Impact of Proinflammatory Cytokine Gene Polymorphisms and Circulating CD3 on Long-Term Renal Allograft Outcome in Egyptian Patients.

The extant study aimed to explore the influence of two cytokines TNF-α - 308 and IFN-γ + 874 gene polymorphism on development of renal transplant rejection and to investigate the feasibility of Th1 cytotoxic immune reaction (CD3). It includes 152 kidney recipients were divided into two subgroups: 76 stable graft functions (SGF) and 76 allograft dysfunctions (AD) compared with 56 healthy individuals as control group. TNF-α - 308 G > A and IFN-γ + 874 A > T genetic polymorphisms were characterized using ARMS-PCR technique. CD3 protein expression was measured using ELISA Kit. The effect on transplant outcome was analyzed where, statistically significant differences of TNF-a-308 G/A were observed between AD group when compared to SGF group (OR = 0.296, 95% CI = 0.091-0.965, p = .031) in AG genotype (intermediate producer genotype). Also, AD group displayed a statistically significant increase of IFN-γ + 874 TT (high producer genotype) when compared to SGF group (OR = 0.290, 95% CI = 0.127-0.665, p = .003). The expression of CD3+ T lymphocytes in recipients with allograft dysfunction was statistically higher than that with stable allograft function and control groups (732 ± 76, 235 ± 51 and 442 ± 50) respectively and (p ≤ 0.001). In conclusion, IFN-γ + 874 T and TNF-α - 308 A alleles are risk alleles for renal transplant rejection and these two single nucleotide polymorphisms (SNPs) may be implicated in the tendency of rejection after renal transplantation. CD3 may be used as non-invasive biomarker in monitoring of rejection and avoid exposing patients for biopsy risks and sampling error.

Hemodynamic Changes of Hepatic & Renal Vessels in Systemic Bacterial Infection with Fever in HCV Related Cirrhosis.

OBJECTIVES: To study the hemodynamic changes of hepatic & renal vessels in systemic bacterial infection with fever in HCV related cirrhosis with possible complications. METHODS: Three groups of patients with systemic bacterial infection with fever were included in the study; group І included 15 patients with decompensated cirrhosis, group ІІ included 15 patients with compensated cirrhosis and group ІІІ included 10 patients without liver affection. Laboratory parameters and Doppler US of hepatic and renal vessels were evaluated during and after subsidence of fever in all patients. RESULTS: Forty patients were enrolled in this prospective study. There were 22 male and 18 female patients. We found that the direction of blood flow in the portal and splenic veins was hepatopetal and the veins were non pulsatile in all cases with no change during and after subsidence of infection. There was no significant difference in portal or splenic vein diameters during and after subsidence of infection in the three studied groups. However, the mean values of portal and splenic veins peak velocities were significantly lower during infection in cirrhotic groups. The mean value of hepatic artery resistive index during fever was significantly higher than after fever in cirrhotic groups. Renal resistive and pulsatility indices were significantly higher during fever in cirrhotic groups. CONCLUSION: Systemic bacterial infection with fever can affect hepatic haemodynamics leading to aggravation of portal hypertension and increasing the risk of complications as variceal bleeding and hepatic encephalopathy and can also affect renal haemodynamics with increased risk of renal impairment.