The soluble urokinase receptor is not a clinical marker for focal segmental glomerulosclerosis

Meijers, Björn; Maas, Rutger; Sprangers, Ben; Claes, Kathleen; Poesen, Ruben; Bammens, Bert; Naesens, Maarten; Deegens, Jeroen K. J.; Dietrich, Ruth; Storr, Markus; Wetzels, Jack F.M.; Evenepoel, Pieter; Kuypers, Dirk

doi:10.1038/ki.2013.505

Cited by 111 publications

(94 citation statements)

References 21 publications

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“…In addition, lower levels were associated with male sex and increased estimated GFR [38]. Findings in other cohorts have raised questions about the role of suPAR in the pathogenesis of proteinuria, its ability to discriminate FSGS from other forms of primary glomerular disease, and its predictive value in identifying recurrent disease post-transplant [39][40][41]. Additional studies are needed to determine the role of this specific molecule in primary FSGS in native kidneys and recurrent disease in renal allografts.…”

Section: Pathogenesismentioning

confidence: 99%

Recurrent focal segmental glomerulosclerosis after kidney transplantation

2015

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Focal segmental glomerulosclerosis (FSGS) is an important cause of glomerular disease in children and adolescents and nearly 50 % of affected patients will progress to endstage kidney disease over a 5 to 10-year period. Unfortunately, there is no established treatment for disease in the native kidney. Moreover, up to 55 % of patients develop recurrent disease after receiving a kidney transplant, with a substantially higher risk in patients who have already experienced recurrent disease in a prior transplant. A number of clinical and laboratory factors have been identified as risk factors for this complication. In addition, new investigations into podocyte biology and circulating permeability factors have shed light on the cause of recurrent the disease. While a number of novel therapeutic agents have been applied in the management of this problem, there still is no proven treatment. In this review, we summarize recent advances in the epidemiology, pathophysiology, and treatment of recurrent FSGS in pediatric patients who have received a kidney transplant.

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Section: Pathogenesismentioning

confidence: 99%

Recurrent focal segmental glomerulosclerosis after kidney transplantation

2015

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“…However, the postulated central role and direct pathological action of suPAR in FSGS is debated intensively. Several studies report lack of differences in suPAR levels between FSGS and other kidney diseases and suggests rather a reduced glomerular filtration as a major cause of increased suPAR in patients with renal disorders [64][65][66][67][68][69]. suPAR is readily detected in both plasma and serum [50,70] and it is also found in urine [50], cerebrospinal fluid [71] and saliva [72].…”

Section: Supar As a Clinical Marker Of Inflammation And Organ Damagementioning

confidence: 99%

Soluble urokinase plasminogen activator receptor—A valuable biomarker in systemic lupus erythematosus?

Enocsson¹,

Sjöwall²,

Wetterö³

2015

Clinica Chimica Acta

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The expression of uPAR is mainly regulated by growth factors and pro-inflammatory cytokines like basic fibroblast growth factor, epidermal growth factor, tumor necrosis factor, interleukin ( suPAR as a clinical marker of inflammation and organ damagePlasma membrane expression of uPAR as well as the levels of circulating suPAR have been investigated in relation to a broad range of conditions and suPAR has been referred to as a "molecular crystal ball" due to its prognostic value in diseases like tuberculosis, HIV, sepsis and cancer [2,6,13,26,58,59]. Further, it has been reported that it reflects overall immune activation and systemic inflammation [2]. suPAR has also emerged as a potential biomarker of fibrosis in chronic liver diseases of diverse etiology [10,11,[60][61][62].Recently, suPAR attracted significant attention in primary focal segmental glomerulosclerosis (FSGS). data from this pilot study revealed significantly higher suPAR levels among patients with moderately or highly elevated SDI after study inclusion, compared to patients without SDI increase (Figure 2).Furthermore, there were higher death rates among patients in the two groups with SDI increase (Figure 2). However, it is well known that present organ damage predicts further organ damage [17,100], and thus, adjustment for SDI at baseline should be performed to reduce the risk of bias. A stepwise linear multiple regression analysis was therefore performed to evaluate the impact of suPAR on future SDI increase. After adjusting for age, sex and SDI at study inclusion, we found suPAR levels to have a significant impact on future SDI increase (p = 0.005, standardized β = 0.20) whereas SDI at study inclusion was excluded from the model. Since recent studies have revealed an inverse correlation between serum suPAR and glomerular filtration [67,68,96], we also included estimated glomerular filtration (eGFR) (calculated by the 4-variable Modification of Diet in Renal Disease StudyGroup formula [101]) in the analysis, but eGFR was not retained in the model. From these results, we suggest that suPAR can actually predict organ damage independent of present SDI score or eGFR, but that a prospective study examining the association between suPAR levels at the time of diagnosis with future SDI would be preferable.In line with these findings, elevated suPAR levels have previously been demonstrated to associate with the risk of developing cancer, cardiovascular disease and type 2 diabetes later in life in the general population [7]. Importantly, these associations were independent of CRP, which is known for its predictive value in cardiovascular disease [7,102].7 Potential roles of suPAR in SLE pathogenesisAssessment of circulating suPAR levels at the clinical laboratory could possibly become a future way to estimate organ damage in SLE, and suPAR would be an even more appealing biomarker candidate if the levels could be mechanistically linked to the disease. The pathogenesis of SLE is notoriously complex and not fully understood, but includes disturbances in t...

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“…18 Ancak daha yeni çalış-malar, suPAR'ın primer FSGS'de etken olduğuna dair kuşkulara yol açmıştır. 19,20 İMMÜNOLOJİK ANORMALLİK NS'nin immün sistemin disregülasyonu sonucu oluştuğuna dair teori en az 30 yıldır mevcuttur. Relaps sırasında hem humoral hem de hücresel immün yanıtlarda anormallik olduğuna dair pek çok rapor mevcuttur.…”

Section: Pri̇mer Glomerüler Defektunclassified

A Brief Overview Of Childhood Nephrotic Syndrome: Review

Zeybek¹,

Gök²

2015

Turkiye Klinikleri J Nephrol

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The soluble urokinase receptor is not a clinical marker for focal segmental glomerulosclerosis

Cited by 111 publications

References 21 publications

Recurrent focal segmental glomerulosclerosis after kidney transplantation

Recurrent focal segmental glomerulosclerosis after kidney transplantation

Soluble urokinase plasminogen activator receptor—A valuable biomarker in systemic lupus erythematosus?

A Brief Overview Of Childhood Nephrotic Syndrome: Review

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