Acquired Bartters Syndrome: A Rare Metabolic Abnormality Induced by Streptomycin

Shazia Durdan^*, Mohammad Shoaib Zaheer, Syed Hasan Amir and Shadab Ahmad Khan
^*Correspondence: Shazia Durdan, Department of Medicine, Jawaharlal Nehru Medical College, A.M.U, Aligarh, India, Email:

Keywords

Acquired Bartter’s Syndrome • Electrolyte wasting • Streptomycin

Introduction

Aminoglycosides, polyvalent cationic antibiotics, are widely prescribed in the treatment of gram negative infections. Aminoglycoside induced nephrotoxicities can have varied presentations such as interstitial nephritis and nonoliguric renal failure [1]. Other less common adverse effects include Fanconi-like syndrome or Bartter syndrome [2]. Aminoglycoside induced renal tubular dysfunction has been reported with gentamicin and tobramycin [3], however, there are only few case reports of bartter’s syndrome associated with streptomycin to the best of our knowledge [4].

Case Presentation

A 38-years-old male, diagnosed as a case of pulmonary tuberculosis, on antituberculous treatment for 1 month presented to our hospital with complains of frequent episodes of vomiting. On admission, his blood pressure was 100/60 mmHg, pulse 105 beats/min, respiratory rate 22 breaths/min, and body temperature 98.2°F. Right upper quadrant tenderness without rebound tenderness was noted. The remainder of the physical examination was unremarkable. Serum biochemistries suggested deranged liver function tests [AST-219 U/L, ALT-42 U/L, ALP-13I U/L, T. Bil-5.1 mg/dl, D. Bil-3.8 mg/dl] however renal function tests and serum electrolytes, were within the normal range. Ultrasonographic scan suggested mildly coarse echo texture of liver with minimal free fluid in perisplenic and interbowel spaces. Alternative causes for elevated liver function tests including alcohol, acetaminophen, viral hepatitis, gallstones, and biliary obstruction were excluded, and a diagnosis of ATTinduced hepatitis was made and subsequently patient was shifted to modified ATT regimen containing Ethambutol, Levofloxacin and Streptomycin. On the fifth day of streptomycin administration, patient reported anorexia, lethargy and generalized weakness. Chvostek and Trousseau signs were although, absent. ECG showed low-voltage QRS complexes. Laboratory investigations revealed pH 7.59, PCO₂ 33 mmHg, PO₂ 160 mmHg, SO₂ 98%, sodium 126 mmol/L, potassium 1.2 mmol/L, serum magnesium 1.05 mg/dl, bicarbonate 32.4 mmol/L, and ionized calcium 0.41 mmol/L suggesting profound hypokalemia, hyponatremia, hypomagnesemia, hypocalcemia, and metabolic alkalosis. Serum immunoreactive parathyroid hormone concentration was elevated secondary to hypocalcemia. These abnormalities persisted for many days as evidenced by Table 1. Streptomycin was subsequently discontinued, and intravenous supplementation of magnesium sulfate, calcium gluconate, and potassium chloride was started, and serum electrolytes returned to normal, as depicted in Table 1.

Discussion

Aminoglycosides are associated with various toxicities including vestibular, cochlear and renal toxicity. Aminoglycoside-induced renal tubular dysfunction can either present as Fanconi-like syndrome with involvement of proximal tubules and manifesting as metabolic acidosis, hypophosphatemia, aminoaciduria and glucosuria as well as frequent elevations in serum creatinine, or as Bartter-like syndrome with distal renal tubule dysfunction, characterized by hypokalemic metabolic alkalosis, hypocalcemia, and hypomagnesemia without a significant elevation of serum creatinine [5]. In our patient, streptomycin-induced Bartterlike syndrome was diagnosed as other causative factors such as poor intake, vomiting, persistent diarrhea, massive glucosuria, and diuretic use were excluded, and the features of Bartter-like syndrome resolved upon withdrawal of streptomycin. Exact mechanisms culminating in aminoglycoside induced Bartter’s syndrome remains elusive; however, it may be similar to hereditary variant of Bartter's disease involving a transporter defect in thick ascending limb of loop of Henle with subsequent renal wasting of Sodium, Potassium, Chloride, Ca, and Magnesium.

Conclusion

This case report highlights the occurrence of Bartter-like syndrome as one of the rare complications of streptomycin therapy emphasizing the fact that streptomycin-induced renal dysfunction may represent significantly underreported cause of Bartter-like syndrome. Thus, acquired Bartterlike syndrome should be kept in mind as a complication of aminoglycoside therapy, and close monitoring of serum and urine electrolytes is warranted during aminoglycoside therapy. Early diagnosis and prompt correction of these electrolyte and acid-base imbalances can reduce the risk of potentially lifethreatening complications.

References

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2. Singh Jaipal, Kamlesh Kumar and Shailesh Mani. “Acquired Bartter Syndrome Following Gentamicin Therapy.” Ind J Nephrol 26 (2016): 461.
3. William Slayton, Dana Anstine, Farahaba Lakhdir and John Sleasman, et al. “Tetany in a Child with AIDS Receiving Intravenous Tobramycin.” South Med J 89 (1996): 1108-1110.
4. Brezis, Mayer. “Metabolic Abnormality Induced by Streptomycin.” Brit Med J 309 (1994): 512.
5. George Alexandridis, Evagelos Liberopoulos and Moses Elisaf. “Aminoglycoside-Induced Reversible Tubular Dysfunction.” Pharmacol 67 (2003): 118-120.