Background: Ultrafiltration is an adjunctive treatment for decompensated heart failure patients with cardiorenal syndrome. The efficacy and safety of ultrafiltration in the patient cohort are still unknown. Methods: We systematically reviewed and evaluated randomized controlled trials, comparing diuretics with ultrafiltration in adult patients with decompensated heart failure and cardiorenal syndrome through January 2014. The primary outcomes were body weight loss and total fluid removal. Results: We identified 8 trials including 608 patients. In a random-effects model, the pooled difference of body weight loss was 1.44 kg between patients receiving ultrafiltration and diuretics (95% CI, 0.29-2.59; p = 0.01). The difference of fluid removal was 1.28 l between groups (95% CI, 0.43-2.12; p = 0.003). The RR for mortality was 0.90 for ultrafiltration compared with diuretics (95% CI, 0.61-1.33; p = 0.60) and the RR for renal function deterioration was 1.29 (95% CI, 0.90-1.85; p = 0.17). There is a trend toward reducing readmission rate in ultrafiltration group. Conclusions: Ultrafiltration is a safe and effective strategy in the treatment of cardiorenal syndrome without increasing the risk of renal deterioration.

Ketamine-associated diseases have been increasing with the rise in ketamine abuse. Ketamine-associated uropathy is one of the most common complications. We investigated the effects of ketamine-associated uropathy on renal health and determined predictors of renal function decline in chronic ketamine abusers. This retrospective cohort study analyzed 51 patients (22 with ketamine-associated hydronephrosis and 29 with ketamine cystitis) from Kaohsiung Veterans General Hospital in Taiwan. Primary renal outcome was end-stage renal disease or estimated glomerular filtration rate decline >30% from baseline. Compared with the ketamine cystitis group, the hydronephrosis group had lower initial and final estimated glomerular filtration rates and higher alkaline phosphatase and gamma-glutamyl transferase levels (p < 0.05). Elevated cholestatic liver enzyme levels correlated with renal dysfunction in ketamine-associated uropathy. The hydronephrosis group had a higher proportion of patients reaching endpoints than the ketamine cystitis group (50% and 7%, respectively, p < 0.001). After adjusting for age, sex, and initial serum creatinine level, hydronephrosis remained an independent risk factor for renal function deterioration. Ketamine-associated hydronephrosis was a poor renal outcome and strong predictor of renal function decline in chronic ketamine abusers. Elevated cholestatic liver enzyme levels correlated with the severity of ketamine-associated uropathy. Ultrasonography screening of these high-risk groups and regular renal function follow-ups are necessary.

Renal fibrosis plays a major role in the progression of renal failure. Determining whether the tubule or the glomerulus is the initiating factor is made difficult by the complexity of disease processes. This Commentary discusses new findings by Grgic et al., who show that acute injury to the renal tubule is sufficient to produce the full spectrum of renal fibrosis.

Patients with renal infarction are vulnerable to thromboembolic complications with poor outcomes. There is limited report concerning the effect of anticoagulant therapy in this population. To assess the impact of anticoagulant therapy on outcomes in patients with renal infarction. A retrospective cohort study of 101 renal infarction patients was conducted. The association between anticoagulant therapy, all-cause mortality, thromboembolic complications and renal outcome was evaluated. Demographic data and comorbidities were collected for analysis. Anticoagulant therapy was treated as a time-dependent variable. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using multivariate Cox proportional hazards models. Fifty-seven (56.4%) patients with renal infarction received anticoagulant therapy during the study period. The all-cause mortality rate was 7.56 per 100 patient-years. Age (HR 1.05, 95% CI 1.02–1.08) was a risk factor for all-cause mortality and anticoagulant therapy was associated with a 92% improved survival (HR 0.08, 95% CI 0.02–0.34). Twelve (11.9%) thromboembolic events occurred following renal infarction. Current smoking (HR 10.37, 95% CI 1.60–67.43) had an adverse effect and anticoagulant therapy (HR 0.14, 95% CI 0.03–0.73) had a significant protective impact on thromboembolic complications. There was no significant association between anticoagulant therapy and long-term renal outcome in renal infarction patients including the monthly change in the estimated glomerular filtration rate (eGFR), the incidence of eGFR reduction of more than 50% and end-stage renal disease. Anticoagulant therapy in patients with renal infarction was associated with better survival and reduced thromboembolic complications.