Impact of Serum Phosphorus on Hemoglobin: A Literature Review

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Fortunata Zirino

DOI: 10.69097/41-04-2024-03

Fortunata Zirino1, Antonella Lipari1, Alessia Tigano1, Alfio Edoardo Giuffrida1, Concetto Sessa1, Dario Galeano1, Ivana Alessandrello1, Roberta Maria Messina1, Roberta Pilato2, Walter Morale1, Vincenzo Calabrese3

1 Unit of Nephrology and Dialysis, P.O. Maggiore “Nino Baglieri”, University of Messina, Messina, Italy
2 Department of General Surgery and Medical-Surgical Specialty, University of Catania, Catania, Italy
3 Unit of Nephrology and Dialysis, Department of Clinical and Experimental Medicine, A.O.U. 'G. Martino', University of Messina, Messina, Italy

Corresponding author:
Vincenzo Calabrese
v.calabrese@outlook.it
telephone number: +39 3208736905

 

Abstract

Phosphorus is a macroelement found in the body, mostly in the bones as crystals of hydroxyapatite. Higher levels are found in patients affected by chronic kidney disease (CKD). Since the early stage of CKD phosphorous excretion is impaired, but the increase of PTH and FGF23 maintains its level in the normal range. In the last decades, the role of FGF23 in erythropoiesis was studied, and now it is well known for its role in anemia genesis in patients affected by conservative CKD. Both Hyperphosphatemia and anemia are two manifestations of CKD, but many studies showed a direct association between serum phosphorous and anemia. Phosphorus can be considered as the common point of more pathogenetic ways, independent of renal function: the overproduction of FGF23, the worsening of vascular disease, and the toxic impairment of erythropoiesis, including the induction of hemolysis.

Keywords: Phosphorus, Hemoglobin, Anemia, Chronic Kidney Disease, FGF23

Introduction

Phosphorus is a macroelement found in the body; 85% of it is deposited in the bone as crystals of hydroxyapatite, 14% in the intracellular compartment as a component of nucleic acids, plasma membranes and involved in all cellular energetic processes, and only 1% is extracellular [1].

Of the latter, 70% is organic phosphorous and 30% is inorganic phosphorous. Inorganic phosphorous can be protein-bound, complexed with sodium, calcium, and magnesium, or circulating as mono- or di-hydrogen forms. About 800 mg of phosphorous is  introduced with the food, and the kidneys filter across the glomerulus about 90% of the daily phosphate load. The residual 10% is excreted by the gastrointestinal system.

Chronic Kidney disease (CKD) impairs phosphorus excretion due to the reduction of the skillful nephron mass. As a consequence of this, parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF-23) are over-secreted from the early stages of CKD, to prevent an increase in serum phosphorous concentration [2].

Both PTH and FGF23 increase phosphorus urinary excretion but, conversely to FGF23, PTH is related to serum calcium due to the relative activation of calcium-sensing receptor (CaSR). Indeed, PTH limits calcium gastrointestinal absorption because it reduces 1,25-dihydroxy vitamin D levels. This negative feedback tray maintains serum calcium and phosphorus within normal ranges in individuals with normal kidney function. The progression of renal disease causes the failure of this equilibrium and hypocalcemia, hyperphosphatemia, and tertiary hyperparathyroidism may occur. 

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