https://doi.org/10.4081/ecj.2025.13710
Telmisartan-induced type 4 renal tubular acidosis: a case report
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Published: 24 June 2025
Hyperkalemia is a common electrolyte disturbance in hospitalized patients, often caused by impaired renal potassium excretion due to hypoaldosteronism. Type 4 Renal Tubular Acidosis (RTA), commonly associated with diabetes mellitus and RAAS-inhibiting medications, is a significant consequence. We report a 56-year-old male with diabetes, hypertension, and coronary artery disease who developed type 4 RTA after starting telmisartan post-hip replacement. His course was complicated by pneumonia and worsening hyperkalemia, with arterial blood gas showing Normal Anion Gap Metabolic Acidosis (NAGMA) and a positive urinary anion gap. Discontinuing telmisartan and initiating hydrocortisone led to significant renal function improvement and potassium normalization. This case highlights the importance of caution when using RAAS inhibitors in high-risk patients and supports hydrocortisone as a viable alternative when fludrocortisone is unavailable.
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Phelps KR, Lieberman RL, Oh MS, et al. Pathophysiology of the syndrome of hyporeninemic hypoaldosteronism. Metabolism 1980;29:186–99. DOI: https://doi.org/10.1016/0026-0495(80)90145-6
Sousa AGP, Cabral JV de S, El-Feghaly WB, et al. Hyporeninemic hypoaldosteronism and diabetes mellitus: pathophysiology assumptions, clinical aspects and implications for management. World J Diabetes 2016;7:101–11. DOI: https://doi.org/10.4239/wjd.v7.i5.101
Farkas J. Non-anion-gap metabolic acidosis (NAGMA). EMCrit Project. Available from: https://emcrit.org/ibcc/nagma/
Galbiati F. Type IV RTA in chronic adrenal insufficiency and concomitant lisinopril treatment. Case Rep Endocrinol 2020;2020:8897112. DOI: https://doi.org/10.1155/2020/8897112
Harris AN, Grimm PR, Lee HW, et al. Mechanism of hyperkalemia-induced metabolic acidosis. J Am Soc Nephrol 2018;29:1411. DOI: https://doi.org/10.1681/ASN.2017111163
Bello CHPRT, Duarte JS, Vasconcelos C, et al. Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review. J Bras Nefrol 2017;39:481-5. DOI: https://doi.org/10.5935/0101-2800.20170086
Palmer BF, Kelepouris E, Clegg DJ. Renal tubular acidosis and management strategies: a narrative review. Adv Ther 2021;38:949–68. DOI: https://doi.org/10.1007/s12325-020-01587-5
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