Prevalence and Risk Factors of Noncontrolled and Resistant Arterial Hypertension in Renal Transplant Recipients

2016 ◽  
Vol 100 (9) ◽  
pp. e54
2015 ◽  
Vol 99 (5) ◽  
pp. 1016-1022 ◽  
Author(s):  
Vetromile Fernando ◽  
Pernin Vincent ◽  
Szwarc Ilan ◽  
Garrigue Valérie ◽  
Delmas Sylvie ◽  
...  

1983 ◽  
Vol 148 (6) ◽  
pp. 1121-1121 ◽  
Author(s):  
P. K. Peterson ◽  
H. H. Balfour ◽  
D. S. Fryd ◽  
R. Ferguson ◽  
R. Kronenberg ◽  
...  

2017 ◽  
Vol 96 ◽  
pp. 7-11 ◽  
Author(s):  
Mohammad Shenagari ◽  
Ali Monfared ◽  
Hadise Eghtedari ◽  
Aydin Pourkazemi ◽  
Tolou Hasandokht ◽  
...  

2010 ◽  
Vol 26 (6) ◽  
pp. 2013-2017 ◽  
Author(s):  
F. Eitner ◽  
I. A. Hauser ◽  
O. Rettkowski ◽  
T. Rath ◽  
K. Lopau ◽  
...  

Acta Medica ◽  
2021 ◽  
pp. 1-10
Author(s):  
Göksel Güven ◽  
Şeref Rahmi Yılmaz ◽  
Tolga Yıldırım ◽  
Fazıl Tuncay Akı ◽  
Yunus Erdem

Objective: Dialysis or renal transplantation are the two treatment options for end-stage renal disease patients. Renal transplantation from an appropriate donor increases survival and quality of life compared to treatment with dialysis. Recent advances in immunosuppressive therapy have significantly improved the success in 1-year graft survival. However, the long-term graft survival remains the same. Therefore, we aimed to determine the underlying causes and risk factors of chronic allograft dysfunction in renal transplant recipients. Materials and Methods: From 2000 to 2012, all consecutive renal transplant recipients followed in our tertiary referral center who underwent renal biopsy due to an increase in serum creatinine level were enrolled. Etiologies of chronic allograft dysfunction were assessed according to pathologic results of renal biopsy specimens and laboratory findings. The immunological and non-immunological risk factors of chronic allograft dysfunction were screened and recorded retrospectively. Results: Eighty (80) renal transplant recipients with a mean age of 38±10 years were included in the study. Delayed graft function (p=0.007), history of acute rejection (p<0.001), positive panel reactive antibody (p=0.033) (Class I (p=0.013), Class II (p=0.006)), positive donor specific antibodies (p=0.001), number of recurrent acute rejections (p<0.001), number of human leukocyte antigens mismatches (p=0.051), cold ischemia time (p=0.001) were found to be risk factors for chronic allograft dysfunction. The donor specific antibodies positivity (p<0.001) and the panel reactive antibody positivity (Class I (p=0.003), Class II (p=0.001)) were significantly higher in patients with antibody mediated rejection than patients without antibody mediated rejection (p=0.002). Conclusion: Delayed graft function, presence and the number of acute rejections, increased cold ischemia time, panel reactive antibody positivity, donor specific antibodies positivity, and the number of human leukocyte antigens mismatches were risk factors for chronic allograft dysfunction.


2015 ◽  
Vol 30 (6) ◽  
pp. 865-872 ◽  
Author(s):  
Hae Min Lee ◽  
In-Ae Jang ◽  
Dongjae Lee ◽  
Eun Jin Kang ◽  
Bum Soon Choi ◽  
...  

2000 ◽  
Vol 11 (9) ◽  
pp. 1735-1743 ◽  
Author(s):  
BERTRAM L. KASISKE ◽  
HARINI A. CHAKKERA ◽  
JOSEPH ROEL

Abstract. Whether the high incidence of ischemic heart disease (IHD) among renal transplant patients can be attributed to the same risk factors that have been identified in the general population is unclear. The risk for major IHD events occurring >1 yr after transplantation among 1124 transplant recipients was estimated by using the risk calculated from the Framingham Heart Study (FHS). The FHS risk predicted IHD (relative risk, 1.28; 95% confidence interval, 1.20 to 1.40; P < 0.001); however, the FHS risk tended to underestimate the risk of IHD for renal transplant recipients. This was largely attributable to increased risks associated with diabetes mellitus and, to a lesser extent, age and cigarette smoking for renal transplant recipients. For men, the relative risks for diabetes mellitus were 2.78 (1.73 to 4.49) and 1.53 for the transplant recipient and FHS populations, respectively; the relative risks for age (in years) were 1.06 (1.04 to 1.08) and 1.05, respectively, and those for smoking were 1.95 (1.20 to 3.19) and 1.69, respectively. For women, the relative risks for diabetes mellitus were 5.40 (2.73 to 10.66) and 1.82, respectively. There was a tendency for the risk associated with cholesterol levels to be higher for transplant recipients, compared with the FHS population, but the risks associated with high-density lipoprotein cholesterol levels and BP appeared to be comparable. Independent of these and other risk factors, the adjusted risk of IHD for the transplant recipient population has decreased. Compared with the era before 1986, transplantation between 1986 and 1992 was associated with a lower relative risk of 0.60 (0.39 to 0.92); transplantation after 1992 was associated with an even lower relative risk of 0.27 (0.11 to 0.63) for IHD. Of concern was the fact that dihydropyridine calcium channel antagonists were associated with an increased risk for IHD (relative risk, 2.26; 95% confidence interval, 1.24 to 4.12; P = 0.008), and this association was independent of other antihypertensive agents and risk factors. Therefore, although the FHS risk predicts IHD after renal transplantation, it tends to underestimate the risks, especially the risk associated with diabetes mellitus. The unexpected finding that dihydropyridine calcium channel antagonists were associated with an increased IHD risk merits further evaluation.


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