Abstract
The kidney has been traditionally considered as one of the two primary target organs in gout (1), but long-term follow-up studies have failed to show a deleterious effect of gout on renal function (2). FNAH is characterized by hyperuricemia or gout, usually appearing at an early age and often in both sexes, associated with progressive renal failure (3–17). The pathogenesis of this syndrome is controversial. Some authors believe that renal deterioration is the result of sustained hyperuricemia because in some patients allopurinol halted the progression of renal insufficiency (8, 16). Most authors, however, have documented the progression of renal disease despite allopurinol therapy (7, 10, 11, 14, 15, 17). We examined the influence of allopurinol on the evolution of renal disease in patients with FNAH.
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© 1995 Springer Science+Business Media New York
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Miranda, M.E. (1995). The Influence of Allopurinol on Renal Deterioration in Familial Nepropathy Associated with Hyperuricemia (FNAH). In: Sahota, A., Taylor, M.W. (eds) Purine and Pyrimidine Metabolism in Man VIII. Advances in Experimental Medicine and Biology, vol 370. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2584-4_15
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DOI: https://doi.org/10.1007/978-1-4615-2584-4_15
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