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Acute kidney injury (AKI) is a frequent complication of hospitalization and is associated with an increased risk of chronic kidney disease (CKD), end-stage renal disease (ESRD), and mortality. While AKI is a known risk factor for short-term adverse outcomes, more recent data suggest that the risk of mortality and renal dysfunction extends far beyond hospital discharge. However, determining whether this risk applies to all patients who experience an episode of AKI is difficult. The magnitude of this risk seems highly dependent on the presence of comorbid conditions, including cardiovascular disease, hypertension, diabetes mellitus, preexisting CKD, and renal recovery. Furthermore, these comorbidities themselves lead to structural renal damage due to multiple pathophysiological changes, including glomeruloscleroses and tubulointerstitial fibrosis, which can lead to the loss of residual capacity, glomerular hyperfiltration, and continued deterioration of renal function. AKI seems to accelerate this deterioration and increase the risk of death, CDK, and ESRD in most vulnerable patients. Therefore, we strongly advocate adequate hemodynamic monitoring and follow-up in patients susceptible to renal dysfunction. Additionally, other potential renal stressors, including nephrotoxic medications and iodine-containing contrast fluids, should be avoided. Unfortunately, therapeutic interventions are not yet available. Additional research is warranted and should focus on the prevention of AKI, identification of therapeutic targets, and provision of adequate follow-up to those who survive an episode of AKI.

Acute kidney injury (AKI) necessitating renal replacement therapy (RRT) is associated with high mortality and increased risk for end stage renal disease. However, it is unknown if this applies to patients with a preliminary unremarkable medical history. The purpose of this study was to describe overall and renal survival in critically ill patients with AKI necessitating RRT stratified by the presence of comorbidity. A retrospective cohort study was performed, between 1994 and 2010, including all adult critically ill patients with AKI necessitating RRT, stratified by the presence of comorbidity. Logistic regression, survival curve and cox proportional hazards analyses were used to evaluate overall and renal survival. Standardized mortality rate (SMR) analysis was performed to compare long-term survival to the predicted survival in the Dutch population. Of the 1067 patients included only 96(9.0%) had no comorbidity. Hospital mortality was 56.6% versus 43.8% in patients with and without comorbidity, respectively. In those who survived hospitalization 10-year survival was 45.0% and 86.0%, respectively. Adjusted for age, sex and year of treatment, absence of comorbidity was not associated with hospital mortality (OR=0.74, 95%-CI=0.47-1.15), while absence of comorbidity was associated with better long-term survival (adjusted HR=0.28, 95%-CI = 0.14-0.58). Compared to the Dutch population, patients without comorbidity had a similar mortality risk (SMR=1.6, 95%-CI=0.7-3.2), while this was increased in patients with comorbidity (SMR=4.8, 95%-CI=4.1-5.5). Regarding chronic dialysis dependency, 10-year renal survival rates were 76.0% and 92.9% in patients with and without comorbidity, respectively. Absence of comorbidity was associated with better renal survival (adjusted HR=0.24, 95%-CI=0.07-0.76). While hospital mortality remains excessively high, the absence of comorbidity in critically ill patients with RRT-requiring AKI is associated with a relative good long-term prognosis in those who survive hospitalization.

Background The predictive value of acute kidney injury (AKI) urinary biomarkers may depend on the time interval following tubular injury, thereby explaining in part the heterogeneous performance of these markers that has been reported in the literature. We studied the influence of timing on the predictive values of tubular proteins, measured before the rise of serum creatinine (SCr) in critically ill, non-septic patients. Methods Seven hundred adult critically ill patients were prospectively included for urine measurements at four time-points prior to the rise in serum creatinine (T = 0, -16, -20 and -24 h). Patients with sepsis and or AKI at ICU entry were excluded. The urinary excretion of the proteins, neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), which are up-regulated in the distal and proximal tubules, respectively, were measured as well as the constitutive cytoplasmatic enzymes, π- and α-glutathione-S-transferase (GST), which are released by the distal and proximal tubules, respectively. Results Five hundred and forty-three subjects were eligible for further analyses; however, 49 developed AKI in the first 48 h. Both NGAL (P = 0.001 at T = -24 vs. non-AKI patients) and KIM-1 (P < 0.0001 at T = 0 vs. non-AKI patients) concentrations gradually increased until AKI diagnosis, whereas π- and α-GST peaked at T = -24 before AKI (P = 0.006 and P = 0.002, respectively vs. non-AKI patients) and showed a rapid decline afterwards. The predictive values at T = -24 prior to AKI were modest for π- and α-GST, whereas NGAL sufficiently predicted AKI at T = -24 and its predictive power improved as the time interval to AKI presentation decreased (area under the receiver operating characteristic curve; AUC = 0.79, P < 0.0001). KIM-1 was a good discriminator at T = 0 only (AUC = 0.73, P < 0.0001). Conclusions NGAL, KIM-1, pi- and alpha-GST displayed unique and mutually incomparable time dependent characteristics during the development of non-sepsis related AKI. Therefore, the time-relationship between the biomarker measurements and the injurious event influences the individual test results.

Because of the delayed rise of serum creatinine concentrations, novel biomarkers such as NGAL, GST and KIM-1 are proposed to detect acute kidney injury (AKI). In this study we evaluated these biomarkers. Twenty-six consecutive adult liver transplantations were evaluated. Markers were measured at four different time points during an intensive care unit admission. Results: Plasma NGAL detected AKI with an optimal area under the curve at 8 h after admission (0.86; p = 0.004) and at 4 h after admission for urinary NGAL (0.80; p = 0.012). The other markers failed to detect AKI. NGAL is a promising biomarker for detecting AKI in patients after liver transplantation.

Identification of risk factors for impaired renal function at hospital discharge in critically ill patients with acute kidney injury (AKI) requiring renal replacement therapy (RRT). A single-center retrospective cohort study was performed evaluating demographic and clinical parameters as potential risk factors for a modest to severely impaired renal function at hospital discharge in patients with AKI requiring RRT in the intensive care unit. Of the 353 patients in our cohort, 90 (25.5%) patients had pre-existing chronic kidney disease (CKD). An estimated glomerular filtration rate (eGFR) ≤60 mL min−1 1.73 m−2 at hospital discharge occurred in 64.0% of which 63.7% without known renal impairment before hospital admission and 8.2% of all cases left the hospital dialysis-dependent. Multivariable logistic regression showed that age (OR = 1.051, P < .001), serum creatinine concentration at start of RRT (OR = 1.004, P < .001) and administration of iodine-containing contrast fluid (OR = 0.830, P = .045) were associated with an eGFR ≤60 mL min−1 1.73 m−2. Furthermore, a medical history of CKD (OR = 5.865, P < .001) was associated with dialysis dependence. Elderly and patients with pre-existing CKD are at a high risk for modest to severely impaired renal function at hospital discharge after AKI requiring RRT.

This report describes a man in his late 50s who underwent donation-after-circulatory-death kidney transplantation in 2012, due to end-stage kidney disease of unknown origin. More than a decade post-transplant, he presented with a progressive decline in graft function after maintenance immunosuppression had been reduced due to multiple skin carcinomas and the prolonged time since transplantation. Kidney biopsy revealed chronic-active tubulointerstitial nephritis with positive immunohistochemical staining for SV40, initially raising suspicion for BK polyomavirus-associated nephropathy. However, quantitative PCR (qPCR) analysis for BKPyV in both plasma and tissue was negative. In contrast, qPCR for JC polyomavirus (JCPyV) was positive in both plasma and biopsy tissue, leading to the diagnosis of JC polyomavirus nephropathy. Despite the reduction of immunosuppressive therapy, the patient experienced ongoing deterioration of graft function. Our report adds to the limited but growing body of literature on JCPyV and emphasises the need for increased clinical awareness and further research into its prevalence, pathogenesis and optimal management in kidney transplant recipients.