Self-reported sleep duration and prediction of proteinuria: a retrospective cohort study.

BACKGROUND: Although multiple studies have shown that sleep duration is a predictor of cardiovascular diseases and mortality, few studies have reported an association between sleep duration and chronic kidney disease. STUDY DESIGN: Retrospective cohort study. SETTING & PARTICIPANTS: 6,834 employees of Osaka University aged 20-65 years who visited Osaka University Healthcare Center for their mandatory annual health examinations between April 2006 and March 2010 and did not have estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m(2), proteinuria, or treatment for self-reported kidney disease. PREDICTOR: Self-reported questionnaires about life style, including sleep duration, and blood and urine testing at the first examinations during the study period. An association between sleep duration and outcome was assessed using multivariate Poisson regression models adjusting for clinically relevant factors. OUTCOME: Time to the development of proteinuria defined as 1+ or higher by dipstick test. RESULTS: Self-reported baseline sleep duration was 6.0 ± 0.9 hours, which reflected the mean sleep duration during a median of 2.5 (25th-75th percentile, 1.4-3.9) years of the observational period. Development of proteinuria was observed in 550 employees (8.0%). A multivariate Poisson regression model clarified that shorter sleep duration, especially 5 or fewer hours, was associated with the development of proteinuria in a stepwise fashion (vs 7 hours; incidence rate ratios of 1.07 [95% CI, 0.87-1.33; P = 0.5], 1.28 [95% CI, 1.00-1.62; P = 0.05], and 1.72 [95% CI, 1.16-2.53; P = 0.007] for 6, 5, and ≤4 hours, respectively), along with younger age, heavier current smoking, trace urinary protein by dipstick test, higher eGFR, higher serum hemoglobin A(1c) level, and current treatment for heart disease. A stepwise association between shorter sleep duration and the development of proteinuria also was verified in 4,061 employees who did not work the night shift. LIMITATIONS: Self-reported sleep duration might be biased. Results in a single center should be confirmed in the larger cohort including different occupations. CONCLUSION: Short sleep duration, especially 5 or fewer hours, was a predictor of proteinuria.

Voriconazole-associated salt-losing nephropathy.

A 74-year-old man was diagnosed with nephrotic syndrome due to focal segmental glomerulosclerosis, and steroid therapy was initiated. Subsequently, he was affected by deep mycosis, and hence, voriconazole (VRCZ) was administered. On the 16th day, he was transferred to our hospital because of somnolence and malaise. His systolic blood pressure was approximately 80 mmHg, and he showed decreased skin turgor, indicating volume depletion. Laboratory analysis revealed hyponatremia and liver dysfunction. Discontinuation of VRCZ and drip infusion of normal saline improved the consciousness disorder, hyponatremia, and liver dysfunction. The levels of antidiuretic hormone (ADH) and plasma renin activity were elevated. This patient showed high excreted urine sodium, despite volume depletion and low serum osmolality. Therefore, this patient was diagnosed with salt-losing nephropathy (SLN). SLN should be considered for treatment of VRCZ-associated hyponatremia, together with syndrome of inappropriate secretion of ADH.

ACE insertion/deletion polymorphism (rs1799752) modifies the renoprotective effect of renin-angiotensin system blockade in patients with IgA nephropathy.

INTRODUCTION: Little is known about genetic predictors that modify the renoprotective effect of renin-angiotensin system (RAS) blockade in IgA nephropathy (IgAN). MATERIALS AND METHODS: The present multicenter retrospective observational study examined effect modification between RAS blockade and three RAS-related gene polymorphisms in 237 IgAN patients, including ACE I/D (rs1799752), AT1R A1166C (rs5186) and AGT T704C (rs699). RESULTS: During 9.9 ± 4.2 years of observation, 63 patients progressed to a 50% increase in serum creatinine level. Only ACE I/D predicted the outcome (ACE DD vs ID/II, hazard ratio 1.86 (95% confidence interval 1.03, 3.33)) and modified the renoprotective effect of RAS blockade (p for interaction between ACE DD and RAS blockade = 0.087). RAS blockade suppressed progression in ACE DD patients but not in ID/II patients (ACE ID/II with RAS blockade as a reference; ID/II without RAS blockade 1.45 (0.72, 2.92); DD without RAS blockade 3.06 (1.39, 6.73); DD with RAS blockade 1.51 (0.54, 4.19)), which was ascertained in a model with the outcome of slope of estimated glomerular filtration rate (p = 0.045 for interaction). CONCLUSION: ACE I/D predicted the IgAN progression and the renoprotective effect of RAS blockade in IgAN patients whereas neither AT1R A1166C nor AGT T704C did.