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Abstract: SA-PO483

Gitelman-Like Syndrome Associated With Chemotherapy With Cisplatin

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical

Authors

  • Diaz Garcia, Juan Daniel, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Alamilla Sanchez, Mario, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Nieto, Julio Cesar, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Ramirez, Irving Gaston, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • López, Claudia Bethzabé, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Yanez Salguero, Valeria, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Ortega, Jose Luis, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Yama Estrella, Martin Benjamin, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Morales Lopez, Enrique Fleuvier, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
  • Velasco Garcia Lascurain, Francisco, Centro Medico Nacional 20 de Noviembre, Mexico City, Mexico City, Mexico
Introduction

Gitelman-like or acquired syndrome is a rare salt-losing tubulopathy similar to thiazides, characterized by severe and chronic hypokalemia associated with metabolic alkalosis and secondary hyperaldosteronism, it is also characteristic of hypomagnesemia and hypocalciuria without a defect in the ability to concentrate urine. Cisplatin is the most widely used antineoplastic agent for the treatment of solid tumors and is a well-known cause of nephrotoxicity.

Case Description

A 38-year-old female with a history of gastric adenocarcinoma was treated with surgery and 12 cycles of cisplatin, adriamycin, and cyclophosphamide, with no history of taking loop diuretics and thiazides. On hospital admission, her vital signs were normal with stable blood pressure and presence of paresthesias in the extremities. Serum creatinine 0.6 mg/dl, BUN 15 mg/dl, hypokalaemia (2.2 mEq/l) and hypomagnesaemia (0.5 mg/dl), with a venous blood gas analysis that reported a pure metabolic alkalosis with pH 7.52, bicarbonate 32 mEq/l , PCO2 38 mmHg, PO2 82 mmHg. Urinary electrolyte levels were requested in 24 hours, demonstrating urinary losses of potassium with hypocalciuria. He required daily treatment with 20 to 80 mEq of KCl orally, 2000 mg of magnesium oxide and 200 mg of spironolactone to maintain his electrolytes within the normal range. , Cisplatin was suspended and chemotherapy was changed. Three months after Cisplatin suspension, the patient reported serum electrolytes within normal limits.

Discussion

The mechanism of cisplatin nephrotoxicity remains uncertain, it is believed that cisplatin can cause DNA damage in the NCCT gene and DCT epithelial apoptosis producing Gitelman-like syndrome. Although this syndrome occurs infrequently, cisplatin causes frequent renal dysfunction. Cisplatin administration in divided doses or as a continuous infusion reduces nephrotoxicity. Immediate replacement of magnesium and potassium deficits reduces the risk of adverse effects. This case demonstrates that cisplatin can have permanent effects on tubular function and can cause significant morbidity. This syndrome should be considered in patients with unexplained electrolyte abnormalities and a history of distant therapy for malignancies.