AI Article Synopsis
- C3 glomerulopathy is a rare kidney disease caused by abnormal activation of the complement system, leading to harmful deposits in the kidneys and frequent recurrence after kidney transplants.
- More than half of kidney transplant recipients experience recurrence of this disease, which is the second most common cause of graft loss after organ rejection.
- Current treatment options include corticosteroids and mycophenolate mofetil, but new anti-complement drugs are being studied, showing promise for improving outcomes in affected transplant patients.
Article Abstract
C3 glomerulopathy is a rare disease, characterized by an abnormal activation of the complement's alternative pathway that leads to the accumulation of the C3 component in the kidney. The disease recurs in more than half of kidney transplant recipients, with a significant impact on graft survival. Recurrence of the primary disease represents the second cause of graft loss after organ rejection. In C3 glomerulopathy, there are several risk factors which can promote a recurrence during transplantation, such as delayed graft function, infection and monoclonal gammopathy. All these events can trigger the alternative complement pathway. In this review, we summarize the impact of C3 glomerulopathy on kidney grafts and present the latest treatment options. The most widely used treatments for the disease include corticosteroids and mycophenolate mofetil, which are already used chronically by kidney transplant recipients; thus, additional treatments for C3 glomerulopathy are required. Currently, several studies using anti-complement drugs (i.e., eculizumab, Ravalizumab, avacopan) for C3 glomerulopathy in kidney transplant patients are ongoing with encouraging results.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11204074 | PMC |
| http://dx.doi.org/10.3390/ijms25126508 | DOI Listing |
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