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Cation Transport, Hypertension and Diabetic Nephropathy

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The Kidney and Hypertension in Diabetes Mellitus

Abstract

The hypothesis that diabetic nephropathy may not simply be a result of the metabolic abnormalities of diabetes, but may require the concomitance of a permissive genetic background, was initially suggested by the incidence pattern of proteinuria in insulin-dependent diabetes [1,2], and was later supported by the observation that renal destiny is often concordant among Type 1 diabetic siblings [3,4]. Family clustering of diabetic nephropathy may occur also in Type 2 diabetes, and closer evidence that this complication may reflect inheritance, independent of that of Type 2 diabetes, is restricted to Pima Indians [5]. Exploring parental history of diabetic nephropathy per se may not be feasible in Type 1 diabetes [6], but addressing the relevance of known genetic factors to renal prognosis is otherwise possible, in the hope to identify suitable markers of predisposition, and to provide clues to the molecular and cellular pathophysiology of diabetic kidney disease. Among the candidate issues, the genetic background predisposing to essential hypertension was more extensively explored and discussed in the past few years. As essential hypertension is known to cluster in families and to be characterised by abnormalities in erythrocyte sodium transport with established genetic components, the hypothesis was probed by examining these variables in diabetic nephropathy, in addition to revisiting the chicken-and-egg relationship of blood pressure with urinary albumin excretion.

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Mangili, R. (1994). Cation Transport, Hypertension and Diabetic Nephropathy. In: Mogensen, C.E. (eds) The Kidney and Hypertension in Diabetes Mellitus. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-6746-9_26

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  • DOI: https://doi.org/10.1007/978-1-4757-6746-9_26

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