Urology - Stone disease Flashcards
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.