URINARY ALBUMIN EXCRETION RATE AND ITS DETERMINANTS AFTER 6 YEARS IN NON-INSULIN-DEPENDENT DIABETIC-PATIENTS

Background. The present study was undertaken to clarify the progressio n of urinary albumin excretion rate (UAER) in non-insulin-dependent di abetic (NIDD) patients 6 years after diagnosis, and to elucidate the r isk factors of nephropathy. Methods. This is a population-based contro lled (baseline) cohort study. The prospective evaluation utilized the diabetic patients as internal controls. The setting was an urban prima ry health care centre. Main outcome measures were the UAER-24 h and fr actional urinary albumin excretion rate (FAG) and their relation to me an blood pressure: haemoglobin Ale, fasting serum insulin and choleste rol and renal size. Results. UAER (mg/24 h) was increased (geometric m ean, quartile 1 and 3) in the diabetic patients at baseline, compared to the non-diabetic control subjects; 21 (10 and 33) versus 12 (8 and 15), P=0.0001 (Wilcoxon's rank test). The UAER-24 h was not increased in diabetic subjects at follow-up; 24 (7 and 49) P=0.3791 versus diabe tic subjects at baseline. Eighteen per cent of normoalbuminuric (UAER <30 mg/24 h) patients developed microalbuminuria (UAER=30-300 mg/24 h) and 3% clinical nephropathy (UAER >300 mg/24 h). Of the microalbuminu ric subjects 19% progressed to clinical nephropathy, 46% remained micr oalbuminuric and 35% remitted to normoalbuminuria. Serum insulin conce ntration, after assessment of confounding factors, measured at the bas eline predicted the UAER for all diabetic subjects at follow-up in mul tiple linear regression analysis in an independent and significant way (P=0.01). Serum insulin concentration (P=0.034) and diuretic therapy (P=0.050) at baseline independently predicted the outcome of the categ orical variable progressor/nonprogressor (n = 22/86) based on the UAER -24 h at baseline and at follow-up. Conclusions. Progression of the UA ER during the first 6 years is found among approximately every fifth N IDD subject who develops either microalbuminuria (from normoalbuminuri a) or clinical nephropathy (from microalbuminuria). The role of serum insulin (insulin resistance) or some factor associated with it, is sug gestive in the genesis of kidney disease.