Impacts of parathyroidectomy on calcium and phosphorus metabolism disorder, arterial calcification and arterial stiffness in haemodialysis patients.

BACKGROUND: Secondary hyperparathyroidism (SHPT) and calcium and phosphorus metabolism disorder are important complications in haemodialysis patients. Parathyroidectomy (PTX) may prevent or delay the progress of vascular calcification in haemodialysis patients. OBJECTIVE: To investigate the impacts of PTX on calcium and phosphorus metabolism, arterial calcification and arterial stiffness in haemodialysis patients with SHPT. METHODS: Twenty-one SHPT-haemodialysis patients were selected for PTX. The preoperative and postoperative 1-year scores of coronary artery calcification were measured via multislice spiral CT, along with the brachial-ankle pulse wave velocity (baPWV), and preoperative and postoperative 1-year indexes such as calcium, phosphorus, calcium-phosphorus product concentration and parathyroid hormone (PTH) level were compared. RESULTS: Compared with the preoperative score, the postoperative 1-year coronary artery calcification score was significantly reduced; the mean baPWVs of the bilateral limbs were reduced; and the levels of serum calcium, phosphorus, calcium-phosphorus product concentration and PTH were all reduced; all differences were statistically significant (P < 0.05). CONCLUSIONS: PTX can be used to correct calcium and phosphorus metabolism disorder, reduce arterial calcification, and improve arterial stiffness.

The association between periodontal conditions, inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis patients.

OBJECTIVES: To analyze the association between periodontal conditions and inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis (HD) patients. MATERIAL AND METHODS: We analyzed 128 HD patients divided into two groups: dentate (n = 103) and edentulous (n=25). The following items were assessed: baseline characteristics, age at the start and duration of HD, biochemical data: C-reactive protein (CRP), serum albumin, calcium, phosphorus, alkaline phosphatase, parathormone. A single dentist performed a complete dental/periodontal examination, including parameters of oral hygiene and gingival bleeding. RESULTS: One person had healthy periodontium, 62.14% of the patients had gingivitis, and 36.9% had moderate or severe periodontitis. The age at HD onset had a positive impact on periodontal status and negatively correlated with the number of teeth. A positive correlation between age and CRP level and negative correlations between age and serum albumin and phosphorus were found. Pocket depth (PD) was negatively correlated with serum albumin. The number of teeth was negatively correlated with serum CRP. CONCLUSIONS: High prevalence and severity of periodontal disease are observed in hemodialysis patients. There is a high probability that periodontal disease may be present at the early stages of chronic kidney disease (CKD) before the hemodialysis onset.

The association between periodontal conditions, inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis patients

Abstract Objectives To analyze the association between periodontal conditions and inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis (HD) patients. Material and Methods We analyzed 128 HD patients divided into two groups: dentate (n = 103) and edentulous (n=25). The following items were assessed: baseline characteristics, age at the start and duration of HD, biochemical data: C-reactive protein (CRP), serum albumin, calcium, phosphorus, alkaline phosphatase, parathormone. A single dentist performed a complete dental/periodontal examination, including parameters of oral hygiene and gingival bleeding. Results One person had healthy periodontium, 62.14% of the patients had gingivitis, and 36.9% had moderate or severe periodontitis. The age at HD onset had a positive impact on periodontal status and negatively correlated with the number of teeth. A positive correlation between age and CRP level and negative correlations between age and serum albumin and phosphorus were found. Pocket depth (PD) was negatively correlated with serum albumin. The number of teeth was negatively correlated with serum CRP. Conclusions High prevalence and severity of periodontal disease are observed in hemodialysis patients. There is a high probability that periodontal disease may be present at the early stages of chronic kidney disease (CKD) before the hemodialysis onset.

A Quick Reference on Phosphorus.

Phosphorus, or phosphate, is the body's major intracellular anion involved in numerous biological processes. Most phosphate is intracellular, with the remaining amount contained within soft tissues and the extracellular space. Parathyroid hormone, calcitriol, calcitonin, and phosphatonins regulate normal phosphate homeostasis by adjusting renal and/or gastrointestinal absorption and/or excretion. Hypophosphatemia occurs secondary to decreased gastrointestinal absorption, transcellular shifts, increased renal excretion, or some combination of these general mechanisms. Hyperphosphatemia results from decreased renal excretion, increased intake or iatrogenic administration, transcellular shifts, or some combination of these.

[Mineral and bone disorders in renal transplantation]. / Métabolisme phosphocalcique et osseux chez le patient transplanté rénal.

The deregulation of bone and mineral metabolism during chronic kidney disease (CKD) is a daily challenge for physicians, its management aiming at decreasing the risk of both fractures and vascular calcifications. Renal transplantation in the context of CKD, with pre-existing renal osteodystrophy as well as nutritional impairment, chronic inflammation, hypogonadism and corticosteroids exposure, represents a major risk factor for bone impairment in the post-transplant period. The aim of this review is therefore to provide an update on the pathophysiology of mineral and bone disorders after renal transplantation.

Management of natural and added dietary phosphorus burden in kidney disease.

Phosphorus retention occurs from higher dietary phosphorus intake relative to its renal excretion or dialysis removal. In the gastrointestinal tract the naturally existing organic phosphorus is only partially (∼60%) absorbable; however, this absorption varies widely and is lower for plant-based phosphorus including phytate (<40%) and higher for foods enhanced with inorganic phosphorus-containing preservatives (>80%). The latter phosphorus often remains unrecognized by patients and health care professionals, even though it is widely used in contemporary diets, in particular, low-cost foods. In a nonenhanced mixed diet, digestible phosphorus correlates closely with total protein content, making protein-rich foods a main source of natural phosphorus. Phosphorus burden is limited more appropriately in predialysis patients who are on a low-protein diet (∼0.6 g/kg/d), whereas dialysis patients who require higher protein intake (∼1.2 g/kg/d) are subject to a higher dietary phosphorus load. An effective and patient-friendly approach to reduce phosphorus intake without depriving patients of adequate proteins is to educate patients to avoid foods with high phosphorus relative to protein such as egg yolk and those with high amounts of phosphorus-based preservatives such as certain soft drinks and enhanced cheese and meat. Phosphorus rich foods should be prepared by boiling, which reduces phosphorus as well as sodium and potassium content, or by other types of cooking-induced demineralization. The dose of phosphorus-binding therapy should be adjusted separately for the amount and absorbability of phosphorus in each meal. Dietician counseling to address the emerging aspects of dietary phosphorus management is instrumental for achieving a reduction of phosphorus load.

FGF-23: the rise of a novel cardiovascular risk marker in CKD.

Elevated plasma levels of the phosphaturic hormone fibroblast growth factor 23 (FGF-23) are a hallmark of chronic kidney disease (CKD)-mineral and bone disorder. FGF-23 allows serum phosphate levels within physiological limits to be maintained in progressive CKD until end-stage renal disease is reached. Despite its seemingly beneficial role in phosphate homeostasis, several prospective studies in dialysis patients and in patients with less advanced CKD associated elevated FGF-23 with poor cardiovascular and renal outcome. Moreover, very recent evidence suggests an adverse prognostic impact of elevated FGF-23 even in subjects without manifest CKD. These epidemiological data are supplemented by laboratory findings that reveal a pathophysiological role of FGF-23 in the pathogenesis of myocardial injury. In aggregate, these clinical and experimental data identify FGF-23 as a promising target of novel therapeutic interventions in CKD and beyond, which should be tested in future clinical trials.

The phosphate binder equivalent dose.

Phosphate binders include calcium acetate or carbonate, sevelamer hydrochloride or carbonate, magnesium and lanthanum carbonate, and aluminum carbonate or hydroxide. Their relative phosphate-binding capacity has been assessed in human, in vivo studies that have measured phosphate recovery from stool and/or changes in urinary phosphate excretion or that have compared pairs of different binders where dose of binder in each group was titrated to a target level of serum phosphate. The relative phosphate-binding coefficient (RPBC) based on weight of each binder can be estimated relative to calcium carbonate, the latter being set to 1.0. A systematic review of these studies gave the following estimated RPBC: for elemental lanthanum, 2.0, for sevelamer hydrochloride or carbonate 0.75, for calcium acetate 1.0, for anhydrous magnesium carbonate 1.7, and for "heavy" or hydrated, magnesium carbonate 1.3. Estimated RPBC for aluminum-containing binders were 1.5 for aluminum hydroxide and 1.9 for aluminum carbonate. The phosphate-binding equivalent dose was then defined as the dose of each binder in g × its RPBC, which would be the binding ability of an equivalent weight of calcium carbonate. The phosphate-binding equivalent dose may be useful in comparing changes in phosphate binder prescription over time when multiple binders are being prescribed, when estimating an initial binder prescription, and also in phosphate kinetic modeling.

Benefits of sevelamer on markers of bone turnover in Taiwanese hemodialysis patients.

BACKGROUND/PURPOSE: Sevelamer hydrochloride is a recently developed phosphate binder, which is a quaternary amine anion exchanger without calcium or aluminum. Sevelamer is effective in controlling hyperphosphatemia without increasing the calcium load in chronic hemodialysis (HD) patients. We investigated whether sevelamer restored bone metabolism in chronic HD patients. METHODS: An 8-week, prospective, open-label, randomized study was conducted after a 2-week washout period in chronic hyperphosphatemic HD patients. This study compared the effect of sevelamer on markers of bone turnover with that of calcium acetate, as stratified by baseline serum intact parathyroid hormone (iPTH) level. RESULTS: There was no difference in the changes of serum phosphorus, calcium-phosphorus product and serum iPTH between the sevelamer and the calcium acetate groups. However, more hypercalcemic events (12%) were documented under calcium acetate treatment. In patients with hypoparathyroidism, calcium acetate treatment decreased serum iPTH at the end of the study, while sevelamer did not. Increased serum alkaline phosphatase levels were found among patients receiving sevelamer treatment compared with those who received calcium acetate treatment. In those patients receiving sevelamer, the serum alkaline phosphatase level was also positively correlated to the sevelamer dosage (r = 0.246, p = 0.013). CONCLUSION: Sevelamer effectively reduces serum phosphorus with a lower incidence of hypercalcemic effects in HD patients. Sevelamer is an effective means of treatment for chronic hyperphosphatemic HD patients, especially those with hypoparathyroidism.

[The French clinician's guide to the Kidney disease: Improving global outcomes (KDIGO) for chronic kidney disease-mineral and bone disorders (CKD-MBD)]. / L'essentiel des nouvelles recommandations des kidney disease: improving global outcomes (KDIGO) pour les désordres du métabolisme minéral et osseux à l'usage du clinicien francophone.

The new recommendations of "Kidney disease: improving global outcomes" for the definition and classification of chronic kidney disease and mineral and bone disorders were released in August 2009. We report the most important of these recommendations and a brief comment from a clinician's point of view. The main points to be noted with regard to the new recommendations are as follows: serum calcium should be in the normal range; phosphorus concentration should be lowered toward the normal range and serum parathyroid hormone (PTH) levels should be two to nine times the upper limit of the normal range; bone remodelling can be assessed using alkaline phosphatase; the use of calcium-phosphorus (Ca x P) product as an index is not recommended anymore; at any stage of CKD, vitamin D deficiency and insufficiency must be corrected; vascular calcification should be detected in a simple way using lateral abdominal radiography and echocardiography; a bone biopsy should be performed before therapy with bisphosphonates; the prescription of dialysate calcium should be individualized within the range of 1.25-1.5 mmol/l; the phosphate binder (calcium- or non-calcium-based) and the other treatments for secondary hyperparathyroidism should be individualized based on a global strategy. A majority of these recommendations are not based on evidence and their feasibility and relevance need to be assessed.

[Disorders of phosphate metabolism].

Serum phosphate is maintained within a certain range by intestinal phosphate absorption, renal phosphate handling, and dynamic equilibrium with the intracellular phosphate or phosphate in bone. Of these, renal phosphate handling is believed to be the main determinant of the serum phosphate level at least in a chronic state. Most of the phosphate filtered from the glomeruli is reabsorbed in proximal tubules through type 2a and 2c sodium-phosphate co-transporters. Therefore, chronic hypophosphatemia and hyperphosphatemia are usually caused by changes in renal phosphate handling. Several humoral factors, including parathyroid hormone and insulin-like growth factor-I, have been known to affect proximal tubular phosphate reabsorption. In addition, fibroblast growth factor 23 (FGF23) was shown to inhibit phosphate reabsorption by suppressing the expression of type 2a and 2c sodium-phosphate co-transporters. FGF23 also reduces the circulatory 1,25-dihydroxyvitamin D [1,25 (OH)2D] level. FGF23 is produced by bone, especially by osteocytes, and works in the kidney by binding to the Klotho-FGF receptor complex. It has been shown that excess actions of FGF23 cause several kinds of hypophosphatemic rickets/osteomalacia with impaired proximal tubular phosphate reabsorption and a rather low 1,25 (OH)2D level. In contrast, deficient actions of FGF23 result in familial hyperphosphatemic tumoral calcinosis with enhanced proximal tubular phosphate reabsorption and high 1,25 (OH)2D. These results indicate that FGF23 is a hormone regulating phosphate and vitamin D metabolism. In addition, several hypophosphatemic and hyperphosphatemic diseases can be classified as endocrine diseases caused by the aberrant actions of FGF23. It is possible that some drugs that modulate the action of FGF23 can be novel therapeutic measures for abnormal phosphate metabolism in the future.

Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23.

In contrast to the regulation of calcium homeostasis, which has been extensively studied over the past several decades, relatively little is known about the regulation of phosphate homeostasis. Fibroblast growth factor 23 (FGF23) is part of a previously unrecognized hormonal bone-parathyroid-kidney axis, which is modulated by PTH, 1,25(OH)(2)-vitamin D (1,25(OH)(2)D), dietary and serum phosphorus levels. Synthesis and secretion of FGF23 by osteocytes are positively regulated by 1,25(OH)(2)D and serum phosphorus and negatively regulated, through yet unknown mechanisms, by the phosphate-regulating gene with homologies to endopeptidases on the X chromosome (PHEX) and by dentin matrix protein 1 (DMP1). In turn, FGF23 inhibits the synthesis of 1,25(OH)(2)D, and it may negatively regulate the secretion of parathyroid hormone (PTH) from the parathyroid glands. However, FGF23 synergizes with PTH to increase renal phosphate excretion by reducing expression of the renal sodium-phosphate cotransporters NaPi-IIa and NaPi-IIc in the proximal tubules. Most insights gained into the regulation of phosphate homeostasis by these factors are derived from human genetic disorders and genetically engineered mice, which are reviewed in this paper.

[Screening and care of chronic renal insufficiency in the elderly population]. / Dépistage et prise en charge de l'insuffisance rénale chronique parmi la population âgée.

The prevalence of chronic renal insufficiency (CRI) increases with age. This growth shall result in it becoming a public health issue for the most elderly In this age group, chronic renal insufficiency primarily stems from diabetes and vascular and glomerular origins. The limiting point is the assessment of the glomerular filtration rate which remains imprecise. Care aims to limit the development of renal insufficiency and to prevent its complications, which are sources of fragility.

[Phosphatonins: novel insights and clinical perspectives]. / Le fosfatine: recenti acquisizioni e possibili evoluzioni nella clinica.

Phosphate plays a vital role in several biological processes including energy and nucleic acid metabolism, cell signaling and bone mineralization. Several endocrine factors coordinately act on the intestine, kidney and bone to maintain their physiological homeostasis. A number of peptides, collectively known as phosphatonins, have recently been identified as regulators of phosphate metabolism in physiological and pathological conditions. These factors--fibroblast growth factors (FGF) 23 and 7, secreted frizzled related protein 4 (sFRP-4), and matrix extracellular phosphoglycoprotein (MEPE)--primarily regulate tubular phosphate reabsorption by acting on the transmembrane expression of SLC34 sodium-phosphate cotransporters. FGF- 23, FGF-7 and sFRP-4 also inhibit the biosynthesis of 1,25(OH)2D3, leading to decreased intestinal phosphate absorption. In this review, we discuss the biological properties of these peptides, their physiological roles, and the alterations in their concentrations in various hypophosphatemic and hyperphosphatemic clinical disorders.

Aporte de calcio en la insuficiencia renal crónica / No disponible

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