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Published ahead of print on April 20, 2005
J Am Soc Nephrol 16: 1909-1919, 2005
© 2005 American Society of Nephrology
doi: 10.1681/ASN.2005010063
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Review

Essential Hypertension, Progressive Renal Disease, and Uric Acid: A Pathogenetic Link?

Richard J. Johnson*, Mark S. Segal*, Titte Srinivas*, Ahsan Ejaz*, Wei Mu*, Carlos Roncal*, Laura G. Sánchez-Lozada{dagger}, Michael Gersch*, Bernardo Rodriguez-Iturbe{ddagger}, Duk-Hee Kang§ and Jaime Herrera Acosta{dagger}

* Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, Florida; {dagger} Department of Nephrology, Instituto Nacional de Cardiología "Ignacio Chávez," México City, México; {ddagger} Renal Service Laboratory, Hospital Universitario and Instituto de Investigaciones Biomédicas, Maracaibo, Venezuela; § Division of Nephrology, Ewha University College of Medicine, Seoul, Korea

Address correspondence to: Dr. Richard Johnson, University of Florida, Section of Nephrology, 1600 SW Archer Road, Gainesville, FL 32610. Phone: 352-392-4008; Fax: 352-392-5465; E-mail: johnsrj{at}medicine.ufl.edu

Hypertension and hypertension-associated ESRD are epidemic in society. The mechanisms responsible for renal progression in mild to moderate hypertension and those groups most at risk need to be identified. Historic, epidemiologic, clinical, and experimental studies on the pathogenesis of hypertension and hypertension-associated renal disease are reviewed and an overview/hypothesis for the mechanisms involved in renal progression is presented. There is increasing evidence that hypertension may exist in one of two forms/stages. The first stage, most commonly observed in early or borderline hypertension, is characterized by salt-resistance, normal or only slightly decreased GFR, relatively normal or mild renal arteriolosclerosis, and normal renal autoregulation. This group is at minimal risk for renal progression. The second stage, characterized by salt-sensitivity, renal arteriolar disease, and blunted renal autoregulation, defines a group at highest risk for the development of microalbuminuria, albuminuria, and progressive renal disease. This second stage is more likely to be observed in blacks, in subjects with gout or hyperuricemia, with low level lead intoxication, or with severe obesity/metabolic syndrome. The two major mechanistic pathways for causing impaired autoregulation at mild to moderate elevations in BP appear to be hyperuricemia and/or low nephron number. Understanding the pathogenetic pathways mediating renal progression in hypertensive subjects should help identify those subjects at highest risk and may provide insights into new therapeutic maneuvers to slow or prevent progression.




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