Africanized Bee Stings and Pathogenesis of Acute Renal Failure
Author(s) -
Ricardo Muñoz-Arizpe,
L. Valencia-Espinoza,
L Velásquez-Jones,
C. Abarca-Franco,
José Domingo Gamboa-Marrufo,
Pedro ValenciaMayoral
Publication year - 1992
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 - 10.1159/000186975
Subject(s) - medicine , pathogenesis , intensive care medicine , nephrology , poison control , medical emergency , pathology , immunology
Ricardo Muñoz-Arizpe, MD, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Col. Doctores, Deleg. Cuauhtémoc, CP 06720, México, DF (México) Dear Sir, Africanized bees (Apis melliferd) are spreading all over the continent since they were inadvertently released in Brazil about three decades ago [1]. Herein we describe a case that survived a massive attack by Africanized bees. The patient developed acute renal failure, but eventually recovered. A 12-year-old boy was the victim of a bee attack in his town (Huitzuco, State of Guerrero), about 200 km south of Mexico City. He lost consciousness during the attack, lasting about 10 min. More than 500 bee stings were found over his face, trunk and extremities. He developed fever, vomiting and hypertension (120/ 100 mm Hg) soon after the attack. Generalized edema, oliguria and gross hematuria developed within a few hours. He was transferred to our hospital the next day. Laboratory reports: hemoglobin 10.9 g/dl (109 g/l), white cell count 32,300/mm3 (32.3 10V1), platelet count 29 × lOVmm3 (29 × 10V1), fibrinogen 395 mg/dl (3.95 g/l), sodium 125 mEq/ 1 (mmol/l), potassium 7.6 mEq/1 (mmol/l), BUN 572 mg/dl (204.2 mmol/l), creatinine 7.2 mg/dl (636.5 μmol/l), immunoglobulins: G 1,330 mg/dl (13.3 g/l), A 131 mg/dl (1.31 g/ 1), M114 mg/dl (1.14 g/l), C3131 mg/dl (1.31 g/ 1), C4 26.0 mg/dl (0.26 g/l), alkaline phosphatase 131 U/1 (2.18 ukat/1) and gamma-gluta-myltransferase 124 U/1 (2.06 ukat/1). Urinaly-sis: sp. gr 1.012, pH 5.5; sediment: protein 3 + ‚ hemoglobin 3 + ‚ 20^10 RBCs/HPF; numerous hemoglobin casts. Fractional excretion of the filtered sodium 3.4%. Peritoneal dialysis was performed and he received intravenous hydrocortisone, 10 mg/ kg daily during 3 consecutive days. He developed a recurrent hemolytic process, with decreasing hemoglobin, increased indirect bili-rubins (1.4 mg/dl, 23 μmol/l) and reduction of haptoglobin to undetectable levels. The hemolytic crisis, together with the thrombo-cytopenia and leukocytosis lasted 2 weeks. The anuric episode lasted 20 days, at the end of which the dialysis was discontinued. A percutaneous renal biopsy showed histopath-ological changes compatible with acute tubular necrosis. The creatinine decreased to 0.5 mg/dl (44.2 μmol/l) and the urinalysis was normal on discharge, 5 weeks after the admission.
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