Leukocyte recruitment and acute renal failure

被引:56
作者
Singbartl, K
Ley, K
机构
[1] Univ Klinikum Munster, Klin & Poliklin Anasthesiol & Operat Intens Med, D-48129 Munster, Germany
[2] Univ Virginia, Cardiovasc Res Ctr, Charlottesville, VA USA
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2004年 / 82卷 / 02期
关键词
kidney failure; acute; leukocytes; neutrophils;
D O I
10.1007/s00109-003-0498-8
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Despite advances in medical technology, acute renal failure (ARF) still represents a major challenge in clinical medicine, as morbidity and mortality have remained unchanged over the past two decades. The pathophysiology of ARF is highly complex and only poorly understood; new insights into the pathophysiology of ARF are therefore of utmost importance to develop better understanding and therapies. Acute tubular necrosis (ATN) is the predominant cause of ARF and often arises as a consequence of septic, toxic, or ischemic insults. The recruitment of leukocytes into the kidney has recently emerged as a key event in the development of experimental ischemic and septic ARF. A few descriptive clinical studies support this idea. However, the clinical relevance of various animal models remains unclear, as does the importance of different leukocyte subsets, and even methodological aspects as how to quantify renal leukocyte recruitment. This review summarizes and critically evaluates experimental findings that provide insight into the role of leukocytes and their recruitment during ARF. We aim to provide a valid description of ARF, illustrate animal models of ARF, review qualitative and quantitative methods to assess renal leukocyte recruitment, and discuss the components of the leukocyte recruitment cascade and their role in ARF.
引用
收藏
页码:91 / 101
页数:11
相关论文
共 96 条
[61]   A2A adenosine receptor-mediated inhibition of renal injury and neutrophil adhesion [J].
Okusa, MD ;
Linden, J ;
Huang, LP ;
Rieger, JM ;
Macdonald, TL ;
Huynh, LP .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2000, 279 (05) :F809-F818
[62]   The inflammatory cascade in acute ischemic renal failure [J].
Okusa, MD .
NEPHRON, 2002, 90 (02) :133-138
[63]   Chemokines and chemokine receptors in leukocyte trafficking [J].
Olson, TS ;
Ley, K .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2002, 283 (01) :R7-R28
[64]   INHIBITION OF NEUTROPHIL MYELOPEROXIDASE ACTIVITY BY SELECTED TISSUES [J].
ORMROD, DJ ;
HARRISON, GL ;
MILLER, TE .
JOURNAL OF PHARMACOLOGICAL METHODS, 1987, 18 (02) :137-142
[65]  
PALLER MS, 1989, J LAB CLIN MED, V113, P379
[66]   Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes [J].
Park, P ;
Haas, M ;
Cunningham, PN ;
Bao, LH ;
Alexander, JJ ;
Quigg, RJ .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2002, 282 (02) :F352-F357
[67]   Selectins: critical mediators of leukocyte recruitment [J].
Patel, KD ;
Cuvelier, SL ;
Wiehler, S .
SEMINARS IN IMMUNOLOGY, 2002, 14 (02) :73-81
[68]   ROLE OF CD11A AND CD11B IN ISCHEMIC ACUTE-RENAL-FAILURE IN RATS [J].
RABB, H ;
MENDIOLA, CC ;
DIETZ, J ;
SABA, SR ;
ISSEKUTZ, TB ;
ABANILLA, F ;
BONVENTRE, JV ;
RAMIREZ, G .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 1994, 267 (06) :F1052-F1058
[69]   Renal ischemic-reperfusion injury in L-selectin-deficient mice [J].
Rabb, H ;
Ramirez, G ;
Saba, SR ;
Reynolds, D ;
Xu, JC ;
Flavell, R ;
Antonia, S .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY, 1996, 271 (02) :F408-F413
[70]   ANTIBODIES TO ICAM-1 PROTECT KIDNEYS IN SEVERE ISCHEMIC REPERFUSION INJURY [J].
RABB, H ;
MENDIOLA, CC ;
SABA, SR ;
DIETZ, JR ;
SMITH, CW ;
BONVENTRE, JV ;
RAMIREZ, G .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 211 (01) :67-73