Case Quiz (August 2020)
A 9-year-old girl presented to the ER with carpopedal spasms and tingling numbness in hands. Patient endorsed tingling sensation in hand since a month which was intermittent and unrelated to wrist movement. She denied history of preceding trauma and swelling in hands. There was no history of similar complaints in the past or any prior surgery. She denied complaints like nausea, vomiting, and diarrhea. Tingling in hands was not associated with paresthesia in other extremities and sensory or motor deficits.
The patient had a past history of night fever, anorexia and weight loss. She was treated as a tuberculous case with no reponse to conventional first-class anti-tuberculous medications and was being treated with the following drugs for two months: amoxicillin-clavulanate, ethionamide, intramuscular capreomycin, linezolid, and para-aminosalicylate (PAS) granules.
Patient was afebrile and her initial vital signs were normal with a pulse of 84/min and blood pressure of 110/70 mm of Hg. On examination, flattening of chest wall on the left side was noted. Trail’s sign was positive with a deviation of the trachea to the left side. On auscultation of lung fields, breath sounds were diminished on the left. These findings suggested presence of tuberculous fibrosis in the left lung. No other stigmata of TB were noted and rest of the physical examination was unremarkable.
Initial blood-work at the time of presentation revealed a low serum calcium level of 6.49 mg/dL. Patient was hospitalized and detailed investigations were done. Other electrolyte abnormalities noted were as follows: serum sodium of 131 mEq/L, potassium of 1.9 mEq/L, chloride of 97 mEq/L, and magnesium of 0.7 mg/dL. Serum albumin was 4 g/dL. Serum creatinine was normal and remained so throughout the course of hospitalization. Her VBG showed pH of 7.5, HCO 3 of 30 mEq/L, and PaCO 2 of 30 mmHg. Routine urine examination revealed a 2–4 pus cells, 1-2 RBCs, and 1-2 epithelial cells, in the absence of proteinuria and glycosuria. Urine calcium/creatinine ratio was 0.49.
Vitamin D and serum parathyroid levels were found to be in the normal range.
Diagnostic tests were done
Case Answer (August 2020)
Acquired Bartter Syndrome Secondary to Aminoglycosides Bartter syndrome is an inherited renal tubulopathy affecting the loop of Henle (ascending limb) that manifests as hypochloremic metabolic alkalosis, hypokalemia, hypercalciuria, and mild hypomagnesemia. Acquired BS is clinically similar to the autosomal dominant phenotypic variant, that is, type 5 Bartter syndrome, which is due to a gain-of-function mutation in the calcium-sensing receptor (CaSR) in the thick ascending limb (TAL) of Henle’s loop.
Aminoglycoside-induced impaired mitochondrial protein synthesis and ATP generation have been hypothesized to be the cause of diffuse renal tubular dysfunction.
Treatment of aminoglycoside-induced Bartter syndrome predominantly consists of symptomatic correction of electrolytes and discontinuation of drug. Indomethacin, potassium-sparing diuretics, and/or aldosterone receptor antagonists have been also recommended,
