A Review on Renal Ischemia and Reperfusion Injury

Öz

Abstract: Kidney disease is one of the outstanding types of diseases that have reduced the quality of life of people in recent years. In particular, damage induced by ischemia-reperfusion leads to varying results, ranging from renal dysfunction to chronic renal failure. Many conditions, such as sepsis, shock, hydronephrosis, open kidney surgery, partial nephrectomy, renal transplantation, or nephron-sparing surgical procedures for renal tumors, may cause ischemic injury in the kidneys. Therefore, many studies are currently under way to reduce and prevent ischemia-reperfusion injury in the kidney. In that studies, attempts have been made to try various methods from the changes of ischemia or reperfusion until the use before or after ischemia-reperfusion of medicines that may be effective in treatment. In this study, we tried to give a general overview of ischemia-reperfusion. Because we can fully understand the complex cellular events that take place from the onset of ischemia to the time of acute or chronic damage can give us new perspectives on the methods to be followed in therapy.

Anahtar Kelimeler

• ischemia,reperfusion,kidney

Böbrek İskemi-Reperfüzyon Hasarı Üzerine Bir Derleme

Öz

Öz: Böbrek hastalıkları son yıllarda insanların yaşam kalitesini düşüren hastalık tipleri arasında önde gelenlerden birisidir. Özellikle iskemi-reperfüzyon tarafından indüklenen hasar, böbrekteki fonksiyon bozukluklarından kronik böbrek yetmezliğine kadar değişebilen sonuçlara yol açmaktadır. Sepsis, şok, hidronefroz, açık böbrek ameliyatları, parsiyel nefrektomi, renal transplantasyon veya renal tümörler için nefron koruyucu cerrahi girişimler gibi bir çok durum böbreklerde iskemik hasara sebep olabilir. Bu yüzden halen böbrekte iskemi-reperfüzyon hasarını azaltmak ve engellemek için pek çok çalışma yürütülmektedir. Bu çalışmalarda iskemi’nin veya reperfüzyon’un süresindeki değişikliklerden, tedavide etkili olabilecek ilaçların iskemi-reperfüzyon öncesi ya da sonrası kullanımlarına kadar pek çok yöntem denenerek sonuç elde edilmeye çalışılmaktadır. Bizde bu çalışmada iskemi-reperfüzyon üzerine genel bir özet çıkarmaya çalıştık. Çünkü iskeminin başlangıcından akut ya da kronik hasarlar oluşuncaya kadar geçen süreçteki karmaşık hücresel olayları tam olarak kavramak tedavide izlenilecek yöntemler hakkında bize yeni bakış açıları kazandırabilir.

Anahtar Kelimeler

• İskemi,reperfüzyon,böbrek,hastalık

Kaynakça

1. [1] Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Cell biology of ischemia/reperfusion injury. Int Rev Cell Mol Biol 2012;298:229-317.
2. [2] Kosieradzki M, Rowinski W. Ischemia/reperfusion injury in kidney transplantation: mechanisms and prevention. Transplantation proceedings 2008;40(10):3279-88.
3. [3] Şener, Göksel, and Yeğen BÇ. "İskemi reperfüzyon hasarı." Klinik Gelişim Derg 22.3 (2009): 5-13.
4. [4] Parks DA, Williams TK, Beckman JS. Conversion of xanthine dehydrogenase to oxidase in iscemic rat intestine: a reevaluation. Am J Physiol. 1988 May; 254 (5 Pt 1): G768-74
5. [5] Di Lisa F, Canton M, Menabò R, Kaludercic N, Bernardi P. Mitochondria and cardioprotection. Heart Fail Rev 2007 déc;12(3-4):249-60.
6. [6] Sugiyama S, Hanaki Y, Ogawa T, Hieda N, Taki K, Ozawa T. The effects of SUN 1165, a novel sodium channel blocker, on ischemia-induced mitochondrial dysfunction and leakage of lysosomal enzymes in canine hearts. Biochem. Biophys. Res. Commun 1988 déc 15;157(2):433-9.
7. [7] Kako K, Kato M, Matsuoka T, Mustapha A. Depression of membrane- bound Na+ -K+ -ATPase activity induced by free radicals and by ischemia of kidney. Am. J. Physiol 1988 févr;254(2 Pt 1):C330-337.
8. [8] Kato M, Kako KJ. Effects of N-(2- ercaptopropionyl)glycine on ischemic-reperfused dog kidney in vivo and membrane preparation in vitro. Mol. Cell. Biochem 1987 déc;78(2):151-9.

9. [9] Roberts BN, Christini DJ. NHE inhibition does not improve Na(+ ) or Ca(2+ ) overload during reperfusion: using modeling to illuminate the mechanisms underlying a therapeutic failure. PLoS Comput Biol 2011 oct;7(10):e1002241.
10. [10] Sanada S, Komuro I, Kitakaze M. Pathophysiology of Myocardial Reperfusion Injury: Preconditioning, Postconditioning and Translational Aspects of Protective Measures. American Journal of Physiology. Heart and Circulatory Physiology [Internet] 2011 août 19 [cité 2011 oct 13]; Available de: http://www.ncbi.nlm.nih.gov/pubmed/21856909
11. [11] Inserte J, Hernando V, Garcia-Dorado D. Contribution of calpains to myocardial ischemia/reperfusion injury. Cardiovascular research [Internet] 2012 juill 10 [cité 2012 août 22]; Available de: http: //www.ncbi.nlm.nih.gov/pubmed/22787134
12. [12] Peng T-I, Jou M-J. Oxidative stress caused by mitochondrial calcium overload. Ann. N. Y. Acad. Sci 2010 juill;1201:183-8. Ischemia-reperfusion: From cell biology to acute kidney injury S11
13. [13] Javadov S, Hunter JC, Barreto-Torres G, Parodi-Rullan R. Targeting the mitochondrial permeability transition: cardiac ischemia-reperfusion versus carcinogenesis. Cell. Physiol. Biochem 2011;27(3-4):179-90
14. [14] Becker LB. New concepts in reactive oxygen species and cardiovascular reperfusion physiology. Cardiovasc. Res 2004 févr 15;61(3):461-70.
15. [15] Alkaitis MS, Crabtree MJ. Recoupling the cardiac nitric oxide synthases: tetrahydrobiopterin synthesis and recycling. Curr Heart Fail Rep 2012 sept;9(3):200-10.
16. [16] Li C, Jackson RM. Reactive species mechanisms of cellular hypoxia-reoxygenation injury. Am. J. Physiol., Cell Physiol 2002 févr;282(2):C227-241.
17. [17] Bayrak O, Bavbek N, Karatas OF, Bayrak R, Catal F, Cimentepe E, et al. Nigella sativa protects against ischaemia/reperfusion injury in rat kidneys. Nephrol. Dial. Transplant 2008 juill;23(7):2206-12.
18. [18] Vanden Hoek TL, Shao Z, Li C, Zak R, Schumacker PT, Becker LB. Reperfusion injury on cardiac myocytes after simulated ischemia. Am. J. Physiol 1996 avr;270(4 Pt 2):H1334-1341.
19. [19] Kadenbach B, Ramzan R, Moosdorf R, Vogt S. The role of mitochondrial membrane potential in ischemic heart failure. Mitochondrion 2011 sept;11(5):700-6.
20. [20] Gustafsson AB, Gottlieb RA. Heart mitochondria: gates of life and death. Cardiovasc. Res 2008 janv 15;77(2):334-43..
21. [21] Kanduc D, Mittelman A, Serpico R, Sinigaglia E, Sinha AA, Natale C, et al. Cell death: apoptosis versus necrosis (review). Int. J. Oncol 2002 juill;21(1):165-70.
22. [22] Gottlieb RA. Cell death pathways in acute ischemia/reperfusion injury. J. Cardiovasc Pharmacol Ther 2011 déc;16(3-4):233-8.
23. [23] Baines CP. How and when do myocytes die during ischemia and reperfusion: the late phase. J. Cardiovasc Pharmacol Ther 2011 déc;16(3-4):239-43.
24. [24] Saikumar P, Dong Z, Weinberg JM, Venkatachalam MA. Mechanisms of cell death in hypoxia/reoxygenation injury. Oncogene 1998 déc 24;17(25):3341-9
25. [25] Reiter RJ, Acuña-Castroviejo D, Tan DX, Burkhardt S. Free radicalmediated molecular damage. Mechanisms for the protective actions of melatonin in the central nervous system. Ann N Y Acad Sci 2001; 939: 200-215.
26. [26] Lopez-Neblina F, Paez-Rollys AJ, Toledo-Pereyra LH. Mechanism of Protection of Verapamil by Preventing Neutrophil Infiltration in the Ischemic Rat Kidney. J SurgRes 1996; 61: 469-472.
27. [27] Frangogiannis NG. Chemokines in ischemia and reperfusion. Thromb Haemost. 2007; 97: 738-747.
28. [28] Thrane AS, Skehan JD, Thrane PS. A novel interpretation of immune redundancy and duality in reperfusion injury with important implications for intervention in ischaemic disease. Med Hypotheses 2007; 68: 1363-1370.
29. [29] García-Villalón AL, Amezquita YM, Monge L, Fernández N, Salcedo A, Diéguez G. Endothelin-1 potentiation of coronary artery contraction after ischemia-reperfusion. Vascul Pharmacol. 2008; 48:109-114.
30. [30] Brezis M, Rosen S. Hypoxia of the renal medulla--its implications for disease. N. Engl. J. Med. 1995 mars 9; 332(10): 647-55.
31. [31] Rauen U, Polzar B, Stephan H, Mannherz HG, de Groot H. Coldinduced apoptosis in cultured hepatocytes and liver endothelial cells: mediation by reactive oxygen species. FASEB J 1999 janv;13(1):155-68.
32. [32] Al-Awqati Q, Oliver JA. Stem cells in the kidney. Kidney international 2002;61(2):387-95.
33. [33] Koo DD, Welsh KI, West NE, Channon KM, Penington AJ, Roake JA, et al. Endothelial cell protection against ischemia/reperfusion injury by lecithinized superoxide dismutase. Kidney Int 2001 août;60(2):786-96.
34. [34] Stolz DB, Ross MA, Ikeda A, Tomiyama K, Kaizu T, Geller DA, et al. Sinusoidal endothelial cell repopulation following ischemia/reperfusion injury in rat liver transplantation. Hepatology 2007 nov;46(5):1464-75.
35. [35] White LE, Cui Y, Shelak CMF, Lie ML, Hassoun HT. Lung endothelial cell apoptosis during ischemic acute kidney injury. Shock 2012 août;38(3):320-7.
36. [36] Faller DV. Endothelial cell responses to hypoxic stress. Clin Exp Pharmacol. Physiol 1999 janv;26(1):74-84.
37. [37] Silva P. Energy and fuel substrate metabolism in the kidney. Semin Nephrol 1990 sept;10(5):432-44.
38. [38] Bagnasco S, Good D, Balaban R, Burg M. Lactate production in isolated segments of the rat nephron. Am J Physiol 1985 avr; 248(4 Pt 2): F522-526.
39. [39] Brezis M, Rosen S, Silva P, Epstein FH. Renal ischemia: a new perspective. Kidney Int 1984 oct;26(4):375-83.
40. [40] Lameire N, Van Biesen W, Vanholder R. Acute kidney injury. Lancet 2008 nov 29;372(9653):1863-5.
41. [41] Kwon O, Hong S-M, Ramesh G. Diminished NO generation by injured endothelium and loss of macula densa nNOS may contribute to sustained acute kidney injury after ischemia-reperfusion. Am J Physiol Renal Physiol 2009 janv;296(1):F25-33.
42. [42] Molitoris BA, Sandoval R, Sutton TA. Endothelial injury and dysfunction in ischemic acute renal failure. Critical care medicine 2002;30(5 Suppl):S235-40.
43. [43] Basile DP, Friedrich JL, Spahic J, Knipe NL, Mang HE, Leonard EC, et al. Impaired endothelial proliferation and mesenchymal transition contribute to vascular rarefaction following acute kidney injury. American journal of physiology [Internet]. Available de: 􀃀 le: //C: \article\21123492.pdf
44. [44] Legrand M, Mik EG, Johannes T, Payen D, Ince C. Renal hypoxia and dysoxia after reperfusion of the ischemic kidney. Molecular medicine (Cambridge Mass.) 2008;14(7-8):502-16.
45. [45] Molitoris BA, Sutton TA. Endothelial injury and dysfunction: role in the extension phase of acute renal failure. Kidney international 2004;66(2):496-9.
46. [46] Lameire N, Van Biesen W, Vanholder R. Acute renal failure. Lancet 2005 févr 29;365(9457):417-30.
47. [47] Blantz RC, Deng A, Miracle CM, Thomson SC. Regulation of kidney function and metabolism: a question of supply and demand. Trans Am Clin Climatol Assoc 2007;118:23-43.
48. [48] Eltzschig HK, Eckle T. Ischemia and reperfusion--from mechanism to translation. Nat Med 2011;17(11):1391-401.
49. [49] Thurman JM. Triggers of in􀃁 ammation after renal ischemia/ reperfusion. Clin Immunol 2007 avr; 123(1):7-13.
50. [50] Jang HR, Ko GJ, Wasowska BA, Rabb H. The interaction between ischemia-reperfusion and immune responses in the kidney. Journal of molecular medicine (Berlin, Germany) [Internet]. 2009; Available de: 􀃀 le: //C: \article\19562316.pdf
51. [51] He CJ, Peraldi MN, Adida C, Rebibou JM, Meulders Q, Sraer JD, et al. Thrombin signal transduction mechanis ms in human glomerular epithelial cells. J Cell Physiol 1992 mars;150(3):475-83.
52. [52] Chambers RC, Laurent GJ. Coagulation cascade proteases and tissue 􀃀 brosis. Biochem Soc Trans 2002 avr;30(2):194-200.
53. [53] Grandaliano G, Monno R, Ranieri E, Gesualdo L, Schena FP, Martino C, et al. Regenerative and proin􀃁 ammatory effects of thrombin on human proximal tubular cells. J Am Soc Nephrol 2000 juin;11(6):1016-25.
54. [54] Gui Y, Loutzenhiser R, Hollenberg MD. Bidirectional regulation of renal hemodynamics by activation of PAR1 and PAR2 in isolated perfused rat kidney. Am J Physiol Renal Physiol 2003 juill;285(1):F95-104.
55. [55] Erlich JH, Boyle EM, Labriola J, Kovacich JC, Santucci RA, Fearns C, et al. Inhibition of the tissue factor-thrombin pathway limits infarct size after myocardial ischemia-reperfusion injury by reducing in􀃁 ammation. Am J Pathol 2000 déc;157(6):1849-62.
56. [56] Hölschermann H, Bohle RM, Schmidt H, Zeller H, Fink L, Stahl U, et al. Hirudin reduces tissue factor expression and attenuates graft arteriosclerosis in rat cardiac allografts. Circulation 2000 juill 18;102(3):357-63.
57. [57] Farivar AS, Delgado MF, McCourtie AS, Barnes AD, Verrier ED, Mulligan MS. Crosstalk between thrombosis and in􀃁 ammation in lung reperfusion injury. Ann Thorac Surg 2006 mars;81(3):1061-7.
58. [58] Favreau F, Thuillier R, Cau J, Milin S, Manguy E, Mauco G, et al. Anti-thrombin therapy during warm ischemia and cold preservation prevents chronic kidney graft 􀃀 brosis in a DCD model. Am J Transplant 2009;10(1):30-9. S12 N. Chatauret et al.
59. [59] Giraud S, Thuillier R, Belliard A, Hebrard W, Nadeau C, Milin S, et al. Direct thrombin inhibitor prevents delayed graft function in a porcine model of renal transplantation. Transplantation 2009;87(11):1636-44.
60. [60] Reiter RJ. Oxidative processes and antioxidant defense mechanisms in the aging brain. FASEB J 1995; 9: 526-533.
61. [61] Karihtala P, Soini Y. Reactive oxygen species and antioxidant mechanisms in human tissues and their relation to malignancies. APMIS 2007;115:81-103.
62. [62] Cherubini A, Ruggiero C, Morand C, Lattanzio F, Dell‘aquila G, Zuliani G, Di Iorio A, Andres-Lacueva C. Dietary antioxidants as potential pharmacological agents for ischemic stroke. Curr Med Chem. 2008; 15: 1236-1248.
63. [63] Mickle DA, Weisel RD. Future directions of vitamin E and its analogues in minimizing myocardial ischemia-reperfusion injury. Can J Cardiol 1993; 9: 89-93.
64. [64] Virág L, Szabó C. The therapeutic potential of poly(ADP-ribose) polymerase inhibitors. Pharmacol Rev 2002; 54: 375-429.
65. [65] Chatauret, N., Badet, L., Barrou, B., & Hauet, T. (2014). Ischemia-reperfusion: From cell biology to acute kidney injury. Progrès en urologie, 24, S4-S12.