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Home :: Renal Calculi

Renal Calculi

Although renal calculi (kidney stones) may form anywhere in the urinary tract, they usually develop in the renal pelvis or the calyces of the kidneys. Such formation follows precipitation of substances normally dissolved in the urine (calcium oxalate, calcium phosphate, magnesium ammonium phosphate or, occasionally, urate or cystine).

Renal calculi vary in size and may be solitary or multiple. They may remain in the renal pelvis or enter the ureter and may damage renal parenchyma; large calculi cause pressure necrosis. In certain locations, calculi cause obstruction, with resultant hydronephrosis, and tend to recur.

Among Americans, renal calculi develop in 1 in 1,000 people, are more common in men (especially those ages 30 to 50) than in women, and are rare in blacks and children. They're particularly prevalent in certain geographic areas, such as the southeastern United States ("stone belt"), possibly because a hot climate promotes dehydration or because of regional dietary habits.


Although the exact cause of renal calculi is unknown, predisposing factors include the following:

  • Dehydration and resultant decreased urine production concentrates calculusforing substances.
  • Infection in tissue provides a site for calculus development; pH changes provide a favorable medium for calculus formation (especially for magnesium ammonium phosphate or calcium phosphate calculi); infected calculi (usually magnesium ammonium phosphate or staghorn calculi) may develop if bacteria serve as the nucleus in calculus formation. Such infections may promote destruction of renal parenchyma.
  • Obstruction can result from urinary stasis (as in immobility from spinal cord injury), which allows calculus constituents to collect and adhere, forming calculi, Obstruction also promotes infection, which, in turn, compounds the obstruction.
  • Metabolic factors that can predispose to renal calculi include hyperparathy roidism, renal tubular acidosis, elevated uric acid (usually with gout), defective metabolism of oxalate, genetic defect in metabolism of cystine, and excessive intake of vitamin D or dietary calcium.

Signs and symptoms

Typical symptoms include sharp mid-back pain, blood in the urine, painful urination, nausea, and vomiting.

Accompanying signs

Other associated signs include fever, chills, hematuria (when calculi abrade a ureter), abdominal distention, pyuria and, rarely, anuria (from bilateral obstruction or unilateral obstruction in the patient with one kidney).


The clinical picture in conjunction with the following diagnostic tests allows a diagnosis:

  • Kidney-ureter-bladder X-rays reveal most renal calculi.
  • Calculus analysis shows mineral content.
  • Excretory urography confirms the diagnosis and determines size and location of calculi.
  • Kidney ultrasonography. an easily performed noninvasive, nontoxic test, detects obstructive changes, such as unilateral or bilateral hydronephrosis.
  • Urine culture of midstrearn specimen may indicate urinary tract infection.
  • Urinalysis may be normal or may show increased specific gravity and acid or alkaline pH suitable for different types of stone formation. Other urinalysis findings include hematuria (gross or microscopic), crystals (urate, calcium, or cystine), casts, and pyuria with or without bacteria and white blood cells.
  • A 24-hour urine collection is evaluated for calcium oxalate, phosphorus, and uric acid excretion levels.
  • Serial blood calcium and phosphorus levels detect hyperparathyroidism and show an increased calcium level in proportion to the normal level of serum protein.
  • Blood protein level determines level of free calcium unbound to protein.
  • Blood chloride and bicarbonate levels may show renal tubular acidosis.
  • Increased blood uric acid levels may indicate gout as the cause.

Diagnosis must rule out appendicitis, cholecystitis, peptic ulcer, and pancreatitis as potential sources of pain.


Because 90% of renal calculi are smaller than 5 mm in diameter, treatment usually consists of measures to promote their natural passage. Along with vigorous hydration, such treatment includes antimicrobial therapy (varying with thecultured organism) for infection; analgesics, such as meperidine, for pain; and diuretics to prevent urinary stasis and further calculus formation. (Thiazides decrease calcium excretion into the urine.)

Prophylaxis to prevent calculus formation includes a low-calcium diet for absorptive hypercalciuria, parathyroidectomy for hyperparathyroidism, and allopurinol and urinary alkalynization for uric acid calculi.

Calculi too large for natural passage may require surgical removal. When a calculus is in the ureter, a cystoscope may be inserted through the urethra and the calculus manipulated with catheters or retrieval instruments. A small-diameter telescope, the ureteroscope, may be inserted through the ureter to remove stones from the ureter and kidney. Extraction of calculi from other areas (kidney calyx, renal pelvis) rarely may necessitate a flank or lower abdominal approach.

Percutaneous ultrasonic lithotripsy and extracorporeal shock-wave lithotripsy shatter the calculus into fragments for removal by suction or natural passage. To prevent recurrence of calculi, the patient will also need teaching before discharge.


If there is a history of stones, fluids should be encouraged to produce adequate amounts of dilute urine (usually 6 to 8 glasses of water per day). Depending on the type of stone, medications or other measures may be recommended to prevent recurrence.

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