Calcium oxalate kidney stones are the most common type of renal calculi. Calcium oxalate and phosphate containing renal calculi represent 80% of the renal calculi cases in USA.
AdvertisementsThe presence of excess urinary oxalate, causes oxalate calculi formation in the kidneys. These kidney calculi may contain calcium oxalate alone or in combination with phosphates. About 80% of the patients with renal calculi are men.
Causes of oxalate stone formationThere are several causes for developing calcium oxalate kidney stones. The foremost reason is having hyperoxaluria, either primary or secondary. Both the hyperoxaluria conditions are discussed briefly hereunder. The causes pertaining to lifestyle are, chronic dehydration, lack of exercise, high intake of animal protein, high intake of sugars, high dietary sodium and consuming food high in oxalates (for example, spinach, rhubarb and nuts).
Certain health conditions like distal renal tubular acidosis, Dent's disease, urinary citrate insufficiency, hyperparathyroidism, Crohn's disease, primary hyperoxaluria, malabsorption of magnesium, renal leak hypercalciuria, absorptive hypercalciuria, idiopathic hypercalciuria or medullary sponge kidney can predispose a person to the development of renal calculi. Patients under chemotherapy for lymphoproliferative or myeloproliferative disorders are likely to develop renal calculi.
Hyperoxaluria (excess oxalate in urine)Hyperoxaluria is a condition wherein excess oxalate is present in urine. Primary hyperoxaluria is caused by three types of genetic mutations. The primary hyperoxaluria type I is due to mutations in AGXT gene, causing AGXT proteins to mistarget mitochondria.
The oxalate calculi formation in primary hyperoxaluria can be severe. The kidneys may get damaged requiring transplants. The oxalosis, oxalate deposition, in the bones, joints and bone marrow may cause skeletal and haematological problems. Liver transplantation in addition to kidney transplant can correct the metabolic defects.
The secondary hyperoxaluria is caused by excessive ingestion, excessive absorption and excessive excretion of oxalate. Ca2+ binds with oxalate in the intestine, rendering both the calcium and oxalate unabsorbable. If the diet is low in calcium, the oxalate present in food can get absorbed and reach kidney. Hence low calcium diets can promote calcium oxalate kidney stone formation. Food rich in animal proteins creates acid load, causing urine acidification, triggers increased excretion of Ca2+ and inhibition of urinary citrate.
Symptoms of calcium oxalate kidney stonesSmall renal calculi may be passed out with urine without symptoms. Calculi larger than 3 mm may block the ureter or pass along the ureter causing extreme pain. The common symptoms of renal calculi include renal colic (radiating pain on the flank or lower back), blood in the urine, pus in the urine, pain while urinating, nausea, vomiting and loss of appetite. The presence of renal colic and blood in urine can help in diagnosing the condition. Confirmative urinalysis, radiographic studies and ultrasound scanning are done to decide on treatment modalities.
Treatment of calcium oxalate kidney stonesFor renal calculus without any symptoms, watchful waiting is advised. If the patient is suffering from renal colic, pain relief medication and active hydration is resorted to. If found necessary intravenous fluids are given to increase urine output to facilitate calculus expulsion with urine. If the calculus is large, less invasive techniques like Extracorporeal shock wave lithotripsy (ESWL), ureteroscopy, ureteroscopic surgery and percutaneous nephrolithotomy are tried.
Prevention of Calcium oxalate kidney stonesThe first step in the treatment oxalate calculus is hydration of the body. It is recommended that sufficient water must be taken to produce at least two liters of urine. Sodium excretion enhances Ca2+ excretion. Potassium reduces sodium excretion. Sufficient intake of magnesium reduces Ca2+ excretion. Urinary citrate inhibits renal calculus formation. Taking potassium citrate helps in inhibiting oxalate renal stones as well as in their dissolution.
Pinheiro VB. et al (citation 10) in their research study reported that oral sodium bicarbonate aided urinary citrate excretion. Grases F. et al (citation 7), in their research study concluded that, when compared to healthy people, kidney stone formers have very low levels of urinary phytate. They suggest that sufficient dietary phytate can increase urinary phytate which in turn inhibit crystallization of calcium oxalate.
David W. Kaufman et al in their research studies reported that Oxalobacter formigenes, a Gram-negative, anaerobic bacterium, metabolizes oxalate in the intestinal tract and that colonization with O. formigenes is associated with a 70% reduction in the risk for being a recurrent calcium oxalate kidney stone former.
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