Red blood cell distribution width (RDW) is an index of red blood cell variability that is usually used to differentiate the cause of anemia. However, clinical evidence for the relationship between RDW and mortality in hemodialysis patients is still lacking. We performed a single center, prospective longitudinal study. During more than 5 years of follow-up in 80 patients undergoing maintenance hemodialysis, 34 patients (42.5%) died. In the Kaplan-Meier curve analyses, higher RDW levels (≥ 14.9%) were significantly associated with all-cause and cardiovascular mortality (log-rank test, P < 0.05, each). In multivariate Cox proportional hazard models, each 1.0% increase in RDW value predicted an estimated 25% higher risk of mortality (P < 0.05) and a 40% higher risk of cardiovascular mortality (P < 0.05). In conclusion, higher RDW value was a significant predictor for all-cause and cardiovascular mortality in patients undergoing maintenance hemodialysis.

Background: Zinc deficiency is highly prevalent and is caused by inadequate dietary intake, malabsorption and removal by treatment in hemodialysis patients. This study investigated the relationship between serum zinc levels and nutritional status in hemodialysis patients. Methods: A cross-sectional study examining 87 hemodialysis patients was performed. The serum concentrations of zinc were studied to evaluate their association with nutritional status, which was assessed by measuring abdominal muscle and fat areas with computed tomography. Results: Serum zinc levels were significantly and positively correlated with subcutaneous and visceral fat areas (r = 0.299, p < 0.01, and r = 0.298, p < 0.01, respectively), but not abdominal muscle areas. Multiple regression analyses demonstrated that serum zinc levels were a significant independent predictor of visceral fat areas (p < 0.01), but not subcutaneous fat areas (p = 0.631). Conclusions: Our findings suggest that serum zinc levels could play a crucial role in determining abdominal fat mass in hemodialysis patients.

Patients on hemodialysis often have carnitine deficiency. We herein report a woman who experienced the dramatic improvement of cardiac dysfunction after intravenous L-carnitine administration. We also investigated the myocardial fatty acid metabolism using I-labeled β-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) single-photon emission computed tomography (SPECT) before and after L-carnitine therapy, and the impaired metabolism was ameliorated. Taken together, these findings indicate that L-carnitine therapy improved cardiac dysfunction via the amelioration of the abnormal myocardial fatty acid metabolism, at least in part.

A 70-year-old man diagnosed with lung adenocarcinoma was referred to our department for an evaluation of acute onset of nephrotic syndrome with acute kidney injury (AKI) after the 7th course of pembrolizumab treatment. Renal biopsy could not be performed, because he needed anticoagulation therapy for venous thrombosis. Pembrolizumab was discontinued, and prednisolone was started. Hemodialysis was also started, because oliguria was not resolved, and dyspnea due to pulmonary congestion appeared even with the high dose of diuretics. Hemodialysis was successfully withdrawn within 5-week duration because of renal function recovery and increase of urine volume. Complete remission was achieved 4 months after initiating prednisolone. He has never experienced hemodialysis again and remains remission of nephrotic syndrome even the dose of prednisolone was tapered for 8 months. Renal pathology in the current case was uncertain. However, minimal change disease seemed to be a plausible cause of nephrotic syndrome with AKI because of a good response to steroid therapy and acute onset of nephrotic syndrome. In addition, renal pathology in all of the reported cases of pembrolizumab-associated nephrotic syndrome with AKI was minimal change disease. Our case shows for the first time that renal function could be reversible with prednisolone in pembrolizumab-associated nephrotic syndrome with severe AKI even after progression of renal failure which needs dialysis.

Background Cisplatin is a highly effective chemotherapeutic agent. However, acute kidney injury (AKI) limits its subsequent use, resulting in poor cancer prognosis. Dipeptidyl peptidase-4 (DPP-4) inhibitors have been reported to attenuate cisplatin-induced AKI in animal models, but the effect in human patients remains to be clarified. We hypothesized that DPP-4 inhibitors can prevent cisplatin-induced AKI in diabetic-cancer patients. Methods We retrospectively reviewed all consecutive cancer patients who were treated with a first cycle of cisplatin-containing regimen between January 2011 and October 2019. We analysed data of diabetic-cancer patients treated with high-dose cisplatin (> 50 mg/m 2)-containing regimens. The change of estimated glomerular filtration rate (eGFR) within 2 weeks after cisplatin treatment was compared between the patients treated with DPP-4 inhibitors and those treated without DPP-4 inhibitors. Results A total of 455 patients were treated with cisplatin during the period. Of these, 34 patients were eligible for the analysis. The change of eGFR was significantly less in the patients treated with DPP-4 inhibitors, compared to those without DPP-4 inhibitors [the percentages of eGFR decline (mean ± SD) was 23.6 ± 20.3% vs 43.1± 20.1%, respectively; P = 0.010]. Furthermore, the incidence of AKI was significantly less in the patients treated with DPP-4 inhibitors (25% vs 64%, respectively; P = 0.026). Conclusions DPP-4 inhibitors may decrease the risk of cisplatin-induced AKI in diabetic patients.