Improvement of cytokine response and survival time by bioartificial kidney therapy in acute uremic pigs with multi-organ dysfunction.
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.
Wang
Hengjin
H
Department of Nephrology, Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, China.
Zhang
Miao
M
Wang
Xiaoyun
X
Mao
Huijuan
H
Ying
Xumin
X
Zhu
Wenbin
W
Sun
Cheng
C
Jiang
Chunming
C
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*
D016207:Cytokines; D004731:Endotoxins; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002245:Carbon Dioxide