Hipertansif ve Normotensif Kronik Üremik Hastalarda Lipid Profili

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1 Hipertansif ve Normotensif Kronik Üremik Hastalarda Lipid Profili Dr. H. Zeki Tonbul 1 'U 1 <ÕOPD] 6HOoXN 1, Dr. Hasan Kaya 1, Dr. Ayla San 1, Dr. Fatih Akçay 2 %X odoõúpd KLSHUWDQVLI YH QRUPRWHQVLI NURQLN UHPLN KDVWDODU DUDVÕQGD OLSLG SURILOL \ Q QGHQ IDUNOÕOÕN EXOXQXS EXOXQPDGÕ ÕQÕ DUDúWÕUPDN DPDFÕ\OD KLSHUWDQVLI VL QRUPRWHQVLI WRSODP NURQLN UHPLOL KDVWD ]HULQGH \DSÕOGÕ %X KDVWDODUÕQ L QRUPRWHQVLI KLSHUWDQVLI NURQLN KHPRGL\DOL] SURJUDPÕQGD LGL.RQWURO JUXEX RODUDN LVH VD OÕNOÕ NLúL DOÕQGÕ *HFH ER\XQFD VDDWOLN DoOÕN VRQUDVÕ DOÕQDQ YHQ ] NDQ UQHNOHULQGH ED]DO LQV OLQ G ]H\L YH VHUXP OLSLG SURILOL WD\LQL \DSÕOGÕ +LSHUWDQVLI YH QRUPRWHQVLI KDVWDODU DUDVÕQGD \Dú RUWDODPDVÕ YH Y FXW NLWOH LQGHNVL \ Q QGHQ QHPOL ELU IDUNOÕOÕN \RNWX +LSHUWDQVLI JUXSWD VHUXP trigliserid, total kolesterol, LDL, VLDL, Apo-B, Lipoprotein-(a) ve insülin düzeyleri normotensif gruba göre QHPOL GHUHFHGH GDKD \ NVHN +'/ G ]H\OHUL LVH GDKD G ú N EXOXQGX +HPRGL\DOL]H JLUHQ YH JLUPH\HQ KDVWDODU DUDVÕQGD GD OLSLG SURILOL \ Q QGHQ IDUNOÕOÕN \RNWX 6RQXo RODUDN KLSHUWDQVLI NURQLN UHPLN KDVWDODUGD OLSLG DQRUPDOOLNOHULQLQ QRUPRWHQVLIOHUGHQ GDKD ID]OD ROGX X WHVSLW HGLOGL %X QHGHQOH KLSHUWDQVLI UHPLN KDVWDODUGD DWHURVNOHUR]XQ GDKD HUNHQ YH FLGGL ER\XWODUGD RUWD\D oõndfd Õ VRQXFXQD YDUÕOGÕ >7XUJXW g]do 7ÕS 0HUNH]L Anahtar Kelimeler: Kronik renal yetmezlik, hipertansiyon, hiperlipidemi, ateroskleroz, hiperinsülinemi Lipid profiles in hypertensive and normotensive chronic uremic patients To elicit whether lipid profile of hypertensive chronic uremic patients was different from those of normotensive patients, this study was performed in 14 hypertensive and 27 normotensive chronic uremic patients. Eighteen patients (9 hypertensive and 9 normotensive) were ongoing regular hemodialysis. Also 12 healthy volunteers was included to the study as control. Basal insulin levels and serum lipid profiles were determined in venous blood samples taken from the patients after 14-hour fasting. There were no any differences between hypertensive and normotensive patients in respect to mean age and body mass index. Serum triglyceride, total-cholesterol, LDL, VLDL, Apo-B, lipoprotein-(a) and insulin levels of the hypertensive patients were significantly higher than those of the normotensive ones. In dialyzed and nondialyzed uremic patients, lipid abnormalities were not different. As a result, it was found that hypertensive chronic uremic patients had greater lipid abnormalities than normotensive patients. Therefore, it may considered that atherosclerosis will occur earlier in hypertensive chronic uremic patients. [Journal of Turgut Özal Medical Center 1997;4(3): ] Key Words: Chronic renal failure, hypertension, hyperlipidemia, atherosclerosis, hyperinsulinemia Kronik renal yetmezlik (KRY)'li hastalarda mortalitenin en önemli nedeni aterosklerotik NDUGL\RYDVN OHU KDVWDOÕNODUGÕU.DUGL\RYDVN OHU KDVWDOÕ D \RO DoDQ HQ QHPOL IDNW UOHU LVH hipertansiyon ve lipid anormallikleridir (1). 1 2 $WDW UN hqlyhuvlwhvl 7ÕS )DN OWHVL øo +DVWDOÕNODUÕ $QDELOLP 'DOÕ (U]XUXP $WDW UN hqlyhuvlwhvl 7ÕS )DN OWHVL %L\RNLP\D $QDELOLP 'DOÕ (U]XUXP 274

2 Tombul HZ, et al. Lipid profiles in chronic uremic patients Üremide lipoprotein lipaz (LPL) aktivitesi D]DOPÕúWÕU %X QHGHQOH NURQLN E EUHN \HWPH]OLNOL KDVWDODUGD HQ VÕN J ]OHQHQ OLSLG DQRUPDOOL L KLSHUWULJOLVHULGHPLGLU øqv OLQ GLUHQFL YH\D GHIHNWLI LQV OLQ FHYDEÕ LOH DUWPÕú SDUDWKRUPRQ VHYL\HOHULQLQ /3/ DNWLYLWHVLQGH D]DOPD\D \RO DoWÕ Õ ELOGLULOPHNWHGLU.5<OL ELUoRN KDVWDGD DoOÕN KLSHULQV OLQHPLVL VDSWDQPÕúWÕU +LSHULQV OLQHPLQLQ KHP KHSDWLN WULJOLVHULW VHQWH]LQL VWLP OH HWWL L KHP GH KLSHUWDQVL\RQD \RO DoWÕ Õ ELOGLULOPHNWHGLU %L] EX odoõúpdpõ]gd KLSHUWDQVLI +7 YH normotensif (NT) kronik üremik hastalarda serum insülin düzeyi ve lipid profilini tayin ederek, insülin düzeyi ve lipid anormallikleri yönünden iki grup DUDVÕQGD IDUOÕOÕN ROXS ROPDGÕ ÕQÕ DUDúWÕUGÕN MATERYAL VE METOD ddoõúpd\d KLSHUWDQVLI NDGÕQ HUNHN YH VL QRUPRWHQVLI NDGÕQ HUNHN WRSODP NURQLN UHPLOL KDVWD LOH VD OÕNOÕ J Q OO NDGÕQ HUNHN DOÕQGÕ <Dú RUWDODPDVÕ +7 JUXSWD \ÕO 17 JUXSWD \ÕO VD OÕNOÕ NRQWUROOHUGH LVH \ÕO LGL +LSHUWDQVLI KDVWDODUGDQ NT'lerden de 9 hasta olmak üzere toplam 18 hasta ortalama 12±4 (8-16) aydan beri haftada 2-3 kez DVHWDWOÕ KHPRGL\DOL]H JLUPHNWH\GL Hasta ve kontroller plazma lipid seviyelerini HWNLOHGL L ELOLQHQ KHUKDQJL ELU KRUPRQ YH\D LODo EHWD bloker, diüretik, androjen, karnitin, antilipemik vb.) NXOODQPÕ\RUODUGÕ $\UÕFD GLDEHWHV PHOOLWXV QHIURWLN sendrom, hipotiroidi veya primer hiperlipidemi gibi KDVWDOÕ Õ RODQODU odoõúpd\d DOÕQPDGÕ +LSHUWDQVLI JUXS LODFD UD PHQ NDQ EDVÕQFÕ NRQWURO DOWÕQGD ROPD\DQ YH\D KHUKDQJL ELU DQWLKLSHUWDQVLI LODo NXOODQPD\DQ KDVWDODUÕ NDSVÕ\RUGX $UWHUL\HO KLSHUWDQVL\RQ WDQÕVÕ :+2 NULWHUOHULQH göre ( mmhg'dan büyük) kondu. Ortalama DUWHUL\HO EDVÕQo 2$% GL\DVWROLN NDQ EDVÕQFÕQD QDEÕ] EDVÕQFÕQÕQ owh ELUL HNOHQHUHN KHVDSODQGÕ +LSHUWDQVLI JUXSWD E EUHN \HWPH]OL LQLQ SULPHU etyolojisi 7 olguda kronik glomerülonefrit (KGN), 4 olguda kronik pyelonefrit (KPN) idi. 3 olguda böbrek \HWPH]OL LQLQ QHGHQL EHOOL GH LOGL 1RUPRWHQVLI JUXSWD LVH E EUHN \HWPH]OL L ROJXODUÕQ QGH.31 QGH.*1 VLQGH DPLORLGR] VRQXFX JHOLúPLúWL ROJXGD ise primer neden bilinmiyordu. +DVWDODUÕQ Y FXW D ÕUOÕNODUÕ ER\ODUÕQÕQ NDUHVLQH E O QHUHN Y FXW NLWOH LQGHNVOHUL 9.ø KHVDS HGLOGL (kg/m 2 *ORPHU OHU ILOWUDV\RQ KÕ]Õ *)+ \Dú Y FXW D ÕUOÕ Õ YH VHUXP NUHDWLQLQ GH HUOHULQL GLNNDWH alan kreatinin klirens formülü ile hesap edildi (10). Serum insülin, parathormon (PTH) ve lipid G ]H\OHULQLQ WD\LQL LoLQ KDVWD YH VD OÕNOÕ NRQWUROOHUGHQ JHFH ER\XQFD VDDWOLN DoOÕN VRQUDVÕ YHQ ] NDQ UQHNOHUL DOÕQGÕ $\UÕODQ VHUXPODU ƒ&gh GHQH\ \DSÕODQD NDGDU VDNODQGÕ Serum trigliserid (TG) ve total kolesterol düzeyleri enzimatik metotla otoanalizörde spektrofotometrik olarak tayin edildi. (Sclavo Inc. &DW 1R YH VÕUDVÕ\OD WLFDUL NLWOHUL NXOODQÕOGÕ +'/NROHVWHURO G ]H\OHULQLQ Oo P LoLQ QFH ]HO o NW U F ELU UHDNWLIOH G ú N YH orn G ú N dansiteli lipoproteinler (LDL ve VLDL) çöktürüldü. Sonra süpernatantdaki HDL-kolesterol düzeyi total kolesterol düzeyinin ölçümünde uygulanan prosedürle otoanalizörde enzimatik olarak (Sclavo Inc. Cat. No: 81430) tayin edildi. Total kolesterol düzeyinden HDL YH /'/NROHVWHURO G ]H\OHULQLQ WRSODPÕ oõnduõodudn VLDL-kolesterol düzeyi hesap edildi. LDL-kolesterol düzeyi ise Friedewald formülü [LDL-kolesterol= Total kolesterol-(hdl-kolesterol+trigliserid / 5)] ile hesap edildi (11). Lipoprotein-(a) düzeyi; Lipoprotein-(a) ticari kitleri (Boehringer Mannheim, Cat. No : ) NXOODQÕODUDN (/,6$ \ QWHPL LOH WD\LQ HGLOGL Apolipoprotein-A1 ve B düzeyleri ise immünotürbidometrik yöntemle (Isolab Inc. USA, &RGH,' YH,' VÕUDVÕ\OD Oo OG Serum insülin düzeyleri enzimatik yöntemle spektrofotometrik olarak (Boehringer Mannheim, Cat. No: ) tayin edildi. Parathormon (PTM-m) düzeyleri; mid-region PTH double-antibody ticari NLWOHUL NXOODQÕODUDN 5,$ LOH Oo OG 6HUXP NUHDWLQLQ YH glukoz düzeylerinin ölçümü ise rutin laboratuvar \ QWHPOHUL LOH \DSÕOGÕ %XOJXODUÕQ GH HUOHQGLULOPHVLQGH $QRYD YDU\DQV DQDOL]L YH VWXGHQWVW WHVWL XQSDLUHG NXOODQÕOGÕ BULGULAR <Dú RUWDODPDVÕ \ Q QGHQ NRQWURO YH KDVWD JUXSODUÕ DUDVÕQGD LVWDWLVWLNVHO RODUDN QHPOL ELU IDUNOÕOÕN \RNWX Journal of Turgut Özal Medical Center 4(3):

3 Kronik üremik hastalarda lipid profili HZ. Tombul ve ark. (p>0.05). Hipertansif ve normotensif üremik hastalar DUDVÕQGD 9.ø \ Q QGHQ KHUKDQJL ELU IDUNOÕOÕN bulunmazken (p>0.05); HT ve NT her iki grupta da 9.ø NRQWUROOHUGHQ QHPOL GHUHFHGH GDKD G ú N W S YH W S VÕUDVÕ\OD LGL +DVWD YH NRQWUROOHUGHNL VHUXP OLSLG SURILOL YH GL HU ED]Õ EXOJXODU 7DEOR GH J U OPHNWHGLU +LSHUWDQVLI YH QRUPRWHQVLI UHPLN KDVWDODU DUDVÕQGD *)+ YH 37+P düzeyi yönünden istatistiksel olarak önemli bir IDUNOÕOÕN PHYFXW GH LOGL S! +LSHUWDQVLI YH normotensif her iki hasta grubunda da PTH-m düzeyleri kontrollerde önemli derecede daha yüksek W S YH W S VÕUDVÕ\OD idi. 1RUPRWHQVLI JUXS LOH NRQWURO JUXEX DUDVÕQGD 2$% TG, kolesterol, HDL, LDL, VLDL, Apo-A1, Apo-B ve insülin düzeyi yönünden istatistiksel olarak önemli ELU IDUNOÕOÕN EXOXQPD]NHQ S! QRUPRWHQVLI üremik hastalarda lipoprotein-(a) düzeyi kontrol grubuna göre önemli derecede daha yüksek bulundu (t=2.66, p<0.02). Hipertansif grupta normotensif gruba ve kontrol grubuna göre serum TG, total-kolesterol, LDL, VLDL, Apo-B, lipoprotein-(a) ve insülin düzeyleri istatistiksel olarak önemli derecede daha yüksek, HDL düzeyleri LVH GDKD G ú N EXOXQGX $ooõn NDQ glikozu ve Apo-A1 G ]H\L \ Q QGHQ LVH KHU o JUXS DUDVÕQGD QHPOL ELU IDUNOÕOÕN WHVSLW HGLOHPHGL S! Hastalar hemodiyalize girenler ve girmeyenler Tablo 1 +DVWD YH NRQWURO JUXSODUÕQGDNL VHUXP OLSLG SURILOL YH GL HU ED]Õ bulgular (X±SD) Parametreler Hipertansif grup (n=14) Normotensif grup (n=27) Kontrol grubu (n=12) GFH (ml/dl) 9.6±7 9.2±5-9.ø NJP 2 ) 22.7± ±2.8 h 25±2.1 OAB (mmhg) 131±7.6 e 90.2± ±8.8 Trigliserid (mg/dl) 188±45 c 145±43 141±33 T. Kolesterol (mg/dl) 225±67 c 159±73 141±58 HDL (mg/dl) 23.5±4.2 a 30.6± ±7.5 LDL (mg/dl) 143±58 a 100±55 89±54 VLDL (mg/dl) 37.3±8.8 d 26.6± ±9.6 Apo-A1 (mg/dl) 20.2±8 20± ±8.8 Apo-B (mg/dl) 248±32 c 212±42 188±43 Lipoprotein-(a) (mg/dl) 31.2±12.7 a 24.3±5.9 f 18.5±7.3 PTH-m (ng/dl) 172±34 176±28 j 37±10 Glukoz (mg/dl) 99.3±9.8 97± ±7.7 øqv OLQ µü/ml) 10.4±3.6 b 8.1± ±2.2 *)+ *ORPHU OHU ILOWUDV\RQ KÕ]Õ 9.ø 9 FXW NLWOH LQGHNVL 2$% 2UWDODPD DUWHUL\HO EDVÕQo D S E S FS G S H p< (Normotensif gruba göre); f: p<0.02, h: p<0.001, j: p< (kontrol grubuna göre). RODUDN LNL\H D\UÕODUDN GH HUOHQGLULOGL LQGH LVH OLSLG SURILOL YH LQV OLQ G ]H\L \ Q QGHQ LNL JUXS DUDVÕQGD QHPOL IDUNOÕOÕ ÕQ ROPDGÕ Õ WHVSLW HGLOGL 7DEOR 7$57,ù0$ 6RQ G QHP E EUHN \HWPH]OLNOL KDVWDODUGD HQ VÕN J U OHQ OLSLG DQRUPDOOL LQLQ KLSHUWULJOLVHULGHPL YH +'/NROHVWHURO G ]H\OHULQGHNL G ú NO N ROGX X WHVSLW HGLOPLúWLU < NVHN SOD]PD WULJOLVHULG VHYL\HOHULQLQ DWHURMHQLN GL HU OLSRSURWHLQOHUL DUWÕUDUDN YH +'/\L G ú UHUHN DWHURJHQH]L KÕ]ODQGÕUGÕ Õ bildirilmektedir (14)..URQLN E EUHN \HWPH]OLNOL ELU orn KDVWDGD DoOÕN KLSHULQV OLQHPLVL YH LQV OLQ GLUHQFL VDSWDQPÕúWÕU Bazal insülin seviyeleri ile serum trigliserid NRQVDQWUDV\RQODUÕ DUDVÕQGD LOLúNL ROGX X YH hiperinsülineminin lipoprotein lipaz aktivitesini azaltarak ve hepatik trigliserid sentezini stimüle ederek hipertrigliseridemi ve lipoprotein DQRUPDOOLNOHULQH \RO DoWÕ Õ WHVSLW HGLOPLúWLU $\UÕFD KLSHULQV OLQHPLQLQ KLSHUWDQVL\RQD GD \RO DoWÕ Õ bildirilmektedir (7, 16-19). ddoõúpdpõ]gd KLSHUWDQVLI NURQLN UHPLN KDVWD grubunda lipid anormalliklerinin normotensif gruba J UH GDKD ID]OD ROGX X WHVSLW HGLOPLúWLU +LSHUWDQVLI grupta serum TG, total-kolesterol, LDL, VLDL, lipoprotein-(a) ve Apo-B düzeyleri normotensif gruba göre önemli derecede daha yüksek, HDL düzeyleri ise GDKD G ú N EXOXQPXúWXU +LSHUWDQVLI KDVWD JUXEXQGD D\QÕ úhnlogh VHUXP ED]DO LQV OLQ G ]H\OHULQLQ GH GDKD \ NVHN ROGX X WHVSLW HGLOPLúWLU 1RUPRWHQVLI UHPLN KDVWD JUXEXQGD LVH VD OÕNOÕ NRQWUROOHUH J UH sadece serum lipoprotein-a düzeyleri daha \ NVHN EXOXQPXúWXU <DSÕODQ odoõúpdodugd VRQ G QHP böbrek yetmezlikli hipertansif hastalarda egzersiz, nifedipin ve prazosin'in serum trigliserid ve insülin düzeylerini G ú UG +'/\L LVH \ NVHOWWL L WHVSLW HGLOPLúWLU % \OHFH KLSHUWDQVLI NURQLN üremik hastalarda antihipertansif tedavi LOH KLSHULQV OLQHPL YH GROD\ÕVÕ\OD OLSLG DQRUPDOOLNOHULQLQ GH G ]HOHFH L J VWHULOPLúWLU %L]GH EX odoõúpdpõ]gd QRUPRWHQVLI UHPLN hastalarda lipid anormalliklerinin hipertansif gruba göre çok daha az 276

4 Tombul HZ, et al. Lipid profiles in chronic uremic patients Tablo 2 'L\DOL]H YH QRQGL\DOL]H UHPLN KDVWDODUÕQ OLSLG profili ve insülin düzeyi yönünden NDUúÕODúWÕUÕOPDVÕ ; 6'. Parametreler Diyalize (n=18) Non-diyalize (n=23) Trigliserid(mg/dl) 163±44 157±42* T. Kolesterol(mg/dl) 182±70 181±65* HDL(mg/dl) 27±8 29±10* LDL(mg/dl) 112±52 117±56* VLDL(mg/dl) 31±9 30±7* Apo-A1(mg/dl) 20.4±8 20±7* Apo-B(mg/dl) 219±35 228±38* Lipoprotein-(a)(mg/dl) 27±8 26±12* øqv OLQµÜ/ml) 8.8±3 8.9±3.1* *: p<0.05 ROGX XQX WHVSLW HWWLN 'L HU WDUDIWDQ 6HQWL YH DUNDGDúODUÕ KLSHUWDQVLI YH QRUPRWHQVLI UHPLN KDVWDODU DUDVÕQGD OLSLG SURILOL \ Q QGHQ IDUNOÕOÕN ROPDGÕ ÕQÕ YH KLSHUWULJOLVHULGHPLQLQ G ú N RUDQGD VDSWDQGÕ ÕQÕ UDSRU HWPLúOHUGLU )DNDW EX odoõúpdgd KDVWDODU KDNNÕQGD D\UÕQWÕOÕ ELOJL YHULOPHPLú YH VHUXP LQV OLQ G ]H\OHUL GH LQFHOHQPHPLúWLU Joven ve ark. ise plazma trigiserid düzeyi 170 PJGOGHQ \ NVHN RODQ KDVWDODUOD EX G ]H\LQ DOWÕQGD RODQ KDVWDODU DUDVÕQGD NDQ EDVÕQFÕ \ Q QGHQ IDUNOÕOÕN EXOXQPDGÕ ÕQÕ ELOGLUPLúOHUGLU $QFDN EX odoõúpdgd YDND VD\ÕVÕ D] Q ROXS LNL JUXS DUDVÕQGD OLSRSURWHLQ OLSD] DNWLYLWHVL \ Q QGHQ GH IDUNOÕOÕN EXOXQDPDPÕúWÕU /'/NROHVWHURO Q EDúOÕFD DSRSURWHLQL $SR% +'/NROHVWHURO Q EDúOÕFD DSRSURWHLQL LVH $SR$GÕU Son dönem böbrek yetmezlikli hastalarda Apo-B düzeyleri normal veya hafifçe yüksek (24,25), Apo-A1 G ]H\OHUL LVH QRUPDO YH\D KDILIoH G ú N EXOXQPXúWXU %L] GH odoõúpdpõ]gd +7 KDVWD JUXEXQGD Apo-B düzeyini yüksek, Apo-A1 düzeyini ise normal bulduk. <DSÕODQ odoõúpdodugd /LSRSURWHLQD LOH DWHURJHQH] DUDVÕQGD VÕNÕ ELU LOLúNL WHVSLW HGLOPLú YH kronik renal yetmezlikli hastalarda serum lipoprotein- D G ]H\OHUL QHPOL GHUHFHGH \ NVHN EXOXQPXúWXU <DNXSR OX YH DUN SURWHLQ ULQLQ GHUHFHVL LOH VHUXP OLSRSURWHLQ D G ]H\OHUL DUDVÕQGD DQODPOÕ ELU LOLúNL WHVSLW HWPLúOHUGLU %L] GH odoõúpdpõ]gd KHP hipertansif hem de normotensif üremik hastalarda VHUXP OLSRSURWHLQD G ]H\LQL VD OÕNOÕ NRQWUROOHUH J UH önemli derecede daha yüksek bulduk. Serum lipid profili üzerine hemodiyalizin etkisi NRQXVXQGD OLWHUDW UGH IDUNOÕ VRQXoODU PHYFXWWXU %L] EX odoõúpdpõ]gd KHPRGL\DOL]H JLUHQ YH JLUPH\HQ UHPLN KDVWDODU DUDVÕQGD VHUXP OLSLG SURILOL \ Q QGHQ QHPOL ELU IDUNOÕOÕN WHVSLW HWPHGLN Sonuç olarak; hipertansif kronik üremik hastalarda lipid anormalliklerinin normotensiflerden daha fazla ROGX X WHVSLW HGLOPLúWLU $\UÕFD KHPRGL\DOL]H JLUHQ YH JLUPH\HQ UHPLN KDVWDODU DUDVÕQGD OLSLG SURILOL \ Q QGHQ IDUNOÕOÕN EXOXQDPDPÕúWÕU % \OHFH hipertansif üremik hastalarda aterosklerozun daha HUNHQ YH FLGGL ER\XWODUGD JHOLúHFH L EX QHGHQOH HWNLQ DQWLKLSHUWDQVLI WHGDYLQLQ VRQ GHUHFH QHPOL ROGX X söylenebilir. KAYNAKLAR 1. Grutzmacher P, Marz W, Peshke B, Gross W, Schoeppe L. Lipoproteins and apolipoproteins during the progression of chronic renal disease. Nephron 1988; 50: Roullet JB, Lacour B, Yvert JP, Prat JJ, Drueke J. Factors of increase in serum triglyceride rich lipoproteins in uremic rats. Kidney Int 1988; 27: Chan MK. Lipid metabolism in renal failure. Clin Biochem 1990; 23: Roullet JB, Lacour B, Yvert JP, Drueke J. Correction by insulin of disturbed triglyceride-rich lipoprotein metabolism in rats with chronic renal failure. Am J Physiol 1986; 250: E $NPDO 0.DVÕP 6( 6ROLPDQ $5 0DVVU\ 6* ([FHVV parathyroid hormone adversely affects lipid metabolism in chronic renal failure. Kidney Int 1990; 37: Chan MK, Varghese Z, Persaud JM, Baillod RA, Moorhead JF. Hyperlipidemia in patients on maintenance hemo and peritoneal dialysis : the relative pathogenetic roles of triglyceride production and triglyceride removal. Clin Nephrol. 1982; 17: Marigliano A, Tedde R, Sechi LA, et al. Insulinemia and blood pressure: Relationship in patients with primary and secondary hypertension and with or without glucose metabolism impairment. Am. J Hyperten. 1990; 3: World Health Organization: Arterial hypertension Report of a WHO Expert Committee. WHO Technical Report Series. 1978: Russel RM. Nutritional Assesment. In: Wyngaarden JB, Smith LH, Bennett JC.(eds.), Cecil Texbook of Medicine (19 th ed.), WB Saunders, Philadelphia 1991: Levely AS, Madaio MP, Perrone RD. Laboratory assement of renal disease: Clearance, urinalysis and renal biopsy. In: Brenner-Rector(ed.), The Kidney, WB Saunders, Philadelphia 1991: Fridewald WT, Levely RI, Frederickson DS. Estimation of the concentration of low density lipoprotein cholesterol in plasma, without use of the preparative centrifuge. Clin. Chem. 1972; 18: Journal of Turgut Özal Medical Center 4(3):

5 Kronik üremik hastalarda lipid profili HZ. Tombul ve ark. 12. Parsy D, Dracon M, Cachera C, Parra HJ, Vanhoutte G, Tacquet A, Fruchart JC. Lipoprotein abnormalities in chronic hemodialysis patients. Nephrol Dial Transplant 1988; 3: Senti M, Romero R, Pedro-Botet J, Pelegri A, Nogues X, Rubies-Prat J. Lipoprotein abnormalities in hyperlipidemic and normolipidemic men on hemodialysis with chronic renal failure. Kidney Int. 1992; 41: Grundy SM. Management of hyperlipidemia of kidney disease. Kidney Int 1990; 37: Chan MK, Varghese Z, Moorhead JF. Lipid abnormalities in uremia, dialysis and transplantation. Kidney Int 1981; 19: Massry SG, Akmal M. Lipid abnormalities, renal failure and parathyroid hormone. Am J Med 1989; 87: %HUJHVLR ) 0RQ]DQÕ * &LXWL 5 6HUUXWR $ %HQXFFL $ )UL]]L V, Salvadori M. Lipids and apolipoproteins change during the progression of chronic renal failure. Clin Nephrol 1992; 38(5): Mak RHK, De Fronzo RA. Glucose and insulin metabolism in uremia. Nephron 1992; 61: DUÕ 5$ 'HPLU 6 $YúDU $ øqv OLQ GLUHQFL YH HVDQVL\HO KLSHUWDQVL\RQ <HQL 7ÕS 'HUJLVL 20. Harter HR, Meltzer VN, Tindira CA, Naumovich AD, Goldberg AP. Comparison of the effects of prazosin versus propranonol on plasma lipoprotein lipids in patients receiving hemodialysis. Am J Med 1986; 80(2A): Riegel W, Horl WH, Heidland A. Long-term effects of nifedipine on carbohydrate and lipid metabolism in hypertansive hemodialyzed patients. Clin Wochenschr 1986; 64(21): Meltzer VN, Goldberg AP, Tindira CA, Naumovich AD, Harter HR. Effects of prazosin and propranonol on blood pressure and plasma lipids in patients undergoing chronic hemodialysis. Am J Cardiol 1984; 53(3): Joven J, Viella E, Ahmad S, Cheung MC, Brunzell JD. Lipoprotein heterogeneity in end-stage renal disease.kidney Int 1993; 43: Ohta J, Matsuda I. Apolipoprotein and lipid abnormalities in uremic children on hemodialysis. Clin Chim Acta 1985; 147: Ron D, Oven I, Aviram M, Better OS, Brook JG. Accumulation of lipoprotein remnants in patients with chronic renal failure. Atherosclerosis 1983; 46: Joven J, Rubies-Prat J, Espinel E, Chacon P, Olmos A, Masdeu S. Apoprotein A-1 and high density lipoprotein subfraction in patients with chronic renal failure receiving hemodialysis. Nephron 1985; 40: Parra HJ, Mejdour H, Cachera C, Dracon M, Tacquet A, Fruchart JC: Lipoprotein-a in patients with chronic renal failure treated by hemodialysis. Clin Chem 1987; 33: Okura Y, Saku K, Hirata K, Zhang B, Liu R, Ogahara S, Naito S, Kajiyama G, Arakawa K. Serum lipoprotein-a levels in maintenance hemodialysis patients. Nephron 1993; 65: Cressman MD, Heyka RJ, Pganini EP, O'Neil J, Skibinski CI, Hoff HF. Lipoprotein-a is an independent risk factor for cardiovascular disease in hemodialysis patients. Circulation 1992; 86: Yavuz M, Güllülü M, Ersoy A, Dilek K, Yurtkuran M. +HPRGL\DOL] KDVWDODUÕQGD VHUXP OLSRSURWHLQ D G ]H\L 7 UN Nefroloji Diyaliz ve Transplantasyon Dergisi 1995; 4(1): <DNXSR OX * 6 OH\PDQODU * g]phq 7 6DSDQ 0 (UVR\ ) Kompanse kronik böbrek yetmezlikli hastalarda serum lipoprotein (a) düzeyi. Türk Nefroloji Diyaliz ve Transplantasyon Dergisi 1996; 5(1): Lacour B, Drueke TB, Lipid metabolism In: Massry SG, Glassock RJ (eds) Texbook of Nephrology, Williams- Wilkins, Baltimore-USA 1989: Attman PO, Alaupovic P: Lipid and apolipoprotein profiles of uremic dyslipoproteinemia-relation to renal function and dialysis. Nephron 1991; 57: <D]ÕúPD $GUHVL Doç. Dr. H. Zeki TONBUL $WDW UN hqlyhuvlwhvl 7ÕS )DN OWHVL øo +DVWDOÕNODUÕ $QDELOLP 'DOÕ / ERZURUM Tel: /