RENAL EXCRETION OF ASCORBIC-ACID IN INSULIN-DEPENDENT DIABETES-MELLITUS

Serum ascorbic acid (AA) is reduced in diabetic patients. Aim of this study was 1) to verify whether such a decrease might be due to an alte red urinary excretion of AA, and 2) whether this latter was modified i n presence of early diabetic nephropathy with microalbuminuria (albumi n excretion rate [AER] > 20 mug/min) in a group of 21 patients affecte d by insulin-dependent (type 1) diabetes mellitus (IDDM) as compared w ith 13 healthy controls matched for sex, age, dietary AA intake, and c reatinine clearance per 1.73 m2 (CCl). Mean serum AA (+/-SD) was lower in diabetics (40.3+/-14 muM/l) than in controls (85.1+/-23.5 muM/l, p =0.0001) and there was no difference between serum AA of patients with or without microalbuminuria. Urinary excretion of AA to creatinine x 100 (UAA/Cr) was higher in micro- (n=6; 4.6+/-1.7) as compared to norm oalbuminurics (n=15, 1.6+/-0.9) or controls (1.5+/-1.2; p=0.0001). For values exceeding renal threshold of tubular AA reabsorption (39 muM) the regression line of serum AA to UAA/Cr was significantly (p=0.001) steeper in diabetics than in controls, suggesting an impaired tubular reabsorption of filtered AA in IDDM. The ratio of AA clearance to CCl was moreoverrelated to AER (r=0.48, p=0.03) and to blood glucose (r=0. 51; p=0.01), being unrelated to uric acid clearance, glycosuria and to urinary excretion of both alanine amino-peptidase and N-acetyl-beta-g lucosaminidase. In conclusion reduced serum AA in IDDM is not explaine d by an augmented UAA/Cr and only early nephropathy appears selectivel y associated with a raised AA urinary escape, likely due to a subclini cal functional tubular damage.