Editing Stones: Epidemiology and Pathogenesis (section)

=== Hyperuricosuria ===
* '''<span style="color:#ff0000">May be associated with pure uric acid calculi or calcium oxalate calculi through heterogenous nucleation</span>'''
** '''Patients with hyperuricosuric calcium nephrolithiasis who form calcium oxalate stones present with normal urinary pH and hyperuricosuria, accompanied sometimes by hypercalciuria'''
** In contrast, those with gouty diathesis, who can form either uric acid or calcium oxalate calculi, have a low fractional excretion of urate (that contributes to hyperuricemia) and low urinary pH (that leads to increased amount of undissociated uric acid)
* '''<span style="color:#ff0000">Causes:</span>'''
*# '''<span style="color:#ff0000">Increased dietary purine intake (most common cause)</span>'''
*# '''<span style="color:#ff0000">Gout</span>'''
*# '''<span style="color:#ff0000">Myeloproliferative and lymphoproliferative disorders</span>'''
*# '''<span style="color:#ff0000">Multiple myeloma</span>'''
*# '''<span style="color:#ff0000">Thalassemia</span>'''
*# '''<span style="color:#ff0000">Hemolytic disorders</span>'''
*# '''<span style="color:#ff0000">Pernicious anemia</span>'''
*# '''<span style="color:#ff0000">Hemoglobinopathies</span>'''
*# '''<span style="color:#ff0000">Secondary polycythemia</span>'''
*# '''<span style="color:#ff0000">Complete or partial hypoxanthine-guanine phosphoribosyltransferase (HGPRT) deficiency</span>'''
*#* Lesch-Nyhan syndrome is an inherited deficiency of the purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase, which leads to the accumulation of hypoxanthine, which is ultimately converted to uric acid
*# '''<span style="color:#ff0000">Overactivity of phosphoribosylpyrophosphate synthetase</span>'''
*# '''<span style="color:#ff0000">Hereditary renal hypouricemia</span>'''