Uticaj proteinurije na poremećaj metabolizma lipoproteina (a)
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- Geoffrey Black
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1 Број 12 ВОЈНОСАНИТЕТСКИ ПРЕГЛЕД Страна 921 O R I G I N A L N I Č L A N A K UDC: : Uticaj proteinurije na poremećaj metabolizma lipoproteina (a) Dejan Petrović*, Radmila Obrenović, Biljana Stojimirović Kliničko-bolnički centar Kragujevac, *Klinika za urologiju i nefrologiju, Kragujevac; Klinički centar Srbije, Institut za medicinsku biohemiju, Institut za urologiju i nefrologiju, Beograd Uvod/Cilj. Proteinurija dovodi do poremećaja metabolizma lipida. Cilj rada bio je da ispita uticaj proteinurije na poremećaj metabolizma lipoproteina (a). Metode. U radu je ispitano 60 bolesnika (odnos mušakaraca i žena M : Ž = 32 : 28), prosečne starosti 37,15±9,85 godina, s prosečnim klirensom endogenog kreatinina 86,27±19,81 ml/min i prosečnim indeksom telesne mase 24,18±2,23 kg/m 2. U zavisnosti od stepena glomerulske proteinurije bolesnici su svrstani u četiri grupe. Prvu grupu, sa proteinurijom manjom od 0,25 g/24 h, činilo je 15 ispitanika (M : Ž = 6 : 9) prosečna starost 34,66±4,82 godine (kontrolna grupa). Drugu grupu, sa proteinurijom 0,25 1,0 g/24 h, činilo je 15 bolesnika sa primarnim glomerulonefritisom (M : Ž = 9 : 6), prosečne starosti 37,87±9,65 godina. Treću grupu, sa proteinurijom 1,0 3,0 g/24 h, činilo je 15 boleslnika sa primarnim glomerulonefritisom (M : Ž = 8 : 7), prosečne starosti 35,67±13,29 godina. Četvrtu grupu, sa proteinurijom većom od 3,0 g/24 h, činilo je 15 bolesnika sa primarnim glomerulonefritisom (M : Ž = 9 : 6), prosečne starosti 40,40±9,75 godina. Kao parametri za procenu uticaja proteinurije na poremećaj metabolizma lipoproteina (a) ispitivani su 24-satna proteinurija, koloidno-osmotski pritisak plazme i koncentracija lipoproteina (a) u serumu. Za statističku analizu dobijenih podataka korišćeni su jednofaktorska parametarska analiza varijanse ANOVA, Kruskal-Wallisov test, Mann-Whitney U test, χ 2 test i Spearmanov test rang korelacije. Rezultati. Bolesnici sa proteinurijom većom od 3,0 g/24 h imali su statistički visoko značajno veće vrednosti lipoproteina (a) u serumu u odnosu na kontrolnu grupu ispitanika i statistički značajno veće vrednosti u odnosu na grupu bolesnika sa proteinurijom od 0,25 do 1,0 g/24 h. Bolesnici sa proteinurijom od 1,0 do 3,0 g/24 h imali su statistički značajno veće vrednosti lipoproteina (a) u serumu u odnosu na kontrolnu grupu ispitanika (proteinurija < 0,25 g/24 h). Između koncentracije albumina u serumu, koloidno osmotskog pritiska i koncentracije lipoproteina (a) u serumu postojala je statistički visoko značajna negativna povezanost. Između 24-satne proteinurije i koncentracije lipoproteina (a) u serumu postojala je statistički visoko značajna pozitivna povezanost. Zaključak. Proteinurija dovodi do poremećaja metabolizma lipoproteina (a). Ključ ne reč i : proteinurija; glomerulonefritis; lipoproteini (a); metabolizam; arterioskleroza. Uvod Kompleks makromolekula u cirkulaciji koji čine glikoprotein po strukturi sličan plazminogenu [apoprotein (a)], kovalentno vezan sa apoproteinom b-lipoproteinom niske gustine LDLs naziva se lipoprotein (a) Lp(a) (1). Postoji više od 30 izooblika apo (a), čija molekulska masa varira između 300 do više od 800 kda. Bolesnici sa izooblicima apo (a) niske molekulske mase (F, B, S 1 i S 2 ) imaju prosečno veću koncentraciju Lp(a) u plazmi u odnosu na bolesnike sa izooblicima apo (a) velike molekulske mase (S 3, S 4 ) (2). Bolesnici sa izooblikom apo (a) niske molekulske mase [LMW apo (a)] i povećanim nivoom Lp(a) imaju veći stepen arterioskleroze na početku hronične slabosti bubrega (2), u odnosu na bolesnike sa apo (a) velike molekulske mase [HMW apo(a)]. U daljem toku bolesti bolesnici sa LMW apo (a) i povećanim nivoom Lp(a) u serumu razvijaju galopirajuću arteriosklerozu, a jačina glomerulske filtracije progresivno opada (2). Petrović D, et al. Vojnosanit Pregl 2005; 62(12):
2 Страна 922 ВОЈНОСАНИТЕТСКИ ПРЕГЛЕД Број 12 Proteinurija (povećani gubitak proteina mokraćom) i razgradnja albumina u ćelijama proksimalnih tubula dovode do hipoalbuminemije. Hipoalbuminemija je odgovorna za smanjenje onkotskog pritiska plazme, podstiče prelazak tečnosti u intersticijumski prostor i stimuliše povećano stvaranje lipoproteina i apoproteina u jetri (2 6). Poremećaj metabolizma lipida kod bolesnika sa proteinurijom rezultat je povećanog stvaranja lipoproteina u jetri i smanjenog klirensa hilomikrona, lipoproteina veoma niske gustine, intermedijarnih lipoproteina i lipoproteina niske gustine (2 6). Hipoalbuminemija, smanjenje koloidno-onkotskog pritiska plazme (KOP) i/ili proteinurija su glavni faktori koji stimulišu povećano stvaranje lipoproteina koji sadrže apo (b) (1, 7). Koncentracija Lp(a) u plazmi je takođe povećana kod g/24 h i indeksom telesne mase (ITM) 27 kg/m 2, koji nisu uzimali imunosupresivne lekove i lekove za lečenje hiperlipoproteinemije. Osnovna obeležja ispitivanja bila su: klirens endogenog kreatinina, 24-satna proteinurija i koncentracija Lp(a) u serumu. U zavisnosti od stepena glomerulske proteinurije bolesnici su podeljeni u četiri grupe: I grupa sa proteinurijom < 0,25 g/24 h (kontrolna grupa), II grupa sa proteinurijom od 0,25 do 1,0 g/24 h, III grupa sa proteinurijom od 1,0 do 3,0 g/24 h i IV grupa sa proteinurijom > 3,0 g/24 h (tabela 1). Dijagnoza glomerulonefritisa postavljena je na osnovu kliničkih i laboratorijskih parametara i potvrđena je biopsijom bubrega i patohistološkim pregledom tkiva bubrega. Tabela 1 Opšti podaci o bolesnicima Grupe proteinurija (g/24 h) Opšti podaci I (< 0,25) II (0,25 1,00) III (1,00 3,00) IV (> 3,00) ґ±sd ґ±sd ґ±sd ґ±sd Broj (n) Pol (m/ž) 6 : 9 9 : 6 8 : 7 9 : 6 Starost (god) 34,66±4,82 37,87±9,65 35,67± 3,29 40,40±9,75 ITM* (kg/m 2 ) 23,28±3,50 24,77±1,53 23,83±1,57 24,83±1,44 Zdravi ispitanici 15 / / / MzGN / MGN / / / 5 MPGN / / / 3 GNMP / FSGS / Primarni glomerulonefritis BPGN** / 2 / / *ITM indeks telesne mase, MzGN mezangioproliferativni glomerulonefritis, MGN membranozni glomerulonefritis, MPGN membranoproliferativni glomerulonefritis, GNMP glomerulonefritis sa minimalnim histološkim promenama, FSGS fokalno segmentna glomeruloskleroza, **BPGN brzo progresivni glomerulonefritis bolesnika sa proteinurijom (7 9). Kod bolesnika sa nefrotskim sindromom nivo Lp(a) u plazmi statistički značajno koreliše sa nivoom albumina u plazmi i težinom proteinurije (1). Povećani nivo Lp(a) je značajan faktor rizika za razvoj kardiovaskularnih bolesti i razvoj i progresiju hronične slabosti bubrega (10 12). Prema National Cholesterol Education Program (NCEP) ciljni nivo Lp(a) kod bolesnika sa proteinurijom i povećanim rizikom za razvoj kardiovaskularnih bolesti treba da bude manji od 30 mg/dl (12). Cilj rada bio je da se ispita uticaj različitog stepena proteinurije na poremećaj metabolizma Lp(a) i utvrdi stepen povezanosti između koncentracije albumina u serumu, koloidno-osmotskog pritiska plazme, 24-satne proteinurije i koncentracije Lp(a) u serumu. Metode Ispitano je 60 bolesnika lečenih u jednogodišnjem periodu, uz primenu Helsinške deklaracije o medicinskim istraživanjima i dobijenu saglasnost bolesnika. U studiju su bili uključeni ispitanici s klirensom endogenog kreatinina većim od 50 ml/min, proteinurijom 10 Krv za određivanje Lp(a) uzimana je natašte, posle sati potpunog gladovanja. Tri nedelje pre ispitivanja bolesnici su obustavili uzimanje lekova za koje je poznato da mogu uticati na nivoe lipida i lipoproteina u krvi. Kreatinin u serumu određivan je pomoću kolorimetrijskog testa, na aparatu Monarch plus IL, Milan, Italy. Normalna koncentracija kreatinina u serumu kod žena iznosi μmol/l, a kod muškaraka μmol/l. Kreatinin u uzorku 24 satne mokraće određivan je istom metodom kao i u serumu, ali sa deset puta većim razblaženjem. Koncentracija albumina u serumu određivana je biuretskom metodom (normalna vrednost albumina g/l). Za kvantitativno određivanje Lp(a) u serumu korišćen je Behring Nephelometer System i N Latex Lp(a) reagens (normalna vrednost Lp(a) iznosi < 30 mg/dl). Proteinurija iz uzorka 24-satne mokraće određivana je kolorimetrijskim testom (normalna količina proteina u uzorku 24-satne mokraće iznosi 150 mg/24 h). Klirens supstancija izračunat je prema formuli: Cx = (Ux Vu) : Px (ml/min), gde je Cx klirens ispitivane supstancije (ml/min), Ux koncentracija ispitivane supstancije u mokraći uzimanoj 24 h (mmol/l), Vu zapremina mokra-
3 Број 12 ВОЈНОСАНИТЕТСКИ ПРЕГЛЕД Страна 923 će uzimane 24 h (l/24 h), a Px koncentracija ispitivane supstancije u plazmi (mmol/l). Koloidno-osmotski pritisak plazme izračunat je na osnovu formule (13): KOP (mmhg) = α(p-alb) 2 + β[alb (P-Alb)]; proteinurija 3,5 g/24 h α = 0,13 i β = 2,07; proteinurija < 3,5 g/24 h α = -1,15 i β = 3,03. P koncentracija ukupnih proteina u plazmi (g/dl), Alb koncentracija albumina u plazmi (g/dl). Normalna vrednost KOP plazme iznosi mmhg. Za statističku analizu dobijenih podataka korišćeni su jednofaktorska parametarska analiza varijanse, Kruskal- Wallisov test, Mann-Whitney U test i Spirmanov test. Prag značajnosti bila je verovatnoća od 0,05 i 0,01. Rezultati Da bi se procenilo stanje funkcije bubrega ispitanicima je određivan klirens endogenog kreatinina. Između ispitivanih grupa bolesnika postoji visoko statistički značajna razlika u prosečnim vrednostima klirensa endogenog kreatinina (jednofaktorska parametarska analiza varijanse). Bolesnici sa proteinurijom 0,25 1,0 g/24 h, 1,0 3,0 g/24 h i proteinurijom > 3,0 g/24 h imaju statistički visoko značajno niže vrednosti klirensa endogenog kreatinina u odnosu na kontrolnu grupu ispitanika (p < 0,01) (tabela 2). Između ostalih grupa ispitanika nije bilo statistički značajne razlike u vrednostima klirensa endogenog kreatinina (p > 0,05) (tabela 2). grupa ispitanika nema statistički značajne razlike u vrednostima albumina i ukupnih proteina (p > 0,05) (tabela 2). Postoji statistički visoko značajna razlika u vrednostima KOP (jednofaktorska parametarska analiza varijanse). Bolesnici sa proteinurijom > 3,0 g/24 h imaju statistički visoko značajno niže vrednosti KOP (p < 0,01) u odnosu na kontrolnu grupu ispitanika i grupe bolesnika sa proteinurijom od 0,25 do 1,0 g/24 h i proteinurijom od 1,0 3,0 g/24 h (tabela 2). Bolesnici sa proteinurijom od 1,0 do 3,0 g/24 h imaju statistički značajno (p < 0,05) niže vrednosti u odnosu na kontrolnu grupu ispitanika (tabela 2). Između ostalih grupa ispitanika nema statistički značajne razlike u vrednostima (p > 0,05) (tabela 2). Između koncentracije albumina u serumu i KOP plazme postoji statistički visoko značajna pozitivna povezanost (p < 0,01). Postoji statistički visoko značajna razlika između ispitivanih grupa bolesnika u prosečnim vrednostima Lp(a) u serumu (Kruskal-Wallisov test). Bolesnici sa proteinurijom od 1,0 do 3,0 g/24 h imaju statistički značajno (p < 0,05) veće vrednosti Lp(a) u serumu u odnosu na kontrolnu grupu ispitanika (proteinurija < 0,25 g/24 h) (tabela 2). Bolesnici sa proteinurijom > 3,0 g/24 h imaju statistički visoko značajno (p < 0,01) veće vrednosti Lp(a) u serumu u odnosu na kontrolnu grupu ispitanika i statistički značajno (p < 0,05) veće vrednosti u odnosu na grupu bolesnika sa proteinurijom od 0,25 do 1,0 g/24 h (tabela 2). Između ostalih grupa ispitanika nema statistički značajne razlike (p > 0,05) u vrednostima Lp(a) u serumu (tabela 2). Tabela 2 Prikaz ispitivanih parametara u zavisnosti od stepena proteinurije Grupe proteinurija (g/24 h) Ispitivani parametri I (< 0,25) II (0,25 1,00) III (1,00 3,00) IV (> 3,00) ґ±sd ґ±sd ґ±sd ґ±sd Klirens kreatinina (ml/min) 99,70±12,94 82,37 ± 21,19 82,85 ± 18,48 80,16 ± 20,80** Ukupni proteini (g/l) 70,00±3,57 70,47±3,94 69,00±3,95 51,60±5,37 Albumin (g/l) 42,93±3,61 41,86±4,27 39,80±2,51 25,13±4,02 Koloidno-osmotski pritisak plazme* (mmhg) 26,44±2,71 26,22±2,94 24,69±2,59 14,73±3,04 Lipoprotein (a) (g/l) 0,14±0,10 0,23±0,27 0,32±0,26 0,35±0,27 Značajnost (p) *p I, II < 0,01; p I, IV < 0,01; p I, IV < 0,01; p I, III < 0,01; p II, IV < 0,01; p II, IV < 0,05; **p I, IV < 0,01; p I, III < 0,05; p I, III < 0,05; p III, IV < 0,01. Između ispitivanih grupa bolesnika postoji statistički visoko značajna razlika u prosečnim vrednostima ukupnih proteina i albumina u serumu (jednofaktorska parametarska analiza varijanse). Bolesnici sa proteinurijom > 3,0 g/24 h imaju statistički visoko značajno niže vrednosti ukupnih proteina i albumina u serumu (p < 0,01) u odnosu na kontrolnu grupu ispitanika, i grupe bolesnika sa proteinurijom od 0,25 do 1,0 g/24 h i proteinurijom od 1,0 do 3,0 g/24 h (tabela 2). Bolesnici sa proteinurijom od 1,0 do 3,0 g/24 h imaju statistički značajno (p < 0,05) niže vrednosti ukupnih proteina u serumu i statistički značajno niže vrednosti albumina u serumu u odnosu na kontrolnu grupu ispitanika (tabela 2). Između ostalih Između koncentracije albumina u serumu, KOP plazme i koncentracije Lp(a) u serumu postoji statistički visoko značajna (p < 0,01) negativna povezanost (tabela 3). Statistički visoko značajna (p < 0,01) pozitivna povezanost postoji između 24-satne proteinurije i koncentracije Lp(a) u serumu (tabela 3). Diskusija Do sada učinjena ispitivanja potvrdila su pretpostavku da proteinurija dovodi do poremećaja metabolizma lipida. Poremećaj metabolizma lipida kod bolesnika sa bolestima
4 Страна 924 ВОЈНОСАНИТЕТСКИ ПРЕГЛЕД Број 12 Tabela 3 Povezanost između koncentracije albumina u serumu, koloidno osmotskog pritiska plazme, 24 h proteinurije i koncentracije lipoproteina (a) u serumu Osnovni statistički Ispitivani parametri parametri Značajnost (p) n x±sd Albumin (g/l) 60 37,43±8,08 ρ = - 0,357 Lipoprotein (a) (g/l) 60 0,26±0,25 p < 0,01 KOP* (mmhg) 60 23,02±5,60 Lipoprotein (a) (g/l) 60 0,26±0,25 Proteinurija (g/24 h) 60 2,14±2,67 Lipoprotein (a) (g/l) 60 0,26±0,25 *KOP koloidno-osmotski pritisak plazme ρ = - 0,353 p < 0,01 ρ = 0,415 p < 0,01 bubrega je nezavisan faktor rizika za razvoj kardiovaskularnih bolesti i progresiju hronične slabosti bubrega. Zbog toga je u ovom radu ispitivan uticaj različitog stepena proteinurije na poremećaj metabolizma Lp(a). Grupe bolesnika sačinjene su prema stepenu proteinurije i ne razlikuju se međusobno po starosnoj dobi, polu i ITM (tabela 1). Bolesnici sa različitim stepenom proteinurije imaju visoko statistički značajno niže vrednosti klirensa endogenog kreatinina u odnosu na kontrolnu grupu (tabela 1). Imajući u vidu da poremećaj metabolizma lipida nastaje kada klirens endogenog kreatinina padne ispod 50 ml/min, a da je ispitivanje uključilo samo bolesnike sa klirensom endogenog kreatinina > 50 ml/min, statistički značajna razlika u vrednostima klirensa endogenog kreatinina nema značajnog uticaja na poremećaj metabolizma lipida (14, 15). Bolesnici sa proteinurijom > 3,0 g/24 h imaju statistički visoko značajno niže vrednosti ukupnih proteina, albumina, KOP plazme i statistički visoko značajno veće vrednosti Lp(a) (tabela 2). Između koncentracije albumina u serumu i KOP plazme postoji statistički visoko značajna pozitivna povezanost. Sl. 1 Povezanost između koncentracije albumina u serumu i KOP plazme Do povećanja Lp(a) kod bolesnika sa nefrotskim sindromom dolazi zbog smanjenja koncentracije albumina u serumu. Gubitak proteina mokraćom podstiče povećano stvaranje proteina u jetri i ima najvažniju ulogu u povećanju koncentracije Lp(a) u serumu kod bolesnika sa bolestima bubrega (2, 5). Kod odraslih bolesnika sa nefrotskim sindromom nivo Lp(a) u plazmi je obrnuto povezan sa nivoom albumina u plazmi i direktno povezan sa težinom proteinurije (1, 2). Između koncentracije albumina u serumu i koncentracije Lp(a) u serumu postoji statistički visoko značajna negativna povezanost, dok između 24-satne proteinurije i koncentracije Lp(a) u serumu postoji statistički visoko značajna pozitivna povezanost (tabela 3), što je u skladu sa rezultatima do sada učinjenih istraživanja (5, 8, 9). Veći stepen proteinurije udružen je sa većim koncentracijama Lp(a) u serumu, što za posledicu ima ubrzani razvoj arterioskleroze i povećanu učestalost kardiovaskularnih bolesti kod bolesnika sa primarnim glomerulonefritisima i proteinurijom. Bolesnici sa povećanom koncentracijom Lp(a) (> 30 mg/dl) imaju 2,7 puta veći rizik od koronarne bolesti srca, u odnosu na bolesnike kod kojih je koncentracija Lp(a) u plazmi < 5 mg/dl (16). Bolesnici sa povećanim nivoom Lp(a) u plazmi i izooblikom apo (a) niske molekulske mase LMW razvijaju galopirajuću arteriosklerozu i progresivno oštećenje bubrega (2). Zbog toga preporuke za praćenje bolesnika sa bolestima bubrega treba da uključe: merenje koncentracije Lp(a) kod svih bolesnika sa bolestima bubrega, određivanje fenotipa apo (a) kod svih bolesnika sa povećanim nivoom Lp(a) i veoma striktno praćenje drugih faktora rizika za arteriosklerozu (anemija, hipertenzija, hiperglikemija, hiperhomocisteinemija) kod svih bolesnika sa povećanim nivoom Lp(a) u serumu (2). Poremećaj metabolizma lipida, kod bolesnika sa proteinurijom je nezavisan faktor rizika za progresiju hronične slabosti bubrega i razvoj kardiovaskularnih komplikacija (17, 18). Zaključak Proteinurija dovodi do poremećaja metabolizma lipida kod bolesnika sa bolestima bubrega. Između 24-satne proteinurije i koncentracije Lp(a) u serumu postoji statistički visoko značajna pozitivna povezanost. Bolesnici sa proteinurijom > 3,0 g/24 h imaju statistički visoko značajno veće vrednosti Lp(a) u serumu u odnosu na kontrolnu grupu is-
5 Број 12 ВОЈНОСАНИТЕТСКИ ПРЕГЛЕД Страна 925 pitanika (proteinurija < 0,25g/24 h). Statistički visoko značajna negativna povezanost postoji između koncentracije albumina u serumu, KOP i koncentracije Lp(a) u serumu. Rano otkrivanje poremećaja metabolizma lipida i pravovremena primena odgovarajuće terapije mogli bi da utiču na usporavanje hronične slabosti bubrega i sprečavanje razvoja pratećih komplikacija. LITERATURA 1. Noto D, Barbagallo CM, Cascio AL, Cefalu AB, Cavera G, Caldarella R, et al. Lipoprotein(a) levels in relation to albumin concentration in childhood nephrotic syndrome. Kidney Int 1999; 55(6): Kronenberg F, Utermann G, Dieplinger H. Lipoprotein(a) in renal disease. Am J Kidney Dis 1996; 27(1): Harris RC, Ismail N. Extrarenal complications of the nephrotic syndrome. Am J Kidney Dis 1994; 23(4): Wheeler DC, Bernard DB. Lipid abnormalities in the nephrotic syndrome: causes, consequences, and treatment. Am J Kidney Dis 1994; 23(3): Sechi LA, Zingaro L, Catena C, Perin A, De Marchi S, Bartoli E. Lipoprotein(a) and apolipoprotein(a) isoforms and proteinuria in patients with moderate renal failure. Kidney Int 1999; 56(3): Wheeler DC. Lipid abnormalities in the nephrotic syndrome: the therapeutic role of statins. J Nephrol 2001; 14 Suppl 4: S Shearer GC, Kaysen GA. Proteinuria and plasma compositional changes contribute to defective lipoprotein catabolism in the nephrotic syndrome by separate mechanisms. Am J Kidney Dis 2001; 37(1 Suppl 2): S Doucet C, Mooser V, Gonbert S, Raymond F, Chapman J, Jacobs C, et al. Lipoprotein(a) in the nephrotic syndrome: molecular analysis of lipoprotein(a) and apolipoprotein(a) fragments in plasma and urine. J Am Soc Nephrol 2000; 11(3): De Sain-Van Der Velden MG, Reijngoud DJ, Kaysen GA, Gadellaa MM, Voorbij H, Stellaard F, et al. Evidence for increased synthesis of lipoprotein(a) in the nephrotic syndrome. J Am Soc Nephrol 1998; 9(8): Wanner C. Importance of hyperlipidaemia and therapy in renal patients. Nephrol Dial Transplant 2000; 15 Suppl 5: : Olbricht CJ. Potential role of lipids in the progression of glomerular diseases. Kidney Blood Press Res 1997; 20(3): : Fried LF, Orchard TJ, Kasiske BL. Effect of lipid reduction on the progression of renal disease: a meta-analysis. Kidney Int 2001; 59(1): Geranton F, Chantrel F, Bouiller M, Muller S, Kolb I, Moulin B, et al. Prediction of colloid osmotic pressure in renal patients. Clin Nephrol 2000; 53(4): Bairaktari E, Elisaf M, Tsolas O, Siamopoulos KC. Serum Lp(a) levels in patients with moderate renal failure. Nephron 1998; 79(3): Attman PO, Alaupovic P, Tavella M, Knight-Gibson C. Abnormal lipid and apolipoprotein composition of major lipoprotein density classes in patients with chronic renal failure. Nephrol Dial Transplant 1996; 11(1): Monzani G, Bergesio F, Ciuti R, Ciciani AM, Martinelli F, Rosati A, et al. Lp(a) levels: effects of progressive chronic renal failure and dietary manipulation. J Nephrol 1997; 10(1): Levey AS. Clinical practice. Nondiabetic kidney disease. N Engl J Med 2002; 347(19): Vogt L, Laverman GD, Dullaart RP, Navis G. Lipid management in the proteinuric patient: do not overlook the importance of proteinuria reduction. Nephrol Dial Transplant 2004; 19(1): 5 8. Rad je primljen 24. IX Abstract Petrović D, Obrenović R, Stojimirović B. Vojnosanit Pregl 2005; 62(12): INFLUENCE OF PROTEINURIA ON THE LIPOPROTEIN (a) METABOLISM DISORDER Background/Aim. Proteinuria causes lipid metabolism abnormalities. The aim of the present study was to examine the influence of proteinuria on the lipoprotein (a) metabolism disorder. Methods. The study included 60 patients of the male-famele ratio (M : F = 32 : 28), mean age 37.15±9.85 years with, the average endogenous creatinine clearance 86.27±19.81 ml/min, and the average body mass index (BMI) 24.18±2.23 kg/m 2. Regarding the level of glomerular proteinuria, the patients were divided into four groups. The first (control) group, with proteinuria levels less than 0.25 g/24h, included 15 patients (M : F = 6 : 9), mean age 34.66±4.82 years, the mean clearance of endogenous creatinine 99.70±12.94 ml/min, and mean BMI 23.28±3.50 kg/m 2. The second group, with proteinuria between 0.25 and 1.0 g/24
6 Страна 926 ВОЈНОСАНИТЕТСКИ ПРЕГЛЕД Број 12 h, includ 15 patients (M : F = 9 : 6) with primary glomerulonephritis, mean age 37.87±9.65 years, the mean clearance of endogenous creatinine 82.85±18.48 ml/min, and mean BMI 23.83±1.57 kg/m 2. The third group includ 15 patients (M : F = 8 : 7) with primary glomerulonephritis, with proteinuria between 1.0 and 3.0 g/24 h, mean age 35.67±13.29 years, the mean clearance of endogenous creatinine 82.85±18.48 ml/min, and mean BMI 23.83±1.57 kg/m 2. The fourth group, with proteinuria higher than 3.0 g/24 h, included 15 patients (M : F = 9 : 6) with primary glomerulonephritis, mean age 40.40±9.75 years, the mean clearance of endogenous creatinine 80.16±20.80 ml/min, and mean BMI 24.83±1.44 kg/m 2. In order to assess the influence of proteinuria on the lipoprotein (a) metabolism abnormalities we investigated 24-hour proteinuria, the colloid osmotic pressure (COP) of plasma, and the serum concentration of lipoprotein (a). The results were statistically analyzed using ANOVA, Kruscal-Wallis test, Mann-Whitney U test, χ 2 test and Spearman test. Results. Statistically, the patients with proteinuria over 3.0 g/24 h had the significantly higher values of lipoprotein (a) in serum as compared to the control group, and the patients with proteinuria about g/24 h. The patients with proteinuria between g/24 h had the statistically significantly higher values of lipoprotein (a) in serum than the control group (proteinuria < 0.25 g/24 h). There was a highly statistically significant negative correlation between serum albumin concentration, COP and the concentration of lipoprotein (a) in serum. There was a highly statistically significant positive correlation between 24-hour proteinuria and the concentration of lipoprotein (a) in serum. Conclusion. Proteinuria leads to the deterioration of lipoprotein (a) abnormalities. K e y w o r d s : proteinuria; glomerulonephritis; lipoprotein (a); metabolism; arteriosclerosis. Correspondence to: Dejan Petrović, Kliničko bolnički centar Kragujevac, Klinika za urologiju i nefrologiju, Odeljenje hemodijalize, Zmaj Jovina 30, Kragujevac, Srbija i Crna Gora. Tel aca96@eunet.yu
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