Severe Hypoglycemia in a Patient with Chronic Renal Failure due to Amyloidosis
Author(s) -
Arzu Topeli̇,
Yunus Erdem,
Ahmet Uğur Yalçin,
Oktay Oymak,
Murat Hayran,
Ünal Yasavul,
Çetin Turgan,
Şali Çaḡlar
Publication year - 1996
Publication title -
the nephron journals/nephron journals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 2235-3186
pISSN - 1660-8151
DOI - 10.1159/000188870
Subject(s) - medicine , hypoglycemia , amyloidosis , chronic renal failure , intensive care medicine , nephrology , kidney disease , diabetes mellitus , endocrinology
Arzu Topeli, Hacettepe Üniversitesi, Tip Fakültesi, İç, Hastahklari Ana Bilim Dali, TR-06100 Ankara (Turkey) Dear Sir, The cause of hypoglycemia in a patient with chronic renal failure (CRF) is a difficult clinical problem since it may be due to various causes, the first thought of is uremia itself. Here we describe a case with severe hypoglycemia in a patient with CRF. A 26-year old male patient with end-stage renal disease was admitted to our medical intensive care unit (MICU) because of upper gastrointestinal (GI) bleeding. He had systemic amyloidosis, diagnosed on rectal biopsy in 1984, secondary to seronegative rheumatoid arthritis since 1982. He had been on a regular hemodialysis program three times weekly since 1985. On admission his blood pressure was 180/100 mm Hg, pulse 104/min, body temperature 36.2°C and physical examination was unremarkable with the exception of a systolic murmur on the mesocardium. Laboratory examination revealed: hemoglobin 8.5 g/dl; blood urea nitrogen 74 mg/dl; creatinine 6.9 mg/dl; Na concentration 136 mgEq/dl; K concentration 4.2 mEq/dl; Ca 8.5 mg/dl on calcium supplement, and P 5.4 mg/dl. GI bleeding was successfully managed with medical therapy and 2 units of packed red blood cells were transfused. During his hospital stay, his plasma glucose levels were noted to be low, with fasting venous blood glucose concentrations of 40 and 45 mg/dl on two separate occasions, though he was asymptomatic. The patient denied any alcohol and drug abuse. Blood samples were taken for basal cortisol and adrenocorticotrophic hormone (ACTH). ACTH stimulation test was done with 250 mg synthetic ACTH (Synacthen; Ciba-Geigy, Basel, Switzerland) administered intramuscularly and plasma cortisol was measured 30 min later. Thyroid-stimulating hormone (TSH), insulin and C-peptide levels were measured after an overnight fast and fasting for 72 h with simultaneous glucose determinations. After stabilization of his GI bleeding, the patient was discharged on his own wish as he refused any other tests while the results of the tests were pending. Two days after discharge he was taken to the emergency room by a family member, in deep coma and unable to respond to even painful stimuli. Blood pressure was 130/ 75 mm
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