Association between serum lipids, polyunsaturated fatty acids, and prognosis in maintenance hemodialysis patients.

INTRODUCTION: Risks of mortality and cardiovascular disease (CVD) are significantly higher in hemodialysis (HD) patients than in the general population, where dyslipidemia is an established risk factor for CVD and mortality. There is no clear conclusion, however, whether dyslipidemia is a significant risk factor for CVD and mortality in HD patients. Similarly, the association between the polyunsaturated fatty acids (PUFAs) and the mortality is not clear in HD patients. METHODS: We retrospectively investigated mortality and CVD events in 420 HD patients. We classified patients into high- and low-lipid groups depending on their lipid levels. Survival rates were calculated using the Kaplan-Meier analysis and evaluated by the log-rank test. The risk estimates were computed using a multivariate Cox proportional hazard analysis. FINDINGS: During their follow-up (June 2011 to June 2016), 151 patients died (37 of CVD), and 112 patients experienced new CVD events. On Kaplan-Meier analysis, the number of all-cause deaths and CVD events were significantly higher in the low HDL-cholesterol group (P < 0.01, log-rank test). Similarly, the number of all-cause deaths was significantly higher in the high eicosapentaenoic acid/arachidonic acid ratio group (P < 0.01, log-rank test). Multivariate Cox proportional analysis showed that HDL-cholesterol was a significant prognostic indicator for new onset of CVD events (low: 0, high: 1, hazard ratio 0.66, 95% confidence interval 0.44-0.97; P = 0.04). DISCUSSION: In HD patients, LDL-cholesterol and non-HDL-cholesterol levels are not associated with mortality or CVD events. The HDL-cholesterol level, however, is an independent predictor of new CVD events even in HD patients.

[Interstitial nephritis induced by mesalazine].

This report concerns the first case in Japan of interstitial nephritis induced by mesalazine, a new therapeutic agent for inflammatory bowel disease, such as ulcerative colitis. Twenty-two cases have already been reported in other countries. The patient, a 27-year-old woman, was treated with mesalazine for her ulcerative colitis at another hospital. At the beginning of her treatment, her serum creatinine level was within the normal range. After 12 months, this level increased up to 5.7 mg/dl. She was then referred to our hospital for renal investigation and therapy. A renal biopsy revealed that severe tubulo-interstitial nephritis had occurred. Her mesalazine treatment was withdrawn and prednisolone was administered. Her serum creatinine level decreased gradually. However, this level remained at about 2.8 mg/dl and stabilized at that level. She was then discharged from the hospital. Glomeruli appeared to have minor glomerular abnormalities except for one globally sclerosed glomerulus as observed by light microscopy. However, IgM and C3 deposition on glomeruli were also observed. Glomerular lesions were suspected from these histological findings. A similar case that showed IgM. C3 depositions in glomeruli has previously been reported. The possibility of glomerular lesions being induced by mesalazine should be further researched. From the summary of reported cases, a delay of diagnosis of interstitial nephritis induced by mesalazine has resulted in permanent irreversible renal failure. Intensive monitoring of renal function is required when a patient is treated with mesalazine.