Corpus ID: 4285004

Diabetes insipidus in uricase-deficient mice: a model for evaluating therapy with poly(ethylene glycol)-modified uricase.

@article{Kelly2001DiabetesII,
  title={Diabetes insipidus in uricase-deficient mice: a model for evaluating therapy with poly(ethylene glycol)-modified uricase.},
  author={S. Kelly and M. Delnomdedieu and M. Oliverio and L. D. Williams and M. G. Saifer and M. R. Sherman and T. Coffman and G. Johnson and M. Hershfield},
  journal={Journal of the American Society of Nephrology : JASN},
  year={2001},
  volume={12 5},
  pages={
          1001-9
        }
}
Uricase-deficient mice develop uric acid nephropathy, with high mortality rates before weaning. Urate excretion was quantitated and renal function was better defined in this study, to facilitate the use of these mice as a model for evaluating poly(ethylene glycol)-modified recombinant mammalian uricases (PEG-uricase) as a potential therapy for gout and uric acid nephropathy. The uric acid/creatinine ratio in the urine of uricase-deficient mice ranges from 10 to >30; on a weight basis, these… Expand

Paper Mentions

Interventional Clinical Trial
The purpose of this study is to determine whether PEG-uricase (a chemically modified recombinant mammalian enzyme that degrades uric acid) is effective in controlling… Expand
ConditionsGout
InterventionBiological
Urate-induced acute renal failure and chronic inflammation in liver-specific Glut9 knockout mice.
Urinary excretion of uric acid, allantoin, and 8-OH-Deoxyguanosine in uricase-knockout mice
PEG-uricase in the management of treatment-resistant gout and hyperuricemia.
Glut9 is a major regulator of urate homeostasis and its genetic inactivation induces hyperuricosuria and urate nephropathy
Uric acid enhances longevity and endurance and protects the brain against ischemia
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