Calcium and Phosphate Handling in Peritoneal Dialysis

Cozzolino, Mario; Gallieni, Maurizio; Chiarelli, Giusy; Brancaccio, Diego

doi:10.1159/000093597

Cited by 8 publications

(7 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These complications are believed to be promoted largely via hyperphosphatemia (36,37). FGF23 has proven to track with PTH levels in advanced CKD, consistent either with a feedback role in response to elevated PTH levels or, alternatively, promoting PTH secretion; the molecular mechanisms of FGF23's effects on parathyroid in vivo have been unclear.…”

Section: Discussionmentioning

confidence: 99%

A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism

Brownstein

Adler²,

Nelson‐Williams³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

220

150

View full text Add to dashboard Cite

Phosphate homeostasis is central to diverse physiologic processes including energy homeostasis, formation of lipid bilayers, and bone formation. Reduced phosphate levels due to excessive renal loss cause hypophosphatemic rickets, a disease characterized by prominent bone defects; conversely, hyperphosphatemia, a major complication of renal failure, is accompanied by parathyroid hyperplasia, hyperparathyroidism, and osteodystrophy. Here, we define a syndrome featuring both hypophosphatemic rickets and hyperparathyroidism due to parathyroid hyperplasia as well as other skeletal abnormalities. We show that this disease is due to a de novo translocation with a breakpoint adjacent to ␣-Klotho, which encodes a ␤-glucuronidase, and is implicated in aging and regulation of FGF signaling. Plasma ␣-Klotho levels and ␤-glucuronidase activity are markedly increased in the affected patient; unexpectedly, the circulating FGF23 level is also markedly elevated. These findings suggest that the elevated ␣-Klotho level mimics aspects of the normal response to hyperphosphatemia and implicate ␣-Klotho in the selective regulation of phosphate levels and in the regulation of parathyroid mass and function; they also have implications for the pathogenesis and treatment of renal osteodystrophy in patients with kidney failure.bone ͉ endocrinology ͉ genetics ͉ phosphorus T he maintenance of normal phosphate homeostasis is critical for diverse biochemical processes in vivo. Its importance is illustrated by disorders featuring hypophosphatemia due to excessive renal phosphate loss. Affected patients develop rickets, a disorder in which abnormal mineralization of bone and growth plate cartilage results in diminished bone strength, deformity, short stature, and bone pain. Rapidly growing bones of the lower extremities generally show the most striking abnormalities (1). Conversely, high phosphate levels may also have adverse physiologic effects. These are most pronounced in patients with chronic kidney disease (CKD) who develop hyperphosphatemia due to impaired renal clearance. These patients develop hyperparathyroidism and renal osteodystrophy.The kidney plays a predominant role in the regulation of serum phosphorus levels. The vast majority of phosphate reabsorption occurs in the proximal tubule and is mediated by the sodium-phosphate cotransporter type IIa (NaPi-IIa), with additional contributions from the related protein NaPi-IIc (2, 3). Parathyroid hormone (PTH) has been considered the major regulator of NaPi-IIa and NaPi-IIc density in the proximal tubular cell apical membrane (3, 4), promoting the rapid removal of NaPi-IIa from the membrane and its subsequent degradation (5). In addition, high phosphate levels are known to promote proliferation of parathyroid cells and enhance PTH secretion and mRNA stability; these effects have been speculated to be mediated by means of reduced serum Ca 2ϩ levels, but the mechanism is uncertain (6-9).More recently, FGF23 and its receptor have been recognized to play fundamental roles in phosphate homeos...

show abstract

Section: Discussionmentioning

confidence: 99%

A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism

Brownstein

Adler²,

Nelson‐Williams³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

220

150

View full text Add to dashboard Cite

show abstract

“…Dans la même étude mexicaine citée précédemment, l'hypoparathyroïdie était plus fréquente et concernait 56.6% des patients en DPCA et 64.2% en DPA [7]. L'hypoparathyroïdie est en effet le trouble minéral et osseux le plus fréquemment retrouvé dans la littérature chez les patients en DP [8]. L'ostéopathie adynamique a été prouvée histologiquement chez 63.2% des patients d'une série espagnole de 57 patients dialysés péritonéaux [9].…”

Section: Prévalence Et Facteurs De Risque Des Troubles Minéraux Et Os...unclassified

“…L'ostéopathie adynamique a été prouvée histologiquement chez 63.2% des patients d'une série espagnole de 57 patients dialysés péritonéaux [9]. De nombreuses études incriminent le diabète comme son principal facteur de risque [7,8,10]. Parmi les autres facteurs de risque on retrouve l'âge, la suppression iatrogène de la PTH par de la vitamine D, l'hypercalcémie, les chélateurs calciques du phosphore ou encore les dialysats riches en calcium [8].…”

Section: Prévalence Et Facteurs De Risque Des Troubles Minéraux Et Os...unclassified

“…De nombreuses études incriminent le diabète comme son principal facteur de risque [7,8,10]. Parmi les autres facteurs de risque on retrouve l'âge, la suppression iatrogène de la PTH par de la vitamine D, l'hypercalcémie, les chélateurs calciques du phosphore ou encore les dialysats riches en calcium [8]. Dans notre série, 2 patientes ont développé une hypoparathyroïdie soit 2.35 %.…”

Section: Prévalence Et Facteurs De Risque Des Troubles Minéraux Et Os...unclassified

“…L'étiologie de la néphropathie reste Une autre complication importante de l'hyperparathyroïdie secondaire est les calcifications vasculaires qui sont associées à la mortalité cardiovasculaire [2,3]. Le premier mécanisme est une précipitation passive de phosphate de calcium dans le système vasculaire secondaire à l'hypercalcémie et l'hyperphosphorémie [8,14]. Le second mécanisme est actif à travers l'hyperphosphorémie qui favorise les calcifications vasculaires en induisant la transformation de cellules musculaires lisses vasculaires en phénotypes ostéochondrogènes et en promouvant la minéralisation de leur matrice cellulaire [3,8].…”

Section: Prévalence Et Facteurs De Risque Des Troubles Minéraux Et Os...unclassified

See 2 more Smart Citations

Mineral and bone disorders in peritoneal dialysis

Houem¹,

Agrou

Saidi

et al. 2022

Bull Dial Domic

View full text Add to dashboard Cite

Introduction Disorders of mineral and bone metabolism are common in dialysis patients and are responsible for an increased risk of fracture, cardiovascular risk and mortality. The mineral and bone disorder most frequently found in peritoneal dialysis (PD) is adynamic osteopathy. The aim of our work is to describe the mineral and bone profile of patients on peritoneal dialysis, to determine the prevalence of hyperparathyroidism in this population and to identify the risk factors associated with it. Material and method This is a cross-sectional study including all our PD patients in whom we analyzed the various clinical, biological, radiological and therapeutic data related to mineral and bone metabolism. We defined hyperparathyroidism by a parathyroid hormone (PTH) ≥ 600pg/ml and we determined the risk factors by comparing two groups : with and without hyperparathyroidism. Results We retained 85 patients whose mean age was 49.18 ± 17.28 years and the sex ratio of 0.77. The seniority in dialysis was 33.31 ± 26.68 months. Median PTH was 668 pg/ml [34-3800] with serum calcium at 87.75±7.52 mg/l, phosphatemia at 54.07±16.69 mg/l and vitamin D at 23.74±11.56 ng/ml. Hyperparathyroidism was found in 60% of patients. The risk factors for hyperparathyroidism noted in our study are: seniority in PD, high PTH before the start of dialysis, and hyperphosphatemia. The short medical follow-up before dialysis seems to play an important role in the development of secondary hyperparathyroidism. Conclusion Hyperparathyroidism is the most frequent mineral and bone disorder in our series. Factors correlated with hyperparathyroidism are length of time on dialysis, hyperphosphatemia and high parathormone levels before the start of dialysis.

show abstract

Calcium, Phosphate, and Renal Osteodystrophy

Vardhan¹,

Hutchison²

2009

Nolph and Gokal’s Textbook of Peritoneal Dialysis

View full text Add to dashboard Cite

Calcium and Phosphate Handling in Peritoneal Dialysis

Cited by 8 publications

References 50 publications

A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism

A translocation causing increased α-Klotho level results in hypophosphatemic rickets and hyperparathyroidism

Mineral and bone disorders in peritoneal dialysis

Calcium, Phosphate, and Renal Osteodystrophy

Contact Info

Product

Resources

About