Follow-up study of glomerular dimensions and cortical interstitium in microalbuminuric type 1 diabetic patients with or without antihypertensive treatment

Background. A decrease in urinary albumin excretion is regularly seen with antihypertensive treatment in patients with diabetic nephropathy. Our study concerns structural data obtained by light microscopy in baseline and follow-up biopsies in antihypertensive treated patients and in a reference group. Methods. Microalbuminuric type 1 diabetic patients with diabetes duration of 6-16 years were studied. Two groups, allocated to treatment with either angiotensin-converting enzyme-inhibitor (group 1, n = 6) or beta-blocker (group 2, n = 6) after the baseline biopsy, were studied in parallel, whereas the reference group (group 3, n = 9), without antihypertensive treatment, was part of a previously completed study. The renal plastic-embedded biopsies were serially sectioned (1 mu m), the sections being used for determining glomerular volume, vascular pole area, and interstitial space expressed as fraction of tubular cortex. Results. A significant increase in glomerular volume (P = 0.04) was seen in group 3 only. Vascular pole area (VPA) and VPA relative to calculated glomerular surface did not show significant changes in any of the groups, only a tendency to increase in VPA in group 3 (P = 0.051). The increase in VPA correlated with systolic blood pressure during the study period (r = 0.49, P = 0.03). Glomerular volume did not correlate with HbA(1C), current diabetic glomerulopathy, or ensuing worsening of glomerulopathy. In group 3 every case showed an increase in interstitium (P = 0.0009), group 2 showed a decrease (P = 0.03), and group 1 showed no change. Increase in interstitial fractional volume correlated with diastolic blood pressure during the study (r = 0.54, P = 0.01). Conclusions. In early microalbuminuria, type 1 diabetic patients show glomerular growth, probably compensatory to the developing glomerulopathy. The increase in interstitial volume fraction: demonstrable in early nephropathy, is further augmented over a few years, but is arrested by antihypertensive treatment.