Phosphorus control in peritoneal dialysis patients
Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment...
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Published in: | Kidney international Vol. 73; no. S108; pp. S152 - S158 |
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01-04-2008
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Abstract | Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean±s.d. age of 55±16 years and mean duration of PD of 33±25 months. Serum calcium (Ca2+), ionized Ca2+, phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D3, 1,25-dihydroxy vitamin D3, total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3±0.65, weekly creatinine clearance 78.5±76.6 l, and daily urine output 550±603 ml day−1. Fifty-five percent of patients had a urine volume of <400 ml day−1. Mean serum phosphorus level was 4.9±1.3 mg per 100 ml, serum Ca2+ 9.4±1.07 mg per 100 ml, iPTH 267±356 pg ml−1, ionized Ca2+ 1.08±0.32 mg per 100 ml, calcium phosphorus (Ca × P) product 39±19 mg2dl−2, 25(OH)D3 8.3±9.3 ng ml−1, 1,25(OH)2D3 9.7±6.7 pg ml−1, total alkaline phosphatase 170±178 U l−1, and bone alkaline phosphatase 71±108 U l−1. While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca2+ level was ≥9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca × P product was >55 mg2dl−2 in 136 patients (26%) and lower than 55 mg2dl−2 in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1±1.4 and 4.5±1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca × P in 73%, serum Ca2+ in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosporus control in the majority of patients. |
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AbstractList | Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean±s.d. age of 55±16 years and mean duration of PD of 33±25 months. Serum calcium (Ca2+ ), ionized Ca2+ , phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D3 , 1,25-dihydroxy vitamin D3 , total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3±0.65, weekly creatinine clearance 78.5±76.6 l, and daily urine output 550±603 ml day-1 . Fifty-five percent of patients had a urine volume of <400 ml day-1 . Mean serum phosphorus level was 4.9±1.3 mg per 100 ml, serum Ca2+ 9.4±1.07 mg per 100 ml, iPTH 267±356 pg ml-1 , ionized Ca2+ 1.08±0.32 mg per 100 ml, calcium phosphorus (Ca × P) product 39±19 mg2 dl-2 , 25(OH)D3 8.3±9.3 ng ml-1 , 1,25(OH)2 D3 9.7±6.7 pg ml-1 , total alkaline phosphatase 170±178 U l-1 , and bone alkaline phosphatase 71±108 U l-1 . While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca2+ level was [greater-than-or-equal-to];9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca × P product was >55 mg2 dl-2 in 136 patients (26%) and lower than 55 mg2 dl-2 in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1±1.4 and 4.5±1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca × P in 73%, serum Ca2+ in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosporus control in the majority of patients.Kidney International (2008) 73, S152-S158; doi:10.1038/sj.ki.5002617 Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean±s.d. age of 55±16 years and mean duration of PD of 33±25 months. Serum calcium (Ca2+), ionized Ca2+, phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D3, 1,25-dihydroxy vitamin D3, total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3±0.65, weekly creatinine clearance 78.5±76.6 l, and daily urine output 550±603 ml day−1. Fifty-five percent of patients had a urine volume of <400 ml day−1. Mean serum phosphorus level was 4.9±1.3 mg per 100 ml, serum Ca2+ 9.4±1.07 mg per 100 ml, iPTH 267±356 pg ml−1, ionized Ca2+ 1.08±0.32 mg per 100 ml, calcium phosphorus (Ca × P) product 39±19 mg2dl−2, 25(OH)D3 8.3±9.3 ng ml−1, 1,25(OH)2D3 9.7±6.7 pg ml−1, total alkaline phosphatase 170±178 U l−1, and bone alkaline phosphatase 71±108 U l−1. While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca2+ level was ≥9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca × P product was >55 mg2dl−2 in 136 patients (26%) and lower than 55 mg2dl−2 in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1±1.4 and 4.5±1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca × P in 73%, serum Ca2+ in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosporus control in the majority of patients. Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean+/-s.d. age of 55+/-16 years and mean duration of PD of 33+/-25 months. Serum calcium (Ca(2+)), ionized Ca(2+), phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D(3), 1,25-dihydroxy vitamin D(3), total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3+/-0.65, weekly creatinine clearance 78.5+/-76.6 l, and daily urine output 550+/-603 ml day(-1). Fifty-five percent of patients had a urine volume of <400 ml day(-1). Mean serum phosphorus level was 4.9+/-1.3 mg per 100 ml, serum Ca(2+) 9.4+/-1.07 mg per 100 ml, iPTH 267+/-356 pg ml(-1), ionized Ca(2+) 1.08+/-0.32 mg per 100 ml, calcium phosphorus (Ca x P) product 39+/-19 mg(2)dl(-2), 25(OH)D(3) 8.3+/-9.3 ng ml(-1), 1,25(OH)(2)D(3) 9.7+/-6.7 pg ml(-1), total alkaline phosphatase 170+/-178 U l(-1), and bone alkaline phosphatase 71+/-108 U l(-1). While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca(2+) level was > or =9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca x P product was >55 mg(2)dl(-2) in 136 patients (26%) and lower than 55 mg(2)dl(-2) in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1+/-1.4 and 4.5+/-1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca x P in 73%, serum Ca(2+) in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosphorus control in the majority of patients. Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate control and its clinical and laboratory associations in a large international group of patients on chronic peritoneal dialysis (PD) treatment. This cross-sectional multicenter study was carried out in 24 centers in three different countries (Canada, Greece, and Turkey) among 530 PD patients (235 women, 295 men) with a mean+/-s.d. age of 55+/-16 years and mean duration of PD of 33+/-25 months. Serum calcium (Ca(2+)), ionized Ca(2+), phosphate, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D(3), 1,25-dihydroxy vitamin D(3), total alkaline phosphatase, and bone alkaline phosphatase concentrations were investigated, along with adequacy parameters such as Kt/V, weekly creatinine clearance, and daily urine output. Mean Kt/V was 2.3+/-0.65, weekly creatinine clearance 78.5+/-76.6 l, and daily urine output 550+/-603 ml day(-1). Fifty-five percent of patients had a urine volume of <400 ml day(-1). Mean serum phosphorus level was 4.9+/-1.3 mg per 100 ml, serum Ca(2+) 9.4+/-1.07 mg per 100 ml, iPTH 267+/-356 pg ml(-1), ionized Ca(2+) 1.08+/-0.32 mg per 100 ml, calcium phosphorus (Ca x P) product 39+/-19 mg(2)dl(-2), 25(OH)D(3) 8.3+/-9.3 ng ml(-1), 1,25(OH)(2)D(3) 9.7+/-6.7 pg ml(-1), total alkaline phosphatase 170+/-178 U l(-1), and bone alkaline phosphatase 71+/-108 U l(-1). While 14% of patients were hypophosphatemic, with a serum phosphorus level lower than 3.5 mg per 100 ml, most patients (307 patients, 58%) had a serum phosphate level between 3.5 and 5.5 mg per 100 ml. Serum phosphorus level was 5.5 mg per 100 ml or greater in 28% (149) of patients. Serum Ca(2+) level was > or =9.5 mg per 100 ml in 250 patients (49%), between 8.5 and 9.5 mg per 100 ml in 214 patients (40%), and lower than 8.5 mg per 100 ml in 66 patients (12%). Ca x P product was >55 mg(2)dl(-2) in 136 patients (26%) and lower than 55 mg(2)dl(-2) in 394 patients (74%). Serum phosphorus levels were positively correlated with serum albumin (P<0.027) and iPTH (P=0.001), and negatively correlated with age (P<0.033). Serum phosphorus was also statistically different (P = 0.013) in the older age group (>65 years) compared to younger patients; mean levels were 5.1+/-1.4 and 4.5+/-1.1 mg per 100 ml, respectively, in the two groups. In our study, among 530 PD patients, accepted uremic-normal limits of serum phosphorus control was achieved in 58%, Ca x P in 73%, serum Ca(2+) in 53%, and iPTH levels in 24% of subjects. Our results show that chronic PD, when combined with dietary measures and use of phosphate binders, is associated with satisfactory serum phosphorus control in the majority of patients. |
Author | Çamsari, T. Dimitriades, A.C. Wu, G. Yavuz, M. Özener, Ç Akçiçek, F. Süleymanlar, G. Ataman, R. Arinsoy, T. Yavuz, A. Evaggelos, D.M. Ateş, K. Yilmaz, M.E. Vlachojannis, G.J. Gültekin, M. Utaş, C. Dombros, N.A. Bozfakioğlu, S. Katopodis, K.P. Oreopoulos, D.G. Akpolat, T. Tam, P. Karayaylali, I. Ersoy, F.F. Stathakis, C.P. Passadakis, P.S. Tsakiris, D.J. |
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ContentType | Journal Article |
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Keywords | dialysis phosphate binders phosphorus control calcium renal osteodystrophy peritoneal dialysis phosphorus |
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References | Ayus, Achinger, Mizani (bb0045) 2007; 71 Nakamoto, Imai, Kawanishi (bb0110) 2001; 17 Block, Hulbert-Shearon, Levin (bb0010) 1998; 31 Martin, Gonzalez (bb0125) 2007; 18 Sugarman, Frederick, Frankenfield (bb0090) 2003; 42 Neves, Graciolli, dos Reis (bb0020) 2007; 71 Sanchez, Bajo, Selgas (bb0175) 2000; 36 Ishimura, Nishizawa, Inaba (bb0180) 1999; 55 Bugg, Jones (bb0075) 1998; 53 Ureña, Prié, Molina-Blétry (bb0135) 2007; 71 Slinin, Foley, Collins (bb0095) 2005; 16 Sawaya, Butros, Naqvi (bb0130) 2003; 64 Taniwaki (bb0015) 2005; 11 Chandna, Farrington (bb0105) 2004; 17 Morishita, Shirai, Kubota (bb0140) 2001; 131 Goodman (bb0160) 2006; 70 Wallot, Bonzel, Winter (bb0155) 1996; 10 Young, Akiba, Albert (bb0100) 2004; 44 Rufino, de Bonis, Martin (bb0030) 1998; 13 Marcen, Teruel, de la Cal (bb0120) 1997; 12 Jean, Chazot, Charra (bb0050) 2006; 21 Ganesh, Stack, Levin (bb0150) 2001; 12 Stoff (bb0080) 1982; 72 Nessim, Jassal, Fung (bb0185) 2007; 71 Eknoyan, Levin, Levin (bb0085) 2003; 42 Weinreich, Passlick-Deetjen, Ritz, for the Collaborators of the Peritoneal Dialysis Multicenter Study Group (bb0165) 1995; 25 Wang, Woo, Sea (bb0070) 2004; 43 Qunibi, Nolan (bb0035) 2004; 66 Musci, Hercz, Uldall (bb0040) 1998; 53 Sanchez, Lopez-Barea, Sanchez-Cabezudo (bb0170) 2004; 19 Alfrey (bb0025) 2004; 90 Young, Albert, Satayathum (bb0060) 2005; 67 Koo, Yoon, Kim (bb0115) 2003; 41 Achinger, Ayus (bb0055) 2005; 67 Winchester, Rotellar, Goggins (bb0065) 1993; 41 Taal, Roe, Masud (bb0145) 2003; 63 Bugg, NC, Jones, JA 1998; 53 Block, GA, Hulbert-Shearon, TE, Levin, NW 1998; 31 Sugarman, JR, Frederick, PR, Frankenfield, DL 2003; 42 Winchester, JF, Rotellar, C, Goggins, M 1993; 41 Alfrey, AC 2004; 90 Wang, AY, Woo, J, Sea, MM 2004; 43 Chandna, SM, Farrington, K 2004; 17 Musci, I, Hercz, G, Uldall, R 1998; 53 Slinin, Y, Foley, RN, Collins, AJ 2005; 16 Ayus, JC, Achinger, SG, Mizani, MR 2007; 71 Marcen, R, Teruel, JL, de la Cal, MA 1997; 12 Ganesh, SK, Stack, AG, Levin, NW 2001; 12 Rufino, M, de Bonis, E, Martin, M 1998; 13 Achinger, SG, Ayus, JC 2005; 67 Young, EW, Akiba, T, Albert, JM 2004; 44 Ureña, T, Prié, D, Molina-Blétry, V 2007; 71 Wallot, M, Bonzel, KE, Winter, A 1996; 10 Neves, KR, Graciolli, FG, dos Reis, LM 2007; 71 Goodman, WG 2006; 70 Ishimura, E, Nishizawa, Y, Inaba, M 1999; 55 Sanchez, C, Lopez-Barea, F, Sanchez-Cabezudo, J 2004; 19 Jean, G, Chazot, C, Charra, B 2006; 21 Nakamoto, H, Imai, H, Kawanishi, H 2001; 17 Sawaya, BP, Butros, R, Naqvi, S 2003; 64 Nessim, SJ, Jassal, SV, Fung, SV 2007; 71 Young, EW, Albert, JM, Satayathum, S 2005; 67 Eknoyan, G, Levin, A, Levin, NW 2003; 42 Martin, KJ, Gonzalez, EA 2007; 18 Morishita, K, Shirai, A, Kubota, M 2001; 131 Qunibi, WY, Nolan, CR 2004; 66 Taniwaki, H 2005; 11 Stoff, JC 1982; 72 Sanchez, MC, Bajo, MA, Selgas, R 2000; 36 Koo, JR, Yoon, JW, Kim, SG 2003; 41 Taal, MW, Roe, S, Masud, T 2003; 63 Weinreich, T, Passlick-Deetjen, J, Ritz, E 1995; 25 Slinin (10.1038/sj.ki.5002617_bb0095) 2005; 16 Nakamoto (10.1038/sj.ki.5002617_bb0110) 2001; 17 Sanchez (10.1038/sj.ki.5002617_bb0175) 2000; 36 Taniwaki (10.1038/sj.ki.5002617_bb0015) 2005; 11 Young (10.1038/sj.ki.5002617_bb0100) 2004; 44 Winchester (10.1038/sj.ki.5002617_bb0065) 1993; 41 Taal (10.1038/sj.ki.5002617_bb0145) 2003; 63 Sanchez (10.1038/sj.ki.5002617_bb0170) 2004; 19 Qunibi (10.1038/sj.ki.5002617_bb0035) 2004; 66 Achinger (10.1038/sj.ki.5002617_bb0055) 2005; 67 Weinreich (10.1038/sj.ki.5002617_bb0165) 1995; 25 Neves (10.1038/sj.ki.5002617_bb0020) 2007; 71 Musci (10.1038/sj.ki.5002617_bb0040) 1998; 53 Koo (10.1038/sj.ki.5002617_bb0115) 2003; 41 Sugarman (10.1038/sj.ki.5002617_bb0090) 2003; 42 Young (10.1038/sj.ki.5002617_bb0060) 2005; 67 Wang (10.1038/sj.ki.5002617_bb0070) 2004; 43 Alfrey (10.1038/sj.ki.5002617_bb0025) 2004; 90 Ayus (10.1038/sj.ki.5002617_bb0045) 2007; 71 Morishita (10.1038/sj.ki.5002617_bb0140) 2001; 131 Ishimura (10.1038/sj.ki.5002617_bb0180) 1999; 55 Nessim (10.1038/sj.ki.5002617_bb0185) 2007; 71 Ganesh (10.1038/sj.ki.5002617_bb0150) 2001; 12 Martin (10.1038/sj.ki.5002617_bb0125) 2007; 18 Bugg (10.1038/sj.ki.5002617_bb0075) 1998; 53 Chandna (10.1038/sj.ki.5002617_bb0105) 2004; 17 Stoff (10.1038/sj.ki.5002617_bb0080) 1982; 72 Block (10.1038/sj.ki.5002617_bb0010) 1998; 31 Jean (10.1038/sj.ki.5002617_bb0050) 2006; 21 Wallot (10.1038/sj.ki.5002617_bb0155) 1996; 10 Goodman (10.1038/sj.ki.5002617_bb0160) 2006; 70 Marcen (10.1038/sj.ki.5002617_bb0120) 1997; 12 Ureña (10.1038/sj.ki.5002617_bb0135) 2007; 71 Rufino (10.1038/sj.ki.5002617_bb0030) 1998; 13 Eknoyan (10.1038/sj.ki.5002617_bb0085) 2003; 42 Sawaya (10.1038/sj.ki.5002617_bb0130) 2003; 64 |
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publication-title: Am J Kidney Dis contributor: fullname: Sea, MM – volume: 64 start-page: 737 year: 2003 end-page: 742 article-title: Differences in bone turnover and intact PTH levels between African American and Caucasian patients with end-stage renal disease publication-title: Kidney Int contributor: fullname: Naqvi, S – volume: 11 start-page: 2472 year: 2005 end-page: 2478 article-title: Aortic calcification in haemodialysis patients with diabetes mellitus publication-title: Nephrol Dial Transplant contributor: fullname: Taniwaki, H – volume: 131 start-page: 3182 year: 2001 end-page: 3188 article-title: The progression of aging in klotho mutant mice can be modified by dietary phosphorus and zinc publication-title: J Nutr contributor: fullname: Kubota, M – volume: 72 start-page: 489 year: 1982 end-page: 495 article-title: Phosphate homeostasis and hypophosphatemia publication-title: Am J Med contributor: fullname: Stoff, JC – volume: 17 start-page: 196 year: 2004 end-page: 201 article-title: Residual renal function: considerations on its importance and preservation in dialysis patients publication-title: Semin Dial contributor: fullname: Farrington, K – volume: 53 start-page: 895 year: 1998 end-page: 902 article-title: Hypophosphatemia: pathophysiology, effects and management on intensive care unit publication-title: Anaesthesia contributor: fullname: Jones, JA – volume: 42 start-page: 1 year: 2003 end-page: 201 article-title: Bone metabolism and disease in chronic kidney disease publication-title: Am J Kidney Dis contributor: fullname: Levin, NW – volume: 12 start-page: 2131 year: 2001 end-page: 2138 article-title: Association of elevated serum PO , Ca × PO product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients publication-title: J Am Soc Nephrol contributor: fullname: Levin, NW – volume: 31 start-page: 607 year: 1998 end-page: 617 article-title: Association of serum phosphorus and calcium × phosphate product with mortality risk in chronic hemodialysis patients: a national study publication-title: Am J Kidney Dis contributor: fullname: Levin, NW – volume: 13 start-page: 65 year: 1998 end-page: 67 article-title: Is it possible to control hyperphosphatemia with diet, without inducing protein malnutrition? 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Snippet | Hyperphosphatemia is independently associated with an increased risk of death among dialysis patients. In this study, we have assessed the status of phosphate... |
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SubjectTerms | Adult Aged Alkaline Phosphatase - blood Biological Transport - physiology calcium Calcium - blood Creatinine - blood Cross-Sectional Studies dialysis Female Humans Hyperphosphatemia - blood Hyperphosphatemia - prevention & control Kidney Failure, Chronic - blood Kidney Failure, Chronic - therapy Male Middle Aged Parathyroid Hormone - blood peritoneal dialysis Peritoneal Dialysis - methods phosphate binders phosphorus Phosphorus - blood phosphorus control renal osteodystrophy |
Title | Phosphorus control in peritoneal dialysis patients |
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