Introduction:
Iron deficiency anaemia is common in chronic kidney disease patients especially those on hemodialysis. In chronic kidney disease patients, chronic inflammation may lead to increased hepcidin production, in turn inhibiting both the uptake of dietary iron and the mobilization of stored iron from the reticuloendothelial system to circulating transferrin.
Iron deficiency anaemia leads to increased gene expression leading to increased iFGF23(intact) along with increased cleavage of FGF23 which decreases iFGF23(intact) and increased cFGF23(cleavage). Hence the nett effect is normal iFGF23 and increased cFGF23.
Ferric Carboxymaltose {FCM} is a stable non-dextran-containing iron formulation developed for rapid IV administration in high doses with controlled delivery of iron into target tissues which is effective and better tolerated than other iron injections in the CKD population.
Recent studies suggest that reduced serum phosphate level in response to intravenous iron is mediated by an acute increase in FGF23. The carbohydrate moiety in Ferric Carboxymaltose leads to decreased cleavage of iFGF23. As iron deficiency itself causes increased expression as well as increased cleavage of iFGF23 and this cleavage being inhibited with FCM, leads to a net increase in expression of iFGF23. This iFGF23 causes increased phosphate excretion by inhibiting NaPi2 co-transporter in the proximal convoluted tubule. It also inhibits 1alpha hydroxylase and decreases 1,25(OH)D3, further decreasing phosphate absorption from gastrointestinal tract. All these lead to hypophosphatemia.
In patients who receive FCM developed
● Transient and asymptomatic reductions in serum phosphate that typically occur within 2 to 4 weeks of treatment.
● Resolves spontaneously within 6 to 12 weeks.
The aim of this study is to assess the impact of a single dose of ferric carboxymaltose {FCM} on iFGF23 and plasma phosphate levels in non-dialysis chronic kidney disease patients.
Methods:
This prospective cohort study enrolled 34 participants with chronic kidney disease stage 3-5 non-dialysis patients (after approval from the Institutional Ethics Committee). The age group of patients was 40 to 80 years and male to female ratio was 1.83:1. Standard haematological and biochemical tests were done which included haemoglobin, phosphorus and Iron studies before including in the study. After written informed consent serum phosphate and iFGF 23 were done. After receiving IV Ferric Carboxymaltose 1 gram, serum phosphate and iFGF23 levels were repeated at 21 days. Statistical analysis was performed using SPSS software, and Spearman's correlation was used to assess the relationships between variables.
Results:
Total 34 patients were enrolled in the study. 11 patients in stage 3, 7 patientsin stage 4 and 17 patients in stage 5 CKD.
Conclusions:
● Treatment of iron deficiency anemia in CKD patients with Ferric Carboxymaltose led to a significant increase in iFGF 23 levels.
● There was a fall in the Serum Phosphate level in this study.
● There was a negative correlation between serum iFGF 23 levels and serum phosphate levels.
● The fall in serum phosphate was significant in stages 3 and 4, whereas increase in iFGF was significant only in Stage 4.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.