Uric acid and left ventricular hypertrophy: another relationship in hemodialysis patients.

BACKGROUND: The impact of serum uric acid (UA) on morbidity and mortality in hemodialysis (HD) patients is quite controversial in relation to the general population. The aim of this study was to evaluate the association of serum UA with both mortality and left ventricular hypertrophy (LVH) in HD patients. METHODS: This longitudinal study enrolled 225 prevalent HD patients who were classified into three groups according to their follow-up-averaged UA (FA-UA) levels: low FA-UA (FA-UA <400 µmol/L), intermediate/reference FA-UA (FA-UA between 400 and 450 µmol/L) and high FA-UA (FA-UA >450 µmol/L). Echocardiography was performed on a nondialysis day and the presence of LVH was defined based on a left ventricular mass index (LVMI) >131 and >100 g/m2 for men and women, respectively. The patients were followed during a 60-month period. RESULTS: The mean FA-UA level was 425 ± 59 µmol/L (range 294-620). There was a consistent association of higher FA-UA with better nutritional status (higher body mass index, normalized protein catabolic rate, creatinine, albumin and phosphorus), higher hemoglobin, but lower C-reactive protein and LVMI. During the 5-year follow-up, 81 patients died (36%) and the main causes of death were cardiovascular (CV) related (70%). When compared with the reference group, the hazard ratio for all-cause mortality was 1.75 [95% confidence interval (CI) 1.02-2.98; P = 0.041] in the low FA-UA group, but there was no significant association with the high FA-UA group. In contrast, FA-UA did not show an association with CV mortality neither with the lower nor with the high FA-UA group. The unadjusted odds ratio (OR) of LVH risk in the low FA-UA compared with the reference FA-UA group was 3.11 (95% CI 1.38-7.05; P = 0.006), and after adjustment for age, gender, diabetes and CV disease, ORs for LVH persisted significantly only in the low FA-UA group [OR 2.82 (95% CI 1.16-6.88,); P = 0.002]. CONCLUSIONS: Low serum UA is a mortality risk factor and is associated with LVH in HD patients. These results are in contrast with the association of UA in the general population and should be the subject of further research.

Primary Failure of the Arteriovenous Fistula in Patients with Chronic Kidney Disease Stage 4/5.

BACKGROUND: An Arteriovenous fistula (AVF) is a creation of the natural blood vessels. It is a "gate of life" for the patients on hemodialysis. AIM: The study aimed to analyze the predictors for primary failure of AVF such as gender, age, number and location of AVF, and primary renal disease in patients with chronic kidney disease (CKD) stage 4/5. MATERIAL AND METHODS: The medical records of 178 created arteriovenous fistulae in patients with CKD stage 4/5, were retrospectively studied. Primary failure of AVF was defined as thrombosis or inability for cannulation of AVF within 3 months. Adequate maturation of AVF was defined as successful cannulation of AVF treatment and blood flow of > 600 ml/min. RESULTS: The mean age of the patients was 59.75 ± 14.65 years, and 65.16% (116/178) were men. Adequate maturation of AVF was achieved in 83.71% (149/178). Primary failure of AVF occurred in 16.29% (29/178) of the created fistulae, while 10.11% (18/178) had early thrombosis. The distal arteriovenous fistulae were significantly more frequently created in male patients (51 vs 18; p = 0.015). The female patients were significantly older than the male patients (63.27 vs 57.86 years; p = 0.018). CONCLUSION: Male gender was associated with better maturation of AVF. The age, number and location of AVF, and primary renal disease in patients with CKD stage 4/5 were not associated with primary failure of AVF.

Cyclosporine nephrotoxicity and early posttransplant hyperkalemia in living-donor renal recipients: report of 4 cases.

OBJECTIVES: Hyperkalemia is an electrolyte disorder that may occur during the first few months after a renal transplant, in patients undergoing cyclosporine immunosuppression. We present our experience with cyclosporine-associated hyperkalemia in living-donor renal transplant recipients, with isolated clinically relevant hyperkalemia soon after surgery. MATERIALS AND METHODS: We report 4 living-donor renal recipients with hyperkalemia soon after transplant. RESULTS: Severe unexpected hyperkalemia (7.5- 9.4 mmol/L) was noted in our patients 12, 20, 22, and 34 days after transplant. The C2 cyclosporine concentration was within recommended range or slightly greater than 1200 ng/mL. The hypertonic glucose/insulin treatment along with potassium diet was without results. A reduction in daily cyclosporine dosages, along with 1- to 2-week administration of fludrocortisone was effective. The patients became normokalemic taking a standard, triple-drug immunosuppression protocol, and were discharged home with normal renal function. There were no repeat episodes of hyperkalemia in any of the patients during 12 months of follow-up. CONCLUSIONS: Cyclosporine should be considered a cause of hyperkalemia in renal transplant recipients. Successful treatment with fludrocortisone confirms that transitional pseudohypoaldosteronism has a potential nephrotoxic effect of cyclosporine. We recommend close monitoring of the cyclosporine concentration and administering fludrocortisone when treating hyperkalemia in renal transplant recipients.