Hypertension is highly prevalent after renal transplantation and has been associated with lower graft survival. Optimum management of post-transplant hypertension remains to be defined. Losartan, a potent, orally active and selective non-peptide blocker of the angiotensin subtype 1 receptor, could represent a useful drug for treating post-transplant hypertension. Recently, a prospective study of 12 weeks treatment with losartan has showed a satisfactory control of arterial hypertension associated with a decrease in proteinuria in this high-risk group of renal transplant patients. A retrospective study was performed to review the role of losartan as a renoprotective agent (evaluating blood pressure and proteinuria) in renal transplant recipients in a long-term follow-up. A total of 150 transplant recipients were included in the study. None of the patients had a serum creatinine >3 mg/dl, or suspected renal artery stenosis, or other severe concomitant diseases. The indication for losartan therapy was hypertension, proteinuria and/or post-transplant erythrocytosis. The values of blood pressure, results of fasting haematology, blood chemistry and total proteinuria in 24-h urine samples were recorded at the time of initiation of losartan therapy, 6 and 3 months before the start, and at 3, 6, 12, 18 and 24 months thereafter. A tendency analysis by linear regression comparing two slopes before and after treatment was realized. A decrease in mean blood pressure and proteinuria, from 106.7+/-0.9 to 98.2+/-2.1 mmHg and from 1253.9+/-188 to 91.2+/-33.7 mg/24 h, P<0.05, respectively, was observed after introduction of losartan. A progressive increase in creatinine clearance was observed after the third month of losartan treatment. No significant changes were seen in haematocrit or serum potassium levels. We can conclude that a progressive decrease in mean arterial pressure associated with a decrease in proteinuria was observed during long-term follow-up. Based on the capacity of losartan to improve renal function, this drug could be decisive for the treatment and prevention of chronic allograft nephropathy.
Diabetic patients on maintenance dialysis often are characterized by a relative parathyroid hormone (PTH) deficiency and a form of renal osteodystrophy with low bone turnover known as adynamic bone. The goal of the present study was to determine whether a reduction in the dialysate calcium concentration would increase the predialysis (basal) PTH and maximal PTH level. Thirty-three diabetic maintenance hemodialysis patients with basal PTH values less than 300 pg/ml were randomized to be dialyzed with either a regular (3.0 mEq/liter or 3.5 mEq/liter, group I) or low (2.25 mEq/liter or 2.5 mEq/liter, group II) calcium dialysate for 1 year. At baseline and after 6 months and 12 months of study, low (1 mEq/liter) and high (4 mEq/liter) calcium dialysis studies were performed to determine parathyroid function. At baseline, basal (I, 126 ؎ 20 vs. II, 108 ؎ 19 pg/ml) and maximal (I, 269 pg/ml ؎ 40 pg/ml vs. II, 342 pg/ml ؎ 65 pg/ml) PTH levels were not different. By 6 months, basal (I, 98 ؎ 18 vs. II, 200 ؎ 34 pg/ml, p ؍ 0.02) and maximal (I, 276 pg/ml ؎ 37 pg/ml vs. II, 529 pg/ml ؎ 115 pg/ml; p ؍ 0.05) PTH levels were greater in group II. Repeated measures analysis of variance (ANOVA) of the 20 patients who completed the entire 12-month study showed that only in group II patients were basal PTH (p ؍ 0.01), maximal PTH ( p ؍ 0.01), and the basal/maximal PTH ratio ( p ؍ 0.03) different; by post hoc test, each was greater ( p < 0.05) at 6 months and 12 months than at baseline. When study values at 0, 6, and 12 months in all patients were combined, an inverse correlation was present between basal calcium and both the basal/maximal PTH ratio (r ؍ ؊0.59; p < 0.001) and the basal PTH (r ؍ ؊0.60; p < 0.001). In conclusion, in diabetic hemodialysis patients with a relative PTH deficiency (1) the use of a low calcium dialysate increases basal and maximal PTH levels, (2) the increased secretory capacity (maximal PTH) during treatment with a low calcium dialysate suggests the possibility of enhanced parathyroid gland growth, and (3) the inverse correlation between basal calcium and both the basal/maximal PTH ratio and the basal PTH suggests that the steady-state PTH level is largely determined by the prevailing serum calcium concentration.
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