Abstract
Obesity is a risk factor for both de novo disease and as a complication of existing chronic kidney disease. Obesity related disease is characterized by albuminuria, glomerulomegaly and secondary focal glomerulosclerosis. Traditionally altered renal hemodynamics causing hyperfiltration and upregulated renin angiotensin system have been associated with these changes. Recently identified circulating factors produced by fat stores such as adiponectin, leptin and inflammatory markers have shown to directly affect the cells in the renal glomeruli and cause pathological changes. Weight loss, blockade of the renin angiotensin system and restoration of adipokine levels may be beneficial to ameliorate the progression of obesity related disease.
Keywords: Obesity, Kidney disease, Adiponectin, Focal sclerosis, Albuminuria, serum cholesterol level, proteinuria, urinalysis, serum, hypertension, Type IV collagen, C57BI/6J, ADIPOKINES, leptin levels, AMPK (5'AMP acti-vated protein kinase), AICAR (5-aminoimidazole-4-carboxamide-1-D-ribonucleoside), NEPH1-3, synaptopodin, actinin-4, zona occludens-1 (ZO1), Adapter protein APPL1, LKB1, AMPK, NOX-4, AICAR, nephrin, Leptin, Hyperleptinemia, TGF-1 expression, glomerulosclerosis, phosphatidylinositol-3-kinase pathway, necrosis factor, (TNF, ), inter-leukin-6 (IL- 6) levels, interleukin -1 (IL-1 ), actin, F-actin, phosphatidylinositol-3-kinase/Akt pathway, JNK/p38-dependent mechanism, 3T3-L1, ICAM-1, VCAM-1, P-selectin, E-selectin, Captopril, Hyperinsulinemia, jun N terminal kinase, GLUT 1, channel 6 (TRPC6), AICAR treatment
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