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What is nephrolithiasis?

Nephrolithiasis (or renal calculi) are concretions formed by precipitations of various urinary solutes in the urinary tract.


What is the most common composition of renal tract stones?

60% of stones are formed from calcium oxalate.
30% are formed from phosphate as a mixture of calcium, ammonium and magnesium (triple phosphate stones are normally caused by an infection).
5% are uric acid.
1% are cystine.


What are the features of oxalate stones?

Calcium oxalate stones account for approximately 60% of urinary calculi. They are spiky, hard and often discoloured by blood.


What do phosphate stones look like?

Phosphate stones are soft, chalky and faceted. Staghorn calculi (most often caused by infection) are composed of triple phosphates of calcium, magnesium and ammonium). Infective stones are sometimes referred to as "struvite stones".


What are the features of urate stones?

Urate stones account for a very small percentage of calculi. They are generally small, hard and pale yellow/ brown in colour.


Who gets renal stones?

Male > female
Stones are more common in early adult life, and more common in Europeans where prevalence is 3%.

The prevalence and incident risk of nephrolithiasis is directly correlated with BMI and weight in both genders.


What are the risk factors for developing urinary calculi?

Strong risk factors include:
- high protein intake
- high salt intake
- white ancestry
- male sex
- dehydration

NB - family hx is only weakly associated with the development of renal stones

Drug causes of calcium stones: loop diuretics, steroids, acetazolamide, theophylline


What is the aetiology of urinary calculi?

Renal stones are crystalline mineral depositions that form from microscopic crystals in the loop of henle, distal nephron or the collecting ducts. This is usually in response to elevated levels of urinary solutes such as calcium, ammonia, uric acid, sodium and oxalate plus reduced levels of stone inhibitors such as citrate and magnesium.

Low urinary volume and and abnormally low or high urine pHs also contribute to the process. All of these can lead to urine supersaturation with stone forming salts and subsequent stone formation. The higher the concentration of 2 ions the more likely they are to precipitate out of solution and form crystals.


What causes crystal deposits to form stones?

The exact pathophysiology that causes crystal deposits to form stones is unknown. There are a number of theories:
1) Nucleation theory - a crystal or foreign body acts as a nucleus for crystallization of supersaturated urine

2) Stone matrix theory - a protein matrix secreted by the renal tubular cells acts as a scaffold for crystallization of supersaturated urine

3) Reduced inhibition theory - reduced urinary levels of naturally occuring inhibitors for crystallization

Dehydration and hypercalciuria are also important. Idiopathic hypercalciuria occurs in 65% of patients with stones.


What causes Staghorn calculi?

Staghorn calculi are triple phosphate calculi that are formed by the action of urease producing organisms (e.g. Proteus, Klebsiella) which produce ammonia and render the urine alkaline. Schistosomiasis predisposes the bladder to calculi (and squamous cell carcinoma!).


What are the effects of urinary tract calculi?

This often depends on the size of the stone. Staghorn calculi are large and fill the renal pelvis and calices. They lead to recurring pyelonephritis and renal parenchymal damage.

Other stones are smaller, ranging in size from a few millimetres to 1-2cm. They cause problems by obstructing the urinary tract. The clinical effect of this depends on the location of the stone. For example, calyceal stones may cause haematuria while bladder stones may cause infection. Chronic bladder stones prediposes to the unusual squamous cell carcinoma.


What is important primary prevention for renal stones?

The most important primary prevention measure for renal stones is adequate hydration. Fluid intake should be at least 2L per day. Dietary factors are also important. Measures should include reducing dietary fat, protein and sodium.


What are the clinical features of renal tract stones?

Again, this depends on the location of the stones, but can be remembered by going from the kidneys to the urethra.
Calyceal stones may be asymptomatic.

Staghorn calculi present with loin pain and upper tract UTI (remember they are infective in origin). This can be associated with a fever, hypotension and tacchycardia (urosepsis). Because of their size they also cause renal destruction by pyelonephritis, pyonephrosis, and hydronephrosis (dilated pelvicalyceal system).

Ureteric stones classically cause renal colic. Classic renal colic is described as acute severe flank pain that radiates to the ipsilateral groin ("loin to groin") or testes. Stones at the junction between the ureter and renal pelvis can cause obstruction and subsequent hydronephrosis, or haematuria and pyelonephritis. Vesico-ureteric obstruction by a stone produces similar symptoms.

Bladder calculi cause bladder irritation leading to haematuria, frequency and pain.

Bladder outflow obstruction causes haematuria and acute retention.


What initial investigations are needed to diagnose nephrolithiasis?

Initial investigations in suspected renal stones should be:

- Bloods: FBC, U&Es, calcium, phosphorus, uric acid and alkaline phosphatase.
- Urinalysis for microscopic haematuria (commonly occurs cf. macroscopic) and crystals*. >10 WBCs per high powered field in urine or pyuria indicates presence of UTI.
- Urine culture for MC&S.
- Urine pH greater than 7 suggests presence of urea splitting organisms such as proteus, pseudomonas or klebsiella, a urine pH of less than 5.5 suggests uric acid stones.

*NB - urine crystals of calcium oxalate, cystine or uric acid may indicate the nature of the stone, but only cystine crystals are pathognomonic of the underlying type of stones


When is a 24 hour urine collection necessary?

24 hour urine collection is not necessary in a patient presenting with stones for the first time. However, it is indicated in a number of cases including recurrent stone formers, those with bilateral or multiple stones, IBD, gout or other crystal arthropathies, primary hyperparathyroidism and children.


When is imaging indicated for stone disease and what is the imaging modality of choice?

If there is a suspicion of nephrolithiasis based on the history, physical examination or lab testes then imaging is indicated.

The imaging modality of choice is a non contrast helical CT scan (NCCT) because it has a high sensitivity and specificity and should be ordered as soon as nephrolithiasis is suspected. It determines presence, size and site of stones and if negative then nephrolithiasis can be ruled out with a high degree of confidence. CT can also be used for patients with known stones who have new onset renal colic because stones commonly move or new ones form.

IVU is used less commonly cf. CT.


When is a plain abdominal KUB film used for renal stones?

These can be used to determine whether stones are radio-opaque and to monitor disease activity. 90% of renal calculi are radio-opaque. The only stones that are not radio-opaque are idinavir and pure uric acid stones.


How should acute renal colic be managed?

It is important to remember that 80% of ureteric stones pass spontaneously. Stones of <4mm will nearly always pass, whereas stones >6mm almost never pass.

The key management in a patient with renal colic and suspected nephrolithiasis is conservative. This includes hydration with crystalloids, pain control with morphine or diclofenac (both IV), and an antiemetic (e.g. ondansetron).


How should patients with confirmed stones but no evidence of obstruction be managed?

Patients with confirmed stones (i.e. on imaging) but with no evidence of obstruction fall into 3 groups. All should have conservative first line treatment with fluids, analgesia and antiemetics as for suspected cases. Adjunct therapy depends on whether there is (i) bacteriuria, (ii) stones <10mm, or (iii) stones >10mm or failed medical therapy.

If bacteriuria is present but no signs of sepsis or obstruction then the patient can be treated with conservative therapy and antibiotics. Empirical antibiotics should be started before receiving sensitivities. This is usually ciprofloxacin or nitrofurantoin or sulfamathoxazole.

Surgical decompression can also be used as a adjunct. in patients with bacteriuria. Drainage is achieved in 2 ways, in the acute setting a urologist can place a ureteric stent past the obstruction to achieve drainage. Alternatively, PCNL can be performed by an interventional radiologist.

Stones that are <10mm can have medical expulsive therapy (MET). This is with an alpha blocker (e.g. tamsulosin) or a calcium channel blocker (e.g. nifedipine) and these are normally given for 4-6 weeks until the stone is cleared.

Finally, stones that are >10mm or failed medical therapy require surgical removal.


What surgical approaches can be used for stones that are >10mm or with failed medical therapy?

This depends on the location of the stones. If the stones are located in the renal pelvis or upper 1/3 of the ureter then percutaneous nephrolithotomy can be used.

Stones in the middle 1/3 of the ureter can be removed by extracorporeal shock wave lithotripsy (ESWL). Stones in the lower 1/3 of the ureter require contact lithotripsy or extraction with a Dormia basket.

Bladder stones require endoscopic retrieval/ destruction.


How should patients with confirmed stones and evidence of obstruction be managed?

This is an emergency situation, as obstructed kidneys are more prone to infection. 1st line management should be fluid resuscitation with crystalloids, pain control with morphine sulphate or ketorolac (both IV) and an antiemetic such as ondansetron.

This should be followed by surgical decompression either by percutaneous nephrostomy or stenting. For stones that fail conservative therapy additional surgical removal is required, again dependant on the location.

Patients with urinary calculi with a fever and other signs of infection need emergency drainage and IV antibiotics. Primary options are with ampicillin or tazosin plus gentamicin (macrolide cover).


What monitoring is required for patients with nephrolithiasis?

Regular fluid intake (of at least 2L) is advised for patients as this is the single most important factor in preventing stone recurrence. This should be accompanied by a low protein and low sodium diet.

Patients with recurrent stones should have 24 hour urine collections to check for metabolic abnormalities.


What are some of the complications that can occur following treatment for urinary tract stones?

1) Post PCNL bleeding - nephrostomy tubes will usually tamponade any bleeding over the first few days, but gross haematuria after PCNL should be evaluated with renal arteriogram to check for an aneurysm.

2) Post ESWL haematoma - occurs because of disruption of blood vessels around and near the kidneys by shock waves.

3) Post ESWL steinstrasse - occurs due to stone fragments obstructing ureter and subsequent fragments not being able to pass.

4) Infection

5) Pneumothorax - may occur from insertion of nephrostomy tube which can pierce the pleural cavity


What is the prognosis of renal stone disease?

The important thing to remember is that nephrolithiasis is a lifelong disease process. Rate of recurrence of nephrolithiasis in first time stone formers is 50% at 5 years and 80% at 10 years. The Return of Kidney Stones (ROKS) nomogram can be used to help predict the risk of recurrent stones.