FAMILIAL RENAL TUBULAR ACIDOSIS
Authors: Russell E. Randall, William H. Targgart
Journal: Annals of Internal Medicine (1961)

Article1 June 1961FAMILIAL RENAL TUBULAR ACIDOSISRUSSELL E. RANDALL JR., WILLIAM H. TARGGART, M.D.RUSSELL E. RANDALL JR.Search for more papers by this author, WILLIAM H. TARGGART, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-6-1108 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAcidosis of renal origin is an increased hydrogen ion concentration due to an impairment in the excretion of titratable acid and/or ammonium ion, to an excessive excretion of bicarbonate, or to a combination of these two defects.1-4While all renal acidosis is presumably tubular in origin, the term "renal tubular acidosis" has come to represent (and will be so used in this text) that syndrome characterized by a hyperchloremic acidosis resulting from marked impairment in the ability to excrete an acid urine.3-15The latter is significantly out of proportion to any impairment in glomerular filtration, and hence is not associated...Bibliography1. SchwartzRelman WBAS: Acidosis in renal disease. New Engl. J. 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FourmanMcCance PRA: Tetany complicating the treatment of potassium deficiency in renal acidosis. Lancet 1: 329, 1955. CrossrefGoogle Scholar38. RiverKushnerArmstrongDubinSlodkiCutting GLDSSHASJHO: Renal tubular acidosis with hypokalemia and muscular paralysis. Metabolism 9: 1118, 1960. MedlineGoogle Scholar39. WeltHollanderBlythe LGWWB: The consequences of potassium depletion. J. Chron. Dis. 11: 213, 1960. CrossrefMedlineGoogle Scholar40. YamahiroReynolds HSTB: Potassium wasting in renal tubular acidosis: a specific tubular defect. Clin. Res. 8: 235, 1960. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication November 29, 1960.From the Medical Services, U. S. Air Force Hospital, Travis Air Force Base, Calif., the University of California Hospital, and the Department of Medicine, University of California, San Francisco, Calif.†Chief of Hospital Service, 1605th U. S. Air Force Hospital, APO 406, New York, N. Y.‡Research Fellow in Gastroenterology, University of Washington School of Medicine, Seattle 5, Wash.Requests for reprints should be addressed to Major Russell E. Randall, Jr., (MC) USAF, Chief, Hospital Service, 1605th U. S. Air Force Hospital, APO 406, New York, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRenal Tubular DisordersDistal Renal Tubular Acidosis (TYPE I, DRTA)Genetics of UrolithiasisRenal tubular acidosis : pathogenesis, diagnosis and treatmentRenal tubular acidosis — a case reportRenal tubular acidosis in childhoodClinical Utilization of Alkaline Phosphatase MeasurementsRenal tubular acidosisFamilial Renal Tubular AcidosisVARDAMAN M. BUCKALEW JR., M.D.Renal tubular acidosisThe Hereditary Renal DiseasesEhlers-Danlos syndrome with renal tuhular acidosis and medullary sponge kidneysFAMILIAL RENAL TUBULAR ACIDOSIS REVISITEDRUSSELL E. RANDALL JR., M.D.Medullary Sponge Kidney with Renal Tubular Acidosis: A Report of 3 CasesRenal Acid-Base Disorders: Pathogenesis and ManagementRenal tubular acidosis presenting with muscle weaknessThe spectrum of hereditary renal diseasesMedical genetics 1961 1 June 1961Volume 54, Issue 6Page: 1108-1116KeywordsApolipoproteinsAttentionBicarbonatesExcretionHospital medicineMedical servicesPyelonephritis Issue Published: 1 June 1961 PDF downloadLoading ...