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Polyglandular Autoimmune Syndrome Presenting as Acute Renal Failure with Severe Hyperkalemia
Author(s) -
Moses Elisaf,
Haralampos Pappas,
Kostas C. Siamopoulos
Publication year - 1996
Publication title -
˜the œnephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000188926
Subject(s) - medicine , hyperkalemia , nephrology , intensive care medicine , kidney disease , cardiology
K.C. Siamopoulos, Associate Professor of Medicine/Nephrology, University of Ioannina,GR-451 10 Ioannina (Greece) Dear Sir, Polyglandular autoimmune syndrome was first described by Schmidt in patients with both Addison’s disease and lymphocyt-ic thyroiditis. The disease has subsequently been expanded to include any combination of adrenal insufficiency, lymphocytic thyroiditis, gonadal dysfunction and diabetes mellitus [1]. Even though prerenal azotemia has been described in patients with Addison’s disease [2, 3], to the best of our knowledge, acute renal failure (ARF) has not yet been reported in patients with Schmidt’s syndrome. A 38-year-old woman was admitted to the hospital because of ARF with severe hyperkalemia. She had developed a generalized vitiligo at the age of 9 years. The patient had been in a stable state of health until 3 months earlier, when anorexia, muscle weakness, somnolence and progressive weight loss developed. Laboratory investigation performed 2 months before the patient’s admission revealed primary hypothyroidism, while the other parameters tested (including serum creatinine) were within normal limits. Thyroxine (75 μg/day) was prescribed. Despite treatment, the symptoms gradually worsened: muscle weakness became prominent, she was unable to move without any help and experienced nausea, vomiting and restlessness. On examination, low blood pressure was found (90/60 mm Hg), and she was admitted to the hospital. Laboratory parameters are shown in table 1. Microscopic examination of a urine sediment was negative and no proteinuria was found. Because of severe hyperkalemia, one session of hemodialysis was performed. Correction of hypovolemia was followed by a progressive improvement in renal function. Glucocorticoid and mineralocorticoid replacement therapy was given and amelioraTable 1. Laboratory parameters of the patient

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