Abstract
Purine nucleotides important for normal cellular metabolism are derived endogenously from de novo synthesis and also from recycling of pre-formed purines via the so-called salvage pathway (Figure 1). The latter pathway contains a number of enzymes, the absence of which can lead to disturbances of purine metabolism and also severe clinical symptoms1. An example is the deficiency of the salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT) which can lead either to the Lesch-Nyhan syndrome or X-linked gout1.
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Simmonds, H.A. et al. (1981). 2, 8-Dihydroxyadeninuria: Or When is a Uric Acid Stone not a Uric Acid Stone?. In: Smith, L.H., Robertson, W.G., Finlayson, B. (eds) Urolithiasis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8977-4_22
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DOI: https://doi.org/10.1007/978-1-4684-8977-4_22
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