Abstract 135: A case of acquired Gitelman syndrome presenting as hypokalemic paralysis and AKI

Introduction: Gitelman syndrome is usually an inherited disorder, it is induced by defect in the thiazide sensitive Na –Cl co-transporter in distal tubules. Case reports on hypokalemia, AKI secondary to GS has been discussed in present case report. Clinical Case: A 18 year old female referred from department of General Medicine as a case of AKI having recurrent hypokalemia. She gave history of hypokalemic paralysis. There was no potential cause of dehydration such as diarrhoea, vomiting, nephrotoxic agent intake or contrast exposure. Family history was negative. During current hospitalization, she was normotensive with normal renal function test. Other electrolyte levels including calcium and routine laboratory parameters were determined to be normal. Kidney dimensions and echogenicity were determined to be normal without hydronephrosis in the urinary system as oer USG finding. Further workup for hypokalemia revealed urine potassium creatinine ratio (17 mmol/g), ABG (pH 7.44, bicarbonate 26.5 mmol/l), urine chloride (111.3 mmol/l) and urine calcium creatinine ratio (0.05 mmol/mmol) respectively with serum Mg (1.7 mg/dl) on lower range. Based on above findings, a diagnosis of Gitelman syndrome has been made. Autoimmune etiology were ruled out. These finding suggested that patient had AKI secondary to hypokalemia. She was started on oral potassium supplementation and magnesium supplementation. Conclusion: GS is a rare tubulopathy transmitted as an autosomal recessive trait. It is caused by mutation in thiazide sensitive Na Cl co-transporter coding gene, SLC12A3. Patients may be referred with hypokalemia, hypomagnesemia and metabolic alkalosis associated muscular weakness and cramping. By contrast, worsening hypokalemia and profound volume depletion as the predisposing factors for ischemic AKI appears to coexist.