Literature DB >> 28873129

Association of Serum Soluble Urokinase Receptor Levels With Progression of Kidney Disease in Children.

Franz Schaefer1, Howard Trachtman2, Elke Wühl1, Marietta Kirchner3, Salim S Hayek4, Ali Anarat5, Ali Duzova6, Sevgi Mir7, Dusan Paripovic8, Alev Yilmaz9, Francesca Lugani10, Klaus Arbeiter11, Mieczyslaw Litwin12, Jun Oh13, Maria Chiara Matteucci14, Jutta Gellermann15, Simone Wygoda16, Augustina Jankauskiene17, Günter Klaus18, Jiri Dusek19, Sara Testa20, Aleksandra Zurowska21, Alberto Caldas Afonso22, Melissa Tracy23, Changli Wei23, Sanja Sever24, William Smoyer25, Jochen Reiser23.   

Abstract

Importance: Conventional methods to diagnose and monitor chronic kidney disease (CKD) in children, such as creatinine level and cystatin C-derived estimated glomerular filtration rate (eGFR) and assessment of proteinuria in spot or timed urine samples, are of limited value in identifying patients at risk of progressive kidney function loss. Serum soluble urokinase receptor (suPAR) levels strongly predict incident CKD stage 3 in adults. Objective: To determine whether elevated suPAR levels are associated with renal disease progression in children with CKD. Design, Setting, and Participants: Post hoc analysis of 2 prospectively followed up pediatric CKD cohorts, ie, the ESCAPE Trial (1999-2007) and the 4C Study (2010-2016), with serum suPAR level measured at enrollment and longitudinal eGFR measured prospectively. In the 2 trials, a total of 898 children were observed at 30 (ESCAPE Trial; n = 256) and 55 (4C Study; n = 642) tertiary care hospitals in 13 European countries. Renal diagnoses included congenital anomalies of the kidneys and urinary tract (n = 637 [70.9%]), tubulointerstitial nephropathies (n = 92 [10.2%]), glomerulopathies (n = 69 [7.7%]), postischemic CKD (n = 42 [4.7%]), and other CKD (n = 58 [6.5%]). Total follow-up duration was up to 7.9 years, and median follow-up was 3.1 years. Analyses were conducted from October 2016 to December 2016. Exposures: Serum suPAR level was measured at enrollment, and eGFR was measured every 2 months in the ESCAPE Trial and every 6 months in the 4C Study. The primary end point of CKD progression was a composite of 50% eGFR loss, eGFR less than 10 mL/min/1.73 m2, or initiation of renal replacement therapy. Main Outcomes and Measures: The primary end point in this study was renal survival, defined as a composite of 50% loss of GFR that persisted for at least 1 month, the start of renal replacement therapy, or an eGFR less than 10 mL/min/1.73 m2.
Results: Of the 898 included children, 560 (62.4%) were male, and the mean (SD) patient age at enrollment was 11.9 (3.5) years. The mean (SD) eGFR was 34 (16) mL/min/1.73 m2. The 5-year end point-free renal survival was 64.5% (95% CI, 57.4-71.7) in children with suPAR levels in the lowest quartile compared with 35.9% (95% CI, 28.7-43.0) in those in the highest quartile (P < .001). By multivariable analysis, the risk of attaining the end point was higher in children with glomerulopathies and increased with age, blood pressure, proteinuria, and lower eGFR at baseline. In patients with baseline eGFR greater than 40 mL/min/1.73 m2, higher log-transformed suPAR levels were associated with a higher risk of CKD progression after adjustment for traditional risk factors (hazard ratio, 5.12; 95% CI, 1.56-16.7; P = .007). Conclusions and Relevance: Patients with high suPAR levels were more likely to have progression of their kidney disease. Further studies should determine whether suPAR levels can identify children at risk for future CKD.

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Year:  2017        PMID: 28873129      PMCID: PMC6121753          DOI: 10.1001/jamapediatrics.2017.2914

Source DB:  PubMed          Journal:  JAMA Pediatr        ISSN: 2168-6203            Impact factor:   16.193


  26 in total

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4.  Usefulness of soluble urokinase plasminogen activator receptor (suPAR) as an inflammatory biomarker in obese children.

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5.  Strict blood-pressure control and progression of renal failure in children.

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3.  Soluble Urokinase Plasminogen Activator Receptor and Decline in Kidney Function in Autosomal Dominant Polycystic Kidney Disease.

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7.  Mechanisms underlying modulation of podocyte TRPC6 channels by suPAR: Role of NADPH oxidases and Src family tyrosine kinases.

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