To study renal tubular reabsorption and tubulo-glomerular balance in diabetic children, glomerular filtration rate (GFR) and tubular reabsorption rates of sodium, glucose, ultrafilterable calcium, and phosphate were measured during fasting in 26 ambulatory type I (insulin-dependent) diabetic children without clinical signs of microangiopathy (age 7–14 yr; duration of diabetes 3–14 yr). Similar measurements were made in 28 healthy school children (age 8–14 yr). Mean GFR in the diabetic children was significantly higher than in the normal children (138 versus 109 ml/min/1.73 m2, P < 0.01). Mean tubular reabsorption rates of sodium, glucose, and calcium were significantly increased in the diabetic subjects (P < 0.001). In contrast, tubular reabsorption rate of phosphate in the diabetic subjects was not enhanced. The renal threshold concentration of phosphate (TmPO4/GFR) was suppressed in the diabetic compared with the healthy subjects (1.23 versus 1.73 mmol/L, P < 0.001). TmP04/GFR was unrelated to circulating parathyroid and growth hormone concentrations but correlated inversely with the reabsorption rate of glucose (r = -0.53, P < 0.01). Sodium reabsorption was closely correlated to GFR in both diabetic (r = 0.99, P < 0.0001) and healthy subjects (r = 1.00, P < 0.0001), and both groups showed identical regression lines. The tubular glucose reabsorption rate was independent of GFR in the diabetics. Tubular calcium and phosphate reabsorptions correlated equally well with sodium reabsorption and with GFR in the diabetic and healthy subjects (P < 0.001). The maximal reabsorption of phosphate relative to GFR was lowered in the diabetic children. Thus, in the diabetic subjects, the tubulo-glomerular balance was maintained for sodium, but not for phosphate.

These findings can be interpreted as a consequence of increased plasma (and ultrafilterate) glucose concentration inhibiting maximal phosphate reabsorption, leading to a stimulation of sodium coupled glucose reabsorption (cotransport), and thereby of solutelinked water reabsorption. The normalization of absolute phosphate reabsorption may be a consequence of the increased reabsorption of sodium. The excess sodium/solute-linked reabsorption is likely to be basic for the mechanism leading to the elevated GFR in the diabetic subjects.

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