Intact Urea Cycle in face of Arginine is required for antiinflammatory balance in TH2 expression. Antiflammatory index could be Th1/Th2 ratio .

This dichotomy also characterizes two alternative states that are often correlated with the course of a disease. The Th1 cytokines are considered proinflammatory cytokines, and they are often correlated with a gaseous messenger known to modulate specific functions of cell populations involved in the immune response. This messenger is nitric oxide (NO), a gaseous metabolite produced by the degradation of amino acid l-arginine by nitric oxide synthase (NOS). NO has been shown to be a crucial host-protective and antimicrobial effector molecule as well as a potential host-destructive mediator in diverse scenarios of immunopathology. Nevertheless, l-arginine may be metabolized by an alternative metabolic pathway. It can also be catalyzed by arginase, which converts l-arginine to l-ornithine and urea. Th2, in contrast to Th1 cytokines, often exhibits anti-inflammatory properties, and their expression has been related to the induction of arginase.

Note that as  arginase is stimulated which promotes Th2, anti-inflammatory activity, ornithine is produced, which of course can be eliminated by the Urea Cycle. If Urea cycle is dysfunctional ornithine backs up and obviously pushes back on arginase performance. This pushes arginine toward inflammatory lines with inducible nitric Acid synthase. This of course could be the explanation of the pathology in the Hepato-renal syndrome