scholarly journals Crystalline nephropathy due to adenine phosphoribosyl transferase deficiency as a cause of renal allograft dysfunction

2020 ◽  
pp. 001-005
Author(s):  
Hegde Umapati ◽  
Mohan Rajapurkar ◽  
Sishir Gang ◽  
Jojera Amit ◽  
Soni Shailesh
Keyword(s):  
Renal Allograft ◽  
Phosphoribosyl Transferase ◽  
Adenine Phosphoribosyl Transferase ◽  
Allograft Dysfunction ◽  
Transferase Deficiency

Minimum allopurinol dose for adenine phosphoribosyl transferase deficiency

2017 ◽  
Vol 59 (10) ◽  
pp. 1097-1098
Author(s):  
Chisato Oyake ◽  
Hirokazu Ikeda ◽  
Masaki Fuyama ◽  
Tsuneki Watanabe ◽  
Keiichi Isoyama
Keyword(s):  
Phosphoribosyl Transferase ◽  
Adenine Phosphoribosyl Transferase ◽  
Transferase Deficiency

Metabolic consequences of adenine-phosphoribosyl transferase deficiency in V79 hamster fibroblasts

1992 ◽  
Vol 203 (2) ◽  
pp. 336-343 ◽  
Author(s):  
Elisabetta Dare' ◽  
Maria Helena Roelofs ◽  
Silvana Simi ◽  
Sofia Pavanello ◽  
Francesco Pilli ◽  
...  
Keyword(s):  
Phosphoribosyl Transferase ◽  
Adenine Phosphoribosyl Transferase ◽  
Transferase Deficiency

scholarly journals Preservation of epoxyeicosatrienoic acid bioavailability prevents renal allograft dysfunction and cardiovascular alterations in kidney transplant recipients

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thomas Duflot ◽  
Charlotte Laurent ◽  
Anne Soudey ◽  
Xavier Fonrose ◽  
Mouad Hamzaoui ◽  
...  
Keyword(s):  
Endothelial Function ◽  
Kidney Transplant ◽  
Plasma Levels ◽  
Renal Allograft ◽  
Transplant Recipients ◽  
Loss Of Function ◽  
Kidney Transplant Recipients ◽  
Allograft Dysfunction ◽  
Allograft Function ◽  
The Impact

AbstractThis study addressed the hypothesis that epoxyeicosatrienoic acids (EETs) synthesized by CYP450 and catabolized by soluble epoxide hydrolase (sEH) are involved in the maintenance of renal allograft function, either directly or through modulation of cardiovascular function. The impact of single nucleotide polymorphisms (SNPs) in the sEH gene EPHX2 and CYP450 on renal and vascular function, plasma levels of EETs and peripheral blood monuclear cell sEH activity was assessed in 79 kidney transplant recipients explored at least one year after transplantation. Additional experiments in a mouse model mimicking the ischemia–reperfusion (I/R) injury suffered by the transplanted kidney evaluated the cardiovascular and renal effects of the sEH inhibitor t-AUCB administered in drinking water (10 mg/l) during 28 days after surgery. There was a long-term protective effect of the sEH SNP rs6558004, which increased EET plasma levels, on renal allograft function and a deleterious effect of K55R, which increased sEH activity. Surprisingly, the loss-of-function CYP2C9*3 was associated with a better renal function without affecting EET levels. R287Q SNP, which decreased sEH activity, was protective against vascular dysfunction while CYP2C8*3 and 2C9*2 loss-of-function SNP, altered endothelial function by reducing flow-induced EET release. In I/R mice, sEH inhibition reduced kidney lesions, prevented cardiac fibrosis and dysfunction as well as preserved endothelial function. The preservation of EET bioavailability may prevent allograft dysfunction and improve cardiovascular disease in kidney transplant recipients. Inhibition of sEH appears thus as a novel therapeutic option but its impact on other epoxyfatty acids should be carefully evaluated.

Pre-transplant hypertension: a major risk factor for chronic progressive renal allograft dysfunction?

1995 ◽  
Vol 10 (7) ◽  
pp. 1206-1211 ◽  
Author(s):  
U. Frei ◽  
R. Schindler ◽  
D. Wieters ◽  
U. Grouven ◽  
R. Brunkhorst ◽  
...  
Keyword(s):  
Risk Factor ◽  
Renal Allograft ◽  
Major Risk Factor ◽  
Allograft Dysfunction
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