1,721,178 research outputs found
Antihypertensive treatment and multifactorial approach for renal protection in diabetes
Type 2 diabetes is reaching epidemic proportions throughout the world, representing the most common cause of ESRD. Early identification of renal impairment associated with diabetes and initiation of renoprotective therapy are imperative. High BP, dyslipidemia, long duration of diabetes, and poor glycemic control are important risk factors; their modification, renal function monitoring, and combined therapies are the current integrated approaches to treat patients with diabetic kidney disease. Strong evidence suggests that achieving target BP goals via inhibition of the renin-angiotensin-aldosterone system confers significant renal protection for diabetic patients. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers lower BP and reduce both the progression of renal damage and adverse cardiovascular events; some important renoprotective actions seem to be independent of the antihypertensive effect. Stringent quality of glycemic control is another key point to prevent onset of nephropathy or slow its progression. Evidence from basic research and clinical trials indicates that hypolipidemic drugs, mainly statins, contribute to modulate the progression of renal damage in diabetes; their use should be considered in any patient with diabetes. Smoking cessation may slow nephropathy progression; given the additional health benefits of stopping smoking, this advice is an important part of the strategy of diabetic nephropathy treatment and prevention. In conclusion, a target-driven, long-term, intensified intervention aimed at multiple risk factors should be recommended in patients with diabetes to preserve their kidney function
Histopathology of diabetic nephropathy.
The clinical manifestations of diabetic nephropathy, proteinuria, increased blood pressure, and decreased glomerular filtration rate, are similar in type 1 and type 2 diabetes; however, the renal lesions underlying renal dysfunction in the 2 conditions may differ. Indeed, although tubular, interstitial, and arteriolar lesions are ultimately present in type 1 diabetes, as the disease progresses, the most important structural changes involve the glomerulus. In contrast, a substantial subset of type 2 diabetic patients, despite the presence of microalbuminuria or proteinuria, have normal glomerular structure with or without tubulointerstitial and/or arteriolar abnormalities. The clinical manifestations of diabetic nephropathy are strongly related with the structural changes, especially with the degree of mesangial expansion in both type 1 and type 2 diabetes. However, several other important structural changes are involved. Previous studies, using light and electron microscopic morphometric analysis, have described the renal structural changes and the structural-functional relationships of diabetic nephropathy. This review focuses on these topics, emphasizing the contribution of research kidney biopsy studies to the understanding of the pathogenesis of diabetic nephropathy and the identification of patients with a higher risk of progression to end-stage renal disease. Finally, evidence is presented that the reversal of established lesions of diabetic nephropathy is possible
Diabetic nephropathy: challenges in pathologic classification.Nat Rev Nephrol (Prec Nat Clin Pract Nephrol), 6: 508-510, 2010
This paper describes the problems associated with the current pathologic classifications of diabetic nephropathy, largely based on studies performed in patients with type 1 diabetes. Compared to type 1 diabetes, renal patholgy in type 2 diabetes is much more heterogeneous
Renal involvment in type 2 diabetes mellitus: prognostic role of proteinuria and morphologic lesions.
Diabetic nephropathy as a model for the use of renal structural endpoints in clinical trials.
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