| 초록 |
Case Study: Objective To describe a rare case of acquired Bartter-like tubulopathy in a patient with systemic lupus erythematosus and secondary Sjögren syndrome, and to highlight the nephrologic clues that support this diagnosis. Methods We reviewed the patient’s clinical presentation, serum and urine biochemical profile, acid-base status, medication history, and response to therapy. Alternative causes of hypokalemic metabolic alkalosis, including gastrointestinal chloride loss, diuretic exposure, and drug-induced tubulopathy, were assessed clinically and excluded. Results A middle-aged Filipino woman with longstanding systemic lupus erythematosus and secondary Sjögren syndrome on hydroxychloroquine and prednisone presented with generalized weakness, bipedal edema, poor concentration, polyuria, and constipation. She had no vomiting, diarrhea, or diuretic use. Laboratory tests showed hypokalemia (2.80 mmol/L), hypomagnesemia (1.48 mg/dL), and metabolic alkalosis (pH 7.49, pCO2 35.9 mmHg, HCO3 27.4 mmol/L) in a normotensive setting. Serum osmolality was 290 mOsm/kg and urine osmolality was 547 mOsm/kg. Urine studies showed inappropriate renal losses with urine potassium of 41.21 mmol/L and urine chloride of 99.74 mmol/L. Spot urine calcium-creatinine ratio was elevated at 1.08, favoring a Bartter-like phenotype. The patient received intravenous and oral potassium and magnesium replacement and was started on spironolactone, while maintenance autoimmune therapy was continued. Serial monitoring showed correction of electrolyte abnormalities with marked clinical improvement. Conclusions Acquired Bartter-like tubulopathy should be considered in patients with autoimmune overlap disease who present with unexplained hypokalemic metabolic alkalosis and persistent urinary electrolyte wasting. Early nephrologic recognition allows timely electrolyte replacement, potassium-sparing therapy, and optimization of control of the underlying autoimmune condition. |