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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]
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]
Additionally, hypercalciuria can contribute to kidney stone formation which may present with flank or back pain that comes and goes. It can be painful to pass kidney stones and in extreme cases cause kidney damage. [2] [3] Patients that both form kidney stones and have hypercalciuria are at increased risk for bone loss leading to osteoporosis. [4]
The term nephrocalcinosis is used to describe the deposition of both calcium oxalate and calcium phosphate. [1] It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. [2] It is caused by multiple different conditions and is determined by progressive kidney dysfunction.
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. Dietary oxalate is an organic ion found in many vegetables, fruits, and nuts. Calcium from bone may also play a role in kidney stone formation.
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. [1]