Chronic Kidney Disease-Mineral Bone Disorder

Moe, Sharon M.

doi:10.1016/b978-1-4377-0987-2.00008-x

Cited by 5 publications

(3 citation statements)

References 430 publications

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“…Furthermore, various hormones such as parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF‐23) play a key role. Normally, both hormones induce increased urinary excretion of phosphate, and PTH also leads to skeletal phosphate resorption, while FGF‐23 decreases renal phosphate reabsorption (Moe, 2010; Nadkarni & Uribarri, 2014; Perwad et al., 2007; Wheeler & Winkelmayer, 2017). However, in this advanced stage of kidney disease (stage 5), these hormones do not longer compensate sufficiently for the continuous input of phosphate from fluid and dietary intake leading to a positive phosphate balance (Galvao et al., 2013; Nadkarni & Uribarri, 2014).…”

Section: Introductionmentioning

confidence: 99%

“…Hyperphosphatemia is associated with severe long‐term consequences in HD patients. For instance, the condition is known to accelerate vascular calcification processes mainly due to an increase in the calcium‐phosphate product (Cozzolino et al., 2001; Moe, 2010). Vascular calcifications are common in HD patients affecting approximately 70%–80% of the patient population (Moe, 2010) and are highly associated with cardiovascular events and premature death (Barreto et al., 2019; Mizobuchi et al., 2009; Moe, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…For instance, the condition is known to accelerate vascular calcification processes mainly due to an increase in the calcium‐phosphate product (Cozzolino et al., 2001; Moe, 2010). Vascular calcifications are common in HD patients affecting approximately 70%–80% of the patient population (Moe, 2010) and are highly associated with cardiovascular events and premature death (Barreto et al., 2019; Mizobuchi et al., 2009; Moe, 2010). Thus, the risk of cardiovascular death is approximately 10–30 times higher in HD patients than in the general population (Ford et al., 2010; London, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of a phosphate kinetics model in hemodialysis therapy—Assessment of the temporal robustness of model predictions

Laursen,

Boel,

Brandi

et al. 2023

Physiological Reports

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In‐depth understanding of intra‐ and postdialytic phosphate kinetics is important to adjust treatment regimens in hemodialysis. We aimed to modify and validate a three‐compartment phosphate kinetic model to individual patient data and assess the temporal robustness. Intradialytic phosphate samples were collected from the plasma and dialysate of 12 patients during two treatments (HD1 and HD2). 2‐h postdialytic plasma samples were collected in four of the patients. First, the model was fitted to HD1 samples from each patient to estimate the mass transfer coefficients. Second, the best fitted model in each patient case was validated on HD2 samples. The best model fits were determined from the coefficient of determination (R2) values. When fitted to intradialytic samples only, the median (interquartile range) R2 values were 0.985 (0.959–0.997) and 0.992 (0.984–0.994) for HD1 and HD2, respectively. When fitted to both intra‐ and postdialytic samples, the results were 0.882 (0.838–0.929) and 0.963 (0.951–0.976) for HD1 and HD2, respectively. Eight patients demonstrated a higher R2 value for HD2 than for HD1. The model seems promising to predict individual plasma phosphate in hemodialysis patients. The results also show good temporal robustness of the model. Further modifications and validation on a larger sample are needed.

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