Sirolimus addition is beneficial for renal allograft dysfunction due to simultaneous acute rejection episode and calcineurin inhibitor nephrotoxicity

2004 ◽  
Vol 36 (9) ◽  
pp. 2668-2670 ◽  
Author(s):  
H.-R. Chang ◽  
M.-H. Lee ◽  
M.-C. Wen ◽  
J.-D. Lian
Keyword(s):  
Acute Rejection ◽  
Renal Allograft ◽  
Calcineurin Inhibitor ◽  
Rejection Episode ◽  
Acute Rejection Episode ◽  
Allograft Dysfunction ◽  
Calcineurin Inhibitor Nephrotoxicity

THE IMPACT OF AN ACUTE REJECTION EPISODE ON LONG-TERM RENAL ALLOGRAFT SURVIVAL (t1/2)1,2

1994 ◽  
Vol 57 (6) ◽  
pp. 857-859 ◽  
Author(s):  
ARTHUE J. MATAS ◽  
KRISTEN J. GILLINGHAM ◽  
WILLIAM D. PAYNE ◽  
JOHN S. NAJARIAN
Keyword(s):  
Acute Rejection ◽  
Renal Allograft ◽  
Rejection Episode ◽  
Acute Rejection Episode ◽  
Allograft Survival ◽  
The Impact

Correlations of Serum and Urine Levels of Neopterin, IL-8, IL-6, IL-6R, Basic Fetoprotein and Hepatocytes Growth Factor with Acute Rejection in kidney Transplantation

Pteridines ◽  
1998 ◽  
Vol 9 (1) ◽  
pp. 22-25
Author(s):  
Tsuneharu Miki ◽  
Shiro Takahara ◽  
Akihiko Okuyma
Keyword(s):  
Acute Rejection ◽  
Rejection Episode ◽  
Stable Condition ◽  
Serum Levels ◽  
Acute Rejection Episode ◽  
Transplant Recipients ◽  
Kidney Transplant Recipients ◽  
Urinary Neopterin ◽  
Basic Fetoprotein ◽  
Urine Levels

Summary Levels of serum- and urinary-neopterin and serum-IL-6 and IL-6R of kidney transplant recipients "Were higher in acute rejection episode than in stable condition. IL-8 serum levels had risen prior to clinical diagnosis of acute rejection episode. Serum HGF levels also increased during acute rejection episode to over 1 ng/ml. Serum-neopterin and IL-6R levels were relatively sensitive for the detection of acute rejection episode.

The Cytochrome P450 3A5 Non-Expressor Kidney Allograft as a Risk Factor for Calcineurin Inhibitor Nephrotoxicity

2018 ◽  
Vol 47 (3) ◽  
pp. 182-190 ◽  
Author(s):  
Suwasin Udomkarnjananun ◽  
Natavudh Townamchai ◽  
Pajaree Chariyavilaskul ◽  
Kroonpong Iampenkhae ◽  
Krit Pongpirul ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Calcineurin Inhibitor ◽  
Cox Regression ◽  
Kidney Tissue ◽  
Acute Rejection Episode ◽  
Genotype 3 ◽  
Kidney Allograft ◽  
Cytochrome P450 3A5 ◽  
Calcineurin Inhibitor Nephrotoxicity ◽  
Donor Genotype

Background: Tacrolimus is mainly metabolized by cytochrome P450 3A5 (CYP3A5), which is expressed in the liver. However, CYP3A5 is also expressed in the kidney tissue and may contribute to local tacrolimus clearance in the kidney allograft. We aimed to evaluate the association between the allograft CYP3A5 genotype and transplant outcomes. Methods: We conducted a retrospective cohort study at the King Chulalongkorn Memorial Hospital, Thailand, comparing 2 groups of donor and recipient CYP3A5 genotypes, the expressor (*1/*1 and *1/*3) and the non-expressor (*3/*3). The primary outcomes were allograft complications including calcineurin inhibitor (CNI) nephrotoxicity and acute rejection episode. Results: Of the 50 enrolled patients, 21 donors were expressors and 29 donors were the non-expressors. Tacrolimus trough concentrations were similar between the 2 genotypes. The incidence of CNI nephrotoxicity was higher in recipients with non-expressor donor genotype compared with the expressor donor genotype (72.4 vs. 33.3%, p = 0.006). CNI nephrotoxicity incidence was not different when recipient’s genotypes were compared. Multivariate analysis from Cox-regression showed a hazard ratio of 3.18 (p = 0.026) for CNI nephrotoxicity in the non-expressor compared with the expressor donor. The recipient CYP3A5 genotypes did not significantly contribute to CNI nephrotoxicity. Kaplan-Meier analysis demonstrated the lowest CNI nephrotoxicity-free survival in recipients with the expressor genotype who received allograft from the non-expressor donors (p = 0.005). Conclusion: In conclusion, our results suggest that donor CYP3A5 non-expressor genotype (*3/*3) is a risk for CNI nephrotoxicity.

scholarly journals Presence of Donor- and Recipient-derived DNA in Cell-free Urine Samples of Renal Transplantation Recipients: Urinary DNA Chimerism

1999 ◽  
Vol 45 (10) ◽  
pp. 1741-1746 ◽  
Author(s):  
Jun Zhang ◽  
Kwok-Lung Tong ◽  
Philip KT Li ◽  
Albert YW Chan ◽  
Chung-Kwong Yeung ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Renal Transplant ◽  
Acute Rejection ◽  
Quantitative Pcr ◽  
Graft Rejection ◽  
Rejection Episode ◽  
Urine Samples ◽  
Acute Rejection Episode ◽  
Organ Donors ◽  
Male Organ

Abstract Background: Previous studies have indicated that microchimerism is present in body tissues, peripheral blood, and plasma of recipients after organ transplantation. We hypothesize that donor-derived DNA may also be present in cell-free urine of renal transplant recipients and that the concentrations of urine DNA may be correlated with graft rejection. Methods: Thirty-one female patients who had renal transplantation were enrolled in the study. In women with male organ donors, the SRY gene on the Y chromosome was used as a marker for donor-derived DNA. Real-time quantitative PCR for the SRY and β-globin genes was carried out on cell-free urinary DNA from these patients. Serial urine samples from a female renal transplant recipient undergoing an acute rejection episode were also collected and analyzed with the β-globin quantitative PCR system. Results: SRY sequences were detected in the urine of 14 of 17 female patients with male organ donors. None of the 14 patients with female organ donors had detectable SRY sequences in urinary DNA. The median fractional concentration of donor-derived DNA was 8.7% (interquartile range, 1.9–26.4%). During the acute rejection episode, urinary concentrations of the β-globin gene were markedly increased, with the concentrations returning rapidly to normal following antirejection treatment. Conclusions: Our results demonstrate that urinary DNA chimerism is present following renal transplantation. The measurement of urinary DNA using quantitative PCR may be useful for the diagnosis and monitoring of graft rejection.

Epigenetic Analysis Demonstrates that Natural Treg Only Infiltrate the Cardiac Allograft During an Acute Rejection Episode

2012 ◽  
Vol 94 (10S) ◽  
pp. 1166
Author(s):  
K. Boer ◽  
A. M.A. Peeters ◽  
A. P.W.M. Maat ◽  
K. Caliskan ◽  
A. H.M.M. Balk ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Rejection Episode ◽  
Cardiac Allograft ◽  
Acute Rejection Episode ◽  
Epigenetic Analysis

scholarly journals The value of urine cytologic examination findings in the diagnosis of the acute renal allograft rejection

2003 ◽  
Vol 60 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Zeljka Tatomirovic ◽  
Radojka Bokun ◽  
Jovan Dimitrijevic ◽  
Ljiljana Ignjatovic ◽  
Anastasija Aleksic ◽  
...  
Keyword(s):  
Acute Rejection ◽  
Allograft Rejection ◽  
Renal Allograft ◽  
Urine Cytology ◽  
Acute Allograft Rejection ◽  
Histological Findings ◽  
Renal Allograft Rejection ◽  
Renal Tubular Cells ◽  
Allograft Dysfunction ◽  
Acute Renal Allograft Rejection

Background. Acute rejection of allograft is one of the most serious complications of renal transplantation that requires fast and precise diagnostic approach. In this paper our experience in cytologic urinalysis as a diagnostic method of the acute renal allograft rejection was reviewed. Methods. The study group included 20 of 56 patients with transplanted kidneys who were assumed for the acute allograft rejection according to allograft dysfunction and/or urine cytology findings. Histological findings confirmed allograft rejection in 4 patients. Urine sediment obtained in cytocentrifuge was air-dried and stained with May-Grunwald-Giemsa. Acute allograft rejection was suspected if in 10 fields under high magnification 15 or more lymphocytes with renal tubular cells were found. Results. Acute transplant rejection occured in 32.1% patients. In 15 patients clinical findings of the acute renal allograft rejection corresponded with cytological and histological findings (in the cases in which it was performed). Three patients with clinical signs of the acute allograft rejection were without cytological confirmation, and in 2 patients cytological findings pointed to the acute rejection, but allograft dysfunction was of different etiology (acute tubular necrosis, cyclosporine nephrotoxicity). In patients with clinical, cytological and histological findings of the acute allograft rejection urine finding consisted of 58% lymphocytes, 34% neutrophilic leucocytes and 8% monocytes/macrophages on the average. The accuracy of cytologic urinalysis related to clinical and histological finding was 75%. Conclusion. Urine cytology as the reliable noninvasive, fast and simple method is appropriate as the a first diagnostic line of renal allograft dysfunction, as well as for monitoring of the graft function.

scholarly journals High rate of acute rejections in renal allograft recipients with thrombophilic risk factors.

1998 ◽  
Vol 9 (7) ◽  
pp. 1309-1313 ◽  
Author(s):  
S Heidenreich ◽  
C Dercken ◽  
C August ◽  
H G Koch ◽  
U Nowak-Göttl
Keyword(s):  
Risk Factors ◽  
Kidney Transplantation ◽  
Acute Rejection ◽  
Renal Allograft ◽  
Vascular Complications ◽  
Acute Rejection Episode ◽  
Renal Transplant Recipients ◽  
Vascular Events ◽  
Factor V Leiden Mutation ◽  
Thrombotic Risk

Inherited and acquired thrombophilic disorders predispose patients for thromboembolic and probably other occlusive vascular events that occur when additional risk factors play in concert. Because acute rejections in renal transplant recipients may reflect vascular events, and an impairment of the fibrinolytic system in immunosuppressed patients has been previously described, the implications of genetic or acquired risk factors of thrombophilia for the occurrence of early acute rejections after kidney transplantation were evaluated. The following risk factors of thrombophilia were determined in 97 patients after cadaveric kidney transplantation: factor V Leiden mutation, protein S, protein C, and antithrombin deficiency. In a retrospective analysis, the prevalence of acute rejections, the histologic classification when rejection episodes had been confirmed by biopsy, and other vascular complications were evaluated. In 21 of the 97 patients, an inherited or acquired risk factor of thrombophilia was detected. Prevalence of acute rejections was 71% in the first 6 mo after transplantation in patients with a thrombophilic disorder and significantly higher compared with patients without thrombophilia (41%; P = 0.017). The distribution of classic risk factors associated with acute rejections, such as number of human leukocyte antigen mismatches or percentage of panel-reactive antibodies, was similar in patients with and without thrombophilia. In the eight patients with thrombophilia and histologically proven acute rejection, four patients had an acute vascular rejection, and in two patients a vascular involvement was suspected. Furthermore, prevalence of cerebral or coronary vascular disease, or venous thromboembolic complications, was significantly higher in patients with a thrombophilic clotting defect (67%) compared with patients with normal hemostasis parameters (28%; P < 0.002). It is concluded that renal allograft recipients with thrombophilia are at risk of developing an acute rejection or other vascular event. Although the determination of thrombotic risk factors was performed at least 3 mo after an acute rejection episode, it can be presumed that acute rejection episodes are associated with subsequent coagulatory abnormalities with further consequences for transplant survival. Thus, pretransplant evaluation of genetic and acquired risk factors of thrombophilia is recommended.

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