Tubular and glomerular function in children after renal transplantation.

Glomerular and tubular function of transplanted kidneys were assessed in 46 children aged 15.7 ± 4.6 yr. 4.2 ± 2.8 yr after renal transplantation. There were 34 cadaveric, and 12 living-related donors. Twelve patients (26%) had acute episodes (acute tubular necrosis, rejection, or urinary tract infection) during follow-up. All patients were on triple immunosuppression. The mean serum creatinine was 1.5 ± 0.6 mg/dL. Creatinine clearance (Ccreat) calculated from a 24-h urine collection was 48.0 ± 19.7 mL/min/1.73 m 2 , and that estimated from the Schwartz formula, 61.0 ± 22.5 mL/min/1.73 m 2 . A positive correlation was found between the calculated and estimated clearances. Mean urine concentrating ability was 487 ± 184 mOsmol/kg, with a value lower than 400 mOsmol/kg in 35% of patients. There was a positive correlation between urine osmolality and estimated Ccreat. Metabolic acidosis (bicarbonate <22 mmol/L) was found in 41% of patients, with relatively alkaline urine and high chloride level. Fractional excretion (FE) of sodium was above 1% in 68% of patients (mean 1.66 ± 1.06%), and FE Mg was above 3% (mean 10.9 ± 5.2%) in 93% of patients. Tubular reabsorption of phosphate (TP)/glomerular filtration rate (GFR) was 3.2 ± 0.8 mg/dL glomerular filtrate (GF). FE K , FE UA , and Ca/creatinine in urine were normal. There were no functional group differences between the cadaveric and living-related kidneys. Significant group differences were found in those with acute episodes and those with a normal course. Estimated Ccreat was 54 ± 20 vs. 67 ± 20 mL/min/1.73 m 2 in the acute episodes and the normal course groups, respectively. Also, the FE NA , FE UA , and FE Mg were higher in the acute episodes group -2.3 ± 1.6, 10.6 ± 4.4, and 14.8 ± 6.5%, respectively, compared with the normal course group -1.4 ± 0.6, 8.2 ± 2.8, and 9.6 ± 4.0%, respectively. There were no between-group differences in plasma bicarbonate, FE K , TP/GFR, and urine osmolality. We believe that most, if not all tubular dysfunctions in the transplanted kidney are secondary to renal failure and interstitial damage from acute episodes and nephrotoxic drugs. These dysfunctions are similar to those in chronic renal failure, where interstitial fibrosis I plays a role in kidney function deterioration.