Renal excretion of ascorbic acid in insulin dependent diabetes mellitus
Seghieri, G.; Martinoli, L.; Miceli, M.; Ciuti, M.; D'Alessandri, G.; Gironi, A.; Palmieri, L.; Anichini, R.; Bartolomei, G.; Franconi, F.
International Journal for Vitamin and Nutrition Research. Internationale Zeitschrift für Vitamin- und Ernahrungsforschung. Journal International de Vitaminologie et de Nutrition 64(2): 119-124
1994
ISSN/ISBN: 0300-9831 PMID: 7960490 Document Number: 438022
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 altered urinary excretion of AA, and 2) whether this latter was modified in presence of early diabetic nephropathy with microalbuminuria (albumin excretion rate (AER) gt 20 mu-g/ min) in a group of 21 patients affected by insulin-dependent (type 1) diabetes mellitus (IDDM) as compared with 13 healthy controls matched for sex, age, dietary AA intake, and creatinine clearance per 1.73 m-2 (CCl). Mean serum AA (+- SD) was lower in diabetics (40.3 +- 14 mu-M/l) than in controls (85.1 +- 23.5 mu-M/l; p = 0. 0001) and there was no difference between serum AA of patients with or without microalbuminuria. Urinary excretion of AA to creatinine times 100 (UAA/Cr) was higher in micro- (n = 6; 4.6 +- 1.7) as compared to normo- albuminurics (n=15; 1.6+-0.9) or controls (1.5 +- 12; p=0.0001). For values exceeding renal threshold of tubular AA reabsorption (39 mu-M) 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 CCI was more over related to AER (r = 0.48, p = 0.03) and to blood glucose (r = 0.51;p = 0.01), being un- related to uric acid clearance, glycosuria and to urinary excretion of both alanine aminopeptidase and N-acetyl-beta-glucosaminidase. In conclusion reduced serum AA in IDDM is not explained by an augmented UAA/Cr and only early nephropathy appears selectively associated with a raised AA urinary escape, likely due to a subclinical functional tubular damage.