Percentage of All Stones

Calcium Oxalate and Phosphate 70

Idiopathic hypercalciuria (50%)

Hypercalciuria and hypercalcemia (10%)

Hyperoxaluria (5%)

••Enteric (4.5%)

••Primary (0.5%)

Hyperuricosuria (20%)

Hypocitraturia

No known metabolic abnormality (15–20%)

Magnesium Ammonium Phosphate (Struvite) 15–20

Uric Acid 5–10

Associated with hyperuricemia

Associated with hyperuricosuria

Idiopathic (50% of uric stones)

Cystine 1–2

Others or Unknown ±5

magnesium ammonium phosphate; (3) 5% to 10% are uric acid stones; and (4) 1% to 2% are made up of cystine. An organic matrix of mucoprotein, making up 1% to 5% of the stone by

weight, is present in all calculi. Although there are many causes for the initiation and propagation of stones, the most important determinant is an increased urinary concentration of the

stones' constituents, such that it exceeds their solubility in urine (supersaturation). A low urine volume in some metabolically normal patients may also favor supersaturation.

Calcium oxalate stones ( Table 20-13 ) are associated in about 5% of patients with both hypercalcemia and hypercalciuria, caused by hyperparathyroidism, diffuse bone disease,

sarcoidosis, and other hypercalcemic states. About 55% have hypercalciuria without hypercalcemia. This is caused by several factors, including hyperabsorption of calcium from the

intestine (absorptive hypercalciuria), an intrinsic impairment in renal tubular reabsorption of calcium (renal hypercalciuria), or idiopathic fasting hypercalciuria with normal parathyroid

function. As many as 20% of calcium oxalate stones are associated with increased uric acid secretion (hyperuricosuric calcium nephrolithiasis), with or without hypercalciuria. The

mechanism of stone formation in this setting involves "nucleation" of calcium oxalate by uric acid crystals in the collecting ducts. Five per cent are associated with hyperoxaluria, either

hereditary (primary oxaluria) or, more commonly, acquired by intestinal overabsorption in patients with enteric diseases. The latter, so-called enteric hyperoxaluria, also occurs in

vegetarians, because much of their diet is rich in oxalates. Hypocitraturia associated with acidosis and chronic diarrhea of unknown cause may produce calcium stones. In a variable

proportion of patients with calcium stones, no cause can be found (idiopathic calcium stone disease).

Magnesium ammonium phosphate stones are formed largely after infections by urea-splitting bacteria (e.g., Proteus and some staphylococci), which convert urea to ammonia. The resultant

alkaline urine causes the precipitation of magnesium ammonium phosphate salts. These form some of the largest stones, as the amounts of urea excreted normally are huge. Indeed, socalled

staghorn calculi occupying large portions of the renal pelvis are almost always a consequence of infection.

Uric acid stones are common in patients with hyperuricemia, such as gout, and diseases involving rapid cell turnover, such as the leukemias. However, more than half of all patients with

urate calculi have neither hyperuricemia nor increased urinary excretion of uric acid. In this group, it is thought that an unexplained tendency to excrete urine of pH below 5.5 may

predispose to uric acid stones, because uric acid is insoluble in relatively acidic urine. In contrast to the radio-opaque calcium stones, uric acid stones are radiolucent.

Cystine stones are caused by genetic defects in the renal reabsorption of amino acids, including cystine, leading to cystinuria. Stones form at low urinary pH.

It can therefore be appreciated that increased concentration of stone constituents, changes in urinary pH, decreased urine volume, and the presence of bacteria influence the formation of

calculi. However, many calculi occur in the absence of these factors; conversely, patients with hypercalciuria, hyperoxaluria, and hyperuricosuria often do not form stones. It has therefore

been postulated that stone formation is enhanced by a deficiency in inhibitors of crystal formation in urine. The list of such inhibitors is long, including pyrophosphate, diphosphonate,

citrate, glycosaminoglycans, osteopontin, and a glycoprotein called nephrocalcin.

Morphology.

Stones are unilateral in about 80% of patients. The favored sites for their formation are within the renal calyces and pelves ( Fig. 20-57 ) and in the bladder. If formed in the renal pelvis,

they tend to remain small, having an average diameter of 2 to 3 mm. These may have smooth contours or may take the form of an irregular, jagged mass of spicules. Often, many stones are

found within one kidney. On occasion, progressive accretion of salts leads to the development of branching structures known as staghorn stones, which create a cast of the pelvic and

calyceal system.

Clinical Course.

Stones are of importance when they obstruct urinary flow or produce ulceration and bleeding. They may be present without producing any symptoms or significant renal damage. In

general, smaller stones are most hazardous, because they may pass into the ureters, producing pain referred to as colic (one of the most intense forms of pain) as well as ureteral

obstruction. Larger stones cannot enter the ureters and are more likely to remain silent within the renal pelvis. Commonly, these larger stones first manifest themselves by hematuria.

Stones also predispose to superimposed infection, both by their obstructive nature and by the trauma they produce.

Date: 2016-04-22; view: 933