In 1856 Ludwig Traube1 proposed a role of the kidney in thepathogenesis of hypertension on the basis that hypertensionand vascular disease were often associated with chronic Bright'sdisease. Subsequent studies by Frederick Mahomed challengedthis idea, since he reported that patients could have hypertensionin the absence of clinical evidence of renal disease.2 Similarly,Gull and Sutton3 reported that the vascular disease characteristicof hypertension, which they termed "arteriocapillary fibrosis,"could occur in the absence of severe renal parenchymal damage.Such observations led to the concept that there was a primary,or "essential," hypertension that was distinct from . . . [Full Text of this Article]
Goldblatt's Hypothesis: A Role for Primary Renal Microvascular Disease
The Vicious Circle of Hypertension, Revisited
Acquired Renal Injury as a Mechanism of Salt-Sensitive Hypertension
Acquired Renal Injury as a General Mechanism of Salt Sensitivity
The Mechanism of Renal Microvascular and Tubulointerstitial Injury
Alterations in Renal VasoconstrictorVasodilator Balance
The Role of Afferent Arteriolopathy in the Development of Salt Sensitivity
Amelioration of Salt Sensitivity by Prevention or Treatment of Renal Injury
A Unified Pathway for the Development of Salt-Sensitive Hypertension
Source Information
From the Division of Nephrology, Baylor College of Medicine, Houston (R.J.J.); the Department of Nephrology, Instituto Nacional de Cardiología I. Chavez, Mexico City, Mexico (J.H.-A.); Scios, Sunnyvale, Calif. (G.F.S.); and the Renal Service and Department of Immunobiology, Hospital Universitario de la Universidad del Zulia, Maracaibo, Venezuela (B.R.-I.).
Address reprint requests to Dr. Johnson at the Division of Nephrology, Baylor College of Medicine, SM-1273, 6550 Fannin St., Houston, TX 77030, or at rjohnson@bcm.tmc.edu.
References
Related Letters:
Salt-Sensitive Hypertension
Haddy F. J., Johnson R. J., Herrera-Acosta J., Schreiner G. F., Rodriguez-Iturbe B.
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N Engl J Med 2002;
347:448-449, Aug 8, 2002.
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