Hyperparathyroidism and Renal Tubular Acidosis
Authors: MARIUS PESSAH
Journal: Annals of Internal Medicine (1974)

Comments1 January 1974Hyperparathyroidism and Renal Tubular AcidosisMARIUS PESSAH, M.D., WILLIAM FRANK, M.D.MARIUS PESSAH, M.D.Search for more papers by this author, WILLIAM FRANK, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-80-1-116_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: The recent NIH conference on hyperparathyroidism (Ann Intern Med79:566-581, 1973) reviewed 57 cases of primary hyperparathyroidism, with weakness, fatigability, polyuria, and polydipsia being prominent symptoms. Of these patients, 24% had reduced serum bicarbonate concentrations and 9% had serum chloride levels greater than 110 meq/litre; 39% had serum chloride levels greater than 107 meq/ litre. Although it was briefly mentioned that this "was probably caused directly by the effect of parathyroid hormone on the kidney," we believe that the association between renal tubular acidosis, or the Fanconi syndrome, and parathyroid disease explains many of the clinical and...References1. MORRISMCSHERRYSHERWOOD REL: Evidence of a pathogenic role of hyperparathyroidism in the renal tubular dysfunction of patients with Fanconi's syndrome (abstract 215). J Clin Invest 49(6) :68A, 1970 Google Scholar2. LEEDRINKARDROSEN DJV: The adult Fanconi syndrome. Medicine {Baltimore) 51:107-138, 1972 CrossrefMedlineGoogle Scholar3. HELLMANAUBARTTER DWF: Evidence for a direct effect of parathyroid hormone on urinary acidification. Am J Physiol 209:643-650, 1965 CrossrefMedlineGoogle Scholar4. GINNSHANBOUR HL: Phosphaturia in magnesium-deficient rats. Am J Physiol 212:1347-1350, 1967 CrossrefMedlineGoogle Scholar5. SHILS M: Experimental human magnesium depletion. Medicine (Baltimore) 48:61-85, 1969 CrossrefMedlineGoogle Scholar1. MULDOWNEYCARROLLDONOHOE FDJ: Correction of renal bicarbonate wastage by parathyroidectomy. Q J Med 40:487-498, 1971 MedlineGoogle Scholar2. MORRIS R: Renal tubular acidosis. N Eng J Med 281: 1405-1413, 1969 CrossrefMedlineGoogle Scholar3. MULDOWNEYDONOHOECARROLL FJD: Parathyroid acidosis in uraemia. Q J Med 41:321-342, 1972 MedlineGoogle Scholar4. MORRISMCSHERRYSEBASTIAN REA: Modulation of experimental renal dysfunction of hereditary fructose intolerance by circulating parathyroid hormone. Proc Natl Acad Sci USA 68:132-135, 1971 CrossrefMedlineGoogle Scholar5. GOLDMASSRYARIEFF LSA: Renal bicarbonate wasting during phosphate depletion; a possible cause of altered acid-base homeostasis in hyperparathyroidism. J Clin Invest 52:2556-2562, 1973 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Department of Medicine Long Island Jewish-Hillside Medical Center New Hyde Park, New York PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe Neuromuscular Manifestations of Primary Hyperparathyroidism in Humans 1 January 1974Volume 80, Issue 1Page: 116-117KeywordsAttentionBicarbonatesChloridesHyperparathyroidismParathyroidParathyroid hormoneRenal diseases Issue Published: 1 January 1974 PDF downloadLoading ...