Sickle-Cell Nephropathy
Authors: VARDAMAN M. BUCKALEW
Journal: Annals of Internal Medicine (1970)

Editorial Notes1 September 1970Sickle-Cell NephropathyVARDAMAN M. BUCKALEW JR., M.D.VARDAMAN M. BUCKALEW JR., M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-73-3-488 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPatients with sickle-cell anemia have a defect in renal concentrating ability. This abnormality has been characterized functionally as an inability to attain normal maximum osmolality levels in response to water deprivation, despite normal tubular water reabsorption during solute diuresis, and a normal diluting mechanism (1, 2). This unique pathophysiologic alteration of the countercurrent mechanism suggests that the defect is due to an abnormality in trapping of solute in the renal papilla. The mechanism of this supposed abnormality in solute trapping by the medulla has been attributed to a poorly defined disorder of vasa recta hemodynamics caused by the presence of...References1. LEVITT M, HOUSER A, and LEVY M: The renal concentrating defect in sickle cell disease. Amer J Med 29:611-622, 1960 CrossrefMedlineGoogle Scholar2. HATCH F, CULBERTSON J, and DIGGS L: Nature of the renal concentrating defect in sickle cell disease. J Clin Invest 46:336-345, 1967 CrossrefMedlineGoogle Scholar3. PERILLIE P and EPSTEIN F: Sickling phenomenon produced by hypertonic solutions: a possible explanation for the hyposthenuria of sicklemia. J Clin Invest 42:570-580, 1963 CrossrefMedlineGoogle Scholar4. MOSTOFI F, VORDER BRUEGGE C, and DIGGS L: Lesions in kidneys removed for unilateral hematuria in sickle cell disease. Arch Path (Chicago) 63:336-351, 1957 MedlineGoogle Scholar5. STATIUS VAN EPS L, PINEDO-VEELS C, and DE VRIES G: Nature of concentrating defect in sickle cell nephropathy. Lancet 1:450-452, 1970 CrossrefMedlineGoogle Scholar6. HO PING KONG H and ALLEYNE G: Defect in urinary acidification in adults with sickle-cell anemia. Lancet 2:954-955, 1968 CrossrefMedlineGoogle Scholar7. KEITEL H, THOMPSON D, and ITANO H: Hyposthenuria in sickle cell anemia: a reversible renal defect. J Clin Invest 35:998-1007, 1956 CrossrefMedlineGoogle Scholar8. LIEF P, SULLIVAN A, and GOLDBERG M: Physiological contributions of thin and thick loops of Henle to the renal concentrating mechanism. J Clin Invest 48:32a, 1969 Google Scholar9. KINCAID-SMITH P, SAKER B, and MCKENZIE I: Lesions in the vasa recta in experimental analgesic nephropathy. Lancet 1:24, 1968 CrossrefMedlineGoogle Scholar10. STEELE T, GYORY A, and EDWARDS K: Renal function in analgesic nephropathy. Brit Med J 2:213-216, 1969 CrossrefMedlineGoogle Scholar11. KINCAID-SMITH P: Pathogenesis of the renal lesion associated with the abuse of analgesics. Lancet 1:859-862, 1967 CrossrefMedlineGoogle Scholar12. DAVIES D: Changes in renal cortex following experimental medullary necrosis. Arch Path (Chicago) 86:377-382, 1968 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: VARDAMAN M. BUCKALEWJR., M.D.Affiliations: Emory University School of Medicine Atlanta, Ga. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byBand 3 mutations, distal renal tubular acidosis, and Southeast Asian ovalocytosis 1 September 1970Volume 73, Issue 3Page: 488-489KeywordsAnemiaHemodynamics ePublished: 1 December 2008 Issue Published: 1 September 1970 PDF downloadLoading ...