Inflammation and oxidation: do they improve after kidney transplantation? Relationship with mortality after transplantation.

UNLABELLED

Patients with chronic kidney disease (CKD) are characterized by a state of inflammation and oxidative stress that seems to improve after kidney transplantation (KT). Nevertheless, there is controversy regarding what is the best marker that better define inflammation and specially oxidative stress.

OBJECTIVE

To evaluate the biomarkers which are associated with improvements in inflammation and lipid peroxidation in patients who have undergone KT. To evaluate the relationship between inflammation, lipid peroxidation and mortality in KT.

PATIENTS

196 KT (between 2003 and 2008). 67.9% men; median age: 51.9 years. Inflammation markers analyzed previous KT and 3 months after KT: c-reactive protein(CRP), interleukin 6(IL-6), tumor necrosis factor alpha(TNFα), soluble tumor necrosis factor receptor alpha(sTNFRα), soluble interleukin-2 receptor (sIL-2R). Lipid peroxidation markers analyzed: oxidized low-density lipoprotein (oxLDL) and anti-oxLDL antibodies. Calculation of glomerular filtration rate after KT: MDRD equation.

RESULTS

Following KT, there is a significant decrease in CRP (p = 0.006), IL-6 (p = 0.0037), TNFα (p < 0.0001), sTNFRα (p < 0.0001) and sIL-2R (p < 0.0001), while levels of oxLDL increase after KT (p < 0.0001) and there is not a significantly difference in anti-oxLDL. 12.8% of the patients had died in 2012. These patients had higher levels of IL-6 (p = 0.011) and sTNFRα (p < 0.006) after KT and a lower MDRD (p < 0.0001), hemoglobin (p = 0.012) and albumin (p = 0.007). We observed no statistically differences in the levels of markers previous KT. Of the patients who died, the 43.5% of them had anti-oxLDL antibody levels greater than 75th percentile (P: 3781 UI/ml, p = 0.028). In the multivariate analysis, age (OR:1.12; p = 0.0129), MDRD (OR:0.92; p = 0.013) and P of anti-oxLDL(OR: 5.19; p = 0.026) were independent risk factors for mortality. Independent risk factors for survival were: P of IL-6 (HR: 2.45; p = 0.027), oxLDL (HR:19.85; p = 0.002) and anti-oxLDL (HR: 9.55; p = 0.003).

CONCLUSIONS

KT improved inflammation but not lipid oxidative state. KT patients who died had a higher inflammatory state (with higher levels of IL-6 and sTNFRα), a worse lipid oxidative state and a worse renal function 3 months after KT. Age, anti-oxLDL and renal function at 3 months after KT were independent risk factors for mortality.