The Role of Growth Factors in Preventing Acute Renal Failure

2007 ◽  
Vol 9 (6) ◽  
pp. 464-468 ◽  
Author(s):  
Marc R. Hammerman ◽  
Steven B. Miller
2000 ◽  
Vol 279 (1) ◽  
pp. F3-F11 ◽  

This review, which is the final installment in a series devoted to controversial issues in acute renal failure (ARF) (3, 47), will examine available information regarding the role of growth factors in ARF. In general, studies in this area have fallen into two broad categories: 1) those that have examined the renal expression of genes encoding growth factors or transcriptional factors associated with the growth response that is induced after ARF, and 2) those that have examined the efficacy of exogenously administered growth factors in accelerating recovery of renal function in experimental models of ARF. Despite the vast amount of information that has accumulated in these two areas of investigation, our understanding of the mechanisms involved in the process of regeneration and repair after ARF, and the role of growth factors in this response, remains rudimentary. This overview, contributed to by a number of experts in the field, is designed to summarize present knowledge and to highlight potentially fertile areas for future research in this area.


1997 ◽  
Vol 12 (8) ◽  
pp. 1560-1563 ◽  
Author(s):  
S. Wang ◽  
R. Hirschberg

2004 ◽  
Vol 19 (1) ◽  
pp. 93-96 ◽  
Author(s):  
Rachita Nanda ◽  
Pramila K. Mishra ◽  
U. K. Das ◽  
S. B. Rout ◽  
P. C. Mohapatra ◽  
...  

2002 ◽  
Vol 36 (9) ◽  
pp. 1466-1470 ◽  
Author(s):  
Donald F Brophy

OBJECTIVE: To examine the role of N-acetylcysteine (NAC) in the prevention of radiocontrast—induced nephropathy (RIN). DATA SOURCES: A literature search of MEDLINE (1966–December 2001) was performed using the following search terms: N-acetylcysteine, nephropathy, acute renal failure, and radiocontrast. STUDY SELECTION: Pertinent English-language animal and human studies were reviewed. DATA SYNTHESIS: Few small animal trials have demonstrated that NAC significantly prevents the development or reduces the severity of acute renal failure. Two human studies demonstrated NAC significantly reduces the occurrence of RIN. CONCLUSIONS: NAC may reduce the occurrence of RIN in high-risk patients. Further large-scale studies are needed to corroborate findings from earlier trials.


1969 ◽  
Vol 131 (2) ◽  
pp. 610-614 ◽  
Author(s):  
F. D. McDonald ◽  
G. Thiel ◽  
D. R. Wilson ◽  
G. F. DiBona ◽  
D. E. Oken

2009 ◽  
Vol 296 (1) ◽  
pp. F135-F144 ◽  
Author(s):  
Renee E. Yura ◽  
S. Gaylen Bradley ◽  
Ganesan Ramesh ◽  
W. Brian Reeves ◽  
Judith S. Bond

Meprin metalloproteases, composed of α and/or β subunits, consist of membrane-bound and secreted forms that are abundantly expressed in proximal tubules of the kidney as well as secreted into the urinary tract. Previous studies indicated that meprin metalloproteases play a role in pathological conditions such as ischemic acute renal failure and urinary tract infection. The aim of this work was to examine the role of meprins in endotoxemic acute renal failure using meprin α knockout (αKO), meprin β knockout (βKO), and wild-type (WT) mice. Differences among the responses of the genotypes were observed as early as 1 h after challenge with 2.5 mg/kg ip Escherichia coli LPS, establishing roles for meprins in the endotoxemic response. Meprin αKO mice displayed lower blood urea nitrogen levels and decreased nitric oxide levels, indicative of a decreased systemic response to LPS compared with WT and meprin βKO mice. Serum cytokine profiles showed lower levels of IL-1β and TNF–α in the meprin αKO mice within 3 h after LPS challenge and confirmed a role for meprins in the early phases of the host response. Meprin αKO mice were also hyporesponsive to LPS administered to the bladder, exhibiting significantly less bladder edema, leukocyte infiltration, and bladder permeability than WT mice. These data indicate that meprin A contributes to the renal and urogenital pathogenesis of endotoxicity.


Author(s):  
Walter Flamenbaum ◽  
John H. Schwartz ◽  
Robert J. Hamburger ◽  
James S. Kaufman

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