Chronic renal failure pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Each kidney is made of approximately one million nephrons. In the event of an injury to the nephrons, the remaining healthy nephrons compensate for the decrease in GFR by hypertrophying and hyperfiltrating. This innate ability of nephrons allows for continued removal of waste products from the body. Over time, this compensation mechanism becomes maladaptive, and the increased filtration pressure in the healthy nephrons leads to distortion of its structural architecture, causing sclerosis and eventual dropout of these nephrons.
Pathophysiology
- The pathophysiology of chronic renal failure involves two broad mechanisms:
- the initiating mechanism responsible for the injury to nephrons and the decrease in their filtration function eg: diabetes, hypertension, immune complex deposition, toxin exposure, inflammation, chronic infections, genetically determined abnormality in development of nephrons.
- a set of compensation mechanisms, involving hypertrophy and hyperfiltration of the remaining healthy nephrons, that are a consequence of the long term reduction of renal mass. This reduction in renal mass occurs regardless of the exact underlying cause.
- This compensation response by the healthy nephrons is mediated by various growth factors, vasoactive hormones, angiogenic factors and cytokines.
- As the disease process progresses, this adaptive response becomes maladaptive and the increased filtration pressure in the healthy nephrons leads to distortion of its structural architecture. This distortion causes sclerosis and the eventual death of these nephrons.
- The renin-angiotensin axis is thought to contribute to the adaptive hypertrophy and sclerosis, the latter, in part, from the action of transforming growth factor β (TGF-β).
- This explains how a long standing disease process affecting the kidneys can eventually lead to decreased renal mass and function over a period of many years.
Pathophysiology of cardiovascular complications
- The excess cardiovascular risk and mortality is demonstrable in early renal disease and in patients with chronic renal failure, with highest relative risk mortality in younger patients.
- This high risk for cardiovascular mortality results from hemodynamic as well as pressure overload, causing left ventricular hypertrophy and cardiomyopathy. Accelerated atherosclerosis and arteriosclerosis also contributes.
- Damage to the large vessels and atherosclerosis is a major contributing factor for high incidence of congestive cardiac failure, ischemic heart disease, left ventricular hypertrophy, cerebrovascular accidents, peripheral artery disease and sudden death.[1]
References
- ↑ London GM (2003). "Cardiovascular disease in chronic renal failure: pathophysiologic aspects". Semin Dial. 16 (2): 85–94. PMID 12641870.