ONE STONE, TWO BIRDS: PATIROMER TARGETS BOTH POTASSIUM AND PHOSPHORUS IN CKD

 

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ONE STONE, TWO BIRDS: PATIROMER TARGETS BOTH POTASSIUM AND PHOSPHORUS IN CKD

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J. Emilio
Sanchez-Alvarez
J. Emilio Sanchez-Alvarez jesastur@gmail.com Hospital Universitario Central de Asturias Nephrology Oviedo Spain *
Nerea Molina nereamolinaA1997@gmail.com Hospital Universitario Central de Asturias Nephrology Oviedo Spain -
David García-Cousillas davidporrua5@gmail.com Hospital Universitario Central de Asturias Nephrology Oviedo Spain -
Enriqueta Gonzalez mariagr.3111@gmail.com Hospital de la Cruz Roja Nephrology Gijón Spain -
Carmen Merino-Bueno carmenmbueno@gmail.com Hospital de Cabueñes Nephrology Gijón Spain -
Eduardo Deras drderas07@gmail.com Hospital Carmen y Severo Ochoa Nephrology Cangas de Narcea Spain -
Catalina Ulloa-Clavijo catalinaulloac@hotmail.com Clínica Universitaria de Navarra Nephrology Pamplona Spain -
Jose Luis Pérez-Canga jlperezcanga@gmail.com Hospital San Agustín Nephrology Avilés Spain -
Pedro Barrera-Baena pedrobb93@gmail.com Hospital de Cabueñes Nephrology Gijón Spain -
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Disorders of bone and mineral metabolism are common in patients with chronic kidney disease (CKD). Elevated serum phosphorus contributes to bone disease, vascular calcification, and higher mortality, so any strategy aimed at lowering it is desirable. Hyperkalemia is also frequent in CKD, particularly in hemodialysis (HD) patients, and is associated with increased morbidity and mortality. Patiromer, a recently introduced potassium binder, may also influence mineral metabolism due to its calcium content.

We conducted a multicenter, prospective, real-world study to assess the effect of patiromer on biochemical parameters of bone and mineral metabolism, particularly serum phosphorus, in CKD stages 3–5. Patiromer was prescribed for chronic hyperkalemia. Epidemiological and clinical data were collected, and serum potassium, calcium, magnesium, and phosphorus levels were analyzed over time.

Fifty-two patients (mean age 71±12 years; 75% male; 63% diabetic; 54% with heart failure; 48% on phosphate binders) were included. Regarding CKD stage, 17% were in stage 3b, 31% in stage 4, 38% in stage 5 (non-dialysis), and 13% on HD. Forty-six patients completed six months of follow-up; two died, two received a kidney transplant, and two were transferred. All patients started patiromer at 8.4 g once daily; only one required dose doubling. Patiromer use led to a 27% reduction in serum potassium (5.9 to 4.6 mEq/L; P<0.001). No significant changes were observed in serum calcium or magnesium. Serum phosphorus decreased by 18% (5.1 to 4.2 mg/dL; P=0.022), without changes in diet or phosphate binder therapy. The decrease in phosphate correlated with baseline phosphate levels (r=0.367; P=0.039). Patiromer was well tolerated; only two patients reported mild constipation, and no treatment discontinuations occurred.

Patiromer is effective and well tolerated for reducing serum potassium in CKD. Its calcium content may also lower serum phosphorus by reducing intestinal phosphorus absorption, similar to calcium-based phosphate binders. Patiromer might therefore have a dual role in CKD management—addressing both hyperkalemia and hyperphosphatemia.

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