Renin-angiotensin-aldosterone system (RAAS) blockers are underutilized in patients with chronic kidney disease (CKD). We aimed to determine barriers against the use of RAAS blockers in these patients. Patients with stage 3-5 CKD referred to Hacettepe University Hospital Nephrology Unit during a 1 year period were evaluated for RAAS blocker use. Two hundred and seventy-nine patients (166 male, 113 female) were analyzed. The mean age of the patients was 56.7 AE 15.2 years, mean serum creatinine was 2.45 AE 1.44 mg/dL, and mean glomerular filtration rate was 33.3 AE 15.1 mL/min. The mean follow-up time was 22.0 AE 21.9 months and the clinical visit number was 4.0 AE 3.5. Angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers were used by 68.8% of all patients and 67.7% of diabetic patients at the time of analysis. In 82.1% of patients, RAAS blockers had either been used earlier or were being used. Hyperkalemia was the principal reason for both not starting and also discontinuing these drugs in patients with CKD. In 37.4% of patients, reasons for not starting RAAS blockers were unclear. This study showed that hyperkalemia is the major barrier against the use of RAAS blockers in patients with CKD. There was, however, a subset of patients who did not receive RAAS blockers even without clear contraindications.

BACKGROUND/OBJECTIVES:In this study, we hypothesized that dietary salt intake may be related with inflammation and albuminuria independently from blood pressure (BP) in non-diabetic hypertensive patients. SUBJECTS/METHODS: A total of 224 patients with primary hypertension were included in the study. Serum C-reactive protein (CRP) levels, 24-h urine sodium and albumin excretion were measured in all patients. The subjects were divided into tertiles according to the level of 24-h urinary sodium excretion: low-salt-intake group (n ¼ 76, mean urine sodium: 111.7 ± 29.1 mmol/24 h), mediumsalt-intake group (n ¼ 77, mean urine sodium: 166.1 ± 16.3 mmol/24 h) and high-salt-intake group (n ¼ 71, mean urine sodium: 263.6±68.3 mmol/24 h). RESULTS: Systolic and diastolic BP measurements of patients were similar in the three salt-intake groups. CRP and urinary albumin levels were significantly higher in high-salt-intake group compared with medium-and low-salt-intake groups (P ¼ 0.0003 and P ¼ 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r ¼ 0.28, P ¼ 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r ¼ 0.21, P ¼ 0.0002). Multiple regression analysis revealed that urinary sodium excretion was an independent predictor of both CRP and albuminuria. CONCLUSIONS: These findings suggest that high salt intake is associated with enhanced inflammation and target organ damage reflected by increased albuminuria in treated hypertensive patients independent of any BP effect. Keywords: albuminuria; hypertension; inflammation; salt intake INTRODUCTION Salt intake is an important factor in the genesis of primary hypertension. Epidemiological and clinical data have showed that high salt intake is associated with increased risk of cardiovascular diseases and stroke. 1 Recent work has provided further evidence that high dietary salt intake may even partly cause blood pressure (BP) -independent target organ damage including left ventricular hypertrophy and microalbuminuria. [2][3][4] Microalbuminuria is a significant predictor of endothelial dysfunction and an independent marker of cardiovascular diseases in patients with primary hypertension. 5,6 Several studies have demonstrated that high salt intake is positively related to urinary albumin excretion and this relation may be independent of BP. 3,4,7 The mechanisms responsible for this effect are unclear. In animal models, dietary salt overload has been demonstrated to contribute to renal injury documented by albuminuria and decreased glomerular filtration rate with a minimally increased arterial pressure. 8,9 Inflammatory mechanisms have been proposed to have a role in this nephrotoxic effect of salt excess. 9-13 The role of inflammation in the initiation and progression of cardiovascular diseases is increasingly recognized. 14,15 Studies in hypertensive individuals have shown increased plasma and vascular tissue levels of C-reactive protein (CRP) and several inflammatory cytokines, suggesting a...

Background:Chronic kidney disease can lead to sarcopenia; however, no study has described sarcopenia in the patients undergoing renal transplantation.Objectives:The aim of the present study was to assess the prevalence of sarcopenia in renal transplant recipients (RTR) and to evaluate the demographic and metabolic risk factors associated with sarcopenia in these patients.Patients and Methods:Sarcopenia was diagnosed by measuring handgrip strength in 166 RTR (68 females and 98 males; mean age, 37.9 ± 11.9 years). Basal metabolic rate, fat mass, free-fat mass, total body water, body mass index, and calf circumference were determined, along with blood biochemistry, vitamin D levels, and glomerular filtration rate.Results:Among 166 patients, sarcopenia was present in 34 (20.5%). Handgrip, basal metabolic rate, free fat mass, and total body water were significantly lower in patients with sarcopenia in comparison with those without sarcopenia. There were no differences between patients with and without sarcopenia in terms of mean time since transplantation, the presence of diabetes mellitus, hypertension, coronary artery disease, hyperlipidemia, glomerular filtration rate, and body mass index. Univariate analysis revealed significant differences between patients with and without sarcopenia with respect to age (mean of 43.70 ± 13.97 and 36.37 ± 10.82 years, respectively; P = 0.007) and 25-OH vitamin D levels (median (IQR) of 12 (2-39) and 17.70 (3-68) μg/L, respectively; P = 0.024). There was a statistically significant positive correlation between vitamin D levels and handgrip strength (r = 0.334; P < 0.001). Multivariate regression analysis determined that age was an independent predictive variable of sarcopenia in RTR (β = 1.060; 95% CI, 1.017-1.105; and P = 0.006).Conclusions:Chronic renal disease contributes to sarcopenia, which may develop at an earlier age in RTR.

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Patients with endothelial dysfunction had significantly higher ambulatory blood pressure values and higher BPV. There was a significant negative correlation between endothelial function and BPV.