UK RADAR TRANSPLANTATION IN FSGS, MCD, AND IgAN

 

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UK RADAR TRANSPLANTATION IN FSGS, MCD, AND IgAN

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David
Pitcher
David Pitcher david.pitcher@ukkidney.org UK Kidney Association RaDaR Bristol United Kingdom *
Alex Mercer alex.mercer@jamco.se JAMCO Pharma Consulting Stockholm Sweden -
Elizabeth Colby liz.colby@bristol.ac.uk University of Bristol Bristol Renal Bristol United Kingdom -
Bruce Hendry bruce.hendry@travere.com Travere Therapeutics Inc. Nephrology San Diego United States -
Jon Barrett jb81@leicester.ac.uk Leicester General Hospital University of Leicester Leicester United Kingdom -
Moin Saleem m.saleem@bristol.ac.uk University of Bristol Royal Hospital for Children Bristol United Kingdom -
Daniel Gale d.gale@ucl.ac.uk University College London Royal Free Hospital London United Kingdom -
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Long term graft survival after renal transplantation varies by primary renal diagnosis and has been correlated with proteinuria (PU). This study of the UK Rare Disease Registry (RaDaR) examines outcomes in patients with primary renal diagnoses of (non-secondary) focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD) and IgA Nephropathy (IgAN) mapped to proteinuria at 1 year post transplant and to the subsequent control of proteinuria.

RaDaR cohorts were identified with primary diagnoses of idiopathic nephrotic syndrome with biopsy-proven FSGS, MCD and IgAN. 2274 patients were identified who had received a first renal transplant since 2005 and 36% of these had proteinuria data available sufficient to quantify UPCR at 1 year post-transplant. Data extraction occurred on 14/08/2025.

 fig1

Figure 1 shows Kaplan-Meier plotted outcomes of transplantation (survival without KF, death or eGFR<15) from date of transplant were superior for IgAN to those in FSGS and MCD patients.  Table 1

Table 1, presenting demography, key characteristics and survival outcomes by diagnosis for patients with PU at 12 months post-transplantation, shows incidence of PU ≥0.3 g/g at this time point in FSGS, MCD and IgAN of 40, 62, 21%, respectively.  

figure2

Figure 2(A-C) shows transplant survival for the 3 diagnoses stratified by PU ≥ or <0.3g/g at one year post transplantation.  In all cases the higher PU group had markedly worse outcomes. The 5 year transplant survival (95% CI) for the higher PU cohorts were 65% (49-77), 66% (56-74) and 59% (27-80) for FSGS, IgAN and MCD respectively.  

figure3

Figure 3(A,B) shows the KM transplant survival for FSGS and IgAN patients respectively with 12 month PU≥0.3g/g stratified by the control of PU in the subsequent 6-24 months, as lowest value <0.3 or ≥0.3g/g (n values for MCD were too low for this analysis). In both FSGS and IgAN the control of proteinuria after 12 months by this simple metric was associated with better outcomes. 

Renal transplant outcomes are better in IgAN patients than those with native diagnoses of FSGS or MCD. This is associated with a lower incidence of PU above 0.3g/g at 12 months. Disease recurrence rates may contribute to these differences. Transplant outcomes in MCD were no better than those in FSGS, despite the younger age of the MCD cohort. For those patients who have PU ≥0.3g/g at 12 months post transplant, outcomes were poor and not correlated with native diagnosis. These data suggest that the development of PU has prognostic significance irrespective of underlying primary glomerular disease. Beyond 12 months, the control of PU appears to be associated with improved outcomes, suggesting the value of interventions that reduce proteinuria.

Kewords