Complications: Renal failure if unrelieved obstruction for > 7 days.
3% of all Americans will suffer from a kidney stone at some time in their life, and half of these people will suffer recurrences over the following ten or more years. It is thus a disease which touches a significant portion of the population.
Normal urine contains predictable amounts of calcium, magnesium, uric acid, and other by-products of metabolism. Normally these substances are in solution and pass into the bladder. Under certain conditions of high saturation, and in a complex chemical environment that is not yet completely understood, the chemicals may crystallize and form a stone-like particle in the kidney. Once formed it stimulates continued crystallization. If the stone remains in the kidney, no symptoms may occur, although there may be microscopic signs of blood in the urine. Once a piece of the stone breaks off and enters the ureter leading to the bladder, prompt spasms occur.
Urine of most normal people is supersaturated with respect to calcium oxalate, so all people can potentially form such stones. Normal urine is not supersaturated with respect to uric acid, cystine or struvite. Conditions that raise calcium oxalate supersaturation raise the risk of calcium oxalate stones. Hypercalciuria and hyperoxaluria are two main clinical examples, and both can result from many diseases. Hyperparathyroidism, renal tubular acidosis, sarcoidosis, vitamin D intoxication, and "idiopathic" hypercalciuria all are causes of hypercalciuria. Hyperoxaluria may be due to overproduction, from hereditary disorders of metabolism, or be acquired from intestinal disease or diet.
Apart from overexcretion, supersaturation can be increased by abnormal interactions between urine ions. Urine citrate forms a soluble salt with calcium that normally reduces free calcium ion levels appreciably; low urine citrate from bowel disease, renal tubular acidosis, and, perhaps, dietary and hereditary causes can raise calcium oxalate supersaturation and promote stones. Normal women excrete more citrate and less calcium than normal men, perhaps a reason why men form stones more often. Low urine pH from hereditary causes or bowel disease promotes uric acid stones; high pH, from alkali, drugs, or renal tubular acidosis increases calcium phosphate supersaturation.
An infection of the urinary tract can cause cellular debris to act as a focus or "seed"on which crystals can form. Bacterial action makes the urine more alkaline, resulting in the deposit of phosphates, which form calcium phosphate stones. Excessive uric acid, increased excretion of calcium by the kidney, combined with an increased insolubility of calcium in the urine, can also cause stones to form. Long-term confinement to bed or even a chronic lack of exercise may encourage mobilization of calcium from bones into the blood, increasing calcium levels in the urine. Similarly, steroids can increase blood and urine calcium levels. An inherited disposition and excess weight can also predispose you to kidney stones.