title: Do metabolic derangements in end-stage polycystic kidney disease differ versus other primary kidney diseases?
abstract: OBJECTIVE
  Autosomal dominant polycystic kidney disease (ADPKD), a systemic disorder caused by mutation in genes encoding polycystins, has been reported to lead to metabolic derangements including new-onset diabetes mellitus after kidney transplantation. We analyzed markers of insulin resistance (IR), inflammation, nutritional status and insulin-like growth factor-1 (IGF-1) in end-stage renal disease (ESRD) patients with ADPKD and ESRD patients with other primary kidney diseases.
  
  
  METHODS
  In a post hoc cross-sectional analysis in 254 non-diabetic CKD 5 patients starting on dialysis, glucose metabolism (insulin, IGF-1, homeostasis model assessment of IR, HOMA-IR), inflammation (high sensitivity C-reactive protein, interleukin-6, and tumour necrosis factor), nutritional status, and bone mineral density (BMD), were assessed. Survival was recorded for median time of 28 months (IQR 15-48 months).
  
  
  RESULTS
  Neither indices of IR, nor IGF-1, inflammatory status, nutritional status, or BMD were different in patients with ADPKD as compared to other aetiologies of ESRD. Kaplan-Meier curves showed better survival among the ADPKD group versus other aetiologies, even after an exclusion of diabetic patients.
  
  
  CONCLUSIONS
  The ESRD phenotype did not differ in ADPKD versus other primary kidney diseases in terms of markers of IR, inflammation, and nutritional status. This argues against the proposition that ADPKD patients are more prone to develop metabolic derangements beyond those generally observed in advanced CKD. However, additional studies are warranted to further elucidate systemic metabolic aspects of ADPKD.
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.|Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Poland.
authors.forename: Magdalena
authors.initials: M
authors.lastname: Jankowska
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Abdul Rashid
authors.initials: AR
authors.lastname: Qureshi
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Peter
authors.initials: P
authors.lastname: Barany
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Olof
authors.initials: O
authors.lastname: Heimburger
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Peter
authors.initials: P
authors.lastname: Stenvinkel
authors.affiliation: Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Bengt
authors.initials: B
authors.lastname: Lindholm
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D015519:Bone Density; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D053208:Kaplan-Meier Estimate; D007676:Kidney Failure, Chronic / Q000097:blood / Q000209:etiology* / Q000401:mortality / Q000628:therapy; D008297:Male; D008875:Middle Aged; D009752:Nutritional Status; D010641:Phenotype; D016891:Polycystic Kidney, Autosomal Dominant / Q000097:blood / Q000150:complications* / Q000401:mortality / Q000628:therapy; D016016:Proportional Hazards Models; D006435:Renal Dialysis; D012307:Risk Factors; D013997:Time Factors; D016896:Treatment Outcome; D055815:Young Adult
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; C583557:IGF1 protein, human; D018836:Inflammation Mediators; D007328:Insulin; D007334:Insulin-Like Growth Factor I
keywords: Autosomal dominant polycystic kidney disease; end-stage renal disease; inflammation; insulin resistance