Diabetic nephropathy 2010 – an omen of change in clinical practice?
Journal Title: Postępy Nauk Medycznych - Year 2011, Vol 24, Issue 4
Abstract
Recently published data on the pathogenesis of glomerular changes in diabetes, and on the outcomes of big randomised clinical trials, stress the importance of strict glycaemia control in preventing diabetic nephropathy. Hyperfiltration does not cause albuminuria in the early phase of diabetic nephropathy. Hyperglycaemia results in over-expression of ACE on the glomerular endothelium and decreases the ACE2 activity on podocytes, which increases angiotensin II and initiates albuminuria. Inhibition of renin-angiotensin system does not prevent diabetic nephropathy, but decreases albuminuria in the early phase of diabetic nephropathy without impeding the progression of the disease. In more advanced stages of diabetic nephropathy inhibition of renin-angiotensin system impedes the progression of renal failure only in hypertensive patients. The decreased inactivation of increased amount of angiotensin II by ACE2 harm the podocyte skeleton, second to the augmented local angiotensin II activity. This results in shedding podocytes into urine /podocyturia/, which uncovers the basal membrane and initiates glomerular hyalinisation and sclerosis. Thus, albuminuria and renal failure are not causally linked to each other, and there is no ground for interpreting albuminuria as a marker of diabetic nephropathy, nor to consider changes in albuminuria a prognostic marker of nephroprotection. Prescribing ACEi and/or ARBs as nephroprotection to every patient with diabetes, which is a routine today, should be limited to patients with coexisting hypertension and albuminuria. The indication to prescribe ACEi/ARBs in preventing macroangiopathy is kept. Controlling hypertension is important for nephroprotection along with controlling glycaemia. The target of therapy is to normalize blood pressure and to keep A1C < 7.0%, also in diabetes type 2. In advanced nephropathy ACEi are especially useful and, in case of intolerance should be replaced with ARBs. The ACE2-mimetics, which are under development, raise hope for further improvement of nephroprotection in diabetes.
Authors and Affiliations
Ryszard Gellert
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