Xanthine urolithiasis

Pais, Vernon M.; Lowe, Gregory Ferrell; Lallas, Costas D.; Preminger, Glenn M.; Assimos, Dean G.

doi:10.1016/j.urology.2005.10.057

Cited by 49 publications

(44 citation statements)

References 15 publications

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“…The resultant increase in xanthine may rarely precipitate xanthine stones. This is typically a concern in patients with inborn errors of uric acid metabolism, and those with extremely high uric acid levels, such as those with the tumor lysis syndrome [48]. Given the much higher prevalence of uric acid nephropathy compared with xanthine nephrolithiasis, it is prudent to utilize allopurinol in patients at risk for tumor lysis syndrome.…”

Section: Treatmentmentioning

confidence: 99%

Uric acid nephrolithiasis

Liebman

Taylor²,

Bushinsky³

2007

Curr Rheumatol Rep

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Uric acid nephrolithiasis is typically found in individuals with a low urine pH and a normal concentration of urinary uric acid. Patients with a history of gout are at greater risk of forming uric acid stones, as are patients with obesity, diabetes, or the complete metabolic syndrome. The unifying renal tubular abnormality of these disorders appears to be the excretion of abnormally acidic urine. This article focuses on the relationship of these disorders to the development of uric acid stones. The diagnosis of uric acid stones can be elusive, because pure uric acid stones are radiolucent on plain radiographs. Ultrasound, or preferably noncontrast helical CT scanning, is required for their detection. The treatment of uric acid stones should focus on alkalinization of the urine with citrate or bicarbonate salts. Additional interventions such as increase in fluid intake and decrease in animal protein ingestion are often beneficial. Patients with documented hyperuricemia often require specific therapy to lower serum uric acid concentration and subsequent excretion.

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Section: Treatmentmentioning

confidence: 99%

Uric acid nephrolithiasis

Liebman

Taylor²,

Bushinsky³

2007

Curr Rheumatol Rep

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“…In hereditary xanthinuria, there is little production of uric acid, and patients present with hypouricemia. Unlike uric acid stones, the rare xanthine and 2,8-dihydroxyadenine (2,8-DHA) stones do not dissolve in an alkaline milieu, and thus, do not respond to therapy with alkali [71]. …”

Section: Discussionmentioning

confidence: 99%

Uric Acid Nephrolithiasis: A Systemic Metabolic Disorder

Wiederkehr

Moe

2011

Clinic Rev Bone Miner Metab

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Uric acid nephrolithiasis is characteristically a manifestation of a systemic metabolic disorder. It has a prevalence of about 10% among all stone formers, the third most common type of kidney stone in the industrialized world. Uric acid stones form primarily due to an unduly acid urine; less deciding factors are hyperuricosuria and a low urine volume. The vast majority of uric acid stone formers have the metabolic syndrome, and not infrequently, clinical gout is present as well. A universal finding is a low baseline urine pH plus insufficient production of urinary ammonium buffer. Persons with gastrointestinal disorders, in particular chronic diarrhea or ostomies, and patients with malignancies with a large tumor mass and high cell turnover comprise a less common but nevertheless important subset. Pure uric acid stones are radiolucent but well visualized on renal ultrasound. A 24 h urine collection for stone risk analysis provides essential insight into the pathophysiology of stone formation and may guide therapy. Management includes a liberal fluid intake and dietary modification. Potassium citrate to alkalinize the urine to a goal pH between 6 and 6.5 is essential, as undissociated uric acid deprotonates into its much more soluble urate form.

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“…This has allowed an extensive evaluation of allopurinol efficacy and safety in HPRTdeficient patients. Several isolated clinical reports of patients with HPRT deficiency have described xanthine lithiasis [15][16][17][18][19][20][21][22][23], or acute gout [24], or have discussed the influence of allopurinol on biochemical variables [25][26][27]. In 8 patients with HPRT deficiency, Kelley et al [4] showed that allopurinol (400-800 mg/d) decreased sUA levels between 48% and 76% after only 48 hours, an effect attributed to a greater sensitivity to the inhibitory effect of allopurinol on xanthine oxidase in HPRT-deficient patients as compared with patients with gout.…”

Section: Discussionmentioning

confidence: 99%