Search

Modern immunosuppressive regimens reduce the acute rejection rate by combining a cornerstone immunosuppressant like tacrolimus or cyclosporine with adjunctive agents like corticosteroids, mycophenolate mofetil (MMF) or azathioprine, often associated with untoward side effects. A 6-month randomized study was conducted in 47 European centers. Triple therapy with tacrolimus (trough levels 5-15 ng/mL), corticosteroids (dosage 10 mg/day) and MMF (1 g/day) was administered for 3 months. From day 92, patients either continued with triple therapy (control, n = 277), or stopped steroids (n = 279), or stopped MMF (n = 277). Surrogate markers for long-term benefits were changes in lipid profiles and occurrence of hematological, gastrointestinal and infectious complications. The 6-month acute rejection incidence (biopsy-proven) was similar in all groups (17.0% vs. 15.1% vs. 14.8%, p = 0.744), although the incidence after month 3 was higher in the steroid stop group than in the two other groups. Mean reductions in total cholesterol (18.9 mg/dL [0.49 mmol/L]) and LDL-cholesterol (8.1 mg/dL [0.21 mmol/L]) between months 4 and 6 were greater in the steroid stop group (p < 0.001). Leukopenia (p = 0.0082), serious CMV infection (p = 0.024), anemia (p = NS) and diarrhea (p = NS) were less frequent in the MMF stop group. In a study population of immunologically low-risk patients' withdrawal of corticosteroids or MMF from a tacrolimus-based therapy at 3 months was feasible. A longer follow-up will be needed to confirm the expected advantages for the long-term outcome and to assess the long-term safety of this minimization of immunosuppressive therapy.

Secondary hyperparathyroidism (HP) is well known complication of long-term uremia. CAPD patients show a peculiar behaviour due to loss of vitamin D metabolites through peritoneum. Severe degrees of hyperparathyroidism may require parathyroidectomy in order to achieve appropriate control. Recently, the possibility of controlling this situation with high oral doses of calcitriol has been communicated. The purpose of this study is to evaluate the effect of this agent on hyperparathyroidism in CAPD patients. Two different groups were constituted according to the length of time on dialysis when HP was detected. All of the patients had i-PTH serum levels five times higher than the normal values (50 pg/ml). During a six month period the daily dose of oral calcitriol was increased in order to achieve a reduction in i-PTH level. The results after this period showed a significant reduction in i-PTH levels (614 +/- 378 to 241 +/- 80 pg/ml) with an average increase in oral calcitriol from 0.16 +/- 0.1 to 0.67 +/- 0.4 with no significant changes in serum calcium or phosphorus. The group with HP at start of dialysis achieved these effects easier and with lower doses of calcitriol. We conclude that moderately high doses of oral calcitriol control secondary hyperparathyroidism in CAPD patients without hypercalcemia.

Three cases are reported of idiopathic IgA nephropathy (Berger's disease) presenting as malignant hypertension, with no data suggesting the underlying glomerulopathy, which was uncovered only after renal biopsy was performed. Comments are made on the validity of the pathological diagnosis, the possible pathogenetic sequence of the association, and on the eventual risks and benefits derived from performing renal biopsy in such patients.

The transport of solutes across the peritoneum may be increased by the topical administration of nitroprusside; the effects of the drug seem to be due to an increase in the number of perfused capillaries and/or in their permeability. We have compared the peritoneal mass transfer coefficients (MTC) for urea, creatinine and parathormone (PTH) under basal conditions and after administration of nitroprusside (4.5 mg/l dialysate) in 15 patients under CAPD therapy. The mean increments of the MTC were 48.8% for urea, 77.5% for creatinine and 323% for PTH. The relative MTC increments for the three molecules (taken in pairs) were: MTCPTH/urea' 2.53 times (mean), MTCPTH/creatinine' 1.7 times, and MTCcreatinine/urea' 0.73-times, with very variable ranges. The overall mean increment (OMI) for all three ratios ranged from -1.25 and +6 times. In six patients, some of the relative increments (and in three of them the OMI) were negative but the epidemiological features of these patients revealed no clear data. The OMI shows a direct correlation with the body surface area and an inverse correlation with the the duration of CAPD and ESRD and with the number of peritonitis episodes, albeit without statistical significance. We conclude that the peritoneal vascular reserve has individual characteristics, and that perhaps the OMI or some other similar index might serve to quantify and characterise it, if our findings are confirmed.