title: Prognostic implications of renal hypertrophy in diabetes mellitus.
abstract: Early in the course of type 1 diabetes mellitus, hypertrophy of the kidney is a consistent finding that is easily diagnosed using current noninvasive methods, especially ultrasonography. Renal functional changes occur in association with hypertrophy, most notably glomerular hyperfiltration. The structural counterpart of this functional change is an early increase in capillary filtration surface area. In most forms of nondiabetic renal hypertrophy, kidney size is closely linked to GFR. In contrast, in diabetes, persistence of hypertrophy after the clinical onset of overt kidney disease (microalbuminuria, hypertension, decreased GFR, etc.) suggests that sustained release of one or more growth factors may continue even after kidney function declines. The fact that growth factors can act in both an autocrine and paracrine fashion raises the possibility that the local effects of such substances may act as local mediators of kidney growth. Failure of renal hypertrophy to reverse following strict glycemic control for a few months may turn out to be an important prognostic indicator of future progression of the renal disease, but this remains to be established. Prospective studies of kidney size in patients with newly diagnosed type 1 diabetes, using accurate noninvasive methods, may be helpful in establishing whether irreversible ("autonomous") hypertrophy of the kidney is indeed a useful prognostic indicator. As therapies are developed that target the different microvascular complications of diabetes (retinopathy, nephropathy, neuropathy), a noninvasive estimation of kidney size may be a cost-effective method of predicting ultimate renal involvement. Since microalbuminuria occurs relatively late in the disease process, early and persistent hypertrophy of the kidney may become a useful prognostic test in the earliest stages of the disease.
authors.affiliation: Department of Medicine, UCLA School of Medicine 90024.
authors.forename: K S
authors.initials: KS
authors.lastname: Kleinman
authors.forename: L G
authors.initials: LG
authors.lastname: Fine
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003920:Diabetes Mellitus / Q000378:metabolism / Q000473:pathology* / Q000628:therapy; D003928:Diabetic Nephropathies / Q000473:pathology* / Q000503:physiopathology; D005919:Glomerular Filtration Rate; D006133:Growth Substances / Q000097:blood; D006801:Humans; D006984:Hypertrophy / Q000473:pathology; D007668:Kidney / Q000473:pathology*; D007684:Kidney Tubules / Q000378:metabolism; D011379:Prognosis
chemical_list: D001786:Blood Glucose; D006133:Growth Substances