Chronic renal failure pathophysiology: Difference between revisions

Jump to navigation Jump to search
Line 3: Line 3:


==Overview==
==Overview==
Each [[kidney]] is made of approximately one million [[nephrons]]. In the event of an injury to the [[nephrons]], the remaining healthy [[nephron]]s compensate for the decrease in [[GFR]] by hypertrophy and hyperfiltration. This innate ability of nephrons allows for continued removal of waste products from the body.
Each [[kidney]] is made of approximately one million [[nephrons]]. In the event of an injury to the [[nephrons]], the remaining healthy [[nephron]]s compensate for the decrease in [[GFR]] by hypertrophy and hyperfiltration. 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==
==Pathophysiology==

Revision as of 13:51, 27 July 2012

Chronic renal failure Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Chronic renal failure from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Chronic renal failure pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Chronic renal failure pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Chronic renal failure pathophysiology

CDC on Chronic renal failure pathophysiology

Chronic renal failure pathophysiology in the news

Blogs on Chronic renal failure pathophysiology

Directions to Hospitals Treating Chronic renal failure

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

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 hypertrophy and hyperfiltration. 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 compromising its filtration function eg: diabetes, hypertension, immune complex deposition, toxin exposure, inflammation, chronic infections, genetically determined abnormality in development of nephrons.
    • a set of mechanisms, involving hypertrophy and hyperfiltration of the remaining healthy nephrons, that are a consequence of long term reduction of renal mass, irrespective of the underlying etiology.
  • This response of 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 increased filtration pressure in the healthy nephrons leads to distortion of its structural architecture, causing sclerosis and eventual dropout 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

References

  1. London GM (2003). "Cardiovascular disease in chronic renal failure: pathophysiologic aspects". Semin Dial. 16 (2): 85–94. PMID 12641870.

Template:WH Template:WS