What is the role of central obesity in the pathophysiology of diabetic nephropathy?

Updated: Oct 09, 2019
  • Author: Vecihi Batuman, MD, FASN; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Answer

Central obesity induces hypertension initially by increasing renal tubular reabsorption of sodium and causing a hypertensive shift of renal-pressure natriuresis through multiple mechanisms, including activation of the sympathetic nervous system and renin-angiotensin-aldosterone system, as well as physical compression of the kidneys. [4] Hypertension, along with increases in intraglomerular capillary pressure and the metabolic abnormalities (eg, dyslipidemia, hyperglycemia) likely interact to accelerate renal injury.

Similar to obesity-associated glomerular hyperfiltration, renal vasodilation, increases in the glomerular filtration rate and intraglomerular capillary pressure, and increased blood pressure also are characteristics of diabetic nephropathy. [5] Increased systolic blood pressure further exacerbates the disease progression to proteinuria and a decline in the glomerular filtration rate, leading to end-stage kidney disease.


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