DEFINITION
Formation of calcium oxalate uroliths within the urinary tract and associated clinical conditions
PATHOPHYSIOLOGY
Presence of hypercalciuria, hyperoxaluria, hypocitraturia, and defective crystal growth inhibitors
Hypercalciuria
In dogs, normocalcemic hypercalciuria is thought to result from either intestinal hyperabsorption of calcium (so-called absorptive hypercalciuria) or reduced renal tubular reabsorption of calcium (so-called renal-leak hypercalciuria). Hypercalcemic hypercalciuria results from excessive glomerular filtration of mobilized calcium, which overwhelms normal renal tubular reabsorptive mechanisms (called resorptive hypercalciuria, since excessive bone resorption is associated with high serum calcium concentrations).
Hyperoxaluria
In humans, hyperoxaluria is associated with inherited abnormalities of excessive oxalate synthesis (i.e., primary hyperoxaluria), excess consumption of foods containing high quantities of oxalate or oxalate precursors, pyridoxine deficiency, and disorders associated with fat malabsorption.
Hypocitraturia
Urine citrate inhibits calcium oxalate urolith formation. By complexing with calcium ions to form the relatively soluble salt calcium citrate, citrate reduces the quantity of calcium available to bind with oxalate. In normal dogs, acidosis is associated with low urinary citrate excretion, whereas alkalosis promotes urinary citrate excretion.
Defective Crystal Growth Inhibitors
In addition to urinary concentration of calculogenic minerals, large-molecular-weight proteins in urine, such as nephrocalcin have a profound ability to enhance solubility of calcium oxalate. Preliminary studies of urine obtained from dogs with calcium oxalate uroliths revealed that nephrocalcin had fewer carboxyglutamic acid residues than nephrocalcin isolated from normal dog urine.
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