2019Turkish Journal of NephrologyOpen access

Acute Kidney Injury Secondary to Rhabdomyolysis in Case with Gitelman Syndrome

Bilal Katipoğlu, İlhan ATEŞ, Nazlı Pelin Aslan, Nisbet Yılmaz

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Abstract

Gitelman syndrome (GS) is a genetically transmitted tubulopathy. It is caused by mutation in the thiazide-sensitive Na-Cl cotransporter–coding gene, SLC12A3. In this case study, we have discussed a patient diagnosed with GS and referred with muscular weakness and cramping complaints due to discontinuing potassium replacement in the follow-up. The patient was diagnosed with rhabdomyolysis and acute kidney injury secondary to hypokalemia upon determination of 2.14 mEq/L potassium, 27.610 U/L creatine kinase, and 3.09 mg/dL creatinine in further examination. Therefore, NaCl 100 cc/h isotonic was administered to the patient in addition to oral and intravenous potassium replacement. The dose of given acetazolamide was 2×250 due to the presence of severe metabolic alkalosis. Clinical and laboratory findings were fully restored to normal levels one week following the initiation of treatment.

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What this paper is about

Gitelman syndrome (GS) is a genetically transmitted tubulopathy. It is caused by mutation in the thiazide-sensitive Na-Cl cotransporter–coding gene, SLC12A3. In this case study, we have discussed a patient diagnosed with GS and referred with muscular weakness and cramping complaints due to discontinuing potassium replacement in the follow-up. The patient was diagnosed with rhabdomyolysis and acute kidney injury secondary to hypokalemia upon determination of 2.14 mEq/L potassium, 27.610 U/L creatine kinase, and 3.09 mg/dL creatinine in further examination. Therefore, NaCl 100 cc/h isotonic was administered to the patient in addition to oral and intravenous potassium replacement. The dose of given acetazolamide was 2×250 due to the presence of severe metabolic alkalosis. Clinical and laboratory findings were fully restored to normal levels one week following the initiation of treatment.

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Available abstract

Gitelman syndrome (GS) is a genetically transmitted tubulopathy. It is caused by mutation in the thiazide-sensitive Na-Cl cotransporter–coding gene, SLC12A3. In this case study, we have discussed a patient diagnosed with GS and referred with muscular weakness and cramping complaints due to discontinuing potassium replacement in the follow-up. The patient was diagnosed with rhabdomyolysis and acute kidney injury secondary to hypokalemia upon determination of 2.14 mEq/L potassium, 27.610 U/L creatine kinase, and 3.09 mg/dL creatinine in further examination. Therefore, NaCl 100 cc/h isotonic was administered to the patient in addition to oral and intravenous potassium replacement. The dose of given acetazolamide was 2×250 due to the presence of severe metabolic alkalosis. Clinical and laboratory findings were fully restored to normal levels one week following the initiation of treatment.

Key concepts: Rhabdomyolysis, Gitelman syndrome, Acute kidney injury, Medicine, Myoglobinuria, Intensive care medicine, Internal medicine, Pediatrics

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