Abstract:Collapsing glomerulopathy (CG) is considered to be a distinct clinicopathologic pattern of proliferative podocyte injury. The clinical significance of CG in renal allograft biopsies is yet not clear due to the scant data on the occurrence of CG in renal transplant recipients. We identified nine cases of CG in allograft biopsies over a period of 2 years. Detailed clinical information, including follow-up data, was collected and histopathological analysis performed. All the nine patients were males with a mean a… Show more
“…Most of the studies have reported that patients with CG eventually develop graft failure over a variable time period. [ 9 10 11 ] We also have observed that 11 (52.38%) out of 21 patients in our study developed graft failure over a period of 2.2 ± 1.7 years.…”
Section: Discussionsupporting
confidence: 74%
“…[ 7 ] CG in renal allografts has been reported in literature in the form of few case reports and small studies [ Table 5 ]. [ 8 9 10 11 ] In the present study, the overall prevalence of CG in renal transplant was 0.83%. However, we report a higher prevalence of 1.4% in the last 4 years, which shows an increasing awareness of disease in recent years.…”
Section: Discussionsupporting
confidence: 43%
“…Other reports showed that CG in allograft can occur anytime from 6 to 98 months after transplantation. [ 9 10 11 12 ] The range of proteinuria in our study was 1.3–6.7 g/24 h and SCr was 1.4–4.6 mg/dl. Swaminathan et al .…”
Section: Discussionmentioning
confidence: 47%
“…[ 9 10 11 ] Plasmapheresis has been attempted to treat / de novo recurrent focal and segmental glomerulosclerosis with little benefit. [ 10 11 ] Thus, prognosis of CG remains dismal. Most of the studies have reported that patients with CG eventually develop graft failure over a variable time period.…”
Collapsing glomerulopathy (CG) is a well-recognized distinct morphological pattern of proliferative parenchymal injury leading to rapid graft failure. We conducted a single-center retrospective study to evaluate the prevalence, clinicopathological features, and prognosis of CG in renal transplant recepient. We analyzed 2518 renal allograft biopsies performed from 2007 to 2015 and correlated their clinicopathological features. The prevalence of CG was 0.83% (21 out of 2518) of allograft biopsies with a higher prevalence of 1.4% during the period from 2012 to 2015. Out of 21 patients, 18 (85.71%) patients had undergone live donor and 3 (14.28%) patients had undergone deceased donor renal transplant. Hypertension was observed in 3 (14.28%) patients. The mean duration of diagnosis for CG was 1.85 ± 1.91 years. Urinalysis revealed microhematuria in 5 (23.8%) patients. The mean 24 h urinary protein excretion was 4.77 ± 5.3 g and serum creatinine was 2.12 ± 1.5 mg/dl. The predominant native kidney diseases in recipients were chronic glomerulonephritis of unknown etiology in 12 (57.14%) patients and hypertensive nephropathy in 3 (14.28%) patients. CG was associated with rejection in 9 (42.85%), calcineurin-inhibitor toxicity in 2 (9.5%), and BK virus nephropathy in 1 patient. All patients received standard triple immunosuppression. Eleven (52.38%) patients developed graft failure over a mean period of 2.2 ± 1.7 years and 6 (28.57%) patients recovered with stable graft function. CG can coexist with viral infection, drug toxicity, rejection, microvascular injury, etc. CG usually presents with moderate to severe proteinuria and may lead to rapid graft dysfunction and subsequent graft failure in most of the patients.
“…Most of the studies have reported that patients with CG eventually develop graft failure over a variable time period. [ 9 10 11 ] We also have observed that 11 (52.38%) out of 21 patients in our study developed graft failure over a period of 2.2 ± 1.7 years.…”
Section: Discussionsupporting
confidence: 74%
“…[ 7 ] CG in renal allografts has been reported in literature in the form of few case reports and small studies [ Table 5 ]. [ 8 9 10 11 ] In the present study, the overall prevalence of CG in renal transplant was 0.83%. However, we report a higher prevalence of 1.4% in the last 4 years, which shows an increasing awareness of disease in recent years.…”
Section: Discussionsupporting
confidence: 43%
“…Other reports showed that CG in allograft can occur anytime from 6 to 98 months after transplantation. [ 9 10 11 12 ] The range of proteinuria in our study was 1.3–6.7 g/24 h and SCr was 1.4–4.6 mg/dl. Swaminathan et al .…”
Section: Discussionmentioning
confidence: 47%
“…[ 9 10 11 ] Plasmapheresis has been attempted to treat / de novo recurrent focal and segmental glomerulosclerosis with little benefit. [ 10 11 ] Thus, prognosis of CG remains dismal. Most of the studies have reported that patients with CG eventually develop graft failure over a variable time period.…”
Collapsing glomerulopathy (CG) is a well-recognized distinct morphological pattern of proliferative parenchymal injury leading to rapid graft failure. We conducted a single-center retrospective study to evaluate the prevalence, clinicopathological features, and prognosis of CG in renal transplant recepient. We analyzed 2518 renal allograft biopsies performed from 2007 to 2015 and correlated their clinicopathological features. The prevalence of CG was 0.83% (21 out of 2518) of allograft biopsies with a higher prevalence of 1.4% during the period from 2012 to 2015. Out of 21 patients, 18 (85.71%) patients had undergone live donor and 3 (14.28%) patients had undergone deceased donor renal transplant. Hypertension was observed in 3 (14.28%) patients. The mean duration of diagnosis for CG was 1.85 ± 1.91 years. Urinalysis revealed microhematuria in 5 (23.8%) patients. The mean 24 h urinary protein excretion was 4.77 ± 5.3 g and serum creatinine was 2.12 ± 1.5 mg/dl. The predominant native kidney diseases in recipients were chronic glomerulonephritis of unknown etiology in 12 (57.14%) patients and hypertensive nephropathy in 3 (14.28%) patients. CG was associated with rejection in 9 (42.85%), calcineurin-inhibitor toxicity in 2 (9.5%), and BK virus nephropathy in 1 patient. All patients received standard triple immunosuppression. Eleven (52.38%) patients developed graft failure over a mean period of 2.2 ± 1.7 years and 6 (28.57%) patients recovered with stable graft function. CG can coexist with viral infection, drug toxicity, rejection, microvascular injury, etc. CG usually presents with moderate to severe proteinuria and may lead to rapid graft dysfunction and subsequent graft failure in most of the patients.
“…Neoplastic conditions like hemophagocytosis syndrome and multiple myeloma, drugs like interferon-α and bisphosphonates (pamidronate) can also lead to CG 17-20. Collapsing glomerulopathy has also been reported as de novo disease post renal transplant 21,22. Occasional genetic/ familial forms have been reported 23.…”
Objectives:To compare the clinico-pathological features of collapsing glomerulopathy (CG) at a tertiary hospital in Saudi Arabia with the world literature.Methods:In a retrospective study, all biopsy-diagnosed cases of CG between 2004-2015 were identified and analyzed, at King Khalid University Hospital, King Saud University, Riyadh. The clinico-pathological findings along with prognosis were reviewed and compared with the reported literature.Results:Thirty-one CG patients were identified, most were adult males. All the CG cases were idiopathic, all Arabs, none HIV positive, none of African descent, and none with a history of drug abuse. The number of glomeruli with collapsing lesions per biopsy ranged from 1 to 9. Other types of FSGS lesions (not otherwise specified and perihilar) were also noted. There was extensive podocyte effacement. Upon treatment, remission (complete/partial) was noted in almost half the patients; around one fourth did not respond to treatment; and one fourth progressed to end stage kidney disease (ESKD). The median time taken to develop ESKD from the time of biopsy diagnosis was 23 months.Conclusion:The clinico-pathological and prognostic correlates of CG in Saudi Arabia are comparable with that of the world literature. The management protocol at our center is the same as that practiced in different parts of the world, and the prognosis is overall poor.
Collapsing focal segmental glomerulosclerosis (cFSGS) in the native kidney is associated with heavy proteinuria and accelerated renal failure. However, cFSGS in the renal allograft is less well characterized. Here we report clinico-pathologic features and APOL1 donor risk genotypes in 38 patients with de novo post-kidney transplant cFSGS. Recipients were 34% female and 26% African-American. Concurrent viral infections and acute vaso-occlusion (including thrombotic microangiopathy, cortical necrosis, atheroembolization, and cardiac arrest with contralateral graft thrombosis) were present in 13% and 29% of recipients, respectively. Notably, 61% of patients had concurrent acute rejection and 47% received grafts from African-American donors, of which 53% carried APOL1 high-risk genotypes. These frequencies of acute rejection and grafts from African-American donors were significantly higher than in our general transplant population (35% and 16%, respectively). Patients had a median serum creatinine of 5.4mg/dl, urine protein/creatinine 3.5 g/g, and 18% had nephrotic syndrome. Graft failure occurred in 63% of patients at an average of eighteen months post-index biopsy. By univariate analysis, donor APOL1 high-risk genotypes, post-transplant time, nephrotic syndrome, and chronic histologic changes were associated with inferior graft survival while acute vaso-occlusion was associated with superior graft survival. Donor APOL1 high-risk genotypes independently predicted poor outcome. Compared to native kidney cFSGS, post-transplant cFSGS had more acute vaso-occlusion but less proteinuria. Thus, de novo cFSGS is associated with variable proteinuria and poor prognosis with potential predisposing factors of African-American donor, acute rejection, viral infection and acute vaso-occlusion. Additionally, donor APOL1 high risk genotypes are associated with higher incidence and worse graft survival.
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