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• W2951533026 abstract "Hyperphosphatemia is a common complication in patients with chronic kidney disease (CKD), particularly in those requiring renal replacement therapy. The importance of controlling serum phosphate has long been recognized based on observational epidemiological studies that linked increased phosphate levels to adverse outcomes and higher mortality risk. Experimental data further supported the role of phosphate in the development of bone and cardiovascular diseases. Recent advances in our understanding of the mechanisms involved in phosphate homeostasis have made it clear that the serum phosphate concentration depends on a complex interplay among the kidneys, intestinal tract, and bone, and is tightly regulated by a complex endocrine system. Moreover, the source of dietary phosphate and the use of phosphate-based additives in industrialized foods are additional factors that are of particular importance in CKD. Not surprisingly, the management of hyperphosphatemia is difficult, and, despite a multifaceted approach, it remains unsuccessful in many patients. An additional issue is the fact that the supposedly beneficial effect of phosphate lowering on hard clinical outcomes in interventional trials is a matter of ongoing debate. In this review, we discuss currently available treatment approaches for controlling hyperphosphatemia, including dietary phosphate restriction, reduction of intestinal phosphate absorption, phosphate removal by dialysis, and management of renal osteodystrophy, with particular focus on practical challenges and limitations, and on potential benefits and harms. Hyperphosphatemia is a common complication in patients with chronic kidney disease (CKD), particularly in those requiring renal replacement therapy. The importance of controlling serum phosphate has long been recognized based on observational epidemiological studies that linked increased phosphate levels to adverse outcomes and higher mortality risk. Experimental data further supported the role of phosphate in the development of bone and cardiovascular diseases. Recent advances in our understanding of the mechanisms involved in phosphate homeostasis have made it clear that the serum phosphate concentration depends on a complex interplay among the kidneys, intestinal tract, and bone, and is tightly regulated by a complex endocrine system. Moreover, the source of dietary phosphate and the use of phosphate-based additives in industrialized foods are additional factors that are of particular importance in CKD. Not surprisingly, the management of hyperphosphatemia is difficult, and, despite a multifaceted approach, it remains unsuccessful in many patients. An additional issue is the fact that the supposedly beneficial effect of phosphate lowering on hard clinical outcomes in interventional trials is a matter of ongoing debate. In this review, we discuss currently available treatment approaches for controlling hyperphosphatemia, including dietary phosphate restriction, reduction of intestinal phosphate absorption, phosphate removal by dialysis, and management of renal osteodystrophy, with particular focus on practical challenges and limitations, and on potential benefits and harms. Hyperphosphatemia is a common complication of patients with CKD, particularly in those with end-stage renal disease (ESRD). In general, high serum phosphate levels are observed only in late stages of CKD. An earlier increase in the course of CKD is prevented by the activation of powerful compensatory mechanisms, including an increase in fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) secretion. Both hormones enhance the fractional excretion of phosphate per functioning nephron, compensating for the progressive loss of functioning nephron mass.1Isakova T. Wahl P. Vargas G.S. et al.Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease.Kidney Int. 2011; 79: 1370-1378Abstract Full Text Full Text PDF PubMed Scopus (606) Google Scholar In advanced CKD, these mechanisms become gradually unable to overcome the continuous input of phosphate from dietary intake, leading to a positive phosphate balance and hyperphosphatemia. The use of certain medications, mainly vitamin D and its active derivatives, may further aggravate the positive balance by increasing intestinal absorption of phosphate. Altered bone metabolism may also play a part in hyperphosphatemia through 2 distinct pathways: on the 1 hand, the increase in bone resorption characteristic of high bone turnover states augments phosphate efflux from bone to blood in advanced CKD stages; on the other hand, the loss of bone buffering capacity characteristic of low bone turnover states decreases the skeletal buffering capacity of increased extracellular phosphate levels already in earlier CKD stages. However, the concentration of serum phosphate is not only the net result of phosphate ingestion, absorption, and excretion. A recent study has demonstrated that the nicotinamide phosphoribosyl transferase (Nampt)/(NAD+) intracellular pathway plays a fundamental role in activity of renal and intestinal phosphate transporters. Thereby it regulates transcellular phosphate shifts independent of oral phosphate ingestion, and contributes to the diurnal variation in serum phosphate concentration.2Miyagawa A. Tatsumi S. Takahama W. et al.The sodium phosphate cotransporter family and nicotinamide phosphoribosyltransferase contribute to the daily oscillation of plasma inorganic phosphate concentration.Kidney Int. 2018; 93: 1073-1085Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar, 3Isakova T. Block G. The phosphate bucket list.Kidney Int. 2018; 93: 1033-1035Abstract Full Text Full Text PDF PubMed Google Scholar Moreover, in some clinical conditions, serum phosphate can vary due to shifts of phosphate from the extracellular to the intracellular space, or vice versa. Most notably, massive cellular shifts of phosphate out of the cells may occur in association with lactic acidosis and diabetic ketoacidosis, causing severe acute hyperphosphatemia. In addition to promoting cellular phosphate exit, metabolic acidosis can diminish glycolysis and therefore cellular phosphate utilization, resulting in an increase in serum phosphate.4O'Connor L.R. Klein K.L. Bethune J.E. Hyperphosphatemia in lactic acidosis.N Engl J Med. 1977; 297: 707-709Crossref PubMed Google Scholar, 5Sternbach G.L. Varon J. Severe hyperphosphatemia associated with hemorrhagic shock.Am J Emerg Med. 1992; 10: 331-332Abstract Full Text PDF PubMed Scopus (5) Google Scholar, 6Kebler R. McDonald F.D. Cadnapaphornchai P. Dynamic changes in serum phosphorus levels in diabetic ketoacidosis.Am J Med. 1985; 79: 571-576Abstract Full Text PDF PubMed Scopus (65) Google Scholar In clinical practice, the deleterious effects of high serum phosphate levels in CKD were underestimated for many years. Despite the well-known contribution of phosphate retention to the development of secondary hyperparathyroidism, it was only in the late 1990s that hyperphosphatemia began to be widely appreciated as a potentially major cardiovascular villain. Using data from the US Renal Data System, Block et al. found an increased risk of death (relative risk, 1.27) associated with serum phosphate levels >6.5 mg/dl. The increased risk remained statistically significant even after adjustment for confounders.7Block G.A. Hulbert-Shearon T.E. Levin N.W. Port F.K. Association of serum phosphorus and calcium x phosphate product with mortality risk in chronic hemodialysis patients: a national study.Am J Kidney Dis. 1998; 31: 607-617Abstract Full Text Full Text PDF PubMed Google Scholar Subsequently, numerous epidemiological studies, both in the general population and in CKD patients, have tightened the knot between phosphate excess and adverse outcomes.8Kestenbaum B. Sampson J.N. Rudser K.D. et al.Serum phosphate levels and mortality risk among people with chronic kidney disease.J Am Soc Nephrol. 2005; 16: 520-528Crossref PubMed Scopus (762) Google Scholar, 9Tonelli M. Sacks F. Pfeffer M. et al.Relation between serum phosphate level and cardiovascular event rate in people with coronary disease.Circulation. 2005; 112: 2627-2633Crossref PubMed Scopus (565) Google Scholar, 10Block G.A. Klassen P.S. Lazarus J.M. et al.Mineral metabolism, mortality, and morbidity in maintenance hemodialysis.J Am Soc Nephrol. 2004; 15: 2208-2218Crossref PubMed Scopus (1863) Google Scholar, 11Voormolen N. Noordzij M. Grootendorst D.C. et al.High plasma phosphate as a risk factor for decline in renal function and mortality in pre-dialysis patients.Nephrol Dial Transplant. 2007; 22: 2909-2916Crossref PubMed Scopus (225) Google Scholar Experimental studies have shed light on the mechanisms by which phosphate may adversely affect the cardiovascular system. Briefly, phosphate may directly contribute to vascular damage by inflammatory actions on the vascular smooth muscle cell, the induction of endothelial dysfunction, and the promotion of vascular calcification.12Martinez-Moreno J.M. Herencia C. de Oca A.M. et al.High phosphate induces a pro-inflammatory response by vascular smooth muscle cells and modulation by vitamin D derivatives.Clin Sci (Lond). 2017; 131: 1449-1463Crossref PubMed Scopus (8) Google Scholar, 13Six I. Maizel J. Barreto F.C. et al.Effects of phosphate on vascular function under normal conditions and influence of the uraemic state.Cardiovasc Res. 2012; 96: 130-139Crossref PubMed Scopus (0) Google Scholar, 14Shanahan C.M. Crouthamel M.H. Kapustin A. Giachelli C.M. Arterial calcification in chronic kidney disease: key roles for calcium and phosphate.Circ Res. 2011; : 109697-109711Google Scholar Furthermore, a high dietary phosphate content may contribute to atherogenesis.15Ellam T. Wilkie M. Chamberlain J. et al.Dietary phosphate modulates atherogenesis and insulin resistance in apolipoprotein E knockout mice–brief report.Arterioscler Thromb Vasc Biol. 2011; 31: 1988-1990Crossref PubMed Scopus (0) Google Scholar Besides its cardiovascular toxicity, hyperphosphatemia has also been linked to a more rapid progression of CKD.11Voormolen N. Noordzij M. Grootendorst D.C. et al.High plasma phosphate as a risk factor for decline in renal function and mortality in pre-dialysis patients.Nephrol Dial Transplant. 2007; 22: 2909-2916Crossref PubMed Scopus (225) Google Scholar, 16Santamaria R. Diaz-Tocados J.M. Pendon-Ruiz de Mier M.V. et al.Increased phosphaturia accelerates the decline in renal function: a search for mechanisms.Sci Rep. 2018; 8: 13701Crossref PubMed Scopus (3) Google Scholar Phosphate excess may also indirectly exert noxious effects, for example, by inhibiting the renal transformation of 25(OH) vitamin D to 1,25(OH)2vitamin D, and by stimulating both FGF23 and parathyroid hormone (PTH) secretion.17Faul C. Amaral A.P. Oskouei B. et al.FGF23 induces left ventricular hypertrophy.J Clin Invest. 2011; 121: 4393-4408Crossref PubMed Scopus (1006) Google Scholar, 18Rodriguez M. Lorenzo V. Parathyroid hormone, a uremic toxin.Semin Dial. 2009; 22: 363-368Crossref PubMed Scopus (0) Google Scholar, 19Wolf M. Update on fibroblast growth factor 23 in chronic kidney disease.Kidney Int. 2012; 82: 737-747Abstract Full Text Full Text PDF PubMed Scopus (218) Google Scholar Based on a large body of clinical and experimental evidence, the control of hyperphosphatemia has emerged as a key element in the management of CKD patients. However, the optimal range for serum phosphate levels in CKD patients is still controversial. The KDOQI guidelines of 2011 suggested that phosphate levels should be kept between 3.5 and 5.5 mg/dl, whereas the subsequent KDIGO guideline of 2009 and its recent update in 2017 opted for a less strict control, suggesting that elevated phosphate levels should be lowered toward the normal range.20Kidney Disease: Improving Global OutcomesKDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF Scopus (153) Google Scholar In daily clinical practice, the management of hyperphosphatemia is based on 4 main strategies: (i) restriction of dietary phosphate intake; (ii) reduction of its intestinal absorption; (iii) phosphate removal by dialysis; and (iv) treatment and prevention of renal osteodystrophy. This review will discuss these treatment approaches, addressing their potential benefits, harms, and limitations in light of the many practical challenges that arise when managing hyperphosphatemia in patients with CKD. Reducing phosphate intake is a widely accepted strategy to aid in the control of hyperphosphatemia. It is a fundamental part of the recommendations issued by both KDIGO and KDOQI guidelines, with a daily phosphate intake of 800 to 1000 mg/d, and a daily protein intake (as the major source of dietary phosphate) of 1.2 g/kg body weight.21Kidney Disease: Improving Global OutcomesKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD-MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar, 22National Kidney FoundationK/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease.Am J Kidney Dis. 2003; 42: S1-S201PubMed Google Scholar However, one should be aware of several important issues when proposing dietary phosphate restriction. First, the bioavailability of phosphate needs to be taken into account, and not the phosphate content of food alone. In general, (i) phosphate bioavailability is very low for plant-derived phosphate, probably due to a lower phosphate:protein ratio and to the fact that phosphate from vegetable origin (phytate) is less well absorbed (usually <50%) because humans do not express the degrading enzyme phytase23Lei X.G. Porres J.M. Phytase enzymology, applications, and biotechnology.Biotechnol Lett. 2003; 25: 1787-1794Crossref PubMed Scopus (0) Google Scholar; (ii) its bioavailability is much greater for processed food; and (iii) its bioavailability appears to be intermediate for animal-derived unprocessed meat. The impact of the source of phosphate was examined in a crossover trial in 9 CKD patients (mean estimated glomerular filtration rate 32 ml/min) that compared vegetarian and meat diets with equivalents nutrients.24Moe S.M. Zidehsarai M.P. Chambers M.A. et al.Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease.Clin J Am Soc Nephrol. 2011; 6: 257-264Crossref PubMed Scopus (237) Google Scholar After 1 week on the vegetarian diet, patients had lower serum phosphorus levels, a trend toward decreased urinary 24-hour phosphorus excretion, and significantly lower FGF23 levels in comparison to patients with the meat-based diet. Second, there are sources of phosphate that are commonly overlooked, mainly from processed foods and medications. Almost all processed foods contain phosphate additives, such as disodium phosphate, monosodium phosphate, and potassium triphosphate, to preserve their color and shelf lives. Inorganic phosphorus, present in phosphate additives, is not protein bound. It dissociates easily in the gut lumen and therefore is more readily absorbed across the intestinal wall. In healthy humans, the fractional absorption rate of phosphate is approximately 70%.25Scanni R. vonRotz M. Jehle S. et al.The human response to acute enteral and parenteral phosphate loads.J Am Soc Nephrol. 2014; 25: 2730-2739Crossref PubMed Scopus (0) Google Scholar A study comparing the phosphate content of similar processed food items with and without additives showed that both total and soluble phosphate content were greater in the foods containing phosphate additives, leading to a 70% higher phosphate uptake per gram of protein.26Benini O. D'Alessandro C. Gianfaldoni D. Cupisti A. Extra-phosphate load from food additives in commonly eaten foods: a real and insidious danger for renal patients.J Ren Nutr. 2011; 21: 303-308Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar Another recent report has estimated that as much as 40% of total phosphate intake may be attributable to phosphate-containing additives.27Calvo M.S. Sherman R.A. Uribarri J. Dietary phosphate and the forgotten kidney patient: a critical need for FDA regulatory action.Am J Kidney Dis. 2019; 73: 542-551Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar This problem seems to be even more worrisome in individuals living in low-income communities.28Gutierrez O.M. Anderson C. Isakova T. et al.Low socioeconomic status associates with higher serum phosphate irrespective of race.J Am Soc Nephrol. 2010; 21: 1953-1960Crossref PubMed Scopus (0) Google Scholar Importantly, dietary intake of inorganic phosphate has been linked to higher carotid-intima thickness.29Itkonen S.T. Karp H.J. Kemi V.E. et al.Associations among total and food additive phosphorus intake and carotid intima-media thickness–a cross-sectional study in a middle-aged population in southern Finland.Nutr J. 2013; 12: 94Crossref PubMed Scopus (0) Google Scholar Furthermore, as the phosphate content in processed foods is often hidden, total phosphate intake is generally underestimated. Additional concern stems from the possible contribution of medication excipients to phosphate overload. The phosphate content of commonly prescribed drugs may be very high, for instance 111.5 mg for 40 mg of paroxetine, 32.6 mg for 10 mg of lisinopril, and 40.1 mg for 10 mg of amlodipine.30Sherman R.A. Ravella S. Kapoian T. A dearth of data: the problem of phosphorus in prescription medications.Kidney Int. 2015; 87: 1097-1099Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar Most importantly, although phosphate lowering by tight dietary restriction is often effective both in predialysis and in dialysis patients,31Combe C. Aparicio M. Phosphorus and protein restriction and parathyroid function in chronic renal failure.Kidney Int. 1994; 46: 1381-1386Abstract Full Text PDF PubMed Google Scholar, 32Combe C. Morel D. de Precigout V. et al.Long-term control of hyperparathyroidism in advanced renal failure by low-phosphorus low-protein diet supplemented with calcium (without changes in plasma calcitriol).Nephron. 1995; 70: 287-295Crossref PubMed Google Scholar, 33Klahr S. The modification of diet in renal disease study.N Engl J Med. 1989; 320: 864-866Crossref PubMed Scopus (110) Google Scholar a beneficial effect on clinical outcomes remains to be demonstrated.33Klahr S. The modification of diet in renal disease study.N Engl J Med. 1989; 320: 864-866Crossref PubMed Scopus (110) Google Scholar Moreover, severe protein restriction increases the risk of malnutrition and eventually poorer outcomes.34Shinaberger C.S. Greenland S. Kopple J.D. et al.Is controlling phosphorus by decreasing dietary protein intake beneficial or harmful in persons with chronic kidney disease?.Am J Clin Nutr. 2008; 88: 1511-1518Crossref PubMed Scopus (205) Google Scholar An alternative strategy for reducing phosphate content of food is the manner of cooking, as cooking procedures have been demonstrated to affect the bioavailability of phosphate by breaking down food structure and changing mineral solubility. In this regard, boiling sliced meat for 30 minutes in soft water reduced its phosphate content by 50%, with no significant changes in the protein content.35Ando S. Sakuma M. Morimoto Y. Arai H. The effect of various boiling conditions on reduction of phosphorus and protein in meat.J Ren Nutr. 2015; 25: 504-509Abstract Full Text Full Text PDF PubMed Google Scholar Finally, recent studies further demonstrated the difficulty of controlling serum phosphate with dietary phosphate restriction. For instance, in a crossover feeding study in 11 CKD patients (estimated glomerular filtration rate 30–45 ml/min per 1.73 m2), a low-phosphate diet (1000 mg/d) lowered serum phosphate levels in comparison to a high-phosphate diet (2500 mg/d), with no change in PTH or FGF23 levels.36Ix J.H. Anderson C.A. Smits G. et al.Effect of dietary phosphate intake on the circadian rhythm of serum phosphate concentrations in chronic kidney disease: a crossover study.Am J Clin Nutr. 2014; 100: 1392-1397Crossref PubMed Google Scholar On the other hand, Chang et al. could not demonstrate any effect of consuming a diet with low content of phosphate additives (11 mg/d) for 3 weeks on serum phosphate and FGF23 levels in patients with CKD stage 2 (mean estimated glomerular filtration rate 79.0 ± 25.3 ml/min per 1.73 m2), although urinary phosphate excretion and serum PTH levels decreased significantly.37Chang A.R. Miller 3rd, E.R. Anderson C.A. et al.Phosphorus additives and albuminuria in early stages of CKD: a randomized controlled trial.Am J Kidney Dis. 2017; 69: 200-209Abstract Full Text Full Text PDF PubMed Google Scholar With that in mind, dietary phosphate restriction in CKD patients requires a rational approach rather than an indiscriminate prescription of reduced dietary protein intake. The nature of dietary phosphate, including hidden sources, should be carefully examined. Appropriate dietary counseling and educational programs involving patients in their own care are important. Encouraging patients to reduce meat consumption and to shift to a grain-based vegetarian diet may allow sufficient protein intake without adversely affecting serum phosphate. Last but not least, it must be stressed that dietary phosphate restriction is difficult to accept and usually insufficient to achieve adequate control of serum phosphate. Therefore, other strategies such as phosphate binders, and phosphate removal by dialysis in patients with ESRD, need to be discussed and prescribed on an individual basis when deemed necessary. All effective phosphate binders reduce the absorption of dietary phosphate in the gastrointestinal tract. The mechanism of action is an exchange of the anion phosphate with an active cation (carbonate, acetate, oxyhydroxide, and citrate) to form a nonabsorbable compound that is excreted in the feces. Insufficient patient adherence is a central problem associated with phosphate binder treatment, given the usually high pill burden, large pill size, and ensuing gastrointestinal adverse events.38Fissell R.B. Karaboyas A. Bieber B.A. et al.Phosphate binder pill burden, patient-reported non-adherence, and mineral bone disorder markers: findings from the DOPPS.Hemodial Int. 2016; 20: 38-49Crossref PubMed Google Scholar Even under supervised study conditions and short follow-up, more than 3 of 4 patients were found to adhere incompletely to phosphate binder prescription.39Van Camp Y.P. Vrijens B. Abraham I. et al.Adherence to phosphate binders in hemodialysis patients: prevalence and determinants.J Nephrol. 2014; 27: 673-679Crossref PubMed Scopus (12) Google Scholar Aluminum-based phosphate binders are among the most effective and best-tolerated chelators as regards acute side effects. In addition, treatment cost is low. However, from the 1970s onward, an increasing number of dialysis patients were found to suffer from severe aluminum intoxication, its major clinical manifestations being encephalopathy, osteomalacia, microcytic anemia, and premature death.40Alfrey A.C. LeGendre G.R. Kaehny W.D. The dialysis encephalopathy syndrome. Possible aluminum intoxication.N Engl J Med. 1976; 294: 184-188Crossref PubMed Google Scholar In the majority of cases, dialysis fluid contamination by aluminum was identified as the main culprit.41Mudge D.W. Johnson D.W. Hawley C.M. et al.Do aluminium-based phosphate binders continue to have a role in contemporary nephrology practice?.BMC Nephrol. 2011; 12: 20Crossref PubMed Scopus (30) Google Scholar Fortunately, this dramatic epidemic could be solved subsequently by using more appropriate, ultrapure water as dialysis fluid.42Davison A.M. Walker G.S. Oli H. Lewins A.M. Water supply aluminium concentration, dialysis dementia, and effect of reverse-osmosis water treatment.Lancet. 1982; 2: 785-787Abstract PubMed Google Scholar However, even in nondialyzed patients with CKD, sporadic cases of aluminum intoxication due to aluminium-containing phosphate binders were reported as well.43Norris K.C. Crooks P.W. Nebeker H.G. et al.Clinical and laboratory features of aluminum-related bone disease: differences between sporadic and epidemic forms of the syndrome.Am J Kidney Dis. 1985; 6: 342-347Abstract Full Text PDF PubMed Google Scholar In this respect, it is noteworthy that citrate has been found to enhance intestinal aluminum absorption considerably, at least in predisposed individuals.44Bakir A.A. The fatal interplay of aluminum and citrate in chronic renal failure: a lesson from three decades ago.Artif Organs. 2015; 39: 87-89Crossref PubMed Scopus (1) Google Scholar Uremic infants and children appear to be at particularly high risk for oral aluminum overload, possibly owing to a more permeable intestinal mucosa at young age.45Foley C.M. Polinsky M.S. Gruskin A.B. et al.Encephalopathy in infants and children with chronic renal disease.Arch Neurol. 1981; 38: 656-658Crossref PubMed Google Scholar Therefore, at present, the prolonged use of aluminium-containing phosphate binders in patients with CKD is strongly discouraged, in accordance with recent clinical practice guidelines.20Kidney Disease: Improving Global OutcomesKDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF Scopus (153) Google Scholar Calcium-based binders (calcium carbonate and calcium acetate) became the binders of choice in the 1980s and 1990s. They were found to be effective and to avoid the serious complications sometimes observed with aluminum-containing compounds.46Janssen M.J. van der Kuy A. ter Wee P.M. van Boven W.P. Aluminum hydroxide, calcium carbonate and calcium acetate in chronic intermittent hemodialysis patients.Clin Nephrol. 1996; 45: 111-119PubMed Google Scholar, 47Jespersen B. Jensen J.D. Nielsen H.K. et al.Comparison of calcium carbonate and aluminium hydroxide as phosphate binders on biochemical bone markers, PTH(1-84), and bone mineral content in dialysis patients.Nephrol Dial Transplant. 1991; 6: 98-104Crossref PubMed Google Scholar Calcium acetate is at least as effective as calcium carbonate in lowering serum phosphate in chronic dialysis patients46Janssen M.J. van der Kuy A. ter Wee P.M. van Boven W.P. Aluminum hydroxide, calcium carbonate and calcium acetate in chronic intermittent hemodialysis patients.Clin Nephrol. 1996; 45: 111-119PubMed Google Scholar, 48Almirall J. Veciana L. Llibre J. Calcium acetate versus calcium carbonate for the control of serum phosphorus in hemodialysis patients.Am J Nephrol. 1994; 14: 192-196Crossref PubMed Google Scholar. However, hypercalcemia episodes have been shown to occur more frequently with calcium acetate.49Pflanz S. Henderson I.S. McElduff N. Jones M.C. Calcium acetate versus calcium carbonate as phosphate-binding agents in chronic haemodialysis.Nephrol Dial Transplant. 1994; 9: 1121-1124Crossref PubMed Scopus (49) Google Scholar In the predialysis setting, calcium acetate was found to be effective in reducing serum phosphorus and intact PTH over a 12-week period in a randomized, double-blind, placebo-controlled trial,50Qunibi W. Winkelmayer W.C. Solomon R. et al.A randomized, double-blind, placebo-controlled trial of calcium acetate on serum phosphorus concentrations in patients with advanced non-dialysis-dependent chronic kidney disease.BMC Nephrol. 2011; 12: 9Crossref PubMed Scopus (0) Google Scholar but calcium carbonate is equally effective.51Fournier A. Moriniere P. Sebert J.L. et al.Calcium carbonate, an aluminum-free agent for control of hyperphosphatemia, hypocalcemia, and hyperparathyroidism in uremia.Kidney Int Suppl. 1986; 18: S114-S119PubMed Google Scholar A key concern with calcium-containing phosphate binders is the rapid achievement of a positive calcium balance due to daily calcium loading.20Kidney Disease: Improving Global OutcomesKDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF Scopus (153) Google Scholar Effectively, in 2 small randomized trials in CKD 3b–4 patients, calcium carbonate supplementation produced a slightly positive calcium balance and did not affect phosphate balance,52Hill K.M. Martin B.R. Wastney M.E. et al.Oral calcium carbonate affects calcium but not phosphorus balance in stage 3-4 chronic kidney disease.Kidney Int. 2013; 83: 959-966Abstract Full Text Full Text PDF PubMed Scopus (131) Google Scholar, 53Spiegel D.M. Brady K. Calcium balance in normal individuals and in patients with chronic kidney disease on low- and high-calcium diets.Kidney Int. 2012; 81: 1116-1122Abstract Full Text Full Text PDF PubMed Scopus (101) Google Scholar although in 1 of these patients it produced a modest reduction in urinary phosphate excretion compared with placebo.52Hill K.M. Martin B.R. Wastney M.E. et al.Oral calcium carbonate affects calcium but not phosphorus balance in stage 3-4 chronic kidney disease.Kidney Int. 2013; 83: 959-966Abstract Full Text Full Text PDF PubMed Scopus (131) Google Scholar The development of ectopic calcification in the media and intima of arterial vessels has been recognized as a major contributing factor for the excess cardiovascular mortality observed in CKD patients.54London G.M. Guerin A.P. Marchais S.J. et al.Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality.Nephrol Dial Transplant. 2003; 18:" @default.
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• W2951533026 title "Strategies for Phosphate Control in Patients With CKD" @default.
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