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 progression of urinary albumin excretion rate (UAER) in non-insulin-dependent diabetic (NIDD) patients 6 years after diagnosis, and to elucidate the risk factors of nephropathy. Methods. This is a population-based controlled (baseline) cohort study. The prospective evaluation utilized the diabetic patients as internal controls. The setting was an urban primary health care centre. Main outcome measures were the UAER-24 h and fractional urinary albumin excretion rate (FAG) and their relation to mean blood pressure: haemoglobin Ale, fasting serum insulin and cholesterol and renal size. Results. UAER (mg/24 h) was increased (geometric mean, 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 diabetic 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 microalbuminuric subjects 19% progressed to clinical nephropathy, 46% remained microalbuminuric and 35% remitted to normoalbuminuria. Serum insulin concentration, after assessment of confounding factors, measured at the baseline predicted the UAER for all diabetic subjects at follow-up in multiple 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 categorical variable progressor/nonprogressor (n = 22/86) based on the UAER-24 h at baseline and at follow-up. Conclusions. Progression of the UAER during the first 6 years is found among approximately every fifth NIDD subject who develops either microalbuminuria (from normoalbuminuria) or clinical nephropathy (from microalbuminuria). The role of serum insulin (insulin resistance) or some factor associated with it, is suggestive in the genesis of kidney disease.