Recurrent Glomerulonephritis after Renal Transplantation: The Clinical Problem

Abstract

Glomerulonephritis (GN) continues to be one of the main causes of end-stage kidney disease (ESKD) with an incidence rating from 10.5% to 38.2%. Therefore, recurrent GN, previously considered to be a minor contributor to graft loss, is the third most common cause of graft failure 10 years after renal transplantation. However, the incidence, pathogenesis, and natural course of recurrences are still not completely understood. This review focuses on the most frequent diseases that recur after renal transplantation, analyzing rate of recurrence, epidemiology and risk factors, pathogenesis and bimolecular mechanisms, clinical presentation, diagnosis, and therapy, taking into consideration the limited data available in the literature. First of all, the risk for recurrence depends on the type of glomerulonephritis. For example, recipient patients with anti-glomerular basement membrane (GBM) disease present recurrence rarely, but often exhibit rapid graft loss. On the other hand, recipient patients with C3 glomerulonephritis present recurrence in more than 50% of cases, although the disease is generally slowly progressive. It should not be forgotten that every condition that can lead to chronic graft dysfunction should be considered in the differential diagnosis of recurrence. Therefore, a complete workup of renal biopsy, including light, immunofluorescence and electron microscopy study, is essential to provide the diagnosis, excluding alternative diagnosis that may require different treatment. We will examine in detail the biomolecular mechanisms of both native and transplanted kidney diseases, monitoring the risk of recurrence and optimizing the available treatment options.

Evaluation of Salivary Indoxyl Sulfate with Proteinuria for Predicting Graft Deterioration in Kidney Transplant Recipients

“…Proteinuria is also a risk factor for death in the first post-transplant year [ 10 ] and cardiovascular diseases in KTRs [ 21 ]. Moreover, there is the association between proteinuria and the recurrence of primary glomerulonephritis [ 22 , 23 ]. Hematuria ( p = 0.07142) and glucosuria ( p = 0.05781) are not risk factors for the deterioration of graft function.…”

Ntrk1 promotes mesangial cell proliferation and inflammation in rat glomerulonephritis model by activating the STAT3 and p38/ERK MAPK signaling pathways

“…Glomerulonephritis is one of the main causes of end-stage renal disease (ESRD) all over the world. The incidence of glomerulonephritis ranges from 10.5% to 38.2% and its prevalence is 17.6%-53.5% [ 1 ]. Mesangial proliferative glomerulonephritis (MsPGN) is characterized by the increased number of cells and extracellular matrix (ECM) in the mesangial region of glomerulus [ 2 ].…”

Benefit of B7-1 staining and abatacept for treatment-resistant post-transplant focal segmental glomerulosclerosis in a predominantly pediatric cohort: time for a reappraisal

“…Treatment of rFSGS has included steroids, plasmapheresis, calcineurin inhibitors, and rituximab [ 7 , 11 , 12 ]. Successful treatment of rFSGS results in 100% 5-year graft survival rate, whereas, failure to effectively treat rFSGS results in a dismal (36.5%) 5-year graft survival rate [ 13 ].…”