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Urinary excretion of n‐acetyl‐β‐ d ‐glucosaminidase and retinol binding protein as alternative indicators of nephropathy in patients with type 1 diabetes mellitus
Author(s) -
Salem Mona A. K.,
ElHabashy Safinaz A.,
Saeid Omayma M.,
ElTawil Mohamed M. K.,
Tawfik Perihan H.
Publication year - 2002
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1034/j.1399-5448.2002.30107.x
Subject(s) - microalbuminuria , medicine , endocrinology , diabetic nephropathy , excretion , urinary system , diabetes mellitus , urine , nephropathy , renal function , retinol binding protein , proteinuria , kidney , retinol , vitamin
Diabetic nephropathy (DN) is usually characterized by glomerular dysfunction, with microalbuminuria as an early indicator. Urinary excretion of smaller molecular weight proteins such as n‐acetyl‐β‐glucosaminidase (β‐NAG) and retinol binding protein (RBP) indicate proximal tubular dysfunction, and may identify diabetic patients at risk of developing diabetic nephropathy. In a trial to assess renal tubular function, urinary excretion of β‐NAG (by colorimetric assay) and RBP (by ELISA) were determined in 59 type 1 diabetic patients (mean age 15 ± 3.2 yr). Of the 59 patients, 11 were microalbuminuric while 48 had normal urinary albumin excretion (UAE). Patients were compared with 40 matched healthy subjects. Diabetic patients with microalbuminuria (n = 11) had concomitant renal tubular disorder indicated by high urinary β‐NAG in all (100%) and RBP in 10 (90.9%) of them. Meanwhile, patients without microalbuminuria (n = 48) had both tubular markers excreted in urine in significantly higher amounts than controls (mean β‐NAG = 6.88 vs. 3.76 U/g Cr, p < 0.001; RBP = 386.6 vs. 151.8 µg/dL, p < 0.001). Among those patients, 29 (61%) had raised urinary β‐NAG activity, and 39 (82%) had increased loss of RBP in urine. A significant correlation was found between urinary β‐NAG and RBP in normoalbuminuric patients (r = 0.66, p < 0.001), as well as between each of the two tubular markers and HbA1c (r = 0.83, p < 0.001). At 30 and 36 months of follow‐up, two out of 48 (4.2%) diabetic patients developed persistent microalbuminuria. Both had elevated baseline HbA1C, and urinary β‐NAG. In conclusion, proximal tubular dysfunction may occur independent of glomerular alteration. Whether tubular markers precede the development of microalbuminuria needs further study.