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  • Title: Urinary proinflammatory cytokine response in renal transplant recipients with polyomavirus BK viruria.
    Author: Sadeghi M, Daniel V, Schnitzler P, Lahdou I, Naujokat C, Zeier M, Opelz G.
    Journal: Transplantation; 2009 Nov 15; 88(9):1109-16. PubMed ID: 19898207.
    Abstract:
    BACKGROUND: Polyomavirus BK (BKV) has emerged as an important complication after kidney transplantation. BKV-associated nephropathy develops in approximately 5% to 8% of renal transplant recipients, and its prognosis is poor. The relationship between urine cytokines and BK viruria in kidney recipients has not been defined. PATIENTS AND METHODS: We compared posttransplant urine cytokine levels of 65 renal transplant outpatients with (BK-positive) or without BK viruria (BK-negative, n=33), low- (n=16) or high-level (n=16) BK viral load (VL), and 24 healthy controls (HCs). Soluble interleukin-1 receptor antagonist (sIL-1RA), interleukin (IL)-2, sIL-2R, IL-3, IL-4, IL-6, sIL-6R, IL-10, IL-17, transforming growth factor-beta2, interferon-gamma, and tumor necrosis factor-alpha levels were determined using commercially available ELISA kits. RESULTS: BK-positive patients showed higher urine IL-3 (P=0.006), sIL-6R (P=0.010), IL-6 (P=0.020), and sIL-1RA (P=0.050) than BK-negative patients. Compared with HCs, BK-negative patients had lower urine sIL-1RA (P=0.003), sIL-6R (P=0.001), and IL-17 (P<0.001), whereas BK-positive patients had higher urine IL-3 (P=0.004) and IL-6 (P=0.001) and lower IL-17 (P<0.001), suggesting cytokine suppression by immunosuppression and upregulation by BK-infection. Urine sIL-6R (P=0.003) and IL-6 (P=0.010) were higher in patients with high VL than in patients with low VL. Additionally, patients with high VL showed higher urine IL-6 (P=0.001), sIL-6R (P=0.001), sIL-1RA (P=0.016), and IL-3 (P=0.047) than BK-negative patients, and higher urine IL-6 (P<0.001) and lower IL-17 (P<0.001) than HCs. CONCLUSION: BK-positive renal transplant recipients, especially those with high VL, showed strong inflammatory cytokine responses with increases of urine sIL-1RA, IL-3, IL-6, and sIL-6R. Our data suggest that monocyte- and Th-2-induced cytokines are involved in the pathogenesis of BKV-associated nephropathy.
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