Abstract

Background: Patients with chronic kidney disease, CK, due to diabetes, DM, and hypertension, HTN, are at risk of rapid progression. The addition of a non-steroidal mineralocorticoid antagonist, finerenone, reduces blood pressure and retards CKD progression. However, it causes a rise in serum potassium, K, of about 0.23 mmol per L. We examined the serum potassium of CKD patients with and without DM by kidney function. Methods: We analyzed data from the Asian Kidney Disease Study. There were 232 CKD patients who underwent measured glomerular filtration rate, GFR, mL per min per 1.73 m2. There were 51 percent male, mean age 58.4, 12.8; 51 percent had DM, 119 of 232, median GFR 47, IQR 29–67. There were 185 of 232 patients using renin-angiotensin system, RAS, blockers. We stratified analyses by groups of K above 4.8, threshold for initiation of finerenone and by GFR above and below 25 where the risks of hyperkalemia is highest. Results: Overall, mean K is 4.35, 0.54. K is negatively associated with GFR; 4.596–0.0048 x GFR; p is 0.0002. There is no difference in serum potassium by use of RAS blockers, 185 of 232. Mean K was higher in DM patients 4.45, 0.58 vs. 4.24, 0.47; P is 0.0023. In patients with GFR below 25, there were 8 of 34 or 23.5 percent with K above 4.8, and 26 of 198 or 13.1% with K above 4.8 and GFR above 25. In DM CKD patients with GFR below 25, 6 of 18 or 33.3 percent had K above 4.8; and 16 of 95 or 16.8 percent had K above 4.8 with GFR above 25. Conclusions: There was 16.8 percent of DM CKD patients with GFR above 25 who had K above 4.8 who would require potassium binders in order to start finerenone.

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