Chronic renal failure pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathophysiologic mechanisms leading to chronic kidney disease stem from the underlying etiologies responsible for the primary renal damage. However; beyond that initial insult, a form of maladaptive systemic and renal response arises that maintains and perpetuates the existing renal disease. Broadly, | The pathophysiologic mechanisms leading to chronic kidney disease stem from the underlying etiologies responsible for the primary renal damage. However; beyond that initial insult, a form of maladaptive systemic and renal response arises that maintains and perpetuates the existing renal disease. Broadly, 3 main mechanisms exist both related in part to the activation of the renin-angiotensin-aldosterone system (RAAS): hyperfiltration, inflammation, and accelerated fibrosis. | ||
===Hyperfiltration=== | ===Hyperfiltration=== | ||
===Inflammation | ===Inflammation=== | ||
===Accelerated Fibrosis=== | |||
==References== | ==References== | ||
Revision as of 01:28, 26 October 2013
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Chronic renal failure Microchapters |
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Chronic renal failure pathophysiology On the Web |
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American Roentgen Ray Society Images of Chronic renal failure pathophysiology |
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Risk calculators and risk factors for Chronic renal failure pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Pathophysiology
The pathophysiologic mechanisms leading to chronic kidney disease stem from the underlying etiologies responsible for the primary renal damage. However; beyond that initial insult, a form of maladaptive systemic and renal response arises that maintains and perpetuates the existing renal disease. Broadly, 3 main mechanisms exist both related in part to the activation of the renin-angiotensin-aldosterone system (RAAS): hyperfiltration, inflammation, and accelerated fibrosis.