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Fluid, electrolyte and acid–base disorders associated with antibiotic therapy

Nature Reviews Nephrology volume 5, pages 193–202 (2009)Cite this article

Abstract

Antibiotics are among the most frequently prescribed drugs in medicine. Their use, however, is often limited by associated renal toxic effects. The most common manifestation of these toxic effects is decreased glomerular filtration rate. However, they can also occur while renal function remains near to normal. This Review focuses on antibiotic-associated fluid, electrolyte and acid–base disorders that do not greatly reduce glomerular filtration. Renal tubules can be affected by antibiotics at various locations. In the proximal tubule, toxic effects of tetracyclines and aminoglycosides can result in complete proximal tubular dysfunction, also known as Fanconi syndrome. Aminoglycosides (and capreomycin) can also affect the loop of Henle and lead to a Bartter-like syndrome. In the collecting ducts, antibiotics can cause a diverse range of disorders, including hyponatremia, hypokalemia, hyperkalemia, renal tubular acidosis, and nephrogenic diabetes insipidus. Causative antibiotics include trimethoprim, amphotericin B, penicillins, ciprofloxacin, demeclocycline and various antitubercular agents. Here, we describe the mechanisms that disrupt renal tubular function. Integrated with the physiology of each successive nephron segment, we discuss the receptors, transporters, channels or pores that are affected by antibiotics. This insight should pave the way for pathophysiology-directed treatment of these disorders.

Key Points

  • Renal tubular function can be affected by antibiotic treatment without a concurrent reduction in glomerular filtration rate

  • Hypokalemia is a frequent complication of antimicrobial therapy

  • Treatment with aminoglycosides can affect renal tubular function in several ways and can lead to hypokalemia, as well as acidosis and alkalosis

  • If unexpected disturbances in electrolyte and/or acid–base balance occur in a patient, their prescribed medications should be carefully checked

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Figure 1: Antibiotics that affect proximal tubule cells.
Figure 2: Antibiotics that affect the thick ascending limb of the loop of Henle.
Figure 3: Antibiotics that affect collecting-duct principal cells.
Figure 4: Antibiotics that affect collecting duct intercalated cells.

References

  1. Rougier, F. et al. Aminoglycoside nephrotoxicity. Curr. Drug Targets Infect. Disord. 4, 153–162 (2004).

    Article  CAS  PubMed  Google Scholar 

  2. Gonzalez, E. et al. Early steroid treatment improves the recovery of renal function in patients with drug-induced acute interstitial nephritis. Kidney Int. 73, 940–946 (2008).

    Article  CAS  PubMed  Google Scholar 

  3. Martinez-Salgado, C., Lopez-Hernandez, F. J. & Lopez-Novoa, J. M. Glomerular nephrotoxicity of aminoglycosides. Toxicol. Appl. Pharmacol. 223, 86–98 (2007).

    Article  CAS  PubMed  Google Scholar 

  4. Rodriguez-Barbero, A., Lopez-Novoa, J. M. & Arevalo, M. Involvement of platelet-activating factor in gentamicin nephrotoxicity in rats. Exp. Nephrol. 5, 47–54 (1997).

    CAS  PubMed  Google Scholar 

  5. Brown, R. S. Potassium homeostasis and clinical implications. Am. J. Med. 77, 3–10 (1984).

    Article  CAS  PubMed  Google Scholar 

  6. Izzedine, H., Launay-Vacher, V. & Deray, G. Antiviral drug-induced nephrotoxicity. Am. J. Kidney Dis. 45, 804–817 (2005).

    Article  CAS  PubMed  Google Scholar 

  7. Knepper, M. A. & Brooks, H. L. Regulation of the sodium transporters NHE3, NKCC2 and NCC in the kidney. Curr. Opin. Nephrol. Hypertens. 10, 655–659 (2001).

    Article  CAS  PubMed  Google Scholar 

  8. Boron, W. F. Acid–base transport by the renal proximal tubule. J. Am. Soc. Nephrol. 17, 2368–2382 (2006).

    Article  CAS  PubMed  Google Scholar 

  9. Igarashi, T. et al. Unraveling the molecular pathogenesis of isolated proximal renal tubular acidosis. J. Am. Soc. Nephrol. 13, 2171–2177 (2002).

    Article  PubMed  Google Scholar 

  10. Giebisch, G., Krapf, R. & Wagner, C. Renal and extrarenal regulation of potassium. Kidney Int. 72, 397–410 (2007).

    Article  CAS  PubMed  Google Scholar 

  11. Davies, J. & Davis, B. D. Misreading of ribonucleic acid code words induced by aminoglycoside antibiotics. The effect of drug concentration. J. Biol. Chem. 243, 3312–3316 (1968).

    CAS  PubMed  Google Scholar 

  12. Schmitz, C. et al. Megalin deficiency offers protection from renal aminoglycoside accumulation. J. Biol. Chem. 277, 618–622 (2002).

    Article  CAS  PubMed  Google Scholar 

  13. Beauchamp, D., Gourde, P. & Bergeron, M. G. Subcellular distribution of gentamicin in proximal tubular cells, determined by immunogold labeling. Antimicrob. Agents Chemother. 35, 2173–2179 (1991).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Bennett, W. M. et al. Microsomal protein synthesis inhibition: an early manifestation of gentamicin nephrotoxicity. Am. J. Physiol. 255, F265–F269 (1988).

    CAS  PubMed  Google Scholar 

  15. Weinberg, J. M., Harding, P. G. & Humes, H. D. Mechanisms of gentamicin-induced dysfunction of renal cortical mitochondria. II. Effects on mitochondrial monovalent cation transport. Arch. Biochem. Biophys. 205, 232–239 (1980).

    Article  CAS  PubMed  Google Scholar 

  16. Ramsammy, L. S., Josepovitz, C. & Kaloyanides, G. J. Gentamicin inhibits agonist stimulation of the phosphatidylinositol cascade in primary cultures of rabbit proximal tubular cells and in rat renal cortex. J. Pharmacol. Exp. Ther. 247, 989–996 (1988).

    CAS  PubMed  Google Scholar 

  17. Powell, J. H. & Reidenberg, M. M. Further studies of the response of kidney lysosomes to aminoglycosides and other cations. Biochem. Pharmacol. 32, 3213–3220 (1983).

    Article  CAS  PubMed  Google Scholar 

  18. Sassen, M. C. et al. Dysregulation of renal sodium transporters in gentamicin-treated rats. Kidney Int. 70, 1026–1037 (2006).

    Article  CAS  PubMed  Google Scholar 

  19. Nix, D. E. et al. Assessment of the enzymuria resulting from gentamicin alone and combinations of gentamicin with various β-lactam antibiotics. Ann. Pharmacother. 31, 696–703 (1997).

    Article  CAS  PubMed  Google Scholar 

  20. Banday, A. A. et al. Time dependent effects of gentamicin on the enzymes of carbohydrate metabolism, brush border membrane and oxidative stress in rat kidney tissues. Life Sci. 82, 450–459 (2008).

    Article  CAS  PubMed  Google Scholar 

  21. Chou, C. L. et al. Acquired Bartter-like syndrome associated with gentamicin administration. Am. J. Med. Sci. 329, 144–149 (2005).

    Article  PubMed  Google Scholar 

  22. Riccardi, D. et al. Localization of the extracellular Ca2+/polyvalent cation-sensing protein in rat kidney. Am. J. Physiol. 274, F611–F622 (1998).

    CAS  PubMed  Google Scholar 

  23. Ward, D. T., McLarnon, S. J. & Riccardi, D. Aminoglycosides increase intracellular calcium levels and ERK activity in proximal tubular OK cells expressing the extracellular calcium-sensing receptor. J. Am. Soc. Nephrol. 13, 1481–1489 (2002).

    Article  CAS  PubMed  Google Scholar 

  24. Ward, D. T. et al. Aminoglycosides induce acute cell signaling and chronic cell death in renal cells that express the calcium-sensing receptor. J. Am. Soc. Nephrol. 16, 1236–1244 (2005).

    Article  CAS  PubMed  Google Scholar 

  25. Gibbons, C. E. et al. Calcium-sensing receptor antagonism or lithium treatment ameliorates aminoglycoside-induced cell death in renal epithelial cells. Biochim. Biophys. Acta 1782, 188–195 (2008).

    Article  CAS  PubMed  Google Scholar 

  26. Alexandridis, G., Liberopoulos, E. & Elisaf, M. Aminoglycoside-induced reversible tubular dysfunction. Pharmacology 67, 118–120 (2003).

    Article  CAS  PubMed  Google Scholar 

  27. Melnick, J. Z., Baum, M. & Thompson, J. R. Aminoglycoside-induced Fanconi's syndrome. Am. J. Kidney Dis. 23, 118–122 (1994).

    Article  CAS  PubMed  Google Scholar 

  28. Ghiculescu, R. A. & Kubler, P. A. Aminoglycoside-associated Fanconi syndrome. Am. J. Kidney Dis. 48, e89–e93 (2006).

    Article  PubMed  Google Scholar 

  29. Etherington, C. et al. Measurement of urinary N-acetyl-β-D-glucosaminidase in adult patients with cystic fibrosis: before, during and after treatment with intravenous antibiotics. J. Cyst. Fibros. 6, 67–73 (2007).

    Article  CAS  PubMed  Google Scholar 

  30. Watanabe, A. et al. Targeted prevention of renal accumulation and toxicity of gentamicin by aminoglycoside binding receptor antagonists. J. Control Release 95, 423–433 (2004).

    Article  CAS  PubMed  Google Scholar 

  31. Nagai, J. & Takano, M. Molecular aspects of renal handling of aminoglycosides and strategies for preventing the nephrotoxicity. Drug Metab. Pharmacokinet. 19, 159–170 (2004).

    Article  CAS  PubMed  Google Scholar 

  32. Hemstreet, B. A. Antimicrobial-associated renal tubular acidosis. Ann. Pharmacother. 38, 1031–1038 (2004).

    Article  PubMed  Google Scholar 

  33. Babu, E. et al. Human organic anion transporters mediate the transport of tetracycline. Jpn J. Pharmacol. 88, 69–76 (2002).

    Article  CAS  PubMed  Google Scholar 

  34. Montoliu, J. et al. Lactic acidosis and Fanconi's syndrome due to degraded tetracycline. Br. Med. J. (Clin. Res. Ed.) 283, 1576–1577 (1981).

    Article  CAS  Google Scholar 

  35. Budkevich, T. V., El'skaya, A. V. & Nierhaus, K. H. Features of 80S mammalian ribosome and its subunits. Nucleic Acids Res. 36, 4736–4744 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Connell, S. R. et al. Ribosomal protection proteins and their mechanism of tetracycline resistance. Antimicrob. Agents Chemother. 47, 3675–3681 (2003).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Wirmer, J. & Westhof, E. Molecular contacts between antibiotics and the 30S ribosomal particle. Methods Enzymol. 415, 180–202 (2006).

    Article  CAS  PubMed  Google Scholar 

  38. Izzedine, H. et al. Drug-induced Fanconi's syndrome. Am. J. Kidney Dis. 41, 292–309 (2003).

    Article  CAS  PubMed  Google Scholar 

  39. Inselmann, G., Balaschke, M. & Heidemann, H. T. Enzymuria following amphotericin B application in the rat. Mycoses 46, 169–173 (2003).

    Article  CAS  PubMed  Google Scholar 

  40. Hebert, S. C: Bartter syndrome. Curr. Opin. Nephrol. Hypertens. 12, 527–532 (2003).

    Article  PubMed  Google Scholar 

  41. Shiah, C. J. et al. Acute muscular paralysis in an adult with subclinical Bartter's syndrome associated with gentamicin administration. Am. J. Kidney Dis. 24, 932–935 (1994).

    Article  CAS  PubMed  Google Scholar 

  42. Landau, D. & Kher, K. K. Gentamicin-induced Bartter-like syndrome. Pediatr. Nephrol. 11, 737–740 (1997).

    Article  CAS  PubMed  Google Scholar 

  43. Pollak, M. R. et al. Autosomal dominant hypocalcaemia caused by a Ca2+-sensing receptor gene mutation. Nat. Genet. 8, 303–307 (1994).

    Article  CAS  PubMed  Google Scholar 

  44. Shin, S. et al. Hypokalemia among patients receiving treatment for multidrug-resistant tuberculosis. Chest 125, 974–980 (2004).

    Article  PubMed  Google Scholar 

  45. Steiner, R. W. & Omachi, A. S. A Bartter's-like syndrome from capreomycin, and a similar gentamicin tubulopathy. Am. J. Kidney Dis. 7, 245–249 (1986).

    Article  CAS  PubMed  Google Scholar 

  46. Ecelbarger, C. A. & Tiwari, S. Sodium transporters in the distal nephron and disease implications. Curr. Hypertens. Rep. 8, 158–165 (2006).

    Article  CAS  PubMed  Google Scholar 

  47. Alexander, R. T., Hoenderop, J. G. & Bindels, R. J. Molecular determinants of magnesium homeostasis: insights from human disease. J. Am. Soc. Nephrol. 19, 1451–1458 (2008).

    Article  CAS  PubMed  Google Scholar 

  48. Nijenhuis, T. et al. Enhanced passive Ca2+ reabsorption and reduced Mg2+ channel abundance explains thiazide-induced hypocalciuria and hypomagnesemia. J. Clin. Invest. 115, 1651–1658 (2005).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. Finton, C. K. et al. Gentamicin-induced hypomagnesemia. Am. Surg. 49, 576–578 (1983).

    CAS  PubMed  Google Scholar 

  50. Elliott, C., Newman, N. & Madan, A. Gentamicin effects on urinary electrolyte excretion in healthy subjects. Clin. Pharmacol. Ther. 67, 16–21 (2000).

    Article  CAS  PubMed  Google Scholar 

  51. Kang, H. S. et al. Aminoglycosides inhibit hormone-stimulated Mg2+ uptake in mouse distal convoluted tubule cells. Can. J. Physiol. Pharmacol. 78, 595–602 (2000).

    Article  CAS  PubMed  Google Scholar 

  52. Fenton, R. A. & Knepper, M. A. Mouse models and the urinary concentrating mechanism in the new millennium. Physiol. Rev. 87, 1083–1112 (2007).

    Article  CAS  PubMed  Google Scholar 

  53. Kamel, K. S. et al. A new classification for renal defects in net acid excretion. Am. J. Kidney Dis. 29, 136–146 (1997).

    Article  CAS  PubMed  Google Scholar 

  54. Mori, H. et al. Hyponatremia and/or hyperkalemia in patients treated with the standard dose of trimethoprim–sulfamethoxazole. Intern. Med. 42, 665–669 (2003).

    Article  CAS  PubMed  Google Scholar 

  55. Perazella, M. A. Trimethoprim is a potassium-sparing diuretic like amiloride and causes hyperkalemia in high-risk patients. Am. J. Ther. 4, 343–348 (1997).

    Article  CAS  PubMed  Google Scholar 

  56. Ahn, Y. H. & Goldman, J. M. Trimethoprim–sulfamethoxazole and hyponatremia. Ann. Intern. Med. 103, 161–162 (1985).

    Article  CAS  PubMed  Google Scholar 

  57. Muto, S. et al. Effect of trimethoprim–sulfamethoxazole on Na+ and K+ transport properties in the rabbit cortical collecting duct perfused in vitro. Nephron Physiol. 102, p51–p60 (2006).

    Article  CAS  PubMed  Google Scholar 

  58. Don, B. R. The effect of trimethoprim on potassium and uric acid metabolism in normal human subjects. Clin. Nephrol. 55, 45–52 (2001).

    CAS  PubMed  Google Scholar 

  59. Eiam-Ong, S., Kurtzman, N. A. & Sabatini, S. Studies on the mechanism of trimethoprim-induced hyperkalemia. Kidney Int. 49, 1372–1378 (1996).

    Article  CAS  PubMed  Google Scholar 

  60. Perazella, M. A. Trimethoprim-induced hyperkalaemia: clinical data, mechanism, prevention and management. Drug Saf. 22, 227–236 (2000).

    Article  CAS  PubMed  Google Scholar 

  61. Reiser, I. W. et al. Reversal of trimethoprim-induced antikaliuresis. Kidney Int. 50, 2063–2069 (1996).

    Article  CAS  PubMed  Google Scholar 

  62. Schreiber, M. et al. Antikaliuretic action of trimethoprim is minimized by raising urine pH. Kidney Int. 49, 82–87 (1996).

    Article  CAS  PubMed  Google Scholar 

  63. Lin, S. H. et al. Reversible voltage-dependent distal renal tubular acidosis in a patient receiving standard doses of trimethoprim sulfamethoxazole. Nephrol. Dial. Transplant. 12, 1031–1033 (1997).

    Article  CAS  PubMed  Google Scholar 

  64. Sawaya, B. P., Briggs, J. P. & Schnermann, J. Amphotericin B nephrotoxicity: the adverse consequences of altered membrane properties. J. Am. Soc. Nephrol. 6, 154–164 (1995).

    CAS  PubMed  Google Scholar 

  65. Wingard, J. R. et al. Clinical significance of nephrotoxicity in patients treated with amphotericin B for suspected or proven aspergillosis. Clin. Infect. Dis. 29, 1402–1407 (1999).

    Article  CAS  PubMed  Google Scholar 

  66. Burges, J. L. & Birchall, R. Nephrotoxicity of amphotericin B, with emphasis on changes in tubular function. Am. J. Med. 53, 77–84 (1972).

    Article  CAS  PubMed  Google Scholar 

  67. Lucas da Silva, P. S., Iglesias, S. B. & Waisberg, J. Hypokalemic rhabdomyolysis in a child due to amphotericin B therapy. Eur. J. Pediatr. 166, 169–171 (2007).

    Article  PubMed  Google Scholar 

  68. Gerkens, J. F. & Branch, R. A. The influence of sodium status and furosemide on canine acute amphotericin B nephrotoxicity. J. Pharmacol. Exp. Ther. 214, 306–311 (1980).

    CAS  PubMed  Google Scholar 

  69. Bernardo, J. F. et al. Potassium depletion potentiates amphotericin-B-induced toxicity to renal tubules. Nephron 70, 235–241 (1995).

    Article  CAS  PubMed  Google Scholar 

  70. Wazny, L. D. & Brophy, D. F. Amiloride for the prevention of amphotericin B-induced hypokalemia and hypomagnesemia. Ann. Pharmacother. 34, 94–97 (2000).

    Article  CAS  PubMed  Google Scholar 

  71. Ural, A. U. et al. Spironolactone: is it a novel drug for the prevention of amphotericin B-related hypokalemia in cancer patients? Eur. J. Clin. Pharmacol. 57, 771–773 (2002).

    Article  CAS  PubMed  Google Scholar 

  72. Mohan, S. et al. Proteinuria lowers the risk of amphotericin B-associated hypokalaemia. J. Antimicrob. Chemother. 60, 690–693 (2007).

    Article  CAS  PubMed  Google Scholar 

  73. Steinmetz, P. R. & Lawson, L. R. Defect in urinary acidification induced in vitro by amphotericin B. J. Clin. Invest. 49, 596–601 (1970).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  74. Barbour, G. L. et al. Vasopressin-resistant nephrogenic diabetes insipidus. A result of amphotericin B therapy. Arch. Intern. Med. 139, 86–88 (1979).

    Article  CAS  PubMed  Google Scholar 

  75. Frokiaer, J. et al. Pathophysiology of aquaporin-2 in water balance disorders. Am. J. Med. Sci. 316, 291–299 (1998).

    CAS  PubMed  Google Scholar 

  76. Butler, W. T. et al. Nephrotoxicity of amphotericin B; early and late effects in 81 patients. Ann. Intern. Med. 61, 175–187 (1964).

    Article  CAS  PubMed  Google Scholar 

  77. Canada, T. W., Weavind, L. M. & Augustin, K. M. Possible liposomal amphotericin B-induced nephrogenic diabetes insipidus. Ann. Pharmacother. 37, 70–73 (2003).

    Article  PubMed  Google Scholar 

  78. Yano, Y., Monteiro, J. L. & Seguro, A. C. Effect of amphotericin B on water and urea transport in the inner medullary collecting duct. J. Am. Soc. Nephrol. 5, 68–74 (1994).

    CAS  PubMed  Google Scholar 

  79. Kim, S. W. et al. Amphotericin B decreases adenylyl cyclase activity and aquaporin-2 expression in rat kidney. J. Lab. Clin. Med. 138, 243–249 (2001).

    Article  CAS  PubMed  Google Scholar 

  80. Hoorn, E. J. & Zietse, R. Combined renal tubular acidosis and diabetes insipidus in hematological disease. Nat. Clin. Pract. Nephrol. 3, 171–175 (2007).

    Article  PubMed  Google Scholar 

  81. El-Sheikh, A. A., Masereeuw, R. & Russel, F. G. Mechanisms of renal anionic drug transport. Eur. J. Pharmacol. 585, 245–255 (2008).

    Article  CAS  PubMed  Google Scholar 

  82. Hirji, M. R. & Mucklow, J. C. Transepithelial water movement in response to carbamazepine, chlorpropamide and demeclocycline in toad urinary bladder. Br. J. Pharmacol. 104, 550–553 (1991).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  83. Kinzie, B. J. Management of the syndrome of inappropriate secretion of antidiuretic hormone. Clin. Pharm. 6, 625–633 (1987).

    CAS  PubMed  Google Scholar 

  84. Brunner, F. P. & Frick, P. G. Hypokalaemia, metabolic alkalosis, and hypernatraemia due to “massive” sodium penicillin therapy. Br. Med. J. 4, 550–552 (1968).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  85. Lipner, H. I. et al. The behavior of carbenicillin as a nonreabsorbable anion. J. Lab. Clin. Med. 86, 183–194 (1975).

    CAS  PubMed  Google Scholar 

  86. Hoorn, E. J. & Zietse, R. Severe hypokalaemia caused by flucloxacillin. J. Antimicrob. Chemother. 61, 1396–1398 (2008).

    Article  CAS  PubMed  Google Scholar 

  87. Bustamante, M. et al. Calcium-sensing receptor attenuates AVP-induced aquaporin-2 expression via a calmodulin-dependent mechanism. J. Am. Soc. Nephrol. 19, 109–116 (2008).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  88. Gordon, J. A. et al. The renal concentrating defect after gentamicin administration in the rat. J. Lab. Clin. Med. 101, 903–910 (1983).

    CAS  PubMed  Google Scholar 

  89. Blazes, D. L. & Decker, C. F. Symptomatic hyperlactataemia precipitated by the addition of tetracycline to combination antiretroviral therapy. Lancet Infect. Dis. 6, 249–252 (2006).

    Article  CAS  PubMed  Google Scholar 

  90. Wiener, M. et al. Lactic acidosis after treatment with linezolid. Infection 35, 278–281 (2007).

    Article  CAS  PubMed  Google Scholar 

  91. De Vriese, A. S. et al. Linezolid-induced inhibition of mitochondrial protein synthesis. Clin. Infect. Dis. 42, 1111–1117 (2006).

    Article  CAS  PubMed  Google Scholar 

  92. Coronado, B. E., Opal, S. M. & Yoburn, D. C. Antibiotic-induced D-lactic acidosis. Ann. Intern. Med. 122, 839–842 (1995).

    Article  CAS  PubMed  Google Scholar 

  93. Halperin, M. L. & Kamel, K. S. D-lactic acidosis: turning sugar into acids in the gastrointestinal tract. Kidney Int. 49, 1–8 (1996).

    Article  CAS  PubMed  Google Scholar 

  94. Fenves, A. Z. et al. Increased anion gap metabolic acidosis as a result of 5-oxoproline (pyroglutamic acid): a role for acetaminophen. Clin. J. Am. Soc. Nephrol. 1, 441–447 (2006).

    Article  CAS  PubMed  Google Scholar 

  95. Peter, J. V. et al. An unusual cause of severe metabolic acidosis. Med. J. Aust. 185, 223–225 (2006).

    PubMed  Google Scholar 

  96. Rolleman, E. J. et al. Guilty as charged: unmeasured urinary anions in a case of pyroglutamic acidosis. Neth. J. Med. 66, 351–353 (2008).

    CAS  PubMed  Google Scholar 

  97. Adler, D. et al. SIADH consecutive to ciprofloxacin intake. Eur. J. Intern. Med. 15, 463–464 (2004).

    Article  PubMed  Google Scholar 

  98. Kushner, J. M., Peckman, H. J. & Snyder, C. R. Seizures associated with fluoroquinolones. Ann. Pharmacother. 35, 1194–1198 (2001).

    Article  CAS  PubMed  Google Scholar 

  99. Chitre, M. M. & Berenson, C. S. Idiosyncratic rifabutin-induced leukopenia and SIADH: case report and review. Pharmacotherapy 21, 493–497 (2001).

    Article  CAS  PubMed  Google Scholar 

  100. Holmes, A. M., Hesling, C. M. & Wilson, T. M. Capreomycin-induced serum electrolyte abnormalities. Thorax 25, 608–611 (1970).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  101. Nakashita, T. & Motojima, S. Case of SIADH caused by ethionamide in a patient with pulmonary tuberculosis [Japanese]. Kekkaku 81, 731–735 (2006).

    PubMed  Google Scholar 

  102. Thiele, A. & Rehman, H. U. Hyperkalemia caused by penicillin. Am. J. Med. 121, e1–e2 (2008).

    Article  CAS  PubMed  Google Scholar 

  103. Barcia, J. P. Hyperkalemia associated with rapid infusion of conventional and lipid complex formulations of amphotericin B. Pharmacotherapy 18, 874–876 (1998).

    CAS  PubMed  Google Scholar 

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  1. Department of Nephrology, Erasmus Medical Centre, Rotterdam, The Netherlands

    R. Zietse, R. Zoutendijk & E. J. Hoorn

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Zietse, R., Zoutendijk, R. & Hoorn, E. Fluid, electrolyte and acid–base disorders associated with antibiotic therapy. Nat Rev Nephrol 5, 193–202 (2009). https://doi.org/10.1038/nrneph.2009.17

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