title: Association of hyperhomocysteinemia with plasma sulfate and urine sulfate excretion in patients with progressive renal disease.
abstract: BACKGROUND
  Plasma total homocysteine (tHcy) level is increased in patients with renal disease, parallel to serum creatinine concentration. In renal failure, the final product of sulfated amino acid metabolism, sulfate, also accumulates as renal function declines. We hypothesized that the elevation in sulfate level could cause hyperhomocysteinemia and tested the relation between tHcy level and both urinary excretion and plasma levels of sulfate.
  
  
  METHODS
  Forty patients with renal disease were divided into three groups: patients without renal failure (nRF; creatinine clearance [CCr] > or = 80 mL/min/1.73 m2 [> or =1.33 mL/s/1.73 m2]), patients with mild renal failure (mRF; 80 > CCr > or = 25 mL/min/1.73 m2 [1.33 > CCr >/ or 0.42 mL/s/1.73 m2]), and patients with severe renal failure (sRF; CCr < 25 mL/min/1.73 m2 [<0.42 mL/s/1.73 m2]). Daily urinary excretion and plasma levels of tHcy, total cysteine (tCys), and sulfate were measured. A healthy control (HC) group also was tested. Serum methionine, taurine, vitamin B12, and folate levels also were determined in patients with renal disease.
  
  
  RESULTS
  Plasma tHcy and sulfate concentrations in the groups with mRF and sRF were greater than in the HC group. Plasma tCys concentrations in the mRF and sRF groups were greater than in the nRF group. Daily urinary Hcy and Cys excretion did not differ among the four groups. Daily urine sulfate and urea nitrogen excretion in the sRF group were significantly less than in the HC and nRF groups. Multiple regression analyses showed that plasma creatinine (beta = 0.40) and sulfate (beta = 0.43) levels were independently associated with plasma Hcy level; among urine parameters, only daily urine sulfate excretion (beta = -0.52) was independently associated with plasma Hcy level.
  
  
  CONCLUSIONS
  The elevated plasma sulfate level, in accordance with renal function, is associated with plasma tHcy level. Decreased sulfate excretion, which might parallel the intake of sulfated amino acid or protein, may increase tHcy levels.
authors.affiliation: Department of Kidney and Dialysis, Hyogo College of Medicine, Nishinomiya, Japan. t-nkns@hyo-med.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Nakanishi
authors.forename: Yoshinaga
authors.initials: Y
authors.lastname: Otaki
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Hasuike
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Nanami
authors.forename: Reiko
authors.initials: R
authors.lastname: Itahana
authors.forename: Koji
authors.initials: K
authors.lastname: Miyagawa
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Nishikage
authors.forename: Masaaki
authors.initials: M
authors.lastname: Izumi
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Takamitsu
mesh_terms: D000704:Analysis of Variance; D003545:Cysteine / Q000097:blood / Q000652:urine; D005260:Female; D006710:Homocysteine / Q000097:blood / Q000652:urine; D006801:Humans; D020138:Hyperhomocysteinemia / Q000097:blood* / Q000209:etiology / Q000503:physiopathology / Q000652:urine*; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000503:physiopathology / Q000652:urine*; D008297:Male; D008875:Middle Aged; D011507:Proteinuria / Q000097:blood / Q000652:urine; D013431:Sulfates / Q000097:blood* / Q000652:urine*; D014508:Urea / Q000652:urine
chemical_list: D013431:Sulfates; D006710:Homocysteine; D014508:Urea; D003545:Cysteine