The Egyptian Journal of Hospital Medicine (April 2012) Vol., 47:

Transcription

1 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Study Of Cadic Valvula Calcification In ESRD Patients On Regula Hemodialysis (A Single Cente Study) AbdelBassit El Shaaawy 1, Mona Hosny 1, Mana Raafat 2 and Nelly Gendy 2 1 Intenal Medicine Deatment, Faculty of Medicine, Ain Shams Univesity; 2 Intenal Medicine Deatment, Theodo Bilhaze Institute. ABSTRACT: Cadiac valve calcification ae common among atients with chonic kidney disease (CKD). Risk factos include alteations in calcium and hoshous metabolism, elevated calcium hoshous oduct and esistent elevations in lasma aathyoid homone (PTH). Echocadiogahy is a simle and inexensive method fo detection of valvula calcifications as suggested by KDIGO guidelines. 60 Patients on egula HD constituted gou A (36 males and 24 females) and 25 healthy voluntees constituted gou B. Gou A was subdivided into: Gou I: 21 atients with no valvula calcification, gou 2: 26 atients with aotic valve calcification and gou 3: 13 atients with aotic and mital valve calcification. Fo all, the following was done: clinical examination, seum Ca, seum P, seum albumin, seum ceatinine, BUN and PTH level in blood. Mmode echo cadiogahy was done fo all. Age, duation of dialysis and duation of 1y kidney disease was highe in gou 2 and 3 comaed to gou 1 ( = ). Calcium was highe in gou 2 than gou 1 ( = 0.09) and gou 3 ( = 0.004) than gou I hoshous was highe in gou 2 and 3 than gou 1 (P = 0.001). P was highe in gou 3 than gou 2 ( = ). Ca x P was highe in gou 2 and 3 than gou 1 ( = ), in gou 3 than gou 2 ( = 0.01) PTH was highe in gou 1 than gou 2 ( = 0.06). Cadiac dysfunction by echocadiogahy was least in gou 1, inceasing in gou 2 and being highest in gou 3. It was found that calcified valve gous has taken highe doses of Calcium and Vitamin D3. We have to take cae on escibing Ca and vitamin D3 to ESRD atients on egula HD. KEY WORDS: Valvula Calcification Ca P PTH Ca x P HEMODIALYSIS. INTRODUCTION: Patients with endstage enal disease in those with nomal enal function (Enesto (ESRD) ae fequently budened with et al., 2003). calcific valvula heat disease (Adagoa et KDIGO ovided a new definition of CKDal., 2004). Valvula involvement in ESRD is MBD: a systemic disode of mineal and most commonly manifested as mital bone metabolism due to CKD, manifested by annula calcification and aotic valve abnomalities of calcium, hoshous, PTH o calcification. Both mital and aotic valve vitamin D metabolism, abnomalities in bone calcification (MAC) occu moe fequently tunove, vascula o othe softtissue and at younge age in those with ESRD than calcification. The evalence and seveity of 190

2 AbdelBassit El Shaaawy et al extaosseous calcification, incease as kidney function deceases (Uhlig et al., 2010). KDIGO ecommended that an echocadiogam can be used to detect the esence o absence of valvula calcification, as easonable altenative to comuted tomogahy based imaging in atients with CKD stages 35 (Moe et al., 2009). Aim of the Wok To detemine the fequency of valvula calcifications in hemodialysis atients using echocadiogahy and its elation to demogahic and laboatoy data. Patient and methods: The study was caied on 60 atients (gou A) with ESRD on egula hemodialysis [24 females (40%) and 36 males (60%) mean age 49 yeas] and 25 healthy contol subjects (gou B), [11 females (44%) and 14 males (56%), mean age yeas]. The study was conducted in hemodialysis unit of Theodo Bilhaz eseach institute between July 2011 and Januay Gou A atients stated hemodialysis fo moe than six months io to the study. Patients wee dialyzed fo 4 hous thee times weekly using high flux filtes and acetate solution as dialysate. All atients had ateiovenous fistula. We excluded fom the study atients having heumatic heat disease, congenital heat disease o heumatic feve histoy. Gou A was divided into 3 subgous accoding to the esence o absence of valvula calcification: Gou 1: Patients with no valvula calcification. Gou 2: Patients with aotic valve calcification only. Gou 3: Patients with both aotic and mital valve calcification in ESRD. Fo all atients and contols the following was done: 1. Full medical histoy and clinical examination. 2. Laboatoy investigations including: a) Seum ceatinine (mg/dl): accoding to the method of Yatzidis (1974). b) Blood uea (mg/dl): accoding to the method of Tobacco et al., (1979). c) Seum calcium (mg/dl): accoding to the method of Renoe et al. (1980). d) Seum hoshous (mg/dl): accoding to the method of Fael (1987). e) Seum albumin (mg/dl): accoding to the method of Doumas et al. ( 1971). f) Paathyoid homone level (ng/ml): accoding to the method of Endas et al. (1989). g) Fo uoses of the study we calculated the value of calcium hoshous oduct (CaxP (mg 2 /dl 2 ). 3. Echocadiogahy: Accoding to the standad otocol, a ofessional skilled cadiologist had efomed echocadiogahic examination to all atients and contol subjects included in the study. M mode, two dimensional echocadiogahy and Dole ultasound studies (ulsed, continuous wave and colou flow imaging) wee efomed using a high esolution (ALT 5000 HDI) scanning device. 191

3 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: We measued aotic oot dimension (AO in mm), valve calcification in ESRD, Right atium dimension (RA in mm), Enddiastolic dimensions (EDD in mm), Endsystolic dimensions (ESD in mm), shotening faction (FS in %), ejection faction (EF in %), inteventicula setum dimensions (IVST d in mm), and osteio wall dimensions in diastole (PWTd in mm). Statistical ackage of social science (SPSS) vesion 15.0 was used fo analysis of data. Data was summaized as mean and standad deviation, Ttest was used fo analysis of two quantitative data and non aametic test (MannWhitney U) was used when data was not symmetically distibuted. Also Peason linea coelation test was used in study valve calcification in ESRD. 4. Statistical methods: * was consideed significant if < 0.05 (S). * was consideed bodeline significance if < (BS). * was consideed highly significant if < 0.01 (HS). * was consideed nonsignificant if > (NS). Table (1): Fequency distibution of demogahic data of gou A Vaiables N % Sex Male Female Pimay kidney disease: Unknown Diabetes mellitus Hyetension Chonic glomeulonehitis Vascula insults: Non Peiheal vascula insult Ischemic heat disease Stoke Aotic calcification Negative Positive Mital calcification Negative Positive Aotic eguge AR Aotic stenosis Mital stenosis Table (2): Comaison of age between gou A and gou B 192

4 AbdelBassit El Shaaawy et al Vaiables Gou A Gou B Age (ys) * Unaied ttest Table (3): Comaison of laboatoy data between gou A and gou B Vaiables Gou A Gou B Uea (mg/dl) * (HS) Ceatinine (mg/dl) * (HS) Albumin (g/day) * (HS) Ca (mg/dl) * (HS) P (mg/dl) * (HS) Ca x P (mg 2 /dl 2 ) * (HS) PTH (mg/dl) * (HS) * Unaied ttest. Table (4): Comaison of laboatoy data between gou A and gou B Vaiables Gou A Gou B AO (mm) RA (mm) * EDD (mm) ESD (mm) * FS (%) EF (%) * IVSTd (mm) * PWTd (mm) * * Unaied ttest. Gou 1 constituted 35% of all atients of gou A and it comised 9 females (42.8%) and 12 males (57.15%), gou 2 constituted 43.33% of all atients of gou A and it comised 12 females (46.15%) and 14 males (53.85%). Gou 3 constituted 21.66% of all atients of gou A and it comised 3 females (23.06%) and 10 males (76.94%). Table (5): Results of valvula calcification and valvula lesions in HD atients Valvula No valvula calcification calcification Numbe (n %) 39 (65%) 21 (35%) Isolated mital valve calcification Isolated aotic valve calcification 26 (66.66%) Mital and aotic valve calcification 13 (33.33%) Mital eguge 17 (43.5%) Mital stenosis Aotic eguge 18 (46.15%) Aotic stenosis Data ae (n %) 193

5 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Table (6): Comaison between hemodialysis atients without valvula calcification (gou 1) and with valvula calcification (gou 2 and 3). Vaiables Gou 1 Gou 2 & 3 (n = 21) (n = 39) Age (yeas) 38.62± ± Duation of hemodialysis (yeas) 2.43± ± Laboatoy data Uea (mg%) Ceatinine (mg%) Albumin (g%) Ca (mg%) P (mg%) Cax P (mg 2 /dl 2 ) PTH (mg%) Echocadiogahic data AO (mm) LA (mm) EDD (mm) ESD (mm) FS(%) EF (%) IVSTd (mm) PWTd (mm) Vascula disease Peiheal vascula disease Ischemic heat disease Stoke No vascula insults Dugs Calcium (mg/day) Alfacalcidol (µg/wk) ± ± ±6 8.20± ± ± ± ± ± ± ± ± ± ± ± (23.8%) 1 (4.8%) 0 (0%) 15 (71.4%) ± ± ± ± ±3 8.62± ± ± ± ±4.5 48± ± ± ± ± ± ± (35.9%) 7 (17.9%) 4 (1%) 14 (35.9%) ± ±0.76 Table (7): Valvula calcification accoding to the etiology of enal disease Etiology of enal disease N = 39 Hyetension 20 (51%) Diabetes 10 (25.6%) Chonic glomeulonehitis 4 (15%) Unknown etiology 5 (12.8%) Table (8): Comaison between gou 1 and gou 2 as egads demogahic data. Vaiables Gou 1 Gou 2 Age (ys) (HS) Duation of imay kidney disease (ys) (HS) Duation of hemodialysis (ys) (HS) * Unaied ttest. 194

6 AbdelBassit El Shaaawy et al Table (9): Comaison between gou 1 and gou 2 as egads laboatoy data Vaiables Gou 1 Gou 2 Uea (mg/dl) (S) Ceatinine (mg/dl) Albumin (g/day) Ca (mg/dl) (HS) P (mg/dl) (HS) Ca x P (HS) (mg 2 /dl ) PTH (mg/dl) (BS) * Unaied ttest. Table (10): Comaison between gou 1 and gou 2 as egads echocadiogahic aametes Vaiables Gou 1 Gou 2 AO (mm) RA (mm) (NS) EDD (mm) (NS) ESD (mm) (NS) FS (%) (NS) EF (%) (S) IVSTd (mm) (NS) PWTd (mm) (NS) * Unaied ttest. Table (11): Comaison between gou 1 and gou 2 as egads dug doses. Vaiables Gou 1 Gou 2 Calcium (mg/dl) (S) Alhacalcifeol (μg) * Unaied ttest (HS) Table (12): Comaison between gou 1 and gou 3 as egads demogahic data. Vaiables Gou 1 Gou 3 Age (ys) (HS) Duation of imay kidney disease (ys) (HS) Duation of hemodialysis (ys) (HS) * Unaied ttest. 195

7 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Table (13): Comaison between gou 1 and gou 3 as egads laboatoy data Vaiables Gou 1 Gou 3 Uea (mg/dl) Ceatinine (mg/dl) Albumin (g/day) Ca (mg/dl) (NS) P (mg/dl) (HS) Cax P (mg 2 /dl 2 ) (HS) PTH (mg/dl) * Unaied ttest. Table (14): Comaison between gou 1 and gou 3 as egads ecvhocadiogahic aametes Vaiables Gou 1 Gou 3 AO (mm) (NS) RA (mm) (NS) EDD (mm) ESD (mm) (S) FS (%) (S) EF (%) (HS) IVSTd (mm) PWTd (mm) (NS) * Unaied ttest. Table (15): Comaison between gou 1 and gou 3 as egads dug doses Vaiables Gou 1 Gou 3 Calcium (mg) (HS) Alhacalcifeol (μg) (HS) * Unaied ttest. 196

8 AbdelBassit El Shaaawy et al Table (16): Comaison between gou 2 and gou 3 as egads demogahic data Vaiables Gou 2 Gou 3 Age (ys) Duation of imay kidney disease (ys) (NS) Duation of hemodialysis (ys) (S) * Unaied ttest. Table (17): Comaison between gou 2 and gou 3 as egads laboatoy data Gou 2 Gou 3 Vaiables Uea (mg/dl) Ceatinine (mg/dl) Albumin (g/day) Ca (mg/dl) (HS) P (mg/dl) (HS) Cax P (mg 2 /dl 2 ) (HS) PTH (mg/dl) (NS) * Unaied ttest. Table (18): aametes Vaiables Comaison between gou 2 and gou 3 as egads echocadiogahic Gou A Gou B AO (mm) (NS) RA (mm) EDD (mm) (NS) ESD (mm) (NS) FS (%) (NS) EF (%) (NS) IVST (mm) PW (mm) * Unaied ttest. Table (19): Comaison between gou 2 and gou 3 as egads dug doses Vaiables Gou 2 Gou 3 Calcium (mg) (S) Alhacalcifeol (μg) (NS) * Unaied ttest. 197

9 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Table (20): Coelation between Ca, P, Cax P, PTH and demogahic data of atients within gou 1. Age (ys) Vaiables Duation of imay kidney disease (ys) Duation of hemodialysis (ys) Coelation coefficient Ca P CaxP PTH * (S) 0.06 (BS) 0.5 (NS) (NS) (NS) 0.5 (NS) * (HS) Peason Linea Coelation test Table (21): Ca (mg/dl) Vaiables Coelation between Ca, P CaxP, PTH, and laboatoy data of atients within gou 1 Coelation Ca P CaxP PTH coefficient * (S) (NS) P (mg/dl) * (S) * (HS) Cax P (mg 2 /dl 2 ) * (HS) 0.07 PTH (mg/dl) (NS) 0.07 Uea (mg/dl) * (S) (BS) (NS) Ceatinine (mg/dl) * (HS) (NS) (NS) 0.02 Albumin (g/day) (NS) Peason Linea Coelation test 198

10 AbdelBassit El Shaaawy et al Table (22): Coelation between Ca, P, CaxP, PTH and echocadiogahic aametes within gou 1 AO (mm) Vaiables Coelation coefficient Ca P CaxP PTH 0.4 (NS) 0.06 (BS) RA (mm) 0.04 (NS) EDD (mm) 0.02 (NS) (NS) (NS) ESD (mm) 0.5 (NS) 0.5 (NS) (NS) 0.08 FS (%) (NS) 0.5 (NS) 0.03 EF (%) 0.5 (NS) (NS) 0.09 IVSTd (mm) (NS) (NS) 0.09 Peason Linea Coelation test Table (23): Coelation between Ca, P, CaxP, PTH and dug doses within gou 1 atients Vaiables Calcium (mg) Coelation coefficient Ca P CaxP PTH (NS) 0.5 (NS) (NS) Alhacalcifeol (μg) Peason Linea Coelation test 199

11 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Table (24): Coelation between Ca, P, CaxP, PTH and demogahic data within gou 2 Age (ys) Vaiables Coelation coefficient Ca P CaxP PTH (NS) (NS) Duation of imay kidney disease (ys) 0.02 (NS) Duation of hemodialysis (ys) (HS) (NS) Peason Linea Coelation test Table (25): Coelation between Ca, P, CaxP, PTH and laboatoy data within gou 2 Ca (mg/dl) Vaiables Coelation coefficient Ca P CaxP PTH (BS) (NS) P (mg/dl) (BS) * (HS) 0.05 Cax P (mg 2 /dl 2 ) (NS) * (HS) 0.05 PTH (mg/dl) Uea (mg/dl) (NS) (NS) Ceatinine (mg/dl) Albumin (g/day) (NS) 0.04 (NS) 0.08 Peason Linea Coelation test 200

12 AbdelBassit El Shaaawy et al Table (26): Coelation between Ca, P, CaxP, PTH and echocadiogahic aametes within gou 2 AO (mm) Vaiables Coelation coefficient Ca P CaxP PTH (NS) RA (mm) (NS) (NS) (NS) (NS) EDD (mm) ESD (mm) FS (%) * (S) * (HS) 0.05 EF (%) (BS) (NS) (S) IVSTd (mm) PWTd (mm) Peason Linea Coelation test Table (27): Coelation between Ca, P, Cax P, PTH and dug doses within gou 2 Vaiables Calcium (mg) Coelation coefficient Ca P CaxP PTH (S) 0.06 (BS) 0.5 (NS) Alhacalcifeol (μg) (S) (NS) (NS) Peason Linea Coelation test 201

13 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Table (28): Coelation between Ca, P, CaxP, PTH and demogahic data within gou 3 Age (ys) Vaiables Coelation coefficient Ca P CaxP PTH (NS) 0.05* (S) Duation of imay kidney disease (ys) 0.5 (NS) 0.01 Duation of hemodialysis (ys) 0.4 (NS) 0.07 Peason Linea Coelation test Table (29): Coelation between Ca, P, CaxP, PTH and laboatoy data within gou 3 Ca (mg/dl) Vaiables Coelation coefficient Ca P CaxP PTH * (HS) 0.06 (BS) (NS) P (mg/dl) * (HS) Cax P (mg 2 /dl 2 ) (BS) PTH (mg/dl) (NS) Uea (mg/dl) * (HS) Ceatinine (mg/dl) * (S) * (HS) Albumin (g/day) (NS) 0.4 (NS) Peason Linea Coelation test 202

14 AbdelBassit El Shaaawy et al Table (30): Coelation between Ca, P, CaxP, PTH and echocadiogahic data within gou 3, Peason Linea Coelation test AO (mm) RA (mm) EDD (mm) ESD (mm) FS (%) EF (%) Vaiables IVSTd (mm) PWTd (mm) Coelation coefficient Ca P CaxP PTH (NS) (NS) (NS) (NS) 0.4 (NS) (BS) (NS) (NS) * (S) * (S) 0.4 (NS) 0.5 (NS) (NS) 0.8 9NS) Table (31): Coelation between Ca, P, CaxP, PTH and dug doses within gou 3 Peason Linea Coelation test Vaiables Coelation coefficient Ca P CaxP PTH Calcium (mg) 0.6 (NS) 0.05 (S) 0.5 (NS) Alhacalcifeol (μg) (NS) * (HS) Table (32): Pedictos of valvula calcification in multile linea egession analysis in hemodialysis atients. Vaiables B * 95% confidence inteval Constant Duation of hemodialysis (ys) CaxP (mg 2 /dl 2 ) EF (%) Age of atients (yeas) R2 = 0.78, SE (standad eo) = 2 * B (standad egession coefficient) 203

15 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: A multile stewise linea egession analysis was efomed to detemine the indeendent factos of valvula calcification in hemodialysis atients. Vaiables significantly associated with valvula calcification and othe known to have effect on valvula calcification wee intoduced in the model. Afte adjustment fo aametes found significant in the univaiate analysis, the indeendent edictos of valvula calcification wee duation of hemodialysis, CaxP oduct, age and educed EF%. We didn't find any significant coelation between Ca, P, CaxP, PTH and age of healthy contols within gou B. We didn't find any significant coelation between Ca, P, CaxP, PTH and laboatoy data within gou B. We didn't find significant coelations between Ca, P, CaxP, PTH and echocadiogahic aametes within gou B. DISCUSSION Lesions of cadiovascula calcification ae also seen in dialysis atients at a much 49.32±10.68) yeas, the fequency of valvula calcification was 39 atients, 26 younge age than in the geneal atients (43.33%) with aotic calcification oulation. Even adults less than 30 yeas of age on dialysis have a high incidence of coonay atey calcification and these lesions ogess at a elatively aid ate (Isido & William, 2002). Calcification of the mital and aotic valves. Valvula calcification is a make of systemic cadiovascula disease in CKDstage 5 atients (Raggi et al., 2011). Echocadiogahy is the gold standad fo assessment of cadiac valve mohology and function. It is non invasive and elatively inexensive. Calcification of the cadiac valves is found in dialysis atients with a evalence fou to five times highe than in the geneal oulation (Staumann et al., 1992; Mazzafeo et al., 1993 and Ribeio et al., 1998). and 13 atients (21.66%) with both aotic and mital calcification. None of the atients had mital calcification only. Also non of ou atients had ulmonay o ticusid valve athology. The esence of valvula calcifications in ESRD atients is emakably high in all ublished seies. Baum et al. (1996), initially studied 49 maintenance HD atients, and identified calcification of mital valve in 59% of case and aotic valve in 55%. Ribeio et al. (1998) found among 92 atients whose mean age was 60 yeas, 44% had mital valve calcifications on echocadiogahy, and 52% had aotic valve calcifications. Nealy 60% of these atients demonstated calcifications of both valves. In othe studies, mital valve calcifications wee In ou esent study on 60 atients on eoted in 45%, and aotic valve egula HD, of age (mean±sd = calcifications in 34% of atients, while 204

16 AbdelBassit El Shaaawy et al both valves wee affected in 21% of the atients studied (Raggi et al., 2002). Valvula thickening and scleosis, is a fequent finding in HD atients. Among such atients, aotic and mital valve scleosis occu in 55 to 69 and 40 to 60 ecent of individuals, esectively (Stinebaugh et al., 1995 and Staumann et al., 1992). In the Jackson cohot of the atheoscleotic isk in communities study (Fox et al., 2004), the Famingham offsing study (Fox et al., 2006), and the Multiethnic study of atheoscleosis (MESA) (Ix et al., 2007) coss sectional associations wee seen between CKD and mital annula calcification. In addition, the cadiovascula health study (CHS) showed a high evalence of CKD in adults with combined mital annula calcification, aotic annula calcification, and aotic valvula stenosis (Baash et al., 2006). Non of ou contol gou had aotic o mital valve calcification. In ou study atients with no calcification ( gou 1 )had a elatively shot hemodialysis duation (mean±sd = 2.43±1.35) yeas, comaed to atients with calcified aotic valve ( gou 2 ) who had a duation on HD (mean±sd = 8.5±2.61) yeas with a highly statistically significant diffeence between both ( = ). Patients with calcified aotic and mital valve ( gou 3) had a hemodialysis duation of (mean±sd = 10.46±2.90) yeas with a highly significant statistical diffeence between gou 3 and gou 1 ( = ) and a statistically significant diffeence between gou 3 and gou 2 ( = 0.04). This means that hemodialysis duation is imlicated in the occuence of cadiac calcification and also imlicated in the e x t e n t o f c a l c i f i c a t i o n. Patients with valvula calcification eceiving hemodialysis, had longe hemodialysis duation (Vokov et al., 2009 and Stozecki et al., 2005), echocadiogahically examined 65 HD atients ages (49±12). Yeas, with duation of HD theay (38±32) months. Valvula calcification wee found in 32 of 65 atients (49%), mital valve calcifications in 10, aotic valve calcifications in 9, and both valves calcifications in 13 atients. In atients with valvula calcification, duation of HD theay was longe. Also Ribeio et al. (1998), study suggests that atients with valvula calcification wee on longtem enal elacement theay. In ou study, age of atients with no calcification was (mean±sd = 38.62±5.54) yeas, while age of atients with calcified aotic valve was (mean±sd = ±9.46) yeas. Age of atients with calcified aotic and mital valve was (mean±sd = 56.15±7.39) yeas. Patients with calcified aotic valve showed a statistically highe age when comaed to atients with no calcification ( = ). The same esult was found on comaing aients with calcified aotic and mital valve and atients with no calcification ( 205

17 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: = 0.001). While atients with calcified aotic valve and atients with calcified aotic and mital calcification didn't show significant diffeence as egads age ( = 0.4). This agees with studies that suggest that valvula calcification is common in old age atients, gou B and gou A didn't show significant diffeence as egads age ( 0.9). Ribeio et al. (1998) eoted that mital valve calcification was associated with age. Ikee et al. (2010) suggested that mital valve calcification was associated with inceased age. Ribeio et al. (1998) eoted that aotic valve calcification was coelated with age. Ikee et al. (2010), detected heat valve calcification using two dimensional echocadiogahy in atients teated with HD thee times a week. In 112 atients, (77 men and 35 women, age (67±10) yeas, duation of HD (95±67) months, aotic and mital valvula calcification wee obseved in 84 (75.0%) and 58 (51.7%) atients, esectively aotic valve calcification was associated with age. Aotic valve calcification is found in 25 to 55 ecent of HD atients occuing 10 to 20 yeas ealie than in the geneal oulation (Nasi et al., 2004) Mital annula calcification occus ealie in atients with chonic enal failue than those without enal dysfunction (Foman et al., 1984). In ou study, 12 atients (20%) of gou A wee diabetic, 10 atients had valvula calcification. Rufino et al. (2003), had a coss sectional obsevational study, atients with valvula calcification wee moe commonly diabetic. In ou study, 27 atients (4%) of gou A, wee hyetensive, 20 atients had valvula calcifications, all of them had a histoy of edialysis hyetension. In ou study we found 20 atients with aotic calcification who had edialysis hyetension, also atients with aotic insufficiency who suffeed fom diabetes wee 4 atients while atients with aotic insufficiency who suffeed fom hyetension wee 9 out of a total of 15 atients with aotic insufficiency. In Ribeio et al. (1998) study atients with valvula calcification had longe duation of edialysis ateial hyetension. Pevious studies have eoted a histoy of hyetension io to stating dialysis as a edicto of valvula calcifications (Baun et al., 1996; Ribeio et al., 1998 and Yoshida et al., 1999). Baun et al. (1996), studied 49 chonic HD atients aged 28 to 74 yeas that wee comaed to 102 nondialysis atients aged 32 to 73 yeas. They assessed calcification of mital and aotic valves. The mital valve was calcified in 59% of dialysis atients, while aotic valve was calcified in55%. They dew attention to hyetension as an imotant isk facto in this ocess. Huting et al. (1994) obseved that mital valvula calcifications was associated with the seveity of edialysis hyetension. 206

18 AbdelBassit El Shaaawy et al Ribeio et al. (1998) study suggests no coelation was found between valvula calcifications and ateial hyetension, but he eoted that aotic valvula calcification was elated with duation of hyetension and with the longe duation of edialysis ateial hyetension. Aotic insufficiency following aotic valve calcification may be due to the ogession of the comlications of hyetension (Kahnooj et al., 2010). Uea level was significantly highe in atients with no calcification as comaed to atients with calcified aotic valve ( 0.04), this is goes with what was exected that uemia is one the isk factos fo calcification. Low seum albumin is not secific fo valvula calcification gous (2 and 3), but also it does affect (gou 1) without calcification, seeming to be a chaacteistic of ESRD and HD. In contast to ou study, Ikee et al. (2010) stated that aotic valve calcification was associated with lowe seum albumin. Ca, P, and CaxP wee highly significantly lowe in gou A than gou B ( = ) but PTH was much highe in gou A ( = ), Ca, P, CaxP, wee significantly lowe in gou 1with no calcification as comaed to gou 2 (with aotic calcification) ( = 0.009, , ) esectively. PTH was significantly highe in gou 1 than gou 2 ( = 0.06), which is against what was exected. P and C ax P oduct wee highe in atients with calcified aotic and mital valve as comaed to atients with no calcification ( = 0.001), which oints to the ole layed by P and CaxP oduct in calcification. At same time, PTh didn't show significant diffeence between the two gous, which means that it has a less imotant ole in valvula calcification (being insignificantly highe in gou 1, = 0.7). Hyehoshatemia may diectly cause o exacebate othe asects of CKDMBD, including seconday hyeaathyoidism, deceased seum calcitiol levels, abnomal bone emodeling and softtissue calcification (Katin et al., 2010). Ca is significantly highe in atients with calcified aotic valve than in atients with calcified aotic and mital valve ( = 0.004). P and CaxP oduct wee much highe in atients with calcified aotic and mital valve than in atients with aotic calcification, again inciminating them of the moe extensive calcification of the heat valves. PTH was insignificantly highe in atients with calcified aotic and mital valve than in atients with calcified aotic valve ( = ). Pesistent elevations in seum calcium and hoshous levels can be aggavated by the lage doses of vitamin D steols used often to teat seconday hyeaathyoidism (Raggi et al., 2011). Taas et al. (2006) studied 90 atients on maintenance HD fo moe than 12 months, 207

19 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: (40%) esented with valvula calcifications and showed highe levels of seum calcium (92.00±7.54 vesus 89.27±6.86 mg/l, = 0.04), hoshous (69.70±18.33 vesus 44.90±12.43 mg/l, ( < 0.001), CaxP oduct ( ± vesus ± mg 2 /L 2, (P < ) as comaed with atients without valvula calcifications. Volkov et al. (2009), eoted that atients with valvula calcification had high seum calcium level. This was not the case in ou study as egads seum calcium. Stozeeki et al. (2005) study showed that no statistical significant diffeences wee found with esect to Ca, P, PTH and mean CaxP oduct in atients with o without valvula calcifications, but the incidence of CaxP oduct above 44.3 mmol 2 /L 2 was highe in valvula calcifications comaed with those without valvula calcifications. Aotic valve calcification was associated with highe seum calcium. Mital valve calcification was not associated with high seum calcium as stated by Ikee et al.(2010). Toun et al. (2005), found that significantly highe hoshate level was obseved in atients with valvula calcifications (5.1±1.4 vesus 4.5±1.4 mg/dl, = 0.04). Rufino et al. (2003) had a coss sectional obsevational study of a cohot of 52 stable atients on maintenance HD fo moe than 12 months. 20 atients (38.4%) esented with valvula calcifications and showed highe levels of seum hoshous comaed to atients without valvula calcifications. In the esence of low calcium, high hoshous, vitamin D deficiency and uemia aathyoid cells leave quiescence (Cozzolino et al., 2009). Small deceases in seum Ca (++) and moe olonged inceases in hoshate stimulate the aathyoid to secete aathyoid homone (Rochelle et al., 2010). Calcium can dive the initial stes in hydoxyaatite fomation and small changes in calcium concentation have ofound effects on calcification of aota(o Neill et al., 2011). Toum et al. (2005), found that CaxP oduct was high in the study oulation (48.6±16.2 vesus 39.8±11.8, = 0.01). Rufino et al. (2003) illustated that a CaxP oduct level > 43 mg 2 /dl 2 was the otimal value in tems of sensitivity and secificity fo edicting the esence of valvula calcification in thei atients oulation. Multile stewise egession analysis selected CaxP as one of the most edictive aametes fo mital calcification (Ribeio et al., 1998). Kahnooj et al. (2010), findings showed that the otimal cutoff oint fo the CaxP. Poduct measuement fo edicting the seveity of aotic valve calcification was 42 mg 2 /dl 2. This discimination level was diffeent in othe studies. Movilli et al. (2005), obtained a beak oint of

20 AbdelBassit El Shaaawy et al mg 2 /dl 2 fo an otimal CaxP oduct discimination value. Volkov et al. (2009), stated that atients with valvula calcification had high blood aathyoid homone level while Ribeio et al. (1998) found no coelation between valvula calcification and aathyoid homone level. Relatively low PTH concentations have been associated with a high evalence of soft tissue and vascula calcification among atients eceiving dialysis (Raggi et al., 2011). Patients with no calcification showed a highe significant doses of calcium and alhacalcidiol than atients with calfied aotic valve ( = 0.04, 0.006) esectively, this is against what was exected. Ca doses was much highe in atients with calcified aotic and mital valve than atients with no calcification ( = ) but alhacalcidiol was significantly lowe in atients with calcified aotic and mital valve and atients with no calcification ( = ). Patients with calcified aotic and mital valve had a highe significant doses of calcium comaed to atients with calcified aotic valve ( =0.03), but alhacalcidiol was nonsignificantly highe in atients with calcified aotic valve than in atients with calcified aotic and mital valve (P = ). Does this oint to calcium dug as a calcification ogession facto wheneve calcification occus. On the contay does alfacalcifeol otect atients with and without calcification fom ogession of calcification by its well known antiinflammatoy effect ove body tissues. Effects of vitamin D such as modulation of an inflammatoy esonse may have a eventive effect (Razzaque, 2011). Inceasing evidence suggests that calcium sulementation may enhance soft tissue calcification and cadiovascula disease in CKDMBD (Peacock, 2010). The thombotic o ulceative changes that occu within heavily calcified valves when exosed to the intacadiac lumen can esult in an euted mass of calcium enteing ciculation. Numeous studies have shown that in animal models of uemia, vascula calcification aeas to be acceleated by the administation of vitamin D (Mizobuchi et al., 2007). Taas et al. (2006) studied 90 atients on maintenance HD fo moe than 12 months, 36 atients (60%) esented with valvula calcification atients with valvula calcification equied highe doses of alfacalcidiol fo teating seconday hyeaathyoidism (0.43±0.60 vesus 1±0.46 μ/day, < ). This was not the case in ou study. On making coelations within gou 1( atients with no calcification), we found a ositive coelation between age and calcium ( = 0.04) which could exlain calcification of eldely valves in ESRD atients on egula HD. We found bodeline significant negative coelation between hoshous and age (P = 0.06). Also calcium had a highly significant ositive coelation 209

21 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: with duation of dialysis. Calcium and hoshous had a negative coelation which is well known. A ositive coelation was found between P and CaxP which suots ou study oinion of inciminating both in the ocess of extaosseous calcification in ESRD on HD, we found a negative coelation of calcium with ceatinine and uea which is well known. In gou 2 (aotic valve calcification), we found a negative highly significant coelation between seum calcium and duation of dialysis which is against inciminating seum calcium in valvula calcification ocess in ESRD on HD. Seum ionized calcium concentation is maintained in a vey limited ange thanks to aathyoid homone (PTH) and the active vitamin D metabolite calcitiol. A deceas in ionized calcium level inactivates the calcium sensoing eceto (CaSR), a membanous otein located incially in the aathyoid glands and the kidney, thus stimulating PTH secetion (Coubebaisse and Soubebielle, 2011). Seum Ca and P in gou 2( with aotic valve calcification ) had a bodeline negative coelation which is well known, P and CaxP oduct had a highly significant ositive coelation ( = ) again suoting the oinion of thei incimination in vavlula calcification ocess. In gou 3( aotic and mital valve calcification ), aathyoid homone had a negative coelation with age ( = 05), which suots that it doesn't lay much a ole in valvula calcification in eldely. We also found highly significant negative coelation of seum Ca and P, which is well known. Against what was exected, we found a ositive bodeline coelation between seum calcium and CaxP oduct. Also against what was exected a non significant ositive coelation was found between seum P and CaxP oduct. Does seum Ca edict CaxP oduct level wheneve valvula calcification is moe extensive o olonged? This does need futhe eseach. We found in gou 3( aotic and mital valve calcification), a highly significant coelation between uea and aathyoid homone. Thee was a negative highly significant coelation between CaxP oduct and ceatinine. Also an invese significant coelation between seum calcium and ceatinine level which is well known. In gou 2 (aotic calcification), thee was a ositive significant coelation between seum calcium level and calcium dose which is edicted and an invese bodeline significant coelation between seum P and calcium dose. We found an invese coelation between seum calcium level and alfacalcidiol dose which may mean that calcium is consumed in valve and vascula calcification all ove the body. In gou 3( aotic and mital calcification ), thee was an indiect significant coelation between seum P and calcium dose, which could inciminate the calcium 210

22 AbdelBassit El Shaaawy et al as a dug encouaging inceases in CaxP oduct and tissue calcification in ESRD on HD with extensive valve calcification. In ou study, atients having aotic calcification wee 39, atients having mital calcification wee 13, 5 atienst had aotic eguge while 5 atients had mital eguge. The est of ou atients had no valvula insufficiency. In ou study, aotic calcification was noted in 65%dialysis atients. The incidence of valvula insufficiency was 3.9% in atients with aotic calcification vesus 0.63% in atients without calcification. Valvula calcification may be associated with aotic egugitation (Voklov et al., 2009). Ribeio et al. (1998), found that aotic calcification was noted in 52% of dialysis atients as comaed to 4% of contols. The evalence of valvula insufficiency was 22% in atients with aotic calcifications vesus 6% in atients without calcification. In ou study none of the atients had stenosis of mital no aotic valves. Valvula calcification may be associated with stenosis of mital and aotic valves (Volkov et al., 2009). Myocadial dysfunction is common just io to the onset of dialysis (Zoccali et al., 2006 and McCullough et al., 2004). Ejection faction was significantly highe in atients with no calcification comaed to atients with aotic valve calcification ( = 0.02) and this is exected. ESD was significantly highe in gou 3( aotic and mital valve calcification ), comaed to gou 1( no calcification) which means some degee of enlagement of venticle in gou 3 ( = 0.02). Also in gou 3, ejection faction and shotening faction ae significantly lowe than gou 1 ( = 0.03 and 0.005) and this shows the elation between calcification and cadiac dysfunction. Thee was no much diffeence in echocadiogahic aametes between gou 2( aotic calcification) and gou 3( aotic and mital calcification) and this means that once calcification haends, changes of echo aametes stats. Cadiovascula calcification is associated with cadiovascula disease and motality among atients eceiving dialysis, and the disode ogesses aidly once established (Raggi et al., 2011). In ou study, 3% of atients had left venticula hyetohy. Tukmen et al. (2008), studied a total of 82 consecutive atients (52 male, mean age 48±12 yeas) undegoing chonic HD teatment fo > 1 yea subjected to echocadiogahy, left venticula hyetohy was detected in 59 (72%) the study atients, Stozecki et al. (2005) found that valvual calcification coexisted with left venticula hyetohy. Left venticula hyetohy (LVM) is the consequence of combined effects of chonic hemodynamic oveload and non hemodynamic biochemical and neuohumoal factos chaacteistic of uemia (Nasi et al., 2004). 211

23 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Left venticula hyetohy is the most fequent cadiac alteation in ESRD (London et al., 2008). LVH has been found in as many as 30 to 45% of atients with CKD. ( Mizobuchi et al., 2007 ). In ou esent study, left atial enlagement was found in (7.8%) the atients. Kocinaj et al. (2009), analyzed data fom 123 atients who wee on egula HD, by means of taditional tansthoacic echocadiogahic examination. The most esented age gou was 60 to 90 yeas old, with edominance of females (56.1%). He found dilated left atium in 26.02% of study atients. In gou 1, we found in ou study a diect ositive coelation between CaxP and aotic valve dimension ( = 0.06), which was exected. Gou 2( aotic calcification), calcium had an invese coelation with ejection faction which was against ou exectations ( = 0.06) also hoshous had a ositive coelation with shotening faction, ( = 0.03) which was against ou exectations. In gou 3, with mital and aotic calcification, CaxP oduct was invesely coelated to inteventicula setal dimension ( = 0.03). Incease in CaxP oduct can be associated with decease in REFERENCE Adagao T (2009). Non invasive evaluation of vascula calcification in CKD atients. KDIGO CKDMBD wok gou. Kidney Int; 76 (sul 113): S1S130. Adagao T, Pies A, Lucas C, et al. (2004). A simle vascula calcification scoe edicts inteventicula setal dimension in case of venticula enlagement. Which may be due to use of high flux dialyses. Ponounced intestitial fibosis is a dominant featue of CKD associated stuctual myocadial emodeling (Ahmed et al., 2007). P and CaxP oduct both had an invese coelation with osteio wall dimension ( = 0.08, = 0.03) esectively, this needs moe eseach by cadiologists as both P and CaxP ae inciminated in tissue calcification in ESRD atients on HD. The extensive intamyocadial fibosis in ESRD atients with elevated aathyoid dhomoen could be esonsible fo attenuation of the hyetohic esonse to essue oveload and the develoment of high stess cadiomyoathy and cadiac failue (London et al., 2002). Conclusion: We had a vey high incidence of valvula calcification (65%) as comaed to othe studies we have to evise ou olicy towads HD teatment using calcium sulement and αcholecalcifeol teatment. Also, we have to evise ou olicy towads the high flux dialyses now. Phoshous and CaxP oduct should be contolled as much as ossible. cadiovascula isk in haemodialysis atients. Nehol Dial Tanslant; 19(6): Ahmed A, Rich MW, Sandes PW, et al. (2007). Chonic kidney disease associated motality in diastolic vesus systolic heat 212

24 AbdelBassit El Shaaawy et al failue: a oensity matched study. Am J Cadiol; 99(3): Baasch E, Gottdiene JS, Maino Lasen EK, Chaves PH, Newman AB (2006). Cadiovascula mobidity and motality in communitydwelling eldely individuals with calcification of the fibous skeleton of the base of the heat and aotoscleosis (The Cadiovascula Health Study). Am J Cadiol; 97(9): Bethesda (2004). US enal data system. USRDS 2004 Annual Data eot. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. Baun J, Oldendof M, Moshage W, et al. (1996). Electon beam comuted tomogahy in the evaluation of cadiac calcification in chonic dialysis atients. Am J Kidney Dis; 27(3): Coubebaisse M, Soubebielle JC (2011). Phoshocalcic metabolism: egulation and exloations]. Nehol The; 7(2): Cozzolino M, Cicei P, Voli EM, Olivi L, Messa PG (2009). Pathohysiology of calcium and hoshate metabolism imaiment in chonic kidney disease. Blood Puif; 27(4): Doumas B, Watson W and Biggs M (1971). Albumin standads and the measuement of seum albumin with bomocesyl geen. Clin Chim Acta; 31:8796. Endas DB, Villanueva R, Sha CF J, Singe FR (1989). Measuement of aathyoid homone. Endocina Metab Clin Noth Am 18(3): Enesto U, Ahmed W, Alet MA (2003). Valvula and eivalvula abnomalities in endstage enal disease. Am J Med Sci; 325(4): Fael EC (1987). Phoshous. In: Pesce AJ, Kalan LA, eds. Methods in clinical chemisty, St Louis: CV Mosby: Foman MB, Vimani R, Robetson RM, Stone WJ (1984). Mital anula calcification in chonic enal failue. Chest; 85(3): Fox CS, Lason MG, Vasan RS, et al. (2006). Cosssectional association of kidney function with valvula and annula calcification: the Famingham heat study. J Am Soc Nehol; 17(2): Fox E, Hakins D, Taylo H, et al. (2004). Eidemiology of mital annula calcification and its edictive value fo coonay events in Afican Ameicans: the Jackson Cohot of the Atheoscleotic Risk in Communities Study. Am Heat J; 148(6): Huting J (1994). Mital valve calcification as an index of left venticula dysfunction in atients with endstage enal disease on eitoneal dialysis. Chest; 105(2): Ikee R, Honda K, Ishioka K, et al. (2010). Diffeences in associated factos between aotic and mital valve calcification in hemodialysis. Hyetens Res; 33(6): Isido B and William G (2002). Cadiovascula clacification in endstage Renal disease.nehol. Dial Tanslant; 17(2): Ix JH, Shliak MG, Katz R, et al. (2007). Kidney function and aotic valve and mital annula calcification in the MultiEthnic Study of Atheoscleosis (MESA). Am J Kidney Dis; 50(3): Kahnooj M, Masoomi M, Nadeinasab A, et al. (2010). Relationshi between calciumhoshous oduct and seveity of valvula heat insufficiency in atients undegoing chonic hemodialysis. The Jounal of Tehan Univesity Heat Cente; 5(2):

25 The Egytian Jounal of Hosital Medicine (Ail 2012) Vol., 47: Katin U, Jeffey S, Byan K, et al. (2010). KDOQI US commentay on the 2009 KDIGO clinical actice Guideline fo the diagnosis, Evaluation, and Teatment of CKDmineal and bone disode (CKDMBD). Ameican Jounal of Kidney Diseases; 55: 5. Kocinaj D, Gashi M, et al. (2009). Echocadiogahic assessment of left atial size in atients with end stage enal disease. Cadiovasc J Af 20(3): London GM (2002). Left venticula alteations and endstage enal disease. Nehol Dial Tanslant; 17 Sul 1:2936. London GM, Machais SJ, Guein AP, et al. (2008). Association of bone activity, calcium load, aotic stiffness, and calcifications in ESRD. J Am Soc Nehol; 19(9): Mazzafeo S, Coen G, Bandini S, et al. (1993). Role of ageing, chonic enal failue and dialysis in the calcification of mital annulus. Nehol Dial Tanslant; 8(4): McCullough PA, Sandbeg KR, Dumle F, Yanez JE (2004). Deteminants of coonay vascula calcification in atients with chonic kidney disease and endstage enal disease: a systematic eview. J Nehol; 17(2): Mizobuchi M, Finch JL, Matin DR, Slatoolsky E (2007). Diffeential effects of vitamin D eceto activatos on vascula calcification in uemic ats. Kidney Int; 72(6): Moe M, Dueke T, Block A et al. (2009). KDIGO clinical actice guideline fo the diagnosis, evaluation, evention, and teatment of chonic kidney disease mineal and bone disode (CKDMBD). Kidney Intenational; 76(sul 113): s22s49. Razzaque MS (2011). The dualistic ole of vitamin D in vascula calcifications. Kidney Int; 79(7): Renoe BW, McDonald JM, Ladenson JH (1980). The effects of stasis with and without execise on fee calcium, vaious cations and Moan A, Katz R, Jenny NS, et al. (2008). Left venticula hyetohy in mild and modeate eduction in kidney function detemined using cadiac magnetic esonance imaging and cystatin C: the multiethnic study of atheoscleosis (MESA). Am J Kidney Dis; 52(5): Movilli E, Feliciani A, Cameini C et al. (2005). A high calciumhoshate oduct is associated with high Ceactive otein concentations in hemodialysis atients. Nehon Clin Pact; 10: Nasi H, Baadaan A, Nadei AS (2004). Close association between aathyoid homone and left venticula function and stuctue in endstage enal failue atients unde maintenance hemodialysis. Acta Med Austiaca; 31(3):6772 O'Neill WC, Lomashvili KA, Malluche HH, Faugee MC, Rise BL (2011). Teatment with yohoshate inhibits uemic vascula calcification. Kidney Int; 79(5): Peacock M (2010). Calcium metabolism in health and disease. Clin J Am Soc Nehol; 5 (1):S2330. Raggi P, Boulay A, ChasanTabe S, et al. (2002). Cadiac calcification in adult hemodialysis atients. A link between endstage enal disease and cadiovascula disease? J Am Coll Cadiol; 39(4): Raggi P, Chetow GM, Toes PU, et al. (2011). The ADVANCE study: a andomized study to evaluate the effects of cinacalcet lus lowdose vitamin D on vascula calcification in atients on hemodialysis. Nehol Dial Tanslant; 26(4): elated aametes. Clin Chim Acta 103: Ribeio S, Ramos A, Bandao A, et al. (1998). Cadiac valve calcification in haemodialysis atients: ole of calcium 214

26 AbdelBassit El Shaaawy et al hoshate metabolism. Nehol Dial Tanslant; 13(8): Rochelle C, Coetti M and Henich W (2010). Valvula Heat Disease in atients with Endstage Renal disease. J Am Soc Nehol; 20: Rufino M, Gacia S, Jimenez A, et al. (2003). Heat valve calcification and calcium x hoshous oduct in hemodialysis atients: analysis of otimum values fo its evention. Kidney Int 85:S Silve J, Levi R (2005). Regulation of PTH synthesis and secetion elevant to the management of seconday hyeaathyoidism in chonic kidney disease. Kidney Int 95:S812 Stinebaugh J, Lavie CJ, Milani RV, Cassidy MM, Figueoa JE (1995). Dole echocadiogahic assessment of valvula heat disease in atients equiing hemodialysis fo endstage enal disease. South Med J; 88(1):6571 Staumann E, Meye B, Misteli M, Blumbeg A, Jenze HR (1992). Aotic and mital valve disease in atients with end stage enal failue on longtem haemodialysis. B Heat J; 67(3): Stozecki P, OdowazSyniewska G, Manitius J (2005). Cadiac valve calcifications and left venticula hyetohy in hemodialysis atients. Ren Fail; 27(6): Taass F, Benjelloun M, Zamd M, et al. (2006). Heat valve calcifications in atients with endstage enal disease: analysis fo isk factos. Nehology (Calton); 11(6): Tobacco A, Meiattini F, Moda E, et al. (1979). Simlified enzymic/coloimetic seum uea nitogen detemination. Clin Chim 25: Toun D, Seze S, Baltali M, et al. (2005). Association of cadiac valve calcification and inflammation in atients on hemodialysis. Ren Fail; 27(2): Tuknen F, Eme A, Ozdemi A, Sevinc C, Eisken E, Yesilcimen K (2008): Relationshi between aotic valve scleosis and left venticula hyetohy in chonic hemodialysis atients. Int Uol Nehol 40 (2): Uhlig K, Bens JS, Kestenbaum B, et al. (2010). KDOQI US commentay on the 2009 KDIGO Clinical Pactice Guideline fo the Diagnosis, Evaluation, and Teatment of CKD Mineal and Bone Disode (CKDMBD). Am J Kidney Dis; 55(5): Volkov MM, Sminov AV, Dobonavov VA, et al. (2009). Heat valve calcification in atients with chonic kidney disease. Klin Med (Mosk); 87(6):3135 Yatzidis H (1974). New method fo diect detemination of tue ceatinine. Clinical Chemisty; 20(9): Yoshida M, Takamatsu J, Yoshida S, et al. (1999). Scoes of coonay calcification detemined by electon beam comuted tomogahy ae closely elated to the extent of diabetessecific comlications. Hom Metab Res; 31(10): Zoccali C, Benedetto FA, Tiei G, et al. (2006). Left venticula systolic function monitoing in asymtomatic dialysis atients: a osective cohot study. J Am Soc Nehol; 17(5):