Some lessons from the studies of renal biopsies in patients with insulin-dependent diabetes mellitus

Michael Mauer, Rudolf W. Bilous, Eileen Ellis, Ralph Harris, Michael W. Steffes

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10 Scopus citations


The authors have studied relationships of renal structure and function in more than 100 patients with insulin-dependent diabetes mellitus (IDDM), aged 13-55 years (mean, 30 years) with diabetes for 1-30 years (mean, 19 years). The authors confirmed the unique nature of the diabetic lesions that, in constellation, occur in no other disease. It was found that increased fractional mesangial volume (Vv Mes) is strongly associated with decreased glomular filtration rate (GFR), proteinuria, and hypertension and that all patients with overt diabetic nephropathy have Vv Mes in excess of 0.35 μm3/μm3. This relationship results from constriction of the capillary lumen and filtration surface as a consequence of increased Vv Mes. Global glomerulosclerosis (scarring) is common in IDDM patients as appears related to ateriolar hyalinosis. Focal segmental glomerulosclerosis is a rare lesion in these patients. Having a single kidney (transplanted IDDM patients) is not associated with accelerated lesion development. The presence or absence of microalbuminuria (MA), per se, does not predict underlying glomerular structure, which may vary from the normal range to a level of pathology bordering on that regularly associated with overt nephropathy. However, when MA is associated with hypertension, or reduced GFR or both, urine albumin excretion (UAE) generally exceeds 40 mg/24 hr, and glomerular pathology is always present. The authors concluded that diabetic nephropathy is a unique renal disorder that cannot be caused by hemodynamic factors alone. The authors further conclude that MA becomes a predictor only when other features of overt nephropathy are already present and that serious diabetic glomerular lesions can be present in patients with normal UAE.

Original languageEnglish (US)
Pages (from-to)197-202
Number of pages6
JournalJournal of Diabetic Complications
Issue number4
StatePublished - 1988

Bibliographical note

Funding Information:
This work was supported by NIH grants AM20742 and DK13083. We thank John Basgen and Tom Groppoli for their excellent technical assistance and Marshall Hoff for his graphics. We thank Ms. Cindy Dawis and Jane Carlson for preparing this manuscript. We appreciate the work of the Clinical Research Center staff in caring for these patients.


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