A single center experience in preemptive kidney transplantation.

Transplantation is recognized as preemptive if it takes place before the initiation of chronic dialysis. This maneuver has the potential to avoid the morbidity and burden of chronic dialysis. From November 2003 to April 2005, 15 (7 male, 8 female) end-stage renal failure patients of mean age 40 +/- 14.8 years received preemptive grafts from 2 living-related and 13 cadaveric donors, constituting 11.5% of all kidney transplantations performed in our center at that time. The period on the waiting list for preemptive recipients, namely, 2 weeks to 6 months (mean, 2.4 months), was significantly shorter than that of other patients (mean, 13.8 months). The mean creatinine clearance calculated from the Cockroft Gault formula and the mean plasma creatinine level in preemptive recipients before transplantation were 12.7 +/- 3.1 mL/min and 6.6 +/- 0.8 mg/dL, respectively. The donors for preemptive and non-preemptive groups of recipients did not differ significantly in respect to age, gender, and renal function. The mean number of mismatches of 3.73 and 3.25 and the mean total ischemic times of 9.53 +/- 5 and 11.2 +/- 5 hours, in preemptive and non-preemptive groups of recipients, respectively. The incidence of delayed graft function (dialysis in the first week after transplantation) was significantly lower among preemptive recipients (20% versus 42%, respectively). The groups did not differ either in respect to the occurrence of acute rejection episodes or graft and patient survivals. In preemptive patients the mean plasma creatinine levels at 3 and 12 months were 1.37 +/- 0.3 and 1.09 +/- 0.3 mg/dL, and in non-preemptive patients 1.7 +/- 0.5 and 1.4 +/- 0.4 mg/dL. In conclusion, these results are promising, confirming the notion that preemptive kidney transplantation is the optimal treatment for end-stage renal disease patients.

Correlation between plasma carnitine, muscle carnitine and glycogen levels in maintenance hemodialysis patients.

Chronic hemodialysis (HD) may lead to losses of carnitine from plasma and muscle. Plasma carnitine does not reflect the body content of carnitine. The purpose of this study was the evaluation of total and free plasma and muscle carnitine concentrations (TPC, FPC, TMC, FMC), muscle glycogen and the relationship between plasma and tissue carnitine content and the basic indices of lipid metabolism in HD patients. The studies were conducted in two groups: the first one consisted of 37 HD patients (19 F, 18 M), the second one served as the control and was composed of 29 (10 F, 19 M) patients with healthy kidneys. Tissue specimens in HD patients were taken during surgery on arterio-venous fistula from brachioradial muscle. Carnitine and glycogen measurements were performed using enzymatic methods according to Cederblad and Huijng respectively. Total cholesterol (CH), HDL-CH, and triglycerides were assayed by enzymatic commercial test system (Boehringer-Mannheim, Germany). To summarise, we found the following phenomena in our HD patients in comparison with the controls: 1) In plasma: similar TPC but decreased FPC levels and FPC/TPC ratio which may suggest free carnitine deficiency. 2) In muscle: significantly lower TMC and FMC levels but normal FMC/ITMC ratio. 3) Negative correlation between TMC and FMC levels and duration of dialysis treatment. 4) No correlation between plasma and muscle camitine concentration. 5) Significantly higher concentration of muscle glycogen which could be explained by the changes in the structure of muscle fibres in HD patients and/or lower physical activity. 6) A positive correlation between FPC/APC or FPC/TPC ratio and HDL-CH in HD patients which may suggest that an appropriate proportion between free and acylcarnitines may influence HDL-CH levels in that population.

Renal allograft protection with angiotensin II type 1 receptor antagonists.

The renal benefits of agents inhibiting the renin-angiotensin-aldosterone system in renal transplant recipients, i.e. preventing the development of chronic graft nephropathy, are supposed but not finally proven. In a double-blind, placebo-controlled, cross-over study, we evaluated the influence of losartan on surrogate markers of tubular injury, urine excretion of transforming growth factor beta-1 (TGF-beta1) and amino-terminal propeptide of type III procollagen (PIIINP) in 16 patients after transplantation. The patients received randomly either losartan (50-100 mg daily) or the beta-blocker carvedilol (12.5-25 mg) for 8 weeks, allowing a placebo washout between treatments. The target office through blood pressure (BP) was below 130/85 mmHg. The BP did not differ in the treatment periods. Losartan significantly decreased N-acetyl-beta-d-glucosaminidase and alfa-1 microglobulin excretion relative to placebo and carvedilol. Urine excretion of TGF-beta1 and PIIINP was significantly lower after losartan. In conclusion, losartan reduces urine excretion of proteins associated with tubular damage and graft fibrosis.