Removal of Blood Ammonia by Hemodialysis.

Kiley, John E.; Welch, Harold F.; Pender, Joseph C.; Welch, Stuart

doi:10.3181/00379727-91-22302

Cited by 64 publications

(29 citation statements)

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“…the expression of urea cycle enzymes or glutamine synthetase in HepG2 cells; Mavri-Damelin et al, 2007;Miyashita et al, 2000), or by the improvement of non-biological systems. Artificial liver devices without a biological component, which rely mostly on binding proteins and compounds to albumin and activated charcoal and remove ammonia by haemodialysis, have had mixed results as regards reducing arterial ammonia concentrations (Kiley et al, 1956;Onodera et al, 2006;Rozga, 2006), although some promising results have been observed in a recent study using selective plasma filtration . Gas permeable hydrophobic membranes; nonporous ion-exchange membranes; ion exchange resins and electrodialysis-based technologies are used to remove ammonia from tissue culture, reviewed in Schneider et al (1996).…”

Section: Discussionmentioning

confidence: 99%

Cells for bioartificial liver devices: The human hepatoma‐derived cell line C3A produces urea but does not detoxify ammonia

Mavri-Damelin

Damelin

Eaton³

et al. 2007

Biotech & Bioengineering

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Extrahepatic bioartificial liver devices should provide an intact urea cycle to detoxify ammonia. The C3A cell line, a subclone of the hepatoma-derived HepG2 cell line, is currently used in this context as it produces urea, and this has been assumed to be reflective of ammonia detoxification via a functional urea cycle. However, based on our previous findings of perturbed urea-cycle function in the non-urea producing HepG2 cell line, we hypothesized that the urea produced by C3A cells was via a urea cycle-independent mechanism, namely, due to arginase II activity, and therefore would not detoxify ammonia. Urea was quantified using (15)N-ammonium chloride metabolic labelling with gas chromatography-mass spectrometry. Gene expression was determined by real-time reverse transcriptase-PCR, protein expression by western blotting, and functional activities with radiolabelling enzyme assays. Arginase inhibition studies used N(omega)-hydroxy-nor-L-arginine. Urea was detected in C3A conditioned medium; however, (15)N-ammonium chloride-labelling indicated that (15)N-ammonia was not incorporated into (15)N-labelled urea. Further, gene expression of two urea cycle genes, ornithine transcarbamylase and arginase I, were completely absent. In contrast, arginase II mRNA and protein was expressed at high levels in C3A cells and was inhibited by N(omega)-hydroxy-nor-L-arginine, which prevented urea production, thereby indicating a urea cycle-independent pathway. The urea cycle is non-functional in C3A cells, and their urea production is solely due to the presence of arginase II, which therefore cannot provide ammonia detoxification in a bioartificial liver system. This emphasizes the continued requirement for developing a component capable of a full repertoire of liver function.

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Section: Discussionmentioning

confidence: 99%

Cells for bioartificial liver devices: The human hepatoma‐derived cell line C3A produces urea but does not detoxify ammonia

Mavri-Damelin

Damelin

Eaton³

et al. 2007

Biotech & Bioengineering

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“…A kidney dialysis machine was used to remove blood ammonia, but this did not result in clinical improvement. 3 Because most of these toxins were thought to be protein-bound and traditional hemodialysis used cellulose membranes impervious to large molecules, polyacrylonitrile membranes were introduced that allowed passage of molecules up to a molecular weight of 15 kDa. Table 1 summarizes the results of the early liver-support therapies introduced in the 1950s and 1960s.…”

Section: Discussionmentioning

confidence: 99%

“…The variation in the cause of the hepatic failure among individual patients from each study makes it hazardous to compare the success rate of the ex vivo liver perfusion technique. In addition, one is tempted to assume that some groups of patients (e.g., those with ALF compared with those with chronic liver disease) may exhibit a better outcome; therefore, we determined neurologic improvement, the percentage decrease in levels of NH 3 or bilirubin before and after perfusion, as well as the mean survival (in days) to compare the results of patients with the same cause from the different groups. Five patients who received eight perfusions have been excluded because they had single-case diseases such as hepatic failure from septic shock, hemochromatosis, acetaminophen intoxication, and primary graft nonfunction.…”

Section: Clinical Outcomementioning

confidence: 99%

Extracorporeal Perfusion for the Treatment of Acute Liver Failure

et al. 2000

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Objective and Summary Background DataBecause of the shortage of available donor organs, death rates from liver failure remain high. Therefore, several temporary liver-assisting therapies have been developed. This article reviews various approaches to temporary liver support as well as immunologic and metabolic developments toward a solution for this problem. MethodsA literature review was performed using Medline and additional library searches to obtain further references. Only articles with a well-defined aim of study and methodology and a clear description of the outcome of the experiments were included. ConclusionsRenewed interest has developed in old and new methods for an extracorporeal approach to the treatment of acute liver failure. Although temporary clinical improvement has been established, further research is needed to achieve a successful long-term clinical outcome. New developments in the field of genetic modification and tissue engineering await clinical application in the near future.

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“…Kiley et al (1956) were the first to employ the dializer for the removal of blood ammonia. Chang (1972) and Gazzard et al (1974) carried out hemoperfusion over coated charcoal in patients with hepatic coma.…”

Section: Discussionmentioning

confidence: 99%