Abstract
Although far more than 50 % of diabetic patients receiving renal replacement therapy have type 2 diabetes [1–5], the renal pathology and natural history of diabetic nephropathy (DN) in type 2 diabetes has been studied much less intensly than in type 1 diabetes and thus many important questions remain unclear. The clinical manifestations of DN, proteinuria, declining GFR and increasing blood pressure, are similar in type 1 and type 2 diabetes [6–7], as they are in many other renal diseases; nevertheless whether these clinical features are the consequences of similar underlying renal lesions is not entirely known. In type 1 diabetes it is generally accepted that glomerulopathy represents the most important structural change, leading to progressive renal function loss [8–13]; concomitantly and roughly proportionally to the degree of glomerulopathy, the arterioles, tubules and interstitium also undergo structural changes, including hyalinosis of the arteriolar wall, thickening and reduplication of tubular basement membranes, tubular atrophy and interstitial expansion and fibrosis [8–14]. These lesions become progressive and severe only when glomerulopathy is far advanced. Quantitative morphometric studies have demonstrated that the lesion most closely related to the decline in renal function in type 1 diabetes is mesangial expansion, caused predominantly by mesangial matrix accumulation [12, 15].
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Fioretto, P., Mauer, M., Nosadini, R. (1998). Renal Structure in Non Insulin Dependent Diabetic Patients with Microalbuminuria. In: Mogensen, C.E. (eds) The Kidney and Hypertension in Diabetes Mellitus. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-6752-0_25
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DOI: https://doi.org/10.1007/978-1-4757-6752-0_25
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