ASSESSMENT OF SOLUBLE ADHESION MOLECULES (sICAM-1, sVCAM-1, sELAM-1) AND COMPLEMENT CLEAVAGE PRODUCTS (sC4d, sC5b-9) IN URINE

Bechtel, Ulrike; Scheuer, R.; Landgraf, R.; König, August; Feucht, Helmut E.

doi:10.1097/00007890-199410270-00008

Cited by 51 publications

(31 citation statements)

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“…Soluble VCAM-1 in plasma is derived from shedding of endothelial cells and has also been related to endothelial dysfunction (26). In the absence of significant excretion of sVCAM-1 in the urine (27), plasma sVCAM-1 concentration can be regarded as a reflection of endothelial release. Finally, microalbuminuria is often regarded as a marker of generalized endothelial dysfunction and has been shown to be independently associated with impaired endothelium-dependent vasodilation (28).…”

Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction Contributes to Renal Function–Associated Cardiovascular Mortality in a Population with Mild Renal Insufficiency

Stam¹,

Guldener²,

Becker³

et al. 2006

Journal of the American Society of Nephrology

229

169

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Mildly impaired renal function is associated with cardiovascular morbidity and mortality. There are indications that endothelial dysfunction and/or chronic inflammation, which play an important role in atherothrombosis, are present in early stages of renal insufficiency. This study investigated whether and to which extent endothelial dysfunction and inflammation were related to renal function and contributed to renal function-associated cardiovascular mortality in a population-based cohort (n ‫؍‬ 613), aged 50 to 75 yr, that was followed with a median duration of 12.5 yr. During follow-up, 192 individuals died (67 of cardiovascular causes). At baseline, renal function was estimated with serum creatinine, the Cockcroft-Gault formula, and the Modification of Diet in Renal Disease equation of GFR (eGFR). Endothelial function was estimated by plasma von Willebrand factor, soluble vascular cell adhesion molecule-1, and the urinary albumin-creatinine ratio. Inflammatory activity was estimated by plasma C-reactive protein and soluble intercellular adhesion molecule-1. Renal function was mildly impaired (mean eGFR 68 ؎ 12 ml/min per 1.73 m 2 ) and independently associated with von Willebrand factor (standardized ␤ ؊0.09; 95% confidence interval [CI] ؊0.18 to ؊0.002; P < 0.05), soluble vascular cell adhesion molecule-1 (standardized ␤ ؊0.14; 95% CI ؊0.22 to ؊0.05; P < 0.01), and albumin-creatinine ratio (standardized ␤ ؊0.15; 95% CI ؊0.23 to ؊0.08; P < 0.001) but not with markers of inflammatory activity. Renal function was inversely associated with cardiovascular and all-cause mortality. The relative risk for cardiovascular mortality but not all-cause mortality associated with renal function decreased from 1.22 to 1.12 per 5 ml/min per 1.73 m 2 decrease of eGFR after adjustment for markers of endothelial dysfunction. In conclusion, endothelial dysfunction was related to renal function and contributed to the excess in cardiovascular mortality in this population-based cohort with mild renal insufficiency.

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Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction Contributes to Renal Function–Associated Cardiovascular Mortality in a Population with Mild Renal Insufficiency

Stam¹,

Guldener²,

Becker³

et al. 2006

Journal of the American Society of Nephrology

229

169

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“…Among those are urinary IL-2, IL-8, and complement fragments such as soluble C4d (15)(16)(17). However, so far these predictors have not been introduced into clinical routine.…”

mentioning

confidence: 99%

Prediction of Acute Renal Allograft Rejection by Urinary Monokine Induced by IFN-γ (MIG)

Hauser¹,

Spiegler²,

Kiss³

et al. 2005

Journal of the American Society of Nephrology

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Early diagnosis of acute allograft rejection (AR) is still decisive for long-term renal allograft survival. The aim of this study was to define the role of the chemokine monokine induced by IFN-␥ (MIG) (CXCL9) and IFN-␥-inducible protein 10 (IP-10) (CXCL10) as early markers of AR in renal transplantation (NTX). In a prospective study, 69 de novo renal transplant recipients were monitored and urine samples were collected after NTX for a median of 29 d. In pH-adjusted urine, MIG and IP-10 were determined by modified ELISA. AR was clinically diagnosed in 15 of 69 recipients and confirmed by biopsy in 14 of 15 AR patients (Banff classification). Corresponding to CXCR3-positive infiltrates in renal tissue, urinary MIG was elevated in 14 of 15 AR patients with a median of 2809 pg/ml (quartile 25% and 75% ‫؍‬ 870 and 13,000; n ‫؍‬ 15), being significantly (P < 0.0001) different from both nonrejecting allograft patients (NO-AR) (median, 25%, and 75%: 96, 1.0, and 161, n ‫؍‬ 54) and healthy controls (median, 25%, and 75%: 144, 19, and 208, n ‫؍‬ 13). Urinary MIG predicted AR with a sensitivity of 93% and a specificity of 89%. In AR and NO-AR groups, MIG values correlated well with IP-10 (P < 0.001). MIG values indicated both imminent rejection and response to successful antirejection therapy. MIG was not related to intercurrent infections or other causes for impairment of renal function. In a multivariate analysis, MIG correlated best (P < 0.001) with AR from all AR-associated parameters. In conclusion, urinary MIG serves as a very sensitive and specific predictor for AR, mirrors response to antirejection therapy, and thus may contribute to improved long-term renal allograft survival.

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“…An increasing number of clinical and experimental studies of renal and cardiac allografts have linked complement activation to alloantigen-independent and -dependent responses. Complement activation occurs during the perioperative period (1-4), acute rejection (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17), and chronic graft dysfunction (18 -21). Split products of early complement components influence the localization, activation, and effector functions of platelets, granulocytes, monocytes, and lymphocytes, while membrane attack complex (MAC), 3 which is formed by the terminal components of complement (C5b-C9), can lead to rapid activation and destruction of target cells (1,4,22).…”

mentioning

confidence: 99%

Membrane Attack Complex Contributes to Destruction of Vascular Integrity in Acute Lung Allograft Rejection

Nakashima

Qian

Rahimi

et al. 2002

The Journal of Immunology

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The lung is known to be particularly susceptible to complement-mediated injury. Both C5a and the membrane attack complex (MAC), which is formed by the terminal components of complement (C5b-C9), can cause acute pulmonary distress in nontransplanted lungs. We used C6-deficient rats to investigate whether MAC causes injury to lung allografts. PVG.R8 lungs were transplanted orthotopically to MHC class I-incompatible PVG.1U recipients. Allografts from C6-sufficient (C6+) donors to C6+ recipients were rejected with an intense vascular infiltration and diffuse alveolar hemorrhage 7 days after transplantation (n = 5). Ab and complement (C3d) deposition was accompanied by extensive vascular endothelial injury and intravascular release of von Willebrand factor. In contrast, lung allografts from C6-deficient (C6−) donors to C6− recipients survived 13–17 days (n = 5). In the absence of C6, perivascular mononuclear infiltrates of ED1+ macrophages and CD8+ T lymphocytes were present 7 days after transplantation, but vascular endothelial cells were quiescent, with minimal von Willebrand factor release and no evidence of alveolar hemorrhage or edema. Lung allografts were performed from C6− donors to C6+ recipients (n = 5) and from C6+ donors to C6− recipients (n = 5) to separate the effects of systemic and local C6 production. Lungs transplanted from C6+ donors to C6− recipients had increased alveolar macrophages and capillary injury. C6 production by lung allografts was demonstrated at the mRNA and protein levels. These results demonstrate that MAC causes vascular injury in lung allografts and that the location of injury is dependent on the source of C6.

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ASSESSMENT OF SOLUBLE ADHESION MOLECULES (sICAM-1, sVCAM-1, sELAM-1) AND COMPLEMENT CLEAVAGE PRODUCTS (sC4d, sC5b-9) IN URINE

Cited by 51 publications

References 0 publications

Endothelial Dysfunction Contributes to Renal Function–Associated Cardiovascular Mortality in a Population with Mild Renal Insufficiency

Endothelial Dysfunction Contributes to Renal Function–Associated Cardiovascular Mortality in a Population with Mild Renal Insufficiency

Prediction of Acute Renal Allograft Rejection by Urinary Monokine Induced by IFN-γ (MIG)

Membrane Attack Complex Contributes to Destruction of Vascular Integrity in Acute Lung Allograft Rejection

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