Free radical ablation for the prevention of post-ischemic renal failure following renal transplantation

Today, management of irreversible renal failure is based primarily on maintenance hemodialysis and renal transplantation with a growing minority of patients treated by peritoneal dialysis. With regard to renal transplantation — the early promise of renal transplantation in the mid 1960's has given way to the realities of the late 1970's. There have been no major changes in the rejection rate of transplanted kidneys in recent years though today's mortality of transplant patients is considerably reduced over what it used to be. Moreover, universally the lack of availability of a sufficient number of organs for transplantation poses a formidable problem. It is all too apparent that current methods of blood purification in uremia are far from optimal. Even though the mortality in maintenance dialysis is relatively low, hemodialysis is characterized by a variety of complications and most maintenance dialysis patients are not optimally rehabilitated.

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A Case of Living-Donor Renal Transplantation for Chronic Renal Failure Caused by Secondary Amyloidosis

Transplantation Proceedings ◽

10.1016/j.transproceed.2011.05.035 ◽

2011 ◽

Vol 43 (6) ◽

pp. 2418-2420 ◽

Cited By ~ 1

Author(s):

K. Sakai ◽

M. Okamoto ◽

K. Koshino ◽

T. Suzuki ◽

S. Nobori ◽

...

Keyword(s):

Renal Failure ◽

Renal Transplantation ◽

Chronic Renal Failure ◽

Living Donor ◽

Secondary Amyloidosis

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Live donor renal transplantation in patients with end-stage renal failure due to IgA nephropathy: clinicopathological assessment

Nephrology ◽

10.1046/j.1440-1797.7.s3.15.x ◽

2002 ◽

Vol 7 ◽

pp. S74-S77

Author(s):

Yu Seun Kim ◽

Hyeon Joo Jeong ◽

Kye Won Kwon ◽

Ho Yung Lee ◽

Dae Suk Han ◽

...

Keyword(s):

Renal Failure ◽

Renal Transplantation ◽

Iga Nephropathy ◽

Live Donor ◽

End Stage Renal Failure ◽

End Stage

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TREATMENT ALTERNATIVES IN RENAL FAILURE AND RENAL TRANSPLANTATION PATIENTS WITH NONOBSTRUCTIVE COLONIC DILATATION

Transplantation Journal ◽

10.1097/00007890-198307000-00008 ◽

1983 ◽

Vol 36 (1) ◽

pp. 37-39 ◽

Cited By ~ 7

Author(s):

WILLIAM E. STRODEL ◽

THOMAS L. DENT ◽

TIMOTHY T. NOSTRANT ◽

FREDERIC E. ECKHAUSER ◽

DARRELL A. CAMPBELL ◽

...

Keyword(s):

Renal Failure ◽

Renal Transplantation ◽

Treatment Alternatives

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Renal transplantation in the first year of life: the treatment of choice for infants with end-stage renal disease.

Journal of the American Society of Nephrology ◽

10.1681/asn.v212s228 ◽

1992 ◽

Vol 2 (12) ◽

pp. S228

Author(s):

J S Najarian ◽

P S Almond ◽

M Mauer ◽

B Chavers ◽

T Nevins ◽

...

Keyword(s):

Renal Failure ◽

Renal Transplantation ◽

Survival Rate ◽

Living Donor ◽

Patient Survival ◽

First Year ◽

End Stage Renal Failure ◽

End Stage ◽

First Year Of Life ◽

Patient Survival Rate

The treatment of choice for end-stage renal failure within the first year of life is controversial. Between September 1970 and February 1991, we performed 28 kidney transplants (27 primary, 1 retransplant, 23 living donor, 5 cadaver) in infants less than 1 yr of age (mean, 7 +/- 2 months; range, 6 wk to 12 months). The 1-yr patient survival rate for living donor recipients was 100% versus 20% for cadaver recipients (P = 0.0001). The 1-yr graft survival rate for living donor recipients was 96% versus 20% for cadaver recipients (P = 0.001). The 1-yr patient survival rate for cyclosporin A (CSA) recipients (N = 12) was 100% versus 75% for non-CSA recipients (P = 0.03). The 1-yr graft survival rate for CSA recipients was 92% versus 75% for non-CSA recipients (P = 0.08). There was no difference in the number of rejection episodes or serum creatinine levels in CSA versus non-CSA recipients. Compared with pretransplant values, the mean posttransplant standard deviation scores (SDS) for height (N = 18), weight (N = 22), and head circumference (N = 8) improved: height SDS from -1.9 to -1.5 (not significant); weight SDS from -2.5 to 0.6 (P less than 0.0005); head circumference SDS from -2.0 to -0.7 (P = 0.01). Because no other renal replacement therapy can match these results, we conclude that renal transplantation is the treatment of choice for infants with end-stage renal failure.

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Demography and survival of patients receiving treatment for chronic renal failure in Australia and New Zealand: report on dialysis and renal transplantation treatment from the Australia and New Zealand dialysis and transplant registry

American Journal of Kidney Diseases ◽

10.1016/0272-6386(95)90641-x ◽

1995 ◽

Vol 25 (1) ◽

pp. 165-175 ◽

Cited By ~ 53

Author(s):

Alexander P.S. Disney

Keyword(s):

Renal Failure ◽

Renal Transplantation ◽

New Zealand ◽

Chronic Renal Failure ◽

Transplant Registry

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Interactions between adenosine and angiotensin II in controlling glomerular filtration

AJP Renal Physiology ◽

10.1152/ajprenal.1985.248.3.f340 ◽

1985 ◽

Vol 248 (3) ◽

pp. F340-F346 ◽

Cited By ~ 13

Author(s):

J. E. Hall ◽

J. P. Granger ◽

R. L. Hester

Keyword(s):

Renal Failure ◽

Angiotensin Ii ◽

Glomerular Filtration ◽

Filtration Rate ◽

Enzyme Inhibitor ◽

Ang Ii ◽

Converting Enzyme ◽

Renal Vasoconstriction ◽

Ischemic Renal Failure ◽

Constrictor Response

This study examined interactions between adenosine (Ado) and angiotensin II (ANG II) in controlling renal blood flow (RBF) and glomerular filtration rate (GFR). In six normal dogs, intrarenal Ado infusion (1.0 mumol/min) transiently decreased RBF, but during sustained Ado infusion RBF increased to 122 +/- 7% of control, although GFR remained at 75 +/- 6% of control. Blockade of ANG II formation with the converting enzyme inhibitor SQ 14225 (n = 6) almost abolished the transient decrease in RBF but did not prevent the sustained fall in GFR caused by Ado. When circulating ANG II was held constant by intravenous infusion of SQ 14225 and 20 ng . kg-1 . min-1 of ANG II (n = 6), Ado transiently decreased RBF but the return of RBF was much slower than in normal dogs and RBF did not increase above control. Maintenance of constant circulating ANG II did not prevent Ado-mediated decreases in GFR. These observations suggest that Ado-mediated reductions in GFR do not depend entirely on ANG II and may be due to dilation of efferent arterioles by Ado. However, the transient renal vasoconstriction caused by Ado depends on ANG II, and data from this study suggest that part of the waning constrictor response to Ado is due to suppression of renin secretion and endogenous ANG II formation. In circumstances where high ANG II levels are maintained (i.e., ischemic renal failure), Ado may be capable of causing sustained renal vasoconstriction.

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