Clinical Pharmacology & Therapeutics · 1972 · 24 citations · 0 references
MedicineNephrologyPharmacologyCalcium HomeostasisMineral MetabolismRenal PathophysiologyDiuretic TherapyRenal DiseaseRenal Drug ClearanceRenal Mineral HandlingRenal PharmacologyUrinary ExcretionDistal Tubular Calcium ReabsorptionDistal Tubule PhysiologyDistal Tubule Sodium TransportMagnesium ExcretionRenal Magnesium ReabsorptionRenal Tubular SecretionTubular Mineral SecretionTubular Sodium Transport
Triamterene administered for 2 weeks to 16 normal volunteers increased the renal clearance of sodium and magnesium without affecting calcium or phosphate excretion. It decreased the uric acid clearance in proportion to the decrease in creatinine clearance. Triamterene induced no significant change in serum calcium, phosphate, or uric acid, but there was a slight increase in serum magnesium. The results support the hypothesis that sodium transport in the distal tubule can be inhibited without affecting calcium reabsorption. The mechanism for the increased blood and urine magnesium is not known but could be both renal and extrarenal. There was no evidence for an inhibition of tubular secretion of uric acid. On the basis of these data, it seems unlikely that triamterene could produce clinically significant hypercalcemia or hyperuricemia in nonazotemic patients. However, magnesium depletion could result from long‐continued use, especially when triamterene is combined with other diuretics which also increase magnesium excretion.