Kidney Function

Background: Serum cystatin C has emerged as a new and potentially more reliable marker of kidney function. However, its utility and performance in patients with acute kidney injury (AKI), particularly for the prediction of dialysis requirement, is not well known.Study Design: Prospective cohort study.Settings & Participants: Adult patients with AKI enrolled at 2 academic medical centers, at time of nephrology consultation.Predictors: Serum cystatin C (primary predictor), serum creatinine, and serum urea nitrogen levels and 24-hour urine output measured at enrollment.Outcomes: The composite of dialysis requirement or in-hospital death.Covariates: Acute Physiology and Chronic Health Evaluation II (APACHE II) score, liver disease, sepsis, and mechanical ventilation.Results: 200 participants were enrolled for this analysis. Mean age was 65 years, 55% were men, and mean APACHE II score was 20. In unadjusted analyses, increases in serum cystatin C (odds ratio [OR], 1.87; 95% confidence interval [CI], 1.36 to 2.59), serum creatinine (OR, 1.53; 95% CI, 1.12 to 2.09), and serum urea nitrogen levels (OR, 1.84; 95% CI, 1.34 to 2.54) were associated with a higher odds (per 1-SD increase) for the composite outcome, whereas greater urine output (OR, 0.56; 95% CI, 0.39 to 0.80) was associated with lower odds. These associations persisted after adjustment for APACHE II score. The addition of serum cystatin C, serum creatinine, and serum urea nitrogen levels or urine output to a basic model entailing APACHE II score, liver disease, sepsis, and assisted mechanical ventilation improved its prediction, evidenced by increases in areas under a receiver operator characteristic curve from 0.816 to 0.829, 0.826, 0.837, and 0.836, respectively. However, there was no significant difference between each of these models.Limitations: Observational study, single serum cystatin C measurement.Conclusion: In patients with AKI, serum cystatin C level performs similarly to serum creatinine level, serum urea nitrogen level, and urine output for predicting dialysis requirement or in-hospital death. Larger studies are needed to confirm these findings.

The coexistence of chronic lymphocytic leukemia (CLL) and nephrotic syndrome was described first by Scott in 1957. The incidence of nephrotic syndrome in patients with CLL is approximately 1% to 2%. Although membranous glomerulonephritis, minimal change, crescentic glomerulonephritis, light-chain deposition disease, amyloidosis, and focal segmental glomerulosclerosis may account for nephrotic syndrome in some instances, the most common lesion is membranoproliferative glomerulonephritis (MPGN). MPGN in the setting of CLL may be caused by cryoglobulinemia, predominantly type II, or be associated with organized immunotactoid deposits made of a monoclonal immunoglobulin G (IgG), classically without cryoglobulinemia and complement activation. The link between CLL and glomerular disease is the monoclonal immunoglobulin produced by the B-cell clone. Furthermore, similar organized deposits with microtubule formation may be found in leukemic lymphocytes and glomeruli of patients with immunotactoid glomerulopathy. The causal relationship between CLL and the glomerulopathy is supported further by parallel improvement of the 2 diseases with chemotherapy.

This review examines US dialysis data, national guidelines, and publications relevant to the early start phenomenon. Kidney International (Source: Medscape Business of Medicine Headlines)