scholarly journals Is serum phosphate a useful target in patients with chronic kidney disease and what is the role for dietary phosphate restriction?

Nephrology ◽  
2017 ◽  
Vol 22 ◽  
pp. 36-41 ◽  
Author(s):  
Nigel D Toussaint ◽  
Stephen G Holt
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Serum Phosphate ◽  
Dietary Phosphate

Phosphate binders in patients with chronic kidney disease: Between the new and the old.

2019 ◽  
pp. 2-3
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Estimated Glomerular Filtration Rate ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Phosphate Binders ◽  
Advanced Chronic Kidney Disease ◽  
Phosphate Retention ◽  
Stage 4 ◽  
Dietary Phosphate

Impaired phosphate excretion by the kidney leads to Hyperphosphatemia. It is an independent predictor of cardiovascular disease and mortality in patients with advanced chronic kidney disease (stage 4 and 5) particularly in case of dialysis. Phosphate retention develops early in chronic kidney disease (CKD) due to the reduction in the filtered phosphate load. Overt hyperphosphatemia develops when the estimated glomerular filtration rate (eGFR) falls below 25 to 40 mL/min/1.73 m2. Hyperphosphatemia is typically managed with oral phosphate binders in conjunction with dietary phosphate restriction. These drugs aim to decrease serum phosphate by binding ingested phosphorus in the gastrointestinal tract and its transformation to non-absorbable complexes [1].

scholarly journals Effects of Dietary Phosphate on Adynamic Bone Disease in Rats with Chronic Kidney Disease – Role of Sclerostin?

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79721 ◽  
Author(s):  
Juliana C. Ferreira ◽  
Guaraciaba O. Ferrari ◽  
Katia R. Neves ◽  
Raquel T. Cavallari ◽  
Wagner V. Dominguez ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Disease ◽  
Adynamic Bone Disease ◽  
Dietary Phosphate ◽  
Adynamic Bone

scholarly journals The effect of attenuating dietary phosphate restriction on blood ionized calcium concentrations in cats with chronic kidney disease and ionized hypercalcemia

2021 ◽  
Vol 35 (2) ◽  
pp. 997-1007 ◽  
Author(s):  
Rebecca F. Geddes ◽  
D. Hendrik N. Broek ◽  
Yu‐Mei Chang ◽  
Vincent Biourge ◽  
Jonathan Elliott ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Ionized Calcium ◽  
Dietary Phosphate

scholarly journals Solubleα-Klotho Serum Levels in Chronic Kidney Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Silverio Rotondi ◽  
Marzia Pasquali ◽  
Lida Tartaglione ◽  
Maria Luisa Muci ◽  
Giusy Mandanici ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Disease ◽  
Clinical Significance ◽  
Serum Levels ◽  
Serum Phosphate ◽  
Renal Tubules ◽  
Ckd Stage ◽  
Tubular Transport ◽  
Negative Effect

Transmembraneα-Klotho (TM-Klotho), expressed in renal tubules, is a cofactor for FGF23-receptor. Circulating soluble-α-Klotho (s-Klotho) results from TM-Klotho shedding and acts on Phosphate (P) and Calcium (Ca) tubular transport. Decreased TM-Klotho, described in experimental chronic kidney disease (CKD), prevents actions of FGF23 and lessens circulating s-Klotho. Thus, levels of s-Klotho could represent a marker of CKD-MBD. To evaluate the clinical significance of s-Klotho in CKD we assayed serum s-Klotho and serum FGF23 in 68 patients (age58±15; eGFR45±21 mL/min). s-Klotho was lower than normal (519±183versus845±330 pg/mL,P<.0001) in renal patients and its reduction was detectable since CKD stage 2 (P<.01). s-Klotho correlated positively with eGFR and serum calcium (Cas) and negatively with serum phosphate (Ps), PTH and FGF23. FGF23 was higher than normal (73±51versus36±11,P<.0002) with significantly increased levels since CKD stage 2 (P<.001). Our data indicate a negative effect of renal disease on circulating s-Klotho starting very early in CKD. Assuming that s-Klotho mirrors TM-Klotho synthesis, low circulating s-Klotho seems to reflect the ensuing of tubular resistance to FGF23, which, accordingly, is increased. We endorse s-Klotho as an early marker of CKD-MBD.

Relationship Between Dietary Phosphate Intake and Biomarkers of Bone and Mineral Metabolism in Australian Adults With Chronic Kidney Disease

2021 ◽  
Author(s):  
Marguerite Conley ◽  
Katrina L. Campbell ◽  
Carmel M. Hawley ◽  
Nicole M. Lioufas ◽  
Grahame J. Elder ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mineral Metabolism ◽  
Phosphate Intake ◽  
Dietary Phosphate

Systematic Review and Meta-analyses of Effects of Phosphate-lowering Agents in Non-dialysis Chronic Kidney Disease

2021 ◽  
pp. ASN.2021040554
Author(s):  
Nicole Lioufas ◽  
Elaine Pascoe ◽  
Carmel Hawley ◽  
Grahame Elder ◽  
Sunil Badve ◽  
...  
Keyword(s):  
Systematic Review ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Outcomes ◽  
Serum Phosphate ◽  
Risk Of Bias ◽  
Lowering Therapy ◽  
Mean Differences ◽  
Meta Analyses

Background: Benefits of phosphate-lowering interventions on clinical outcomes in patients with chronic kidney disease (CKD) are unclear; systematic reviews have predominantly involved dialysis patients. This study aimed to summarize evidence from randomized controlled trials (RCTs) concerning benefits and risks of non-calcium-based phosphate-lowering treatment in non-dialysis CKD. Methods: We conducted a systematic review and meta-analyses of RCTs involving noncalcium-based phosphate-lowering therapy compared to placebo, calcium-based binders, or no study medication, in adults with CKD not on dialysis or post-transplant. RCTs had ≥3 months follow up and outcomes included biomarkers of mineral metabolism, cardiovascular parameters, and adverse events. Outcomes were meta-analyzed using the Sidik-Jonkman method for random effects. Unstandardized mean differences were used as effect sizes for continuous outcomes, with common measurement units and Hedge's g standardized mean differences (SMD) otherwise. Odds ratios were used for binary outcomes. Cochrane risk of bias and GRADE assessment determined the certainty of evidence. Results: Twenty trials involving 2,498 participants (median sample size 120, median follow up 9 months) were eligible for inclusion. Overall, risk of bias was low. Compared with placebo, non calcium-based phosphate binders reduced serum phosphate (12 trials, weighted mean difference -0.37, 95% CI -0.58,-0.15 mg/dL, low certainty evidence) and urinary phosphate excretion (8 trials, SMD -0.61, 95% CI -0.90,-0.31, low certainty evidence), but resulted in increased constipation (9 trials, log odds ratio [OR] 0.93, 95% CI 0.02, 1.83, low certainty evidence) and greater vascular calcification score (3 trials, SMD 0.47, 95% CI 0.17, 0.77, very low certainty evidence). Data for effects of phosphate-lowering therapy on cardiovascular events (log OR 0.51 [95% CI -0.51, 1.17]) and death were scant. Conclusions: Non-calcium-based phosphate-lowering therapy reduced serum phosphate and urinary phosphate excretion, but there was an unclear effect on clinical outcomes and intermediate cardiovascular end-points. Adequately powered RCTs are required to evaluate benefits and risks of phosphate-lowering therapy on patient-centered outcomes.

scholarly journals Can we IMPROVE cardiovascular outcomes through phosphate lowering in CKD? Rationale and protocol for the IMpact of Phosphate Reduction On Vascular End-points in Chronic Kidney Disease (IMPROVE-CKD) study

BMJ Open ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. e024382 ◽  
Author(s):  
Nicole Lioufas ◽  
Nigel D Toussaint ◽  
Eugenia Pedagogos ◽  
Grahame Elder ◽  
Sunil V Badve ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Compliance ◽  
Left Ventricular ◽  
Serum Phosphate ◽  
Lanthanum Carbonate ◽  
Cardiovascular Morbidity And Mortality ◽  
Fgf 23 ◽  
The Impact

IntroductionPatients with chronic kidney disease (CKD) are at heightened cardiovascular risk, which has been associated with abnormalities of bone and mineral metabolism. A deeper understanding of these abnormalities should facilitate improved treatment strategies and patient-level outcomes, but at present there are few large, randomised controlled clinical trials to guide management. Positive associations between serum phosphate and fibroblast growth factor 23 (FGF-23) and cardiovascular morbidity and mortality in both the general and CKD populations have resulted in clinical guidelines suggesting that serum phosphate be targeted towards the normal range, although few randomised and placebo-controlled studies have addressed clinical outcomes using interventions to improve phosphate control. Early preventive measures to reduce the development and progression of vascular calcification, left ventricular hypertrophy and arterial stiffness are crucial in patients with CKD.Methods and analysisWe outline the rationale and protocol for an international, multicentre, randomised parallel-group trial assessing the impact of the non-calcium-based phosphate binder, lanthanum carbonate, compared with placebo on surrogate markers of cardiovascular disease in a predialysis CKD population—the IMpact of Phosphate Reduction On Vascular End-points (IMPROVE)-CKD study. The primary objective of the IMPROVE-CKD study is to determine if the use of lanthanum carbonate reduces the burden of cardiovascular disease in patients with CKD stages 3b and 4 when compared with placebo. The primary end-point of the study is change in arterial compliance measured by pulse wave velocity over a 96-week period. Secondary outcomes include change in aortic calcification and biochemical parameters of serum phosphate, parathyroid hormone and FGF-23 levels.Ethics and disseminationEthical approval for the IMPROVE-CKD trial was obtained by each local Institutional Ethics Committee for all 17 participating sites in Australia, New Zealand and Malaysia prior to study commencement. Results of this clinical trial will be published in peer-reviewed journals and presented at conferences.Trial registration numberACTRN12610000650099.

scholarly journals P0898VITAMIN C STATUS MODIFIES PARATHYROID HORMONE SECRETION IN NON-DIALYZED CHRONIC KIDNEY DISEASE PATIENTS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Ryuta Fujimura ◽  
SHOGO SHIBATA ◽  
Takechiyo Tokuda ◽  
Ayako Tanaka ◽  
Aya Mizumoto ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Vitamin C ◽  
Secondary Hyperparathyroidism ◽  
Hormone Secretion ◽  
Serum Vitamin ◽  
Serum Phosphate ◽  
Vitamin C Deficiency

Abstract Background and Aims Among patients with chronic kidney disease (CKD) at predialysis stage, there is a high incidence of secondary hyperparathyroidism. Metabolic changes associated with secondary hyperparathyroidism lead to renal osteodystrophy, including osteitis fibrosa, ectopic calcification, cardiovascular disease, and the risk of death, and serum parathyroid hormone levels are influenced by nutritional variables. Non-dialyzed CKD patients are especially prone to vitamin C deficiency because of dietary restrictions and malnutrition. Vitamin C is an important antioxidant and relates to the development and maintenance of bone tissues. However, the contribution of vitamin C deficiency to parathyroid hormone secretion is unknown. Here, we performed a single-center cross-sectional study in order to assess association of serum vitamin C and parathyroid hormone in non-dialyzed CKD patients. Method We had 280 consecutive patients who underwent serum vitamin C and serum intact parathyroid hormone (iPTH) measurement for screening purposes from January 1st, 2013 to November 30th, 2017. We analysed a total of 128 patients (71.3±11.6 year-old, 80 males) who had an estimated glomerular filtration rate (eGFR) that remained less than 60 mL/min/1.73m2 after 152 patients were excluded because of vitamin C or vitamin D supplementation, age &lt;20 years, dialysis, positive serostatus for HIV, hepatitis B or hepatitis C, chronic infection, or cancer. Results Twenty-three percent of the patients (n=29) had vitamin C levels&lt; 2.0 μg/mL (a range seen in very deficient subjects), 53% (n=68) had levels between 2.0 and 5.5 μg/mL, and 31 patients (24%) had vitamin C levels &gt;5.5 μg/mL, which is considered the upper limit of normal for the healthy population. Log(iPTH) significantly correlated with age (r=-0.238, p=0.00672), log(eGFR) (r=-0.625, p&lt;0.0001), serum calcium (r=-0.609, p&lt;0.0001), and serum phosphate (r=0.41, p&lt;0.0001), and had a tendency to correlate with serum albumin (r=-0.146, p=0.101). Low serum vitamin C was associated with higher serum iPTH (P=0.0005, one-way analysis of variance). In a multiple linear regression model with log(iPTH) as the dependent variable, and age, gender, log(eGFR), serum levels of calcium, phosphate, albumin, and vitamin C as independent variables, the inverse relationship of log(iPTH) and serum vitamin C was confirmed (R2 = 0.568, adjusted R2 = 0.543, P&lt;0.0001), along with other parameters influencing iPTH levels, including age, log(eGFR), serum calcium, and serum phosphate. Low vitamin C levels were also associated with increased serum alkaline phosphatase (r=-0.209, p=0.0179), a further indicator of the impact of vitamin C status on bone metabolism. Conclusion Vitamin C deficiency is prevalent in a significant proportion of non-dialyzed CKD patients. Low vitamin C levels contribute to secondary hyperparathyroidism, leading to increased bone turnover. This novel observation may result from effects of vitamin C on vitamin D metabolism, vitamin D binding in target tissues, and cAMP-linked signalling pathways in bone and parathyroid gland. Therapeutic intervention with supplemental vitamin C for secondary hyperparathyroidism might be a good strategy.

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