TUBULOPATHY WITH MACROALBUMINURIA DUE TO DIABETIC NEPHROPATHY AND PRIMARY GLOMERULONEPHRITIS

Tubular damage is a recognized feature of both overt diabetic nephropa thy and glomerulonephritis. However, the pattern and mechanism of tubu lar damage in the two clinical settings remain unclear. Two groups of patients with macroalbuminuria (albuminuria > 300 mg/day) were studied . Group 1 comprised 41 patients with biopsy proven primary glomerulone phritis and group 2 comprised 28 patients with clinical diabetic nephr opathy due to insulin dependent diabetes mellitus. Serum creatinine, c reatinine clearance, glomerular proteinuria (albuminuria and transferr inuria), markers of tubular damage such as urinary excretion of lysoso mal enzyme (N-acetyl glucosaminidase), brush border enzymes (leucine a minopeptidase and gamma-glutamyl transferase) and retinol binding prot ein (tubular protein) were measured. Both groups were comparable in se rum creatinine, creatinine clearance, glomerular proteinuria and excre tion of N-acetyl-glucosaminidase. However, a significantly higher degr ee of tubular brush border enzymuria and a lower level of tubular prot einuria were seen in group 1 than in group 2. In group 1, albuminuria correlated to tubular enzymuria and tubular proteinuria. However, ther e was no correlation in diabetic patients between parameters of glomer ular and tubular damage or dysfunction. The data presented suggested t hat the pattern of tubulopathy is different in patients with comparabl e degree of macroalbuminuria due to diabetic nephropathy and glomerulo nephritis. Moreover, in diabetic nephropathy contrary to glomeruloneph ritis, markers of tubular damage are unrelated to glomerular proteinur ia. This may suggest different mechanisms of tubular damage in the two clinical settings. We recommend that in all patients with proteinuria , particularly those with diabetic nephropathy, markers of renal tubul ar damage may be useful in monitoring the course of their disease.