Cyclosporin A (CsA) causes tubular dysfunction characterized by polyuria, calcium wasting, distal tubular acidosis and hyperkalemia. The hypercalciuria induced by cyclosporine administration is associated with an inhibition of calbindin D_28k expression. It has also been shown that chronic metabolic alkalosis increased the expression of Ca²⁺ transport proteins accompanied by diminished urine Ca²⁺ excretion. The aim of this study was to determine the effect of acidbase status on CsA-induced hypercalciuria. Experiments were performed on male Sprague-Dawley rats. Metabolic alkalosis and acidosis was induced by adding 0.28 mol/L NaHCO₃ and 0.28 mol/L NH₄Cl in the drinking water for 7 days. Seven days after NaHCO₃ or NH₄Cl administration, rats were treated with CsA (25 mg/kg, i.p.) daily for 14 days. To estimate glomerular filtration rate (GFR) over time, animals were placed in metabolic cages. Fractional urinary calcium excretion was determined by EasyLyte calcium analyzer. The CsA group showed decreased serum calcium and Creatinine clearance, increased fractional urinary calcium excretion compared to control group. Creatinine clearance experiments demonstrated that metabolic alkalosis alone did not affect GFR, but significantly prevented increase in fractional urinary calcium excretion induced by CsA, whereas chronic metabolic acidosis resulted in the exact opposite effects. Fully understanding the mechanisms of CsA-induced renal injury is essential for nephrologists. In this study metabolic alkalosis reduced CsA-induced hypercalciuria. Further studies are needed to elucidate whether this effect may be achieved pharmacologically by the expression of Ca²⁺ transport proteins.