title: Role of haptoglobin phenotype in end-stage kidney disease.
abstract: BACKGROUND
  We recently reported that haptoglobin (Hp) phenotype 1-1 is protective against the development of nephropathy in normal creatinine diabetics. In the present study, we sought to determine if Hp phenotype also plays a role in renal deterioration by determining Hp phenotypes in a consecutive series of patients with chronic renal failure (CRF) in hemodialysis (HD) and predialysis clinics.
  
  
  METHODS
  Three hundred and ninety-two patients on HD for less than 2 years and 182 predialysis patients (creatinine clearance time [CCT] <35 ml/min) were subjected to Hp phenotyping. Age, gender and presence of diabetes or hypertension were recorded. Patients were stratified according to age (above and below 60 years) and severity of renal dysfunction (CRF or HD).
  
  
  RESULTS
  We observed a markedly lower prevalence of the Hp 1-1 phenotype in HD patients under 60 years of age compared to patients with CRF or compared to the general population. This was not due to differences in the threshold for dialysis initiation among patients with different Hp types or to decreased survival of patients with Hp 1-1 prior to entering HD. In HD patients 60 years and over, Hp 1-1 prevalence was increased, as observed with other diseases in this age group.
  
  
  CONCLUSIONS
  The prevalence of Hp 1-1 is decreased in HD patients less than 60 years of age. This may be due to a fundamental difference in the rate of renal deterioration in patients with different Hp types. In addition, Hp 1-1 may provide a protective effect against mortality in elderly patients.
authors.affiliation: Department of Nephrology, Rambam Medical Center, Haifa, Israel. burbea@rambam.health.gov.il
authors.forename: Zvi
authors.initials: Z
authors.lastname: Burbea
authors.forename: Farid
authors.initials: F
authors.lastname: Nakhoul
authors.forename: Shai
authors.initials: S
authors.lastname: Rosenberg
authors.forename: Roaa
authors.initials: R
authors.lastname: Zoabi
authors.forename: Karl
authors.initials: K
authors.lastname: Skorecki
authors.forename: Irit
authors.initials: I
authors.lastname: Hochberg
authors.forename: Rachel
authors.initials: R
authors.lastname: Miller-Lotan
authors.forename: Sidney
authors.initials: S
authors.lastname: Benchetrit
authors.forename: Joshua
authors.initials: J
authors.lastname: Weissgarten
authors.forename: Aaron
authors.initials: A
authors.lastname: Knecht
authors.forename: David
authors.initials: D
authors.lastname: Tovbin
authors.forename: Nina S
authors.initials: NS
authors.lastname: Levy
authors.forename: Andrew P
authors.initials: AP
authors.lastname: Levy
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001835:Body Weight / Q000235:genetics / Q000502:physiology; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D005260:Female; D006242:Haptoglobins / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000235:genetics* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D015995:Prevalence; D006435:Renal Dialysis / Q000379:methods
chemical_list: D006242:Haptoglobins; D003404:Creatinine