus conference on cardio-renal syndromes (CRS) was held in Venice Italy, in September 2008 under the auspices of the Acute Dialysis Quality Initiative (ADQI). The following topics were matter of discussion after a systematic literature review and the appraisal of the best available evidence: definition/classification system; epidemiology; diagnostic criteria and biomarkers; prevention/protection strategies; management and therapy. The umbrella term CRS was used to identify a disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Different syndromes were identified and classified into five subtypes. Acute CRS (type 1): acute worsening of heart function (AHF–ACS) leading to kidney injury and/or dysfunction. Chronic cardio-renal syndrome (type 2): chronic abnormalities in heart function (CHF-CHD) leading to kidney injury and/or dysfunction. Acute reno-cardiac syndrome (type 3): acute worsening of kidney function (AKI) leading to heart injury and/or dysfunction. Chronic reno-cardiac syndrome (type 4): chronic kidney disease leading to heart injury, disease, and/or dysfunction. Secondary CRS (type 5): systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. Consensus statements concerning epidemiology, diagnosis, prevention, and management strategies are discussed in the paper for each of the syndromes. [ABSTRACT FROM PUBLISHER]

Background. In adult cardiac surgery, the predictive value for AKI of neutrophil gelatinase-associated lipocalin (NGAL) appears to have wide variability. The choice of definition of acute kidney injury (AKI) might, at least in part, account for such variability. [ABSTRACT FROM PUBLISHER]

Background. The RIFLE classification scheme for acute kidney injury (AKI) is based on relative changes in serum creatinine (SCr) and on urine output. The SCr criteria, therefore, require a pre-morbid baseline value. When unknown, current recommendations are to estimate a baseline SCr by the MDRD equation. However, the MDRD approach assumes a glomerular filtration rate of ∼75 mL/min/1.73 m2. This method has not been validated. [ABSTRACT FROM PUBLISHER]