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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Hyperphosphatemia in dialysis: which binder?

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Carlo Alfieri1, Fabio Malberti2, Sandro Mazzaferro3, Maurizio Gallieni4, Domenico Russo5, Piergiorgio Messa1, Mario Cozzolino6

1 Fondazione IRCCS Ca’ Granda – Ospedale Maggiore Policlinico Milano & Università degli Studi di Milano
2 Divisione di Nefrologia e Dialisi, ASST Cremona
3 Sapienza Università di Roma & Ospedale Policlinico Umberto I
4 Presidio Ospedaliero San Carlo Borromeo, ASST Santi Paolo e Carlo, Milano & Università degli Studi di Milano
5 Dipartimento di Sanità Pubblica Università degli Studi Federico II. Napoli
6 Presidio Ospedaliero San Paolo, ASST Santi Paolo e Carlo, Milano & Università degli Studi di Milano

Autore Corrispondente
Mario Cozzolino, MD, PhD, FERA, FASN
Renal Division
Department of Health Sciences
University of Milan,
San Paolo Hospital
20142, Milano ITALY
Phone: 00390281844215
E-mail:  Mario.cozzolino@unimi.it

 

Abstract

Several studies have evidenced the association between high serum phosphorus concentrations and adverse events especially in patients on dialysis.

Recent K-DIGO guidelines suggest lowering elevated phosphate levels toward the normal range. This goal should be achieved by combining dietary counseling, optimizing dialysis procedures and prescribing phosphate binders.

Despite the availability of several binders, the “ideal” phosphate binder that combines high efficacy, low pills burden, minimal side effects and low cost is still not available.
In clinical practice it is crucial to reach a high patient’s compliance to therapy. The pill burden is the most relevant factor contributing to low compliance. This is the case of phosphate binder therapy that represents almost 50% of total pills prescribed to patients on dialysis.
It has been evidenced an association between pills of phosphate binder and poor control of phosphorus and PTH.
In recent years sucroferric oxyhydroxide is available as a new phosphate binder. Its
peculiarity is an high phosphate binding capability that requires prescription of low number of pills per day. This characteristic has been confirmed by several randomized controlled trials. These trials have also evidenced that sucroferric oxyhydroxide may cause some gastrointestinal side effects. There is an ongoing study to confirm in “the real world” the incidence of side effects reported by controlled trials.

Key words: Phosphate; Binder; Secondary Hyperparathyroidism

Sorry, this entry is only available in Italian.

Lo scenario attuale

Le alterazioni del metabolismo minerale, ed in particolare l’iperfosforemia, sono riconosciute oggi fattori di rischio importanti per l’incremento della morbilità e mortalità dei pazienti affetti da malattia renale cronica, sia durante le fasi iniziali che nelle fasi più avanzate di malattia (1, 2).  Il controllo del bilancio fosforico rappresenta pertanto un punto cardine nel trattamento di questi pazienti.

 

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CKD-MBD in Peritoneal Dialysis

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Anna Rachele Rocca, Tania Gnerre Musto, Sandro Mazzaferro

Dipartimento di Scienze Cardiovascolari Respiratorie Nefrologiche Anestetiche e Geriatriche. Sapienza Università di Roma

Autore Corrispondente:
Anna Rachele Rocca
Dipartimento di Scienze Cardiovascolari Respiratorie Nefrologiche Anestetiche e Geriatriche. Sapienza Università di Roma
Viale del Policlinico 155
00100 Roma, Italia
Tel/Fax 0649974293
E-mail: racheleroc@gmail.com

 

Abstract

CKD-MBD is a systemic disorder of the mineral and bone metabolism as a result of CKD. The clinical relevance of this syndrome has led to the identification of the biochemical targets to be achieved in order to improve the outcome of the patient. However, in hemodialysis (HD) and peritoneal dialysis (DP) patients, these targets are not reached. Hyperphosphatemia is a predictor of cardiovascular and all-cause mortality. In DP the removal of phosphorus (P) occurs by diffusion and convection, with a contribution of ultrafiltration of about 11%. P clearance is time dependent, with differences between CAPD and APD and depending on membrane transport characteristics. Residual renal function plays a key role in the P balance. Calcium (Ca) clearance in PD depends on the calcium levels, calcium concentration in dialysate and ultrafiltration. Positive Ca balance brings to Adynamic Bone Disease. Several bone-derived substances, some of them with hormonal action, have shed new light on the bone- cardiac axis. The hormonal functions of bone are likely to be related to histological lesions that develop during chronic renal failure. Compared to the past, recent data show less obvious differences in bone histomorphometry parameters between HD patients and PD patients. However, in PD patients fewer fractures are reported, probably due to different bone quality.

Key Words: CKD-MBD, peritoneal dialysis, calcium, phosphorus, Adynamic Bone Disease

Sorry, this entry is only available in Italian.

Nel corso degli ultimi anni numerose evidenze scientifiche hanno mostrato una stretta correlazione tra i disordini del metabolismo minerale, le anomalie ossee, le calcificazioni extrascheletriche e l’aumento della morbilità e mortalità nei pazienti con malattia renale cronica (1). La tradizionale definizione di osteodistrofia renale non esprimeva in maniera completa questa sindrome complessa che invece è stata riconosciuta tale e ha preso il nome di CKD-Mineral Bone Disorders (Madrid 2005). Pertanto il termine CKD-MBD definisce un disordine sistemico del metabolismo minerale ed osseo dovuto alla malattia renale cronica che si manifesta in presenza di una sola o una combinazione delle seguenti condizioni: alterazioni dei parametri di laboratorio (calcemia, fosforemia, PTH, vitamina D); anomalie nel turnover, nella mineralizzazione, nel volume, nella crescita lineare o nella resistenza dell’osso; calcificazioni vascolari o dei tessuti molli (2). 

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