Diabetic Nephropathy

Diabetic nephropathy is a glomerular sclerosis and fibrosis caused by metabolic and hemodynamic changes in diabetes mellitus. It manifests itself in a slowly progressive albuminuria with worsening of hypertension and renal insufficiency. Diagnosis is based on history, physical examination, urine findings and the albumin / creatinine ratio in urine. The treatment consists in strict blood sugar control, Angiotensinhemmung (by administration of ACE inhibitors and / or angiotensin receptor blockers) and the control of blood pressure as well as the lipids.

(Diabetes mellitus (DM): Diabetic nephropathy.)

Diabetic nephropathy is a glomerular sclerosis and fibrosis caused by metabolic and hemodynamic changes in diabetes mellitus. It manifests itself in a slowly progressive albuminuria with worsening of hypertension and renal insufficiency. Diagnosis is based on history, physical examination, urine findings and the albumin / creatinine ratio in urine. The treatment consists in strict blood sugar control, Angiotensinhemmung (by administration of ACE inhibitors and / or angiotensin receptor blockers) and the control of blood pressure as well as the lipids. (Diabetes mellitus (DM). Diabetic nephropathy) Diabetic nephropathy (DN) is the most common cause of nephrotic syndrome in adults. Diabetic nephropathy is the leading cause of end stage renal disease in the US. (N. D. Übers .: and Europe), responsible for up to 80% of cases. The prevalence of renal insufficiency is probably about 40% among patients with type 1 diabetes mellitus. The prevalence of renal failure in patients with diabetes mellitus type 2 is usually indicated by 20-30%, but this figure is probably low. Kidney failure is especially common in certain ethnic groups, such as dark-skinned, Mexican Americans, Polynesians and Pima Indians. Other risk factors include the following: the duration and extent of hyperglycemia hypertension dyslipidemia cigarette smoking Some polymorphisms that the renin-angiotensin-aldosterone axis relate to family history of diabetic nephropathy Genetic variables (reduced number of glomeruli) Since a Type 2 diabetes often has existed for several years before it is detected, a nephropathy often <10 years developed after the diabetes was diagnosed. Kidney failure usually requires ? 10 years after the onset of nephropathy to develop. Pathophysiology The pathogenesis starts with disease of the small vessels. The pathophysiology is complex and involves the glycosylation of proteins, hormonal influence release of cytokines (eg. As transforming growth factor beta), deposits in the mesangial matrix and changes in glomerular hemodynamics. The hyperfiltration early functional disorder, is only a relative predictor of the development of kidney failure. Hyperglycemia leads to glycosylation of glomerular proteins that are responsible for the proliferation of mesangial cells and the matrix expansion and vascular endothelial damage. The glomerular basement membrane thickens classically. Lesions of diffuse or nodular glomerulosclerosis intercapillary are unmistakable. Areas of nodular glomerulosclerosis can be described as Kimmelstiel-Wilson lesions. There are also an interstitial fibrosis and tubular atrophy. It comes to the pronounced hyalinisation the afferent and efferent arterioles and atherosclerosis. Only the mesangial matrix expansion appears to correlate with the progression to ESRD. Diabetic nephropathy (mesangial cell proliferation and matrix expansion) Figure provided by Agnes Fogo, M.D., and the American Journal of Kidney Disease, Atlas of Renal Pathology (see www.ajkd.org). var model = {thumbnailUrl: '/-/media/manual/professional/images/diabetic_nephropathy_mesangial_cell_proliferation_and_matrix_expansion_high_de.jpg?la=de&thn=0&mw=350' imageUrl: '/-/media/manual/professional/images/diabetic_nephropathy_mesangial_cell_proliferation_and_matrix_expansion_high_de.jpg?la = de & thn = 0 ', title:' Diabetic nephropathy (mesangial cell proliferation and matrix expansion), 'description' u003Ca id = "v38396911 " class = ""anchor "" u003e u003c / a u003e u003cdiv class = ""para "" u003e u003cp u003eMesangialzellproliferation and matrix expansion with endothelial manifest here as thickened glomerular basement membranes with no apparent immune complex deposits (PAS staining

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