The urinary tract system consists of two kidneys which filter the blood extracting water, urea, mineral salts, toxins, and other waste products. Urine is created and is transported from the kidneys through the ureters that connect the kidneys to the bladder. The urethra then carries urine from the bladder to the outside of the body.

Kidney Stone Formation
Kidney stones are made of different types of crystals. Most are (1) calcium oxalate, (2) calcium phosphate, (3) a combination of calcium oxalate and calcium phosphate, (4) magnesium ammonium phosphate, also known as struvite or infection stones, (5) uric acid, (6) cystine, and (7) miscellaneous types such as occur with drug metabolites.

Genetically inherited disorders account for some stone formation. High protein and salt intake increase the risk of calcium stone formation. High purine diets (meat, fish, chicken) lower urinary pH and cause increased excretion of uric acid. Vitamin B6 deficiency leads to increased formation and excretion of oxalate. Dehydration, excessive vitamin C intake, calcium supplementation, and calcium containing antacids may also lead to stone formation. Also, geography plays a part with more stones noted in the southeast, also known as the stone belt.

Calcium Stones
Calcium oxalate develops in acid urine (pH less than 6.0). Calcium phosphate develops in alkaline urine (pH greater than 7.2). Calcium phosphate stones are also associated with urinary tract infection, Renal Tubular Acidosis (RTA) and hyperparathyroidism. Hypercalciuria or increased calcium in the urine may lead to calcium stone formation. Often times the blood calcium level is normal even though there is elevated calcium in the urine. This may be the result of intestinal hyperabsorption of calcium. Renal leak hypercalciuria occurs when there is impaired reabsorption of calcium in the kidney, leading to hypercalciuria even in a fasting state with no intake of calcium. Resorptive hypercalciuria, which is seen in hyperparathyroidism, is characterized by increased bone breakdown and increase in serum calcium level.

Citrate plays a big part in calcium stone formation. It forms a soluble salt with calcium and inhibits the formation of calcium oxalate and calcium phosphate crystals. Anything that leads to hypocitrauria or low levels of urinary citrate increases the chance of developing stones. Chronic diarrhea, renal tubular acidosis (RTA), diets high in protein and salt, low levels of blood potassium often associated with thiazide diuretics are all associated with hypocitrauria.

Oddly enough, calcium stones may develop in patients who excrete too much uric acid (hyperuricosuria). When urine is less than pH 5.5, uric acid crystals develop and calcium crystals then begin layering around this crystal to form a calcium oxalate stone. Hyperuricosuria develops in chronic diarrhea, high purine intake, and is associated with tumor lysis after chemotherapy or radiation.

Oxalate forms an insoluble complex with calcium to develop a calcium oxalate stone. High levels of oxalate in the urine, or hyperoxaluria, is even more important to stone formation than high levels of calcium or hypercalciuria. Excessive intake of food and drink containing oxalate leads to calcium oxalate stones. Also, excessive intake of Vitamin C which is metabolized to oxalate may lead to hyperoxaluria and an increase in stone formation.

Enteric hyperoxaluria is seen in inflammatory bowel disease, bowel resection, and small bowel bypass procedures. With these conditions there is an increase in bile salt and fatty acids that combine with calcium leading to increased oxalate available for absorption. With increased intestinal absorption of oxalate, there is an increase in urinary oxalate leading to formation of calcium oxalate stones. These patients also have low urinary citrate and magnesium as a result of chronic metabolic acidosis due to chronic diarrhea. All these factors lead to calcium oxalate stone formation.

Uric Acid Stones
Uric acid is an end product of purine metabolism. It’s the same crystal that causes gout, an arthritic condition. Foods high in purines are red meat, fish, and chicken. The solubility of uric acid depends on the acidity or alkalinity of the urine. In acid urine, pH less than 5.5, uric acid crystals precipitate leading to stone formation. If urine is alkaline, uric acid remains soluble and doesn’t precipitate out. Knowledge of this fact is the basis of the medical treatment of uric acid stones.

Magnesium Ammonium Phosphate Stones
These stones are also call triple phosphate, struvite, or infection stones. These stones develop when the urine pH is higher than 7.2 and ammonia is present in the urine. Bacteria that produce urease act on the urea present in urine to form ammonia, bicarbonate, and carbonate ion. The most common bacteria associated with struvite stones is proteus, but other bacteria such as staph aureus, klebsiella pneumoniae, and pseudamonas may also be implicated. Since females are more susceptible to urinary tract infection, struvite stones occur more often in females than males with a ratio of 2:1.

Cystine Stones
Cystinuria is an autosomal recessive disorder that causes impaired renal tubular reabsorption of cystine, ornithine, lysine, and arginine. This leads to increased urinary excretion of these compounds, but the only one that forms stones is the cystine.

Crixivan Stones
One of the most common protease inhibitors used to treat HIV disease is crixivan or indinavir sulfate. Urinary stones have been associated with the use of crixivan.