Kidney Stones

Renal calculi or kidney stones are formed by the deposition of certain chemicals in the kidneys, particularly calcium oxalate, calcium phosphate and uric acid. Levels of these chemicals in the blood are normally controlled by biochemical feedback mechanisms, and any excess is excreted through the kidneys. Failure of this mechanism or high dietary levels of these compounds can result in saturation of the urine resulting in deposition in the kidneys.

Stones are thought to start as small crystals which continue to grow as more chemical is deposited. Crystal formation is normally prevented in healthy kidneys; however in some instances this defence mechanism fails allowing growth of stones.
Most kidney stones are formed from calcium, particularly calcium oxalate. About 10% are formed from uric acid, particularly in patients with acid urine. Cystine calculi occur only in patients with cystinuria. Magnesium ammonium phosphate calculi (struvite) indicate the infection with urea splitting bacteria such as Proteus.
Urinary calculi may vary in size from grain of sand to golf ball. They may stay lodged in the kidney or pass from the kidney, through the ureter to the bladder, and eventually through the urethra to be voided in urine. Smaller stones may be passed without incident. The passage of larger stones into the ureter with subsequent acute obstruction,  urinary tract dilation, and spasm is associated with classic renal colic. Renal colic is characterized by undulating cramps and severe pain and may be accompanied by nausea and vomiting.
As the stone travels through the ureter, the pain moves from the flank to the lower abdomen, down to the groin, and eventually to the scrotal or labial areas.
The most important risk factor for urinary calculi is hereditary hypercalciuria (an inherited predisposition to excrete large amounts of calcium in the urine). Other conditions which predispose to stone formation include hyperparathyroidism, sarcoidosis, vitamin D toxicity and renal tubular acidosis. High levels of oxalate in urine may be primary or caused by excessive ingestion of foods such as rhubarb, spinach or cocoa, or excess oxalate absorption caused by enteric diseases.