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Stone Disease of the Urinary Tract
Introduction
Stones may occur in all parts of the urinary tract, including the pelvicalyceal system of the kidney, the ureter, the bladder and sometimes even the urethra. Stones most commonly provoke symptoms caused by obstruction or by predisposing to urinary tract infections.
Upper tract calculi are much more common than bladder calculi and the incidence is rising. Stones range from the uncommon staghorn calculus , which fills the pelvicalyceal system, to small stones developing in the pelvicalyceal system that can migrate and obstruct the ureter. Acute ureteric obstruction causes severe pain and presents as the surgical emergency ureteric colic . Most stone disease is, however, asymptomatic or else presents nonurgently to the outpatient clinic.
Stone disease (urolithiasis) in childhood is now rare in developed countries. The peak incidence occurs between 20 and 50 years of age, and declines slowly thereafter ( Fig. 37.1 ). The life time risk of urolithiasis is 10% to 15% in Western countries and up to 25% in the Middle East. Males are affected nearly twice as often as females. There is also a high incidence of recurrent stones; if preventative measures are not used, the risk is around 10% at 1 year, 33% at 5 years and 50% at 10 years.
Pathophysiology of Stone Disease
Stones are often formed from a mixture of chemical substances and minerals (e.g., calcium and oxalate), when their concentration exceeds their solubility in urine. Intermittent periods of supersaturation caused by dehydration, medical conditions or following meals, can lead to the earliest phase of crystal formation ( nucleation ). Crystals coalesce into groups ( aggregation ), and act as nucleus for further stone formation. Promoters of stone formation are low urine volume, low urine pH, calcium, sodium, oxalate, and urate. Lack of crystallisation inhibitors in the urine also plays a role in stone formation. Inhibitors of stone formation include citrate, magnesium, Tamm-Horsfall protein and glycosaminoglycans. Table 37.1 provides a simple classification showing the relative frequency of stone types and their important clinical characteristics and aetiology. Calcium is present in over 80%, as oxalate or phosphate compounds or both. The aetiology of stone disease is multifactorial in most cases.
TABLE 37.1
Chemical Composition, Clinical Features and Aetiology of Urinary Tract Stones
| Chemical Composition | % | Clinical Features | Aetiology |
|---|---|---|---|
| Calcium oxalate | 70%–80% | Three types of stone are described:
|
Most cases are idiopathic; predisposing factors include urinary stasis, infection and foreign bodies Some are caused by metabolic disorders, which lead to excess urinary excretion of calcium or oxalate:
|
| Mixed calcium oxalate and phosphate stones | 10% | As earlier | Some are caused by disorders associated with hypercalcaemia, for example, sarcoidosis, multiple metastases, multiple myeloma, milk-alkali syndrome, overtreatment with vitamin D |
| Pure calcium phosphate stones | 1% | As earlier | Some of these patients excrete abnormally large amounts of calcium, possibly as a result of increased absorption (idiopathic hypercalciuria but without hypercalcaemia) |
| Magnesium ammonium phosphate (struvite/infection stones) | 10%–15% | Typically large ‘staghorn’ calculi of pelvicalyceal system and some bladder stones | Chronic infection with organisms capable of producing urease, typically Proteus . Urease splits urea, forming ammonia if the urine is alkaline |
| Uric acid | 5%–10% | Stones tend to absorb yellow and brown pigments. Pure stones are radiolucent | Occur in primary gout and hyperuricaemia following chemotherapy for leukaemias or myeloproliferative disorders. Childhood urate bladder stones occur in some developing countries when urine pH is low |
| Cystine or xanthine | 1% | Excess urinary excretion of cystine or xanthine. Pure stones are radiolucent | Autosomal recessive inherited disorders |
Predisposing Factors for Stone Disease
A specific predisposing factor can be detected in some cases. These include chronic infection, urinary stasis and foreign bodies, and are summarised in Box 37.1 .
BOX 37.1
Predisposing Factors in Stone Formation
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Stasis of urine, particularly when associated with infection—for example, congenital abnormalities, hydronephrosis, chronic obstruction (e.g., benign prostatic hyperplasia, neurogenic bladder)
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Chronic urinary infection (urea-splitting organisms, e.g., Proteus cause alkaline urine and the development of magnesium–ammonium–phosphate stones, typically the ‘staghorn’ calculi of the renal pelvis
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Excess urinary excretion of stone-forming substances—for example, idiopathic hypercalciuria (calcium stones), hyperparathyroidism (calcium stones), hyperoxaluria (oxalate stones), gout (uric acid stones), cystinuria (cystine stones), xanthinuria (xanthine stones)
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Foreign bodies—for example, fragments of catheter tubing, self-inserted artefacts, parasites (schistosome ova), fragments of diseased tissue (e.g., renal papillary necrosis)
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Dietary—for example, high animal protein intake and high salt diet
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Obesity—associated with lower urinary pH, which can promote uric acid stones
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Dehydration—lower volume, concentrated urine encourages crystallisation
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Bowel or digestive disorders—can affect absorption of calcium and water
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Family or personal history of stones
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Prolonged immobility—leads to skeletal decalcification and increased serum calcium levels
Calcium-Containing Stones
In patients with calcium-containing stones, specific underlying abnormalities are rarely discovered. Some patients excrete excessive calcium ( idiopathic hypercalciuria ) without being hypercalcaemic; in these, there may be increased intestinal absorption of calcium leading to increased urinary excretion.
Stones Caused by Excessive Urinary Excretion of a Stone Constituent
A minority of patients have an underlying disorder responsible for excessive urinary excretion of the main constituent of the stone. Examples include hyperparathyroidism (calcium), hyperoxaluria (oxalate), gout (uric acid), cystinuria (cystine stones) and xanthinuria (xanthine stones).
Clinical Features of Stone Disease
The clinical problem of discrete urinary stones should not be confused with calcification of the renal parenchyma, which can be a feature of tuberculosis and medullary sponge kidney. These and similar diseases can usually be diagnosed by their characteristic x-ray appearance.
The clinical presentation of stones depends on the size, morphology and site of the stone(s). Many cause no symptoms but represent a potentially serious problem. Other stones produce marked pathological effects, which present with acute or chronic symptoms or are discovered incidentally on investigation of unrelated symptoms. The presentation of urinary tract stones is summarised in Box 37.2 .
BOX 37.2
Presentation of Stones in the Urinary Tract
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Incidental finding on x-ray or computed tomography (CT)
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Loin pain
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Ureteric colic
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Painful passage of small stones via urethra
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Symptoms of infection (cystitis, pyelonephritis)
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Haematuria
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Impaired renal function
Urinary tract stones produce their injurious effects in three main ways:
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by obstructing urinary flow;
-
by predisposing to infection;
-
by causing local tissue irritation and damage.
Obstruction of Urinary Flow
Pelvicalyceal Obstruction
Obstruction of renal calyces causes local urinary obstruction ( hydrocalyx ) and can lead to chronic or recurrent loin pain. Similar pain may also be caused by chronic, incomplete obstruction of the pelviureteric junction (PUJ) or ureter. The result is hydronephrosis , that is, dilatation of the renal pelvis, both intrarenal and extrarenal. Severe obstruction may lead to progressive renal parenchymal damage and impaired renal function; the patient may develop renal failure if both kidneys are affected.
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