Renal functional reserve in calcium channel blocker-treated hypertensive recipients of kidney transplant.

Renal functional reserve during infusion of an amino acid solution was examined in 12 cyclosporin-treated kidney recipients at 1 (T1) and 8 months (T2) after transplantation. Patients were retrospectively divided into six normotensive (NT) and six hypertensive recipients (HT) maintained on monotherapy with a calcium channel blocker. Baseline glomerular filtration rates (GFR) were similar in NT and HT at T1 and T2. Renal functional reserve was identical in NT and HT at T1 (15 +/- 7 vs 18 +/- 13 ml/min/1.73 m2) but significantly greater in HT at T2 (11 +/- 5 vs 23 +/- 10 ml/min/1.73 m2; P < 0.05). At T2, baseline proximal tubule outflow (lithium clearance) was greater in HT (26 +/- 8 vs 16 +/- 3 ml/min/1.73 m2; P < 0.05), whereas fractional proximal reabsorption was less (54 +/- 11% vs 67 +/- 5%; P < 0.05). These results indicate that: (i) hypertensive recipients on calcium channel blocker therapy do not exhibit permanent glomerular hyperfiltration until 8 months after transplantation, and have a reduced proximal reabsorption; (ii) measurement of amino acid-stimulated GFR and renal functional reserve is a more sensitive method than that of baseline GFR for evaluating renal function and the effects of therapy in kidney recipients.

[Non-neoplastic hypercalcemia]. / Hypercalcémies non néoplasiques.

Hypercalcaemia is a frequent situation in clinical practice. An earlier detection is facilitated by routine analysis of serum calcium. The clinical manifestations depend on severity and the rate of onset of hypercalcaemia. Paucisymptomatic and asymptomatic presentations are the most frequent. Causes of hypercalcaemia are numerous and the mechanisms are various. PTH and vit. D play a preponderant part. In first of all iatrogenic cause are eliminated (all vit D preparations, thiazide diuretics, milk-alkali syndrome). Among non neoplastic hypercalcaemia primary hyperparathyroidism is the first diagnosis. Nephrolithiasis and asymptomatic forms are the most frequent presentations actually. The biochemical profile is not always typical. Generally the association of echography and tomodensitometry lead to the topographic diagnosis. Parathyroid surgical exploration is often necessary in difficult cases. Secondary, the other rare causes of hypercalcaemia are studied: sarcoidosis and granulomatosis disease, thyrotoxicosis and dome endocrinopathies, immobilisation hypercalcaemia, familial hypocalciuric, hypercalcaemia. All of this causes of hypercalcaemia are potentially reversible.