title: Improvement of cytokine response and survival time by bioartificial kidney therapy in acute uremic pigs with multi-organ dysfunction.
abstract: OBJECTIVE
  To explore whether bioartificial kidney (BAK) ameliorates cytokine response and biochemical indices, and prolongs the survival time in acute uremic pigs with multiple organ dysfunction syndrome (MODS).
  
  
  METHODS
  Hybridized pigs suffering from MODS and acute renal failure (ARF) were treated with BAK (Group A, n=6) or sham-BAK containing no cells (Group B, n=6), or received no treatment (Group C, n=5). Data on blood pressure, hepatic and renal function, IL-10, TNF-α, arterial blood gas, and survival time of all the pigs was recorded.
  
  
  RESULTS
  Mean arterial pressure (MAP, mmHg) responded more rapidly and reached higher values in Group A (91.82 ± 5.73) compared with Groups B and C at 24 hours (p<0.01). The peak level of serum IL-10 (pg/mL) in Group A (249.57 ± 43.51) was significantly higher than in Groups B and C (132.06 ± 17.53, 104.25 ± 13.42, p<0.01). Serum TNF-α level (pg/mL) in Group A dropped gradually to 402.91 ± 32.47 at 24 hours, and showed a significant discrepancy compared with those before treatment (537.16 ± 38.45) and Group B (512.94 ± 19.5, p<0.05). There was no difference in plasma endotoxin and serum IL-6 between pre-treatment and post-treatment in Groups A and B. BAK treatment, however, resulted in a significant decline in IL-6/IL-10 ratios. The average survival time (hours) in Group A (113.01 ± 14.32) was significantly longer, prolonged by 35.93% and 63.90% compared to Groups B and C (p<0.01), respectively.
  
  
  CONCLUSIONS
  The addition of renal tubule cell therapy to hemofiltration in an acutely uremic animal model with MODS altered systemic cytokine balance, ameliorated MAP, and prolonged survival time.
authors.affiliation: Department of Nephrology, Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
authors.forename: Hengjin
authors.initials: H
authors.lastname: Wang
authors.forename: Miao
authors.initials: M
authors.lastname: Zhang
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Wang
authors.forename: Huijuan
authors.initials: H
authors.lastname: Mao
authors.forename: Xumin
authors.initials: X
authors.lastname: Ying
authors.forename: Wenbin
authors.initials: W
authors.lastname: Zhu
authors.forename: Cheng
authors.initials: C
authors.lastname: Sun
authors.forename: Chunming
authors.initials: C
authors.lastname: Jiang
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D000818:Animals; D021522:Bioartificial Organs; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000097:blood; D016207:Cytokines / Q000097:blood*; D004195:Disease Models, Animal; D004731:Endotoxins / Q000097:blood; D006440:Hemofiltration; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007687:Kidney Tubules, Proximal / Q000473:pathology / Q000637:transplantation*; D007688:Kidneys, Artificial; D018374:LLC-PK1 Cells; D009102:Multiple Organ Failure / Q000097:blood / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*; D013552:Swine; D013997:Time Factors; D023822:Tissue Engineering; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D014511:Uremia / Q000097:blood / Q000276:immunology / Q000503:physiopathology / Q000628:therapy*
chemical_list: D016207:Cytokines; D004731:Endotoxins; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002245:Carbon Dioxide