Urolithiasis
Updates to Article Attributes
Urolithiasis refers to the presence of calculi anywhere along the course of the urinary tracts. For the purpose of the article the terms urolithiasis, nephrolithiasis and renal or kidney stones are used interchangeably, although some authors have slightly varying definitions of each.
See main articles: ureteric calculi and bladder stones for further discussion of these.
Epidemiology
Most patients tend to present between 30-60 years of age 1.
The lifetime incidence of renal stones is high, seen in as many as 5% of women and 12% of males. By far the most common stone is calcium oxalate, however the exact distribution of stones depends on the population and associated metabolic abnormalities (e.g. struvite stones are more frequently encountered in women, as urinary tract infection as more common) 8.
Clinical presentation
Although some renal stones remain asymptomatic, most will result in pain. Small stones that arise in the kidney are more likely to pass into the ureter where they may result in renal colic. Haematuria, although common, may be absent in ~15% of patients 1.
Pathology
The composition of urinary tract stones varies widely depending upon metabolic alterations, geography and presence of infection, and their size varies from gravel to staghorn calculi. The more common composition of stones include:
- calcium oxalate +/- calcium phosphate: ~75%
- struvite (triple phosphate): 15%
- pure calcium phosphate: 5-7%
- uric acid: 5-8%
- cystine: 1%
Certain risk factors have been identified including 8:
- low fluid intake
- urinary tract malformations:
-
urinary tract infections
- especially with urease producing bacteria (see below)
- urease hydrolyses urea to ammonium thus increasing urinary pH
- cystinuria: congenital disorder
- hypercalciuria: most common metabolic abnormality
- high sodium intake
- primary hyperparathyroidism
- hypervitaminosis D
- Cushing syndrome
- sarcoidosis
- milk-alkali syndrome
- hyperoxaluria
- high dietary oxalate (vegetarians)
- low gut absorption of calcium, leading to increased absorption of oxalate
- low dietary intake of calcium
- malabsorption / ileal disease (e.g. Crohn disease) resulting in fats binding calcium
- hypocitruria
- usually idiopathic
- renal tubular acidosis (type 1)
- chronic diarrhoea
- hyperuricosuria
- idiopathic/familial
- gout
- myeloproliferative diseases
- high dietary protein intake
Calcium containing stones
Most renal calculi contain calcium, usually in the form of calcium oxalate (CaC2O4) and often mixed with calcium phosphate (CaPO4) 1,6. In most instances no specific cause can be identified, although most patients have idiopathic hypercalcuria without hypercalcaemia.
Brushite is a unique form of calcium phosphate stones that tends to recur quickly if patients are not treated aggressively with stone prevention measures and are resistant to treatment with shock wave lithotripsy.
Interestingly hyperuricosuria is also associated with increased calcium containing stone formation, and is thought to be related to the the uric acid crystals acting as a nidus on which calcium oxalate and calcium phosphate can precipitate 6.
Rarely the underlying cause is primary oxaluria, a liver enzyme deficiency leading to massive cortical and medullary medullary nephrocalcinosis and,and renal failure.
Struvite stones
Struvite (magnesium ammonium phosphate) stones are usually seen in the setting of infection with urease producing bacteria (e.g. Proteus, Klebsiella, Pseudomonas and Enterobacter), resulting in hydrolysis of urea into ammonium and increase in the urinary pH 6,10. They can grow very large and form a cast of the renal pelvis and calices resulting in so-called staghorn calculi. The struvite accounts for approximately 70% of these calculi, and is usually mixed with calcium phosphate thus rendering them opaque. Uric acid and cystine are also found as minor components.
Uric acid
Hyperuricosuria is not always associated with hyperuricoaemia, and is seen in a variety of settings (see above), although in most instances uric acid stones occur in patients with no identifiable underlying aetiology 6. Uric acid crystals form and remain insoluble at acidic urinary pH (below 5).
Cystine stones
Cystine stones are also formed in acidic urine, and are seen in patients with congenital cystinuria.
Others
- Indinavir stones
- pure matrix stones
Radiographic features
These depend on stone composition, and vary according to modality. The much greater sensitivity of CT to tissue attenuation means that some stones radiolucent on plain radiography are nonetheless radiopaque on CT.
Plain film
Calcium containing stones are radiopaque
- calcium oxalate +/- calcium phosphate
- struvite (triple phosphate) - usually opaque but variable
- pure calcium phosphate
Lucent stones include
- uric acid
- cystine
- Indinavir stones
- pure matrix stones
Fluoroscopy
Intravenous urography (IVU) is a traditional contrasted radiographic study of the renal parenchyma, pelvicalyceal system, ureters and the urinary bladder. This exam has been largely replaced by CT.
CT
On CT almost all stones are opaque, but vary considerably in density.
- calcium oxalate +/- calcium phosphate: 400-600HU
- struvite (triple phosphate): usually opaque but variable
- pure calcium phosphate: 400-600HU
- uric acid: 100-200HU
- cystine: opaque
Two radiolucent stones are worth mentioning 11:
- Indinavir stones - (anti-retroviral drug) radiolucent and usually undetectable on CT 5
- pure matrix stones
Ninety-nine percent of renal tract calculi are visible on CT KUB. Given that one of the commonest sites for a stone to become lodged is the vesicoureteric junction, some centres perform the study in the prone position to establish if the stone is retained within the intravesical component of the ureter or has already passed into the bladder itself.
Dual energy CT
DECT is a technique allowing determination of calculus composition, by assessing stone attenuation at two different kVp levels. Each CT vendor has its own algorithms for the use of dual energy CT for assessing stone composition.
Ultrasound
Ultrasound is frequently the first investigation of the renal tract, and although by no means as sensitive as CT, it is often able to identify calculi. Small stones and those close to the corticomedullary junction can be difficult to reliably identify. Ultrasound compared to CT KUB reference showed a sensitivity of only 24% in identifying calculi. Nearly three-quarters of calculi not visualised were 3mm or less in size.13. Features include 7:
- echogenic foci
- acoustic shadowing
- twinkle artefact on color Doppler
- color comet-tail artefact 9
Treatment and prognosis
Treatment depends on the location of the stone, composition and size.
Irrespective of stone composition, patients who present with renal colic require assessment. Approximately 90% of stones less than 4mm are likely to pass down the ureter and into the bladder, and thus often require no more than analgesia and hydration 1. This is of course provided that the kidney is not obstructed and infected in which case a percutaneous nephrostomy should be performed on an emergency basis to save the organ and prevent sepsis.
Calcium stones
Small asymptomatic stones in the kidney can be safely ignored, and if patients maintain good states of hydration, the risk of recurrent symptoms can be dramatically reduced 10. In all settings a search for a possible underlying cause of hyperoxaluria/hypercalcuria should be sought and if present corrected when possible.
Larger stones may be treated with:
Struvite stones
Struvite stones are usually large (staghorn calculi) and result from infection. These stones need to be treated surgically and the entire stone removed, including small fragments, as otherwise these residual fragments act as a reservoir for infection and recurrent stone formation.
Uric acid stones
Uric acid stones usually are the result of low urinary pH, and hydration and elevation of urinary pH to approximately 6 is usually sufficient (note rendering the urine too alkali (e.g. >pH 6.5) may result in calcium stone formation) 10.
Cystine stones
Cystine stones may be difficult to treat and are difficult to shatter with ESWL. Hydration and alkalinisation are usually first line therapy.
Complications
Recognised complications include:
- spontaneous extravasation: spontaneous rupture of renal pelvis (SRRP) +/- urinoma formation 4
- recurrent urinary tract infections / pyelonephritis
- impaction of the stone along the ureter may result in hyrdoureter/hydronephrosis
Differential diagnosis
The differential of renal calculi is essentially that of abdominal calcifications. On CT there is usually little confusion as not only is CT exquisitely sensitive in detecting stones, but their location can also be precisely noted.
Thus the differential diagnosis is predominantly on plain film, and to a lesser degree ultrasound.
- cholethiasis overlying right kidney
- pancreatic calcification
- phleboliths
- calcified mesenteric lymph nodes
- renal artery calcification 7
- intrarenal gas (only a differential for ultrasound)
- acoustic shadow is usually 'dirtier'
- gas typically more mobile than stones
-<p><strong>Urolithiasis</strong> refers to the presence of calculi anywhere along the course of the <a href="/articles/urinary-tracts">urinary tracts</a>. For the purpose of the article the terms urolithiasis, nephrolithiasis and renal or kidney stones are used interchangeably, although some authors have slightly varying definitions of each. </p><p>See main articles: <a title="Ureteric calculi" href="/articles/ureteric-calculi">ureteric calculi</a> and <a href="/articles/bladder-calculus">bladder stones</a> for further discussion of these.</p><h4>Epidemiology</h4><p>Most patients tend to present between 30-60 years of age <sup>1</sup>. </p><p>The lifetime incidence of renal stones is high, seen in as many as 5% of women and 12% of males. By far the most common stone is calcium oxalate, however the exact distribution of stones depends on the population and associated metabolic abnormalities (e.g. struvite stones are more frequently encountered in women, as <a href="/articles/urinary-tract-infection">urinary tract infection</a> as more common) <sup>8</sup>.</p><h4>Clinical presentation</h4><p>Although some renal stones remain asymptomatic, most will result in pain. Small stones that arise in the kidney are more likely to pass into the ureter where they may result in renal colic. Haematuria, although common, may be absent in ~15% of patients <sup>1</sup>.</p><h4>Pathology</h4><p>The composition of urinary tract stones varies widely depending upon metabolic alterations, geography and presence of infection, and their size varies from gravel to <a href="/articles/staghorn-calculi">staghorn calculi</a>. The more common composition of stones include:</p><ul>- +<p><strong>Urolithiasis</strong> refers to the presence of calculi anywhere along the course of the <a href="/articles/urinary-tracts">urinary tracts</a>. For the purpose of the article the terms urolithiasis, nephrolithiasis and renal or kidney stones are used interchangeably, although some authors have slightly varying definitions of each. </p><p>See main articles: <a href="/articles/ureteric-calculi">ureteric calculi</a> and <a href="/articles/bladder-calculus-1">bladder stones</a> for further discussion of these.</p><h4>Epidemiology</h4><p>Most patients tend to present between 30-60 years of age <sup>1</sup>. </p><p>The lifetime incidence of renal stones is high, seen in as many as 5% of women and 12% of males. By far the most common stone is calcium oxalate, however the exact distribution of stones depends on the population and associated metabolic abnormalities (e.g. struvite stones are more frequently encountered in women, as <a href="/articles/urinary-tract-infection">urinary tract infection</a> as more common) <sup>8</sup>.</p><h4>Clinical presentation</h4><p>Although some renal stones remain asymptomatic, most will result in pain. Small stones that arise in the kidney are more likely to pass into the ureter where they may result in renal colic. Haematuria, although common, may be absent in ~15% of patients <sup>1</sup>.</p><h4>Pathology</h4><p>The composition of urinary tract stones varies widely depending upon metabolic alterations, geography and presence of infection, and their size varies from gravel to <a href="/articles/staghorn-calculi">staghorn calculi</a>. The more common composition of stones include:</p><ul>
- +<li>urinary tract malformations:<ul>
- +<li><a title="Horseshoe kidney" href="/articles/horseshoe-kidney">horseshoe kidney</a></li>
- +<li><a title="Duplex collecting system" href="/articles/duplex-collecting-system">duplex collecting system</a></li>
- +</ul>
- +</li>
-<li>high dietary oxalate</li>- +<li>high dietary oxalate (vegetarians) </li>
-</ul><h5>Calcium containing stones</h5><p>Most renal calculi contain calcium, usually in the form of calcium oxalate (CaC<sub>2</sub>O<sub>4</sub>) and often mixed with calcium phosphate (CaPO<sub>4</sub>) <sup>1,6</sup>. In most instances no specific cause can be identified, although most patients have idiopathic hypercalcuria without hypercalcaemia. </p><p>Brushite is a unique form of calcium phosphate stones that tends to recur quickly if patients are not treated aggressively with stone prevention measures and are resistant to treatment with shock wave lithotripsy. </p><p>Interestingly hyperuricosuria is also associated with increased calcium containing stone formation, and is thought to be related to the the uric acid crystals acting as a nidus on which calcium oxalate and calcium phosphate can precipitate <sup>6</sup>. </p><p>Rarely the underlying cause is <a href="/articles/primary-oxaluria">primary oxaluria</a>, a liver enzyme deficiency leading to massive <a href="/articles/medullary-nephrocalcinosis">medullary nephrocalcinosis</a> and renal failure.</p><h5>Struvite stones</h5><p>Struvite (magnesium ammonium phosphate) stones are usually seen in the setting of infection with urease producing bacteria (e.g. <em>Proteus, Klebsiella, Pseudomonas </em>and<em> Enterobacter</em>), resulting in hydrolysis of urea into ammonium and increase in the urinary pH <sup>6,10</sup>. They can grow very large and form a cast of the renal pelvis and calices resulting in so-called <a href="/articles/staghorn-calculi">staghorn calculi</a>. The struvite accounts for approximately 70% of these calculi, and is usually mixed with calcium phosphate thus rendering them opaque. Uric acid and cystine are also found as minor components. </p><h5>Uric acid</h5><p>Hyperuricosuria is not always associated with hyperuricoaemia, and is seen in a variety of settings (see above), although in most instances uric acid stones occur in patients with no identifiable underlying aetiology <sup>6</sup>. Uric acid crystals form and remain insoluble at acidic urinary pH (below 5).</p><h5>Cystine stones</h5><p>Cystine stones are also formed in acidic urine, and are seen in patients with congenital <a href="/articles/cystinuria">cystinuria</a>.</p><h4>Radiographic features</h4><p>These depend on stone composition, and vary according to modality. The much greater sensitivity of CT to tissue attenuation means that some stones radiolucent on plain radiography are nonetheless radiopaque on CT.</p><h5>Plain film</h5><p>Calcium containing stones are radiopaque</p><ul>- +</ul><h5>Calcium containing stones</h5><p>Most renal calculi contain calcium, usually in the form of calcium oxalate (CaC<sub>2</sub>O<sub>4</sub>) and often mixed with calcium phosphate (CaPO<sub>4</sub>) <sup>1,6</sup>. In most instances no specific cause can be identified, although most patients have idiopathic hypercalcuria without hypercalcaemia. </p><p>Brushite is a unique form of calcium phosphate stones that tends to recur quickly if patients are not treated aggressively with stone prevention measures and are resistant to treatment with shock wave lithotripsy. </p><p>Interestingly hyperuricosuria is also associated with increased calcium containing stone formation, and is thought to be related to the the uric acid crystals acting as a nidus on which calcium oxalate and calcium phosphate can precipitate <sup>6</sup>. </p><p>Rarely the underlying cause is <a href="/articles/primary-hyperoxaluria">primary oxaluria</a>, a liver enzyme deficiency leading to massive cortical and medullary <a href="/articles/medullary-nephrocalcinosis">nephrocalcinosis</a>,and renal failure.</p><h5>Struvite stones</h5><p>Struvite (magnesium ammonium phosphate) stones are usually seen in the setting of infection with urease producing bacteria (e.g. <em>Proteus, Klebsiella, Pseudomonas </em>and<em> Enterobacter</em>), resulting in hydrolysis of urea into ammonium and increase in the urinary pH <sup>6,10</sup>. They can grow very large and form a cast of the renal pelvis and calices resulting in so-called <a href="/articles/staghorn-calculi">staghorn calculi</a>. The struvite accounts for approximately 70% of these calculi, and is usually mixed with calcium phosphate thus rendering them opaque. Uric acid and cystine are also found as minor components. </p><h5>Uric acid</h5><p>Hyperuricosuria is not always associated with hyperuricoaemia, and is seen in a variety of settings (see above), although in most instances uric acid stones occur in patients with no identifiable underlying aetiology <sup>6</sup>. Uric acid crystals form and remain insoluble at acidic urinary pH (below 5).</p><h5>Cystine stones</h5><p>Cystine stones are also formed in acidic urine, and are seen in patients with congenital <a href="/articles/cystinuria">cystinuria</a>.</p><h5>Others</h5><ul>
- +<li>Indinavir stones </li>
- +<li>pure matrix stones</li>
- +</ul><h4>Radiographic features</h4><p>These depend on stone composition, and vary according to modality. The much greater sensitivity of CT to tissue attenuation means that some stones radiolucent on plain radiography are nonetheless radiopaque on CT.</p><h5>Plain film</h5><p>Calcium containing stones are radiopaque</p><ul>
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