Immunoglobulin M and C1q mesangial labeling in IgA nephropathy

Welch, Thomas R.; McAdams, James

doi:10.1016/s0272-6386(98)70021-6

Cited by 15 publications

(9 citation statements)

References 8 publications

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“…41 This may explain the increased renal IgM deposition in those with low C4 levels and the negative correlation between serum C4 and renal deposition of IgM in the current study. The gradually accumulated renal IgM deposition is associated with heavy proteinuria, 42 crescents formation, 43,44 increased mesangial matrix as well as mesangial and perimesangial electron-dense deposits 45 leading to a poor outcome in IgAN. 46 We presumed that the lectin pathway may not be activated sufficiently under the condition of C4 deficiency, which protect the glomeruli from the initial injury at the time of renal biopsy.…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics of IgA nephropathy associated with low complement 4 levels

Zhu

Lin

et al. 2014

Renal Failure

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Objective: C4 deficiency is the most commonly inherited immune disorder in human. The present study investigated the characteristics of the IgAN patients with low serum C4 levels.Methods: We performed a prospective observational study. Clinical as well as histopathologic parameters were assessed. A Kaplan-Meier survival analysis was performed concerning the primary outcome defined as the serum creatinine increased 1.5-fold from baseline. The prognostic significances of clinical and histopathologic parameters were determined using Cox proportional hazards models. Results: Five-hundred twelve biopsy proven IgAN cases were available for analysis with a median follow-up of 38.4 months. Ninety-nine cases (19.34%) presented with low C4 levels (LowC4 group) and the other 413 cases did not (NlowC4 group). At the time of renal biopsy, renal injury was lighter in the LowC4 group compared with the NlowC4 group. Renal C4 deposition was significantly decreased while IgM deposition was increased in the LowC4 group. A correlation analysis shows that lower C4 levels were associated with better renal presentations at biopsy. However, the risk of developing the primary outcome was significantly greater in those with low C4 levels. Specifically, during the follow-up period, the risk of developing primary outcome was nearly ten folds higher in those with low C4, compared to those without low C4. Conclusion: There is a high prevalence of low C4 levels in IgAN patients. These patients with low C4 levels exhibited better renal presentations at the time of renal biopsy, whereas might be associated with a poor prognosis.

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Section: Discussionmentioning

confidence: 99%

Clinical characteristics of IgA nephropathy associated with low complement 4 levels

Zhu

Lin

et al. 2014

Renal Failure

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“…C1q, in particular, is a high molecular weight negatively changed protein, frequently identified with heavy proteinuria. We have shown that C1q labeling in nephrotic syndrome [18]and in IgA nephropathy [19]is a nonspecific consequence of proteinuria. Complete immunohistochemical and ultrastructural analysis is critical before labeling a glomerular protein a ‘deposit’.…”

Section: Evidence Of Complement Activation In Glomerulonephritismentioning

confidence: 99%

The Complement System in Renal Diseases

Welch¹

2001

Nephron

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The complement system has long been recognized as having a role in immune glomerular disease. This review provides an update on this association, some strategies for the clinical testing of complement in disease, and a brief commentary on current research directions. Evidence of complement activation in glomerulonephritis comes from characteristic patterns of a decrease in the serum concentrations of specific components, some of which are virtually diagnostic of certain nephritides. These patterns are often accompanied by the presence of complement components in the glomeruli and the detection of complement breakdown products in the circulation. In certain diseases, circulating complement-activating substances can be detected. Although there are over 20 complement proteins, clinical analysis is most often directed at C3 and C4, with occasional measurement of B and C5. Recently, a variety of mechanisms for complement-induced injury has been recognized. These mechanisms go far beyond simple passive lysis of erythrocytes, the earliest functional effect of complement studied. The role of such mechanisms in renal disease is just beginning to be studied. Local synthesis of complement components in the kidney may play a role both in host defense and in the promotion of interstitial inflammation and scarring. Such mechanisms will likely be defined more precisely with the availability of animals with specific complement deficiencies. Ultimately, an understanding of the role of complement in renal disease may permit specific targeted inhibition of one or more complement functions as a form of therapy.

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“…Thomas et al . reported IgM and C1q mesangial labelling to correlate with heavy proteinuria, but not with a poor outcome in childhood IgAN 5 . Espinosa et al .…”

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confidence: 94%