Serum suPAR in patients with FSGS: trash or treasure?

Maas, Rutger; Deegens, Jeroen K. J.; Wetzels, Jack F.M.

doi:10.1007/s00467-013-2452-5

Cited by 73 publications

(62 citation statements)

References 60 publications

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“…Current candidates for the recurrent FSGS factor, reviewed recently (44), include cardiotrophinlike cytokine factor 1 (45), apoA1b (an isoform of ApoA1) (46), anti-CD40 antibody (47), and serum urine-type plasminogen activator receptor (suPAR) (48). The role of suPAR remains controversial (49). suPAR levels were reported in FSGS and other primary glomerular diseases (50).…”

Section: Primary Fsgsmentioning

confidence: 99%

Focal Segmental Glomerulosclerosis

Rosenberg

Kopp

2017

CJASN

434

366

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Focal segmental glomerulosclerosis (FSGS) is a leading cause of kidney disease worldwide. The presumed etiology of primary FSGS is a plasma factor with responsiveness to immunosuppressive therapy and a risk of recurrence after kidney transplant-important disease characteristics. In contrast, adaptive FSGS is associated with excessive nephron workload due to increased body size, reduced nephron capacity, or single glomerular hyperfiltration associated with certain diseases. Additional etiologies arenow recognized asdrivers of FSGS: high-penetrance geneticFSGSdue to mutations in one of nearly 40 genes, virus-associated FSGS, and medication-associated FSGS. Emerging data support the identification of a sixth category: APOL1 risk allele-associated FSGS in individuals with sub-Saharan ancestry. The classification of a particular patient with FSGS relies on integration of findings from clinical history, laboratory testing, kidney biopsy, and in some patients, genetic testing. The kidney biopsy can be helpful, with clues provided by features on light microscopy (e.g., glomerular size, histologic variant of FSGS, microcystic tubular changes, and tubular hypertrophy), immunofluorescence (e.g., to rule out other primary glomerulopathies), and electron microscopy (e.g., extent of podocyte foot process effacement, podocyte microvillous transformation, and tubuloreticular inclusions). A complete assessment of renal histology is important for establishing the parenchymal setting of segmental glomerulosclerosis, distinguishing FSGS associated with one of many other glomerular diseases from the clinical-pathologic syndrome of FSGS. Genetic testing is beneficial in particular clinical settings. Identifying the etiology of FSGS guides selection of therapy and provides prognostic insight. Much progress has been made in our understanding of FSGS, but important outstanding issues remain, including the identity of the plasma factor believed to be responsible for primary FSGS, the value of routine implementation of genetic testing, and the identification of more effective and less toxic therapeutic interventions for FSGS.

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Section: Primary Fsgsmentioning

confidence: 99%

Focal Segmental Glomerulosclerosis

Rosenberg

Kopp

2017

CJASN

434

366

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“…32 This interesting finding is currently under debate. 53,54 Another observation making uPAR particularly interesting in relation to SLE is that uPAR stimulates efferocytosis, i.e.…”

Section: Discussionmentioning

confidence: 99%

Soluble urokinase plasminogen activator receptor levels reflect organ damage in systemic lupus erythematosus

Enocsson

Wetterö

Skogh

et al. 2013

Translational Research

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Compared to healthy controls, serum suPAR levels were significantly elevated in SLE patients. No association was recorded regarding suPAR levels and SLE disease activity in cross-sectional or consecutive samples. However, a strong association was observed between suPAR and SDI (p<0.0005). Considering distinct SDI domains, renal, neuropsychiatric, ocular, skin and peripheral vascular damage had significant impact on suPAR levels.This study is the first to demonstrate an association between serum suPAR and irreversible organ damage in SLE. Further studies are warranted to evaluate suPAR and other biomarkers as predictors of evolving organ damage.

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“…The postulated circulating factor has not yet been identified yet. Recent findings suggest a role for cardiotrophin‐like cytokine factor 1 (CLC‐1),3 whereas the experimental findings concerning soluble urokinase‐type plasminogen activator receptor (suPAR) in the pathogenesis of FSGS in humans remain conflicting 6, 7. Here, we report on successful transplantation of a deceased donor renal allograft that failed in the first recipient due to fulminant recurrent primary FSGS and successful kidney retransplantation in the first recipient employing pretreatment with ofatumumab.…”

Section: Case Reportmentioning

confidence: 94%

Successful management of recurrent focal segmental glomerulosclerosis

Kienzl-Wagner

Rosales

Scheidl

et al. 2018

American Journal of Transplantation

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Primary focal segmental glomerulosclerosis (FSGS) recurs in up to 55% of patients after kidney transplantation. Herein we report the successful management of recurrent FSGS. A 5‐year‐old boy with primary FSGS received a deceased donor renal transplant. Immediate and fulminant recurrence of FSGS caused anuric graft failure that was resistant to plasmapheresis and rituximab. After exclusion of structural or immunologic damage to the kidney by repeated biopsies, the allograft was retrieved from the first recipient on day 27 and transplanted into a 52‐year‐old second recipient who had vascular nephropathy. Immediately after retransplantation, the allograft regained function with excellent graft function persistent now at 3 years after transplant. After 2 years on hemodialysis, the boy was listed for kidney retransplantation. To prevent FSGS recurrence, pretreatment with ofatumumab was performed. Nephrotic range proteinuria still occurred after the second transplantation, which responded, however, to daily plasma exchange in combination with ofatumumab. At 8 months after kidney retransplantation graft function is good. The clinical course supports the hypothesis of a circulating permeability factor in the pathogenesis of FSGS. Successful ofatumumab pretreatment implicates a key role of B cells. Herein we provide a description of successful management of kidney failure by FSGS, carefully avoiding waste of organs.

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Serum suPAR in patients with FSGS: trash or treasure?

Cited by 73 publications

References 60 publications

Focal Segmental Glomerulosclerosis

Focal Segmental Glomerulosclerosis

Soluble urokinase plasminogen activator receptor levels reflect organ damage in systemic lupus erythematosus

Successful management of recurrent focal segmental glomerulosclerosis

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