Effects of Cyclosporine on Tubular Acidification Function in Patients with Idiopathic Uveitis

Abstract

Renal tubular acidification function was studied in 12 patients treated with cyclosporine (Cy) for idiopathic uveitis (IU) and in 5 patients with IU not treated with Cy. After intravenous bicarbonate loading fractional bicarbonate excretion was similar in both groups indicating normal proximal tubular acidification function. Plasma renin activity, plasma aldosterone and transtubular potassium gradient were similar in both groups. Distal hydrogen ion secretion evaluated by the ability to increase urine-blood (U-B) pCC₂ in a highly alkaline urine was impaired in Cy-treated patients (31.8 ± 3.2 mm Hg) as compared to controls (47.9 ± 0.5 mm Hg) (p < 0.005). We conclude that Cy therapy is associated with a distal acidification defect with a low U-B pCO₂gradient during sodium bicarbonate loading. Because none of our Cy-treated patients spontaneously developed overt metabolic acidosis one could classify them as having an incomplete form of distal tubular acidosis.

Hypocitraturia as a risk factor for nephrocalcinosis after kidney transplantation

“…Kidney grafts experience tubular damage due to the tubulotoxic side effects of calcineurin inhibitors, through ischemic injury during transplantation or due to chronic rejection [5,13,14,15,16,17,18]. The major problem of tubular dysfunction is renal tubular acidosis [5,13].…”

Nitric Oxide Production Modulates Cyclosporin A-Induced Distal Renal Tubular Acidosis in the Rat

“…dRTA, which is accompanied by hyperchloremia and hyperkalemia, is a serious adverse effect in patients with organ transplantation (Stahl et al, 1986;Heering and Grabensee, 1991) and idiopathic uveitis (Aguilera et al, 1992) and in animals (JaramilloJuarez et al, 2000) treated with CsA. In the clinical situation, RTA is diagnosed from the urinary findings obtained from oral NH 4 Cl challenge tests (Rose, 1994); however, there are few studies that evaluate in vivo tubular function in animal models (Jaramillo-Juarez et al, 2000).…”

Cyclosporine-associated hyperkalemia: report of four allogeneic blood stem-cell transplant cases

“…This was the case with our third patient who showed a simultaneous deterioration of renal function and increased blood CsA levels. On the other hand, CsA may cause isolated increase in serum potassium concentration because of mechanisms other than decreased glomerular filtration rate (19). In the present four cases, hyperkalemia developed despite adequate renal function and no antibiotic therapy that would cause hyperkalemia was used during this time.…”