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Renal Diseases
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
The principles of management of renal osteodystrophy are: Correction of acidosis using sodium bicarbonate.Phosphate restriction by control of dietary intake and the use of a phosphate binder (e.g. calcium carbonate to maintain plasma phosphate within the normal range for age).Supplements of oral 1-α-hydroxycholecalciferol or 1,25 dihydroxycholecalciferol to maintain the PTH within normal range, if not achieved by control of plasma phosphate. This may require the total calcium to be maintained at the upper end of the normal range. Total calcium is a measurement of bound, ionised and complexed calcium. The proportion may increase in CKD, reflected by total hypercalcaemia. However, if the ionised calcium is within the normal range, treatment with vitamin D analogues may continue.
Answers
Published in John D Firth, Professor Ian Gilmore, MRCP Part 2 Self-Assessment, 2018
John D Firth, Professor Ian Gilmore
Hydroxylated vitamin D suppresses PTH expression and alfacalcidol should be considered for prophylaxis against renal bone disease and progressive hyperparathyroidism. However, the obvious abnormality is that the patient’s serum phosphate level is elevated and the priority must be to reduce this. Calcium acetate would be the most reasonable choice of phosphate binder here: it should be taken with (or just before) meals and may offer advantages over calcium carbonate, especially in patients with reduced gastric acidity. Aluminium-containing phosphate binders carry the risk of aluminium accumulation and neurological side effects and are no longer used (except in rare instances). Sevelamer is only clearly indicated if calcium-containing binders cannot be used because the calcium level (or calcium-phosphate product) are undesirably high. Parathyroidectomy is not indicated: the patient only has a mildly elevated level of PTH that is likely to improve with better phosphate control.
Chronic Renal Failure
Published in Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George, The Scientific Basis of Urology, 2010
There are a number of phosphate binders currently available, which fall into two categories: calcium-based binders (calcium acetate and calcium carbonate) and non-calcium-based binders (sevelamer hydrochloride and lanthanum carbonate). Use of the calcium-based preparations is limited by the fact that patients with CKD should not take in more than 2 g of elemental calcium per day, as this may again promote vascular calcification.
Estimating hospital inpatient cost-savings with sucroferric oxyhydroxide in patients on chronic hemodialysis in five European countries: a cost analysis
Published in Journal of Medical Economics, 2021
Jose Antonio Herrero, Mario Salomone, Antonio Ramirez de Arellano, Thilo Schaufler, Sebastian Walpen
Given that hyperphosphatemia increases the risk of vascular calcification, cardiovascular events, cardiovascular mortality and hospitalizations5–9, and hyperphosphatemia is associated with higher all-cause and cardiovascular mortality37,38, reducing mortality and hospitalizations is an important public health goal that also promotes efficient use of healthcare resources. Traditional phosphate binders pose a high pill burden and low tolerability leading to poor adherence and mild-to moderate benefits in achieving and maintaining serum phosphate levels targets20,39,40. Moreover, calcium-based phosphate binders contribute to an increase in calcium phosphate product, associated with high risk of cardiovascular disease41–43. Newer iron-containing phosphate binders therefore offer potential benefits, such as a lower pill burden with SO and improved iron parameters with ferric citrate, and the biggest challenge to efficacy for these newer phosphate binders is non-adherence44. Data reporting the distinct benefits of phosphate binders on hard outcomes such as mortality or hospitalizations are, however, scarce44,45.
Endocrine fibroblast growth factors as potential biomarkers for chronic kidney disease
Published in Expert Review of Molecular Diagnostics, 2020
Yuichiro Kondo, Hirotaka Komaba, Masafumi Fukagawa
If the implicated toxicity of FGF23 in CKD patients is not confirmed in future studies, the value of FGF23 as a biomarker will be less clear. FGF23 initially emerged as a sensitive biomarker of phosphate metabolism in CKD patients, but current evidence is not sufficient to support this possibility. In our experience, there are not a few patients who show very high FGF23 levels, together with normo- or even hypophosphatemia. For such patients, tightening dietary phosphate restriction or intensifying phosphate binder therapy may not be justified based on the current evidence and clinical guidelines. It is also noteworthy that the cost for measuring FGF23 is much higher than that of phosphorus, which could be a major obstacle in performing repeated measurements for assessing the trends of changes. Last but not least, it should be mentioned that FGF23 levels could be affected by many factors other than serum phosphorus or dietary phosphorus intake, such as PTH, calcium, active vitamin D treatment, iron deficiency, inflammation, and erythropoiesis [26–31,36–38]. Thus, clinicians would be uncertain about what to do when they encounter a patient who shows very high FGF23 levels. These concerns limit the potential of FGF23 as a biomarker of phosphate metabolism.
Calciphylaxis-as a drug induced adverse event
Published in Expert Opinion on Drug Safety, 2019
Ignacio Portales-Castillo, Daniela Kroshinsky, Cindy K. Malhotra, Roberta Culber-Costley, Mario Gennaro Cozzolino, Shelly Karparis, Charles L. Halasz, Jeremy Goverman, Harold J. Manley, Rajeev Malhotra, Sagar U. Nigwekar
Increased serum phosphate levels and serum calcium-phosphate product levels are a common risk factor found in case control studies [16,41,42]. Phosphate binders which serve to decrease serum phosphate levels can contain or not contain calcium. A randomized trial evaluating the effect of phosphate binders on CKD found that although they were effective in decreasing phosphorus levels, there was an increased risk of vascular calcification in the coronaries and aorta [54]. Unfortunately, the study was not powered to examine the differences between calcium and non-calcium containing binders. There is a case report associating the use of calcium containing phosphate binders with calciphylaxis [55]. The hypothesized mechanisms to explain this are positive calcium balance and alkalinization [56]. In contrast sevelamer, a non-calcium phosphate binder, has been shown to increase serum fetuin-A levels when compared to calcium binders [57]. It has also been associated with better clinical outcomes [58]. In a large case-control study, phosphate binder therapy at hemodialysis initiation was not statistically significant with increased odds of subsequent development of calciphylaxis; however, trends towards increased odds were noted for both calcium and non-calcium based binder treatments [13]. Multiple case-control studies in patients with calciphylaxis have not found a consistent increase in the odds of calciphylaxis with phosphate binders.