Effect of hcv virus on insulin resistance in post renal transplant patients role of tnf alpha

Abstract EN

New-onset diabetes mellitus (PTDM) is a common complication of kidney transplantation and is associated with increases in graft loss, morbidity and mortality.

Numerous epidemiological studies have also reported a higher prevalence of type 2 diabetes mellitus (DM2) in subjects infected by HCV.

The aim of this work is to study the relation between insulin resistance and virus load in HCV + ve renal transplant patients with and without diabetes and to investigate the role of TNF-alpha. Patient and methods: Patients: this study included 79 renal transplant patients, divided into 4 groups; Group I: 20 HCV + ve diabetic patients, Group II: 23 HCV + ve non-diabetic patients, Group III: 20 HCV–ve diabetic patients, Group IV: 16 controls HCV-ve non-diabetic transplant patients.

To all patients, the following were done; fasting serum glucose, HOMA method for insulin resistance, ALT and AST, TNF -α measurements, anti-HCV antibodies (ELISA), and HCV RNA quantitative PCR.

All HCV + ve patient had HCV before renal transplantation, and all are receiving cyclosporine (CSA), Mycophenolate mofetil (MMF) or Azathioprine (AZA), and steroids. Results showed that HOMA index showed highly significant increase in patients with HCV, HCV + DM and DM (GI, GII, GIII), compared with control (GIV) (p<0.001).

Furthermore, patients with HCV + DM had statistically significant higher levels of HOMA index compared to those of DM alone (p<0.001).

Serum TNF-alpha levels showed also highly significant increase in patients with HCV and HCV + DM (GI, GII) compared with patients with D.M alone and to control group (p<0.001).

HCV RNA load showed a significant correlation with both HOMA index and TNF-alpha levels (r= 0.811 and 0.848, respectively) (p<0.001).

In conclusion this study showed that HCV + ve renal transplant patients is associated with insulin resistance.

And the degree of insulin resistance is directly proportional to the virus load.

The mechanism of insulin resistance may be through increased TNF-alpha secretion, which showed also significant correlation with virus load.