Non-dipper status and left ventricular hypertrophy as predictors of incident chronic kidney disease.

We have hypothesized that non-dipper status and left ventricular hypertrophy (LVH) are associated with the development of chronic kidney disease (CKD) in non-diabetic hypertensive patients. This study included 102 patients with an estimated glomerular filtration rate (eGFR) ≥ 60 mL/min/1.73 m(2). Ambulatory blood pressure monitoring and echocardiography were performed at the beginning of the study, and the serum creatinine levels were followed. During the average follow-up period of 51 months, CKD developed in 11 patients. There was a significant difference in the incidence of CKD between dippers and non-dippers (5.0% vs 19.0%, P < 0.05). Compared to patients without CKD, patients with incident CKD had a higher urine albumin/creatinine ratio (52.3 ± 58.6 mg/g vs 17.8 ± 29.3 mg/g, P < 0.01), non-dipper status (72.7% vs 37.4%, P < 0.05), the presence of LVH (27.3% vs 5.5%, P < 0.05), and a lower serum HDL-cholesterol level (41.7 ± 8.3 mg/dL vs 50.4 ± 12.4 mg/dL, P < 0.05). Based on multivariate Cox regression analysis, non-dipper status and the presence of LVH were independent predictors of incident CKD. These findings suggest that non-dipper status and LVH may be the therapeutic targets for preventing the development of CKD in non-diabetic hypertensive patients.

A case report of crescentic glomerulonephritis associated with Hantaan virus infection.

Although various glomerular diseases in hantavirus infection have been reported, an association between hantavirus infection and crescentic glomerulonephritis has not been described. Herein, we report a case of immune complex-mediated crescentic glomerulonephritis in a 70-year-old man with Hantaan virus infection.

A more appropriate cardiac troponin T level that can predict outcomes in end-stage renal disease patients with acute coronary syndrome.

PURPOSE: Cardiac troponin T (cTnT), a useful marker for diagnosing acute myocardial infarction (AMI) in the general population, is significantly higher than the usual cut-off value in many end-stage renal disease (ESRD) patients without clinically apparent evidence of AMI. The aim of this study was to evaluate the clinical usefulness of cTnT in ESRD patients with acute coronary syndrome (ACS). MATERIALS AND METHODS: Two hundred eighty-four ESRD patients with ACS were enrolled between March 2002 and February 2008. These patients were followed until death or June 2009. Medical records were reviewed retrospectively. The cut-off value of cTnT for AMI was evaluated using a receiver operating characteristic (ROC) curve. We calculated Kaplan-Meier survival curves, and potential outcome predictors were determined by Cox proportional hazard analysis. RESULTS: AMIs were diagnosed in 40 patients (14.1%). The area under the curve was 0.98 in the ROC curve (p<0.001; 95% CI, 0.95-1.00). The summation of sensitivity and specificity was highest at the initial cTnT value of 0.35 ng/mL (sensitivity, 0.95; specificity, 0.97). Survival analysis showed a statistically significant difference in all-cause and cardiovascular mortalities for the group with an initial cTnT ≥0.35 ng/mL compared to the other groups. Initial serum cTnT concentration was an independent predictor for mortality. CONCLUSION: Because ESRD patients with an initial cTnT concentration ≥0.35 ng/mL have a poor prognosis, it is suggested that urgent diagnosis and treatment be indicated in dialysis patients with ACS when the initial cTnT levels are ≥0.35 ng/mL.

Urinary TGF-beta1 as an indicator of antiproteinuric response to angiotensin II receptor blocker in proteinuric renal diseases.

BACKGROUND: Angiotensin II receptor blockers (ARBs) reduce proteinuria, however, with large inter-individual variability. The present study investigated whether urinary transforming growth factor-beta1 (TGF-beta1) might predict the antiproteinuric efficacy of ARB in non-diabetic chronic renal disease. METHODS: Non-diabetic patients with proteinuria (>1 g/day) received 50 mg of losartan daily followed by 100 mg in two treatment periods, each lasting 12 weeks. Clinical parameters and urinary TGF-beta1 levels were measured at baseline and during the treatment period. RESULTS: In the whole group of patients, losartan treatment effectively decreased proteinuria. However, considerable differences existed among individual antiproteinuric responses. Good (n=34) or low (n=15) responders showed average proteinuria reduction of 69% or 17% from baseline, respectively. Both groups showed similar baseline biochemical and renal parameters and comparable degree of mean arterial blood pressure (MAP) reduction. However, the low responders were older and showed significantly higher baseline urinary TGF-beta1 levels. On multiple regression analysis, age, baseline urinary TGF-beta1 and % reduction in urinary TGF-beta1 and % reduction in MAP significantly predicted antiproteinuric response to losartan therapy. CONCLUSION: The present data suggest that the determination of baseline urinary TGF-beta1 could be an useful indicator of short-term antiproteinuric response to ARB treatment in non-diabetic nephropathy.