Renal calculi

Renal calculi: Excerpt from Professional Guide to Diseases (Eighth Edition)

Renal calculi or nephrolithiasis (commonly called kidney stones) may form anywhere in the urinary tract but usually develop in the renal pelvis or the calyces of the kidneys. Calculi formation follows precipitation of substances normally dissolved in the urine, such as calcium oxalate, calcium phosphate, magnesium ammonium phosphate or, occasionally, urate or cystine. (See How urine pH affects calculi formation.) 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.

Causes and incidence

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

❑ Dehydration: Decreased urine production concentrates calculus-forming substances.

❑ Infection: Infected, damaged tissue serves as a site for calculus development; pH changes provide a favorable medium for calculus formation (especially for magnesium ammonium phosphate or calcium phosphate calculi); or infected calculi (usually magnesium ammonium phosphate or staghorn calculi) may develop if bacteria serve as the nucleus in calculus formation. Infections may promote destruction of renal parenchyma.

❑ Obstruction: Urinary stasis (as in immobility from spinal cord injury) allows calculus constituents to collect and adhere, forming calculi. Obstruction also promotes infection, which, in turn, compounds the obstruction.

❑ Metabolic factors: These factors may predispose to renal calculi: hyperparathyroidism, 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.

Among Americans, renal calculi develop in 2% to 10% of the population, with people living in southeastern states having an increased risk. They’re more common in males (especially those ages 30 to 40) than in females by a 3:1 ratio. They’re rare in children.

Some types of calculi tend to be familial; some are associated with other conditions, such as bowel disease, ileal bypass for obesity, or renal tubule defects. Calcium calculi are most common, accounting for over 75% of all calculi, and are two to three times more common in males, usually appearing between ages 20 and 30. The calcium may combine with other substances, such as oxalate (the most common substance), phosphate, or carbonate, to form the stone. Oxalate is present in certain foods. Diseases of the small intestine increase the tendency to form calcium oxalate calculi. Recurrence is likely.

Uric acid calculi are also more common in males and make up about 6% of all calculi. These calculi are associated with gout and chemotherapy. Cystine calculi, which make up about 2% of all calculi, may form in people with cystinuria, a hereditary disorder affecting both males and females. Struvite calculi, accounting for about 15% of all calculi, are mainly found in females as a result of a urinary tract infection (UTI). They can grow very large and may obstruct the kidney, ureter, or bladder.

Indavir stones appear in patients with human immunodeficiency virus who are treated with the protease inhibitor indinavir.

Signs and symptoms

Clinical effects vary with size, location, and etiology of the calculi. Pain, the key symptom, usually results from obstruction; large, rough calculi occlude the opening to the ureter and increase the frequency and force of peristaltic contractions. The pain of classic renal colic travels from the costovertebral angle to the flank, to the suprapubic region and external genitalia. The intensity of this pain fluctuates and may be excruciating at its peak. If calculi are in the renal pelvis and calyces, pain may be more constant and dull. Back pain (from calculi that produce an obstruction within a kidney) and severe abdominal pain (from calculi traveling down a ureter) may also occur. (See Types of renal calculi.) Nausea and vomiting usually accompany severe pain.

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).

Diagnosis

Diagnosis is based on the clinical picture and the following tests:

❑ Computed tomography scan or magnetic resonance imaging are highly sensitive for identifying hydronephrosis and detecting small renal and urethral stones.

❑ Excretory urography may be used for diagnosis of obstruction by urinary calculus.

❑ Kidney-ureter-bladder X-rays reveal most renal calculi.

❑ Calculus analysis shows mineral content.

CONFIRMING DIAGNOSIS Excretory urography confirms the diagnosis and determines size and location of calculi.

❑ Kidney ultrasonography is an easily performed, noninvasive, nontoxic test to detect obstructive changes such as hydronephrosis.

❑ Urine culture of midstream sample may indicate UTI.

❑ 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 increased calcium level in proportion to normal serum protein.

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.

Treatment

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 the cultured 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, allopurinol for uric acid calculi, and daily administration of ascorbic acid by mouth to acidify the urine.

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. Extraction of calculi from other areas (kidney calyx, renal pelvis) 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.

Special considerations

Patient care includes confirming the diagnosis, facilitating passage of the stone, and prevention of future occurrences.

❑ To aid diagnosis, maintain a 24- to 48-hour record of urine pH, with nitrazine pH paper; strain all urine through gauze or a tea strainer, and save all solid material recovered for analysis.

❑ To facilitate spontaneous passage, encourage the patient to walk if possible. Also promote sufficient intake of fluids to maintain a urine output of 3 to 4 L/day (urine should be very dilute and colorless). To help acidify urine, offer fruit juices, particularly cranberry juice. If the patient can’t drink the required amount of fluid, supplemental I.V. fluids may be given. Record intake and output and daily weight to assess fluid status and renal function.

❑ Stress the importance of proper diet and compliance with drug therapy. For example, if the patient’s stone is caused by a hyperuricemic condition, advise him (or whoever prepares his meals) to avoid foods high in purine. Restrict protein to 60 g/day to decrease calcium and uric acid, and limit sodium to 3 to 4 g/day. Oxalate foods are restricted.

❑ If surgery is necessary, give reassurance by supplementing and reinforcing what the surgeon has told the patient about the procedure. The patient is apt to be fearful, especially if surgery includes removal of a kidney, so emphasize the fact that the body can adapt well to one kidney. If he’s to have an abdominal or flank incision, teach deep-breathing and coughing exercises.

❑ After surgery, the patient will probably have an indwelling catheter or a nephrostomy tube. Unless one of his kidneys was removed, expect bloody drainage from the catheter. Never irrigate the catheter without a physician’s order. Check dressings regularly for bloody drainage, and know how much drainage to expect. Immediately report suspected hemorrhage (excessive drainage, rising pulse rate). Use sterile technique when changing dressings or providing catheter care.

❑ Watch for signs of infection (rising fever, chills), and give antibiotics as ordered. To prevent pneumonia, encourage frequent position changes, and ambulate the patient as soon as possible. Have him hold a small pillow over the operative site to splint the incision and thereby facilitate deep-breathing and coughing exercises.

❑ Before discharge, teach the patient and his family the importance of following the prescribed dietary and medication regimens to prevent recurrence of calculi. Encourage increased fluid intake. If appropriate, show the patient how to check his urine pH, and instruct him to keep a daily record. Tell him to immediately report symptoms of acute obstruction (pain, inability to void).

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Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

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More About This Book: Title: Professional Guide to Diseases (Eighth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2005 ISBN: 1-58255-370-X

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