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Oxalate. The buildup of oxalate in the body causes increased renal excretion of oxalate (hyperoxaluria), which in turn results in kidney and bladder stones.Stones cause urinary obstruction (often with severe and acute pain), secondary infection of urine and eventually kidney damage. [2]
Careful dietary decisions should be taken since a deficient calcium intake diet accompanies the risk of excessive bone loss and can increase the absorption of dietary oxalates, found in many leafy greens and vegetables, which combine with calcium in the intestines, [29] and form oxalate kidney stones. [8]
A favorable outcome is more likely if a kidney transplant is complemented by a liver transplant, given the disease originates in the liver. [citation needed] Secondary hyperoxaluria is much more common than primary hyperoxaluria, and should be treated by limiting dietary oxalate and providing calcium supplementation. [citation needed]
In kidney stones, calcium oxalate is the most common mineral type (see nephrolithiasis). Uric acid is the second most common mineral type, but an in vitro study showed uric acid stones and crystals can promote the formation of calcium oxalate stones.
Between 1% and 15% of people globally are affected by kidney stones at some point. [14] [15] In 2015, they caused about 16,000 deaths worldwide. [16] Some of the oxalate in urine is produced by the body. Calcium and oxalate in the diet play a part but are not the only factors that affect the formation of calcium oxalate stones.
The authors of the paper hypothesized that acute oxalate nephropathy is an underdiagnosed cause of kidney failure and suggested thorough examination of patient dietary history in cases of unexplained kidney failure without proteinuria (an excess of protein in the urine) and with large amounts of calcium oxalate in urine sediment. [18]