title: Urine but not serum soluble urokinase receptor (suPAR) may identify cases of recurrent FSGS in kidney transplant candidates.
abstract: BACKGROUND
  Recently, serum soluble urokinase receptor (suPAR) has been proposed as a cause of two thirds of cases of focal segmental glomerulosclerosis (FSGS). It was noted to be uniquely elevated in cases of primary FSGS, with higher levels noted in cases that recurred after transplantation. It is also suggested as a possible target and marker of therapy.
  
  
  METHODS
  We studied serum and urine suPAR from pretransplantation banked samples from 86 well-characterized kidney transplant recipients and 10 healthy controls to determine its prognostic utility. Causes of native kidney disease were primary FSGS, diabetic nephropathy, membranous nephropathy, immunoglobulin A nephropathy, and autosomal dominant polycystic kidney disease. suPAR was measured using a commercially available enzyme-linked immunosorbent assay kit. Urinary suPAR was indexed to creatinine.
  
  
  RESULTS
  Both serum and urine suPAR correlated with proteinuria and albuminuria. Serum suPAR was found to be elevated in all transplant candidates with advanced renal disease compared with healthy controls and could not differentiate disease diagnosis. Urine suPAR was elevated in cases of recurrent FSGS compared with all other causes of end-stage renal disease. Recurrent FSGS cases had substantially higher proteinuria compared with all other cases. However, elevated urinary suPAR showed a trend in providing additional prognostic information beyond proteinuria in the small cohort of recurrent FSGS cases.
  
  
  CONCLUSIONS
  In advanced renal disease, elevated serum suPAR is not unique to FSGS cases. Urinary suPAR appears to be higher in cases of FSGS destined for recurrence and merits further evaluation.
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA.
authors.forename: Carlos R
authors.initials: CR
authors.lastname: Franco Palacios
authors.forename: John C
authors.initials: JC
authors.lastname: Lieske
authors.forename: Hani M
authors.initials: HM
authors.lastname: Wadei
authors.forename: Andrew D
authors.initials: AD
authors.lastname: Rule
authors.forename: Fernando C
authors.initials: FC
authors.lastname: Fervenza
authors.forename: Nikolay
authors.initials: N
authors.lastname: Voskoboev
authors.forename: Vesna D
authors.initials: VD
authors.lastname: Garovic
authors.forename: Ladan
authors.initials: L
authors.lastname: Zand
authors.forename: Mark D
authors.initials: MD
authors.lastname: Stegall
authors.forename: Fernando G
authors.initials: FG
authors.lastname: Cosio
authors.forename: Hatem
authors.initials: H
authors.lastname: Amer
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016022:Case-Control Studies; D005260:Female; D005923:Glomerulosclerosis, Focal Segmental / Q000097:blood / Q000209:etiology* / Q000652:urine*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000601:surgery; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D011507:Proteinuria / Q000097:blood / Q000652:urine; D055293:Receptors, Urokinase Plasminogen Activator / Q000097:blood / Q000378:metabolism*; D012008:Recurrence; D012995:Solubility
chemical_list: D015415:Biomarkers; C524898:PLAUR protein, human; D055293:Receptors, Urokinase Plasminogen Activator