Effect of Intravenous Ferric Carboxymaltose Treatment on Serum Phosphorus Levels in Non-Dialysis Patients with Chronic Kidney Disease: A Retrospective Observational Study

Abstract

ABSTRACT Objective: Anemia is common in chronic kidney disease (CKD), particularly when the glomerular filtration rate (GFR) falls below 30 mL/min/1.73m2. Iron deficiency exacerbates anemia, and intravenous ferric carboxymaltose (FCM) is frequently used due to its rapid iron delivery and low risk of hypersensitivity. However, FCM has been linked to hypophosphatemia, with limited data in non-dialysis CKD patients. This study evaluated the occurrence of hypophosphatemia and changes in serum phosphorus after FCM therapy in this population. Methods: We retrospectively analyzed 113 adult non-dialysis CKD patients (stages 3A–5) who received intravenous FCM for iron deficiency anemia between 2022 and 2023. Patients had baseline and 1-month serum phosphorus and creatinine measurements; those with dialysis, acute infection, malignancy, active inflammation, phosphate binder use, or documented malnutrition were excluded. Phosphorus changes were compared across CKD stages, and factors associated with hypophosphatemia (<2.5 mg/dL) were assessed using paired t-tests, one-way ANOVA, correlation, and regression analyses. Results: Baseline mean phosphorus was 3.62 ± 1.10 mg/dL, creatinine 2.35 ± 1.42 mg/dL, and eGFR 30.16 ± 13.59 mL/min/1.73m2. FCM administration resulted in a modest but statistically significant decrease in serum phosphorus to 3.49 ± 1.05 mg/dL (mean change: −0.137 mg/dL, p < 0.001). Serum phosphorus decreased across all CKD stages, and the magnitude of reduction did not differ significantly between stages. Hypophosphatemia (<2.5 mg/dL) occurred in 12.3% of patients, most frequently in stages 3 and 4, with no cases observed in stage 5. Those who developed hypophosphatemia had significantly lower baseline phosphorus than those who did not (3.04 ± 0.69 vs. 3.71 ± 1.13 mg/dL, p = 0.005). Phosphorus change correlated with baseline phosphorus (r = 0.488, p < 0.001) but not with baseline creatinine (p = 0.077). No significant associations were found with age, gender, parathyroid hormone, vitamin D, or hemoglobin. Conclusion: In non-dialysis CKD patients, FCM causes a small but significant decline in serum phosphorus, with clinically significant hypophosphatemia being uncommon. Lower baseline phosphorus increases susceptibility, underscoring the need for pre-treatment assessment and targeted post-treatment monitoring. While advanced CKD may confer lower risk due to impaired phosphate excretion, these results should be interpreted cautiously given the retrospective design and absence of mineral metabolism markers. Findings may inform individualized iron therapy strategies and support the inclusion of phosphorus monitoring in CKD anemia management protocols.

Keywords

• Chronic Kidney Disease
• Non-Dialysis
• Ferric Carboxymaltose
• Hypophosphatemia
• Phosphate Metabolism

Hemodiyaliz Dışı Kronik Böbrek Hastalarında İntravenöz Ferrik Karboksimaltoz Tedavisinin Serum Fosfor Düzeylerine Etkisi

Öz

ÖZ Amaç: Anemi, özellikle glomerüler filtrasyon hızı (GFR) 30 mL/dk/1.73m2 nın altına düştüğünde, kronik böbrek hastalığında (KBH) yaygındır. Demir eksikliği anemiyi daha da kötüleştirir ve intravenöz ferrik karboksimaltoz (FCM), hızlı demir verilmesi ve düşük aşırı duyarlılık riski nedeniyle sıklıkla kullanılmaktadır. Ancak, FCM’nin hipofosfatemi ile ilişkili olduğu bildirilmiştir ve hemodiyaliz dışı KBH hastalarında bu konuda sınırlı veri bulunmaktadır. Bu çalışma, bu popülasyonda FCM tedavisi sonrası hipofosfatemi görülme sıklığını ve serum fosforundaki değişiklikleri değerlendirmiştir. Yöntem: 2022–2023 yılları arasında demir eksikliği anemisi nedeniyle intravenöz FCM alan 113 erişkin hemodiyaliz dışı KBH hastası (evre 3A–5) retrospektif olarak analiz edildi. Hastaların tedavi öncesi ve 1 ay sonraki serum fosfor ve kreatinin ölçümleri vardı; diyaliz, akut enfeksiyon, malignite, aktif inflamasyon, fosfat bağlayıcı kullanımı veya belgelenmiş malnütrisyonu olanlar dışlandı. Fosfor değişiklikleri KBH evrelerine göre karşılaştırıldı, hipofosfatemi (<2.5 mg/dL) ile ilişkili faktörler eşleştirilmiş t-testi, tek yönlü ANOVA, korelasyon ve regresyon analizleri ile değerlendirildi. Bulgular: Başlangıçta ortalama fosfor 3.62 ± 1.10 mg/dL, kreatinin 2.35 ± 1.,42 mg/dL ve eGFR 30.16 ± 13.59 mL/dk/1.73m2 idi. FCM uygulaması serum fosforunda hafif fakat istatistiksel olarak anlamlı bir düşüşe yol açtı: 3.49 ± 1.05 mg/dL (ortalama değişim: −0.137 mg/dL, p < 0.001). Serum fosforu tüm KBH evrelerinde azaldı ve azalma derecesi evreler arasında anlamlı farklılık göstermedi. Hipofosfatemi (%12.3) en sık evre 3 ve 4’te görüldü, evre 5’te hiç vaka gözlenmedi. Hipofosfatemi gelişenlerin başlangıç fosfor düzeyleri anlamlı olarak daha düşüktü (3.04 ± 0.69 vs. 3.71 ± 1.13 mg/dL, p = 0.005). Fosfor değişimi, başlangıç fosfor düzeyi ile koreleydi (r = 0.488, p < 0.001), ancak başlangıç kreatinin ile ilişki saptanmadı (p = 0.077). Yaş, cinsiyet, paratiroid hormonu, D vitamini veya hemoglobin ile anlamlı ilişki bulunmadı. Sonuç: Hemodiyaliz dışı KBH hastalarında FCM, serum fosforunda küçük fakat anlamlı bir düşüşe neden olmaktadır; klinik olarak anlamlı hipofosfatemi nadirdir. Düşük başlangıç fosforu, duyarlılığı artırmaktadır; bu nedenle tedavi öncesi değerlendirme ve hedeflenmiş tedavi sonrası takip önemlidir. İleri evre KBH, fosfat atılımının bozulması nedeniyle daha düşük risk oluşturabilir; ancak retrospektif tasarım ve mineral metabolizması belirteçlerinin yokluğu göz önünde bulundurulmalıdır. Bulgular, kişiselleştirilmiş demir tedavi stratejilerine katkı sağlayabilir ve KBH anemi yönetim protokollerine fosfor izleminin dahil edilmesini destekleyebilir.

Anahtar Kelimeler

• Kronik Böbrek Hastalığı
• Hemodiyaliz Dışı
• Ferrik Karboksimaltoz
• Hipofosfatemi
• Fosfat Metabolizması

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