title: Tubular secretion of creatinine in autosomal dominant polycystic kidney disease: consequences for cross-sectional and longitudinal performance of kidney function estimating equations.
abstract: BACKGROUND
  Autosomal dominant polycystic kidney disease (ADPKD) is characterized by renal tubular cell proliferation and dedifferentiation, which may influence tubular secretion of creatinine (CCr[TS]).
  
  
  METHODS
  Diagnostic test study.
  
  
  METHODS
  We therefore investigated CCr(TS) in patients with ADPKD and controls and studied consequences for the performance of glomerular filtration rate (GFR) estimating equations.
  In patients with ADPKD and healthy controls, we measured GFR as (125)I-iothalamate clearance while simultaneously determining creatinine clearance.
  
  
  METHODS
  24-hour urinary albumin excretion.
  
  
  RESULTS
  In 121 patients with ADPKD (56% men; mean age, 40 ± 11 [SD] years) and 215 controls (48% men; mean age, 53 ± 10 years), measured GFR (mGFR) was 78 ± 30 and 98 ± 17 mL/min/1.73 m(2), respectively, and CCr(TS) was 15.9 ± 10.8 and 10.9 ± 10.6 mL/min/1.73 m(2), respectively (P < 0.001). The higher CCr(TS) in patients with ADPKD remained significant after adjustment for covariates and appeared to be dependent on mGFR. Correlation and accuracy between mGFR and CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) estimated GFR (eGFR) were 0.95 and 99%, respectively; between mGFR and MDRD (Modification of Diet in Renal Disease) Study eGFR, they were 0.93 and 97%, respectively. Values for bias, precision, and accuracy were similar or slightly better than in controls. In addition, change in mGFR during 3 years of follow-up in 45 patients with ADPKD correlated well with change in eGFR.
  
  
  CONCLUSIONS
  Cross-sectional, single center.
  
  
  CONCLUSIONS
  CCr(TS) in patients with ADPKD is higher than that in controls, but this effect is limited and observed at only high-normal mGFR. Consequently, the CKD-EPI and MDRD Study equations perform relatively well in estimating GFR and change in GFR in patients with ADPKD.
authors.affiliation: Division of Nephrology, Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
authors.forename: Edwin M
authors.initials: EM
authors.lastname: Spithoven
authors.forename: Esther
authors.initials: E
authors.lastname: Meijer
authors.forename: Wendy E
authors.initials: WE
authors.lastname: Boertien
authors.forename: Steef J
authors.initials: SJ
authors.lastname: Sinkeler
authors.forename: Hilde
authors.initials: H
authors.lastname: Tent
authors.forename: Paul E
authors.initials: PE
authors.lastname: de Jong
authors.forename: Gerjan
authors.initials: G
authors.lastname: Navis
authors.forename: Ron T
authors.initials: RT
authors.lastname: Gansevoort
mesh_terms: D000328:Adult; D003404:Creatinine / Q000652:urine*; D003430:Cross-Sectional Studies; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000502:physiology*; D006801:Humans; D007677:Kidney Function Tests / Q000379:methods* / Q000639:trends; D007684:Kidney Tubules / Q000378:metabolism*; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D016891:Polycystic Kidney, Autosomal Dominant / Q000175:diagnosis* / Q000652:urine*
chemical_list: D003404:Creatinine
keywords: Autosomal dominant polycystic kidney disease (ADPKD); creatinine; estimated glomerular filtration rate (eGFR); measured GFR; tubular secretion of creatinine