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Type 4 renal tubular acidosis in a kidney transplant recipient

We report a case of a 66-year-old diabetic patient who presented with muscle weakness 2 weeks after kidney transplantation. Her immunosuppressive regimen included tacrolimus, mycophenolate mofetil, and steroids. She was found to have hyperkalemia and normal anion gap metabolic acidosis. Tacrolimus l...

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Detalles Bibliográficos
Autor principal: Kulkarni, Manjunath
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Chang Gung University 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6138773/
https://www.ncbi.nlm.nih.gov/pubmed/27105603
http://dx.doi.org/10.1016/j.bj.2015.08.008
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author Kulkarni, Manjunath
author_facet Kulkarni, Manjunath
author_sort Kulkarni, Manjunath
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description We report a case of a 66-year-old diabetic patient who presented with muscle weakness 2 weeks after kidney transplantation. Her immunosuppressive regimen included tacrolimus, mycophenolate mofetil, and steroids. She was found to have hyperkalemia and normal anion gap metabolic acidosis. Tacrolimus levels were in therapeutic range. All other drugs such as beta blockers and trimethoprim – sulfamethoxazole were stopped. She did not respond to routine antikalemic measures. Further evaluation revealed type 4 renal tubular acidosis. Serum potassium levels returned to normal after starting sodium bicarbonate and fludrocortisone therapy. Though hyperkalemia is common in kidney transplant recipients, determining exact cause can guide specific treatment.
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spelling pubmed-61387732018-09-27 Type 4 renal tubular acidosis in a kidney transplant recipient Kulkarni, Manjunath Biomed J Correspondence We report a case of a 66-year-old diabetic patient who presented with muscle weakness 2 weeks after kidney transplantation. Her immunosuppressive regimen included tacrolimus, mycophenolate mofetil, and steroids. She was found to have hyperkalemia and normal anion gap metabolic acidosis. Tacrolimus levels were in therapeutic range. All other drugs such as beta blockers and trimethoprim – sulfamethoxazole were stopped. She did not respond to routine antikalemic measures. Further evaluation revealed type 4 renal tubular acidosis. Serum potassium levels returned to normal after starting sodium bicarbonate and fludrocortisone therapy. Though hyperkalemia is common in kidney transplant recipients, determining exact cause can guide specific treatment. Chang Gung University 2016-02 2016-03-29 /pmc/articles/PMC6138773/ /pubmed/27105603 http://dx.doi.org/10.1016/j.bj.2015.08.008 Text en © 2016 Chang Gung University. Publishing services by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Correspondence
Kulkarni, Manjunath
Type 4 renal tubular acidosis in a kidney transplant recipient
title Type 4 renal tubular acidosis in a kidney transplant recipient
title_full Type 4 renal tubular acidosis in a kidney transplant recipient
title_fullStr Type 4 renal tubular acidosis in a kidney transplant recipient
title_full_unstemmed Type 4 renal tubular acidosis in a kidney transplant recipient
title_short Type 4 renal tubular acidosis in a kidney transplant recipient
title_sort type 4 renal tubular acidosis in a kidney transplant recipient
topic Correspondence
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6138773/
https://www.ncbi.nlm.nih.gov/pubmed/27105603
http://dx.doi.org/10.1016/j.bj.2015.08.008
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