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Nephrosclerosis Clinical Presentation

  • Author: Fernando C Fervenza, MD, PhD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Mar 30, 2015
 

History

Patients may present with hypertension, its complications (eg, heart failure, stroke), and/or symptoms of uremia. In most patients, hypertension is present for many years (usually >10 y), with evidence of periods of accelerated or poorly controlled BP.

Features suggesting the diagnosis of hypertensive nephrosclerosis are as follows:

  • Black race
  • Hypertensive retinal changes
  • Left ventricular hypertrophy
  • Long-standing or very severe hypertension
  • Proteinuria less than 0.5 g/d
  • Hypertension diagnosed prior to the onset of proteinuria
  • Hypertension preceding renal dysfunction
  • No evidence of another renal disease
  • Biopsy findings compatible with the diagnosis
Next

Physical

Upon physical examination, evidence of hypertension-related target organ damage includes hypertensive changes in the retinal vessels and signs of left ventricular hypertrophy.

Hemorrhages or exudates are characteristic of accelerated hypertension, and papilledema is a feature of malignant hypertension.

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Causes

No specific causes for hypertensive nephrosclerosis are known.

A gene that predisposes to hypertensive renal injury has been identified in rats. To date, however, no specific hypertensive ESRD-associated gene has been identified in humans. It must be noted that the APOL1 gene variant can increase the risk of renal disease progression in African American hypertensive patients, but the mechanism by which it causes progression of renal disease is unknown and it is unclear whether the gene variant causes hypertension other than by causing renal disease first.

Correct identification of hypertensive nephrosclerosis susceptibility genes requires accurate hypertensive nephrosclerosis phenotyping. The major impediment to establishing a reliable hypertensive nephrosclerosis phenotype is the absence of strong clinical criteria to distinguish hypertensive nephrosclerosis from other renal diseases. Genetic approaches to hypertensive nephrosclerosis require careful scrutiny of clinical diagnoses before assigning phenotypes to study subjects.

See also Pathophysiology.

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Contributor Information and Disclosures
Author

Fernando C Fervenza, MD, PhD Professor of Medicine, Mayo Graduate School of Medicine; Consulting Staff, Department of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic

Fernando C Fervenza, MD, PhD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Coauthor(s)

Stephen C Textor, MD 

Stephen C Textor, MD is a member of the following medical societies: American Association for the Advancement of Science, American Heart Association, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

David Rosenthal, MD Staff Nephrologist, Department of Nephrology, Kaiser Permanente

David Rosenthal, MD is a member of the following medical societies: American Society of Hypertension

Disclosure: Nothing to disclose.

Ladan Zand, MD Fellow in Nephrology, Department of Internal Medicine, Division of Nephrology, Mayo Medical School

Ladan Zand, MD is a member of the following medical societies: American College of Physicians, American Society of Nephrology, Canadian Medical Association, Ontario Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, International Society of Nephrology, American Society for Biochemistry and Molecular Biology, American Federation for Medical Research, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa

Disclosure: Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Chike Magnus Nzerue, MD, FACP Professor of Medicine, Associate Dean for Clinical Affairs, Meharry Medical College

Chike Magnus Nzerue, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

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Nephrosclerosis. The glomerular tuft is shrunken, with wrinkling of the capillary walls (asterisk), global glomerular sclerosis (arrow), and complete obliteration of the capillary loops and glomerular ischemia (periodic acid-Schiff stain at 250X magnification).
Nephrosclerosis. Glomerulus with wrinkling of glomerular basement membranes accompanied by reduction of capillary lumen diameter (silver stain at 400X magnification).
Nephrosclerosis. Hyaline arteriosclerosis with hyaline deposits (arrows) (trichrome stain at 250X magnification).
Nephrosclerosis. Fibrointimal proliferation of the arcuate artery (periodic acid-Schiff stain at 150X magnification).
 
 
 
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