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SHELDON C. SOMMERS, M.D.; GORDON B. ROBBINS, M.D.; DAVID S. BABIN, M.D.; CLAIRE T. KNAACK, M.D

Arch Intern Med. 1962;110(4):505-510.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

How pyelonephritis and hypertension may be interrelated is conjectural. Some progress in understanding this complex situation has followed more widespread investigations of renal hypertension and establishment of better pathological diagnostic criteria.^1,2 Opinions regarding pathogenesis of the hypertension that complicates chronic pyelonephritis generally favor either the Goldblatt renin-angiotensin mechanism or the Grollman renoprival theory.^3,4 Hypertension with unilateral pyelonephritis is sometimes cured by a nephrectomy, which is considered clear evidence of a causal relationship.⁵

In human renal hypertension the juxtaglomerular apparatus, the evident site where renin is stored and secreted, has attracted increased attention.⁶ Hypertrophy and hyperplasia of the renal juxtaglomerular cells characterize most instances of surgically curable Goldblatt type renal hypertension.⁷ Among 30 such cases so far analyzed, 4 had significant amounts of associated pyelonephritis.^7,8 In each the inflammation was localized to wedge-shaped segments of the renal cortex and medulla. The only morphologic alteration found . . . [Full Text PDF of this Article]

Author Affiliations
LA JOLLA, CALIF.

From the Departments of Pathology, Scripps Memorial Hospital, La Jolla, Calif.; Massachusetts Memorial Hospitals, Boston, and Boston University School of Medicine.

Footnotes
Submitted for publication May 24, 1962; accepted June 13.

Presented in part before the American Society of Experimental Pathology, Atlantic City, April 13, 1961.

Aided by U.S. Public Health Service Grants FG-281 and FG-481, and U.S. Public Health Service Grant 2G-267.

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