TY - JOUR
T1 - Post-transplant nephrotic syndrome
T2 - A comprehensive clinicopathologic study
AU - Yakupoglu, Ulkem
AU - Baranowska-Daca, Elzbieta
AU - Rosen, Daniel
AU - Barrios, Roberto
AU - Suki, Wadi N.
AU - Truong, Luan D.
PY - 2004/6
Y1 - 2004/6
N2 - Background. Post-transplant (Tx) nephrotic syndrome (NS) is not well defined. Methods. Seventy-four renal transplant recipients with NS were studied. Results. Biopsies showed chronic allograft nephropathy (CAN) in 31 patients; recurrent glomerular disease (GN) in 15, de novo GN in 18, and undetermined GN in 9. NS developed 0.25 to 384 months post-Tx and was treated with angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) in 18 patients; calcium channel blockers in 25; or both drugs in 31. NS remitted in 24% of cases 2 to 28 months after onset, and this persisted in all except 3 patients. The remission rate was lowest (9%) for CAN and highest (47%) for de novo GN. Compared with persistent NS, those with remission showed higher prevalence of de novo GN (53% vs. 17%), lower prevalence of CAN (18% vs. 50%), earlier onset of NS (39 vs. 59 months), lower serum SCr at onset (2.3 vs. 2.9 mg/dL), and higher incidence of treatment with ACE or ARB. The 5-year graft loss rates for CAN, recurrent and de novo GN were 57%, 36%, and 23%, respectively. Compared with the functioning grafts, the failed grafts showed higher prevalence of CAN (60% vs. 16%), lower prevalence of de novo GN (12% vs. 46%), earlier onset of NS (47 vs 65 months post-Tx), higher serum SCr at onset (3.3 vs. 2.0 mg/dL), lower prevalence of remission of NS (5% vs. 48%), and higher proteinuria at follow-up (5.1 vs. 2.5 g/day). Graft survival improved with NS remission (88% vs. 18%). Conclusion. Post-Tx NS displays distinctive clinicopathologic features with pathogenetic and therapeutic implications.
AB - Background. Post-transplant (Tx) nephrotic syndrome (NS) is not well defined. Methods. Seventy-four renal transplant recipients with NS were studied. Results. Biopsies showed chronic allograft nephropathy (CAN) in 31 patients; recurrent glomerular disease (GN) in 15, de novo GN in 18, and undetermined GN in 9. NS developed 0.25 to 384 months post-Tx and was treated with angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB) in 18 patients; calcium channel blockers in 25; or both drugs in 31. NS remitted in 24% of cases 2 to 28 months after onset, and this persisted in all except 3 patients. The remission rate was lowest (9%) for CAN and highest (47%) for de novo GN. Compared with persistent NS, those with remission showed higher prevalence of de novo GN (53% vs. 17%), lower prevalence of CAN (18% vs. 50%), earlier onset of NS (39 vs. 59 months), lower serum SCr at onset (2.3 vs. 2.9 mg/dL), and higher incidence of treatment with ACE or ARB. The 5-year graft loss rates for CAN, recurrent and de novo GN were 57%, 36%, and 23%, respectively. Compared with the functioning grafts, the failed grafts showed higher prevalence of CAN (60% vs. 16%), lower prevalence of de novo GN (12% vs. 46%), earlier onset of NS (47 vs 65 months post-Tx), higher serum SCr at onset (3.3 vs. 2.0 mg/dL), lower prevalence of remission of NS (5% vs. 48%), and higher proteinuria at follow-up (5.1 vs. 2.5 g/day). Graft survival improved with NS remission (88% vs. 18%). Conclusion. Post-Tx NS displays distinctive clinicopathologic features with pathogenetic and therapeutic implications.
KW - Chronic allograft nephropathy
KW - De novo glomerular diseases
KW - Graft failure
KW - Heavy proteinuria
KW - Post-transplant nephrotic syndrome
KW - Recurrent glomerular diseases
KW - Remission
KW - Renal transplant biopsy
UR - http://www.scopus.com/inward/record.url?scp=2442714899&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2442714899&partnerID=8YFLogxK
U2 - 10.1111/j.1523-1755.2004.00655.x
DO - 10.1111/j.1523-1755.2004.00655.x
M3 - Article
C2 - 15149349
AN - SCOPUS:2442714899
VL - 65
SP - 2360
EP - 2370
JO - Kidney international
JF - Kidney international
SN - 0085-2538
IS - 6
ER -