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Changes in Serum and Urinary Potassium Handling Associated with Renin-Angiotensin-Aldosterone System Inhibitors in Advanced Chronic Kidney Disease Patients

Objective This study aimed to (i) compare the extent of urinary potassium (K(+)) excretion in addition to the changes in serum K(+) concentration: and (ii) clarify the association between changes in serum K(+) concentration, urinary K(+) excretion, and acid-base status with or without renin-angioten...

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Detalles Bibliográficos
Autores principales: Ueda, Yuichiro, Ookawara, Susumu, Miyazawa, Haruhisa, Ito, Kiyonori, Hirai, Keiji, Hoshino, Taro, Morishita, Yoshiyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6820673/
https://www.ncbi.nlm.nih.gov/pubmed/31695981
http://dx.doi.org/10.7759/cureus.5561
Descripción
Sumario:Objective This study aimed to (i) compare the extent of urinary potassium (K(+)) excretion in addition to the changes in serum K(+) concentration: and (ii) clarify the association between changes in serum K(+) concentration, urinary K(+) excretion, and acid-base status with or without renin-angiotensin-aldosterone system (RAAS) inhibitors in patients with advanced chronic kidney disease (CKD) stages. Methods Six hundred and ninety-one patients with advanced CKD (CKD G3b, 161; G4, 271; G5, 259) were retrospectively evaluated. Differences in serum K(+) concentration, urinary K(+) excretion, and serum sodium and chloride differences (Na(+)−Cl(-)) were compared among patients with RAAS inhibitors, RAAS inhibitors and diuretic agents, and without either medication in each CKD stage. Results Serum K(+) concentrations in patients with RAAS inhibitors were significantly higher than in those with RAAS inhibitors and diuretics in CKD stage G3b and the other two treatment groups in CKD stage G4. Urinary K(+) excretion among the three groups did not differ significantly in each CKD stage. Serum Na(+)−Cl(-) differences in patients with RAAS inhibitors were significantly smaller than in those with RAAS inhibitors and diuretics in CKD stages G3b (p = 0.006) and the other two groups in CKD stage G4 (vs. RAAS inhibitors and diuretics, p <0.001; vs. without either medication, p = 0.008). Conclusion Our study demonstrated that RAAS inhibitor use might be associated with hyperkalemia via not decreased urinary K(+) excretion but rather K(+) redistribution from intracellular to extracellular fluid induced by the progression of metabolic acidosis in patients with advanced CKD, particularly stages G3b and G4.