1060 DEFECTIVE RENAL TUBULAR FUNCTION IN DIABETIC CHILDREN CAUSING HYPERCALCIURIA AND AN INCREASED URINARY pH

Abstract

In a group of 47 diabetic children 19 had a urinary calcium excretion above 5.2 mg/kg/24 hr or 2 SD above the mean (2.4 mg/kg/24 hr) of a control group of 58 healthy children.In 13 of these 19 children the hypercalciuria was independent of the degree of glucose excretion and persisted on follow-up. In fasting urine samples the calcium/creatinine ratio of the hypercalciuric group (0.21±0.11, mean ± SD) differed (p<.001) from that of the normo-calciuric group (0.08±0.06), also the urinary pH of the hypercalciuric group (6.27±0.74) differed (p<.05) from that of the normocalciuric group (5.57±0.40). The blood pH, bicarbonate, glucose and the serum fosfate, ionised calcium, alkaline fosfatase, iPTH, hCT, hGH were not different. After an oral calcium load the urinary cAMP and the TmP/GFR increased (p<.05 and p<.01 respectively) in the hypercalciuric group but not the urinary calcium/creatinine ratio. Indomethacin lowered (p<.02) the calcium/creatinine ratio in fasting urine samples of 10 hypercalciuric children from 0.32±0.18 to 0.17±0.15 but not that of the normocalciuric children. The correlation between the excretion of sodium and the calcium/creatinine ratio was significant in the normocalciuric group, but became only so in the hypercalciuric group after indomethacin administration. It is suggested that prostaglandins contribute to a defective renal tubular function causing hypercalciuria in these diabetic children.