Section 1: Epidemiology and aetiology
The lifetime risk of kidney stones is 1-15 per cent, with the risk affected by race, age, gender and geography. An average GP practice may therefore see more than 100 patients a year with colic, although some may present directly to A&E.
Stones typically affect adults aged 20-50 years and are more common in men than women (in a 3:2 ratio), although the prevalence among women appears to be increasing.1
Caucasians are affected more often than other racial groups; stone disease has a higher prevalence in hot or dry climates, although it is also relatively common in the more temperate climates of the US, Scandinavia or the UK. Obesity is also considered to be a risk factor.2
The most significant underlying cause for stone formation is dehydration, which is sometimes related to more sedentary occupations in the UK. Theories of stone growth include supersaturation (precipitation of the solute if a certain concentration is exceeded), nucleation and aggregation and balance of inhibitors (for example, citrate) versus promoters of growth.
Stone formation is due to precipitation in a solute due to dehydration in most cases.
Plain KUB demonstrating a large proximal ureteric stone and stent
Classification of urinary tract calculi may be by position (renal, ureteric or bladder) or by composition (idiopathic, metabolic or infective stones).
Metabolic stones may be divided into calcium stones - the commonest being calcium oxalate, others being calcium phosphate and mixed oxalate/phosphate stones - or non- calcium stones, for example uric acid or cystine.
In the absence of symptoms of renal stones or specific risk factors, for example previous stones, recurrent infections or haematuria, further investigation is not manadatory in patients found to have calcium oxalate crystals on microscopy.
Infection stones, sometimes known as 'struvite' stones are made of magnesium ammonium (calcium) phosphate, and are typically associated with bacteria such as Proteus or Klebsiella species.
Patients with a history of inflammatory bowel disease or urinary diversion are at risk of stone formation for reasons such as changes in calcium metabolism, dehydration, stasis and altered bowel function.
Rarely, patients may be taking medication that directly promotes stone formation - for example, indinavir, triamterene or the migraine drug topiramate, although this is very unusual.
Section 2: Diagnosis
The classic symptom of renal colic is typically loin pain with radiation anteriorly towards the groin; however the pain may be located more anteriorly, such as the iliac fossa, for example.
The patient may collapse with the severity of this pain, which is colicky in nature, sometimes with associated vomiting.
Previous history of stones is important as patients often recognise the symptoms themselves. Direct questions about comorbidity - asthma, peptic ulcer, diabetes mellitus - and allergy to medication, shellfish or contrast media are integral in order to guide choice of analgesia and imaging.
Basic tests should include urinalysis, blood tests and imaging.
A urinary dipstick is mandatory, typically for red cells and information on whether nitrite positive; the urinary pH can help with diagnosing acidic stones.
For example, urate and cystine stones are associated with acidic pH, and they are sometimes treated by dissolution therapy (for example, alkalinisation).
MSU should be sent for pathology to see if there is any growth of organisms.
Formal microscopy remains the gold standard for assessment of red cells in the urine, although in acute renal colic a dipstick is sensitive enough to help support a clinical impression of renal pathology.
Blood tests include FBC and renal function. All patients with first presentation of stone should have serum calcium and urate measured. Although hypercalcaemia is not common, detection of this should alert one to possible underlying causes such as hyperparathyroidism.
Similarly, elevated serum uric acid should be excluded, and managed with allopurinol if detected.
A plain KUB X-ray should be the initial imaging test in all cases. There is debate as to whether a non-contrast CT KUB should replace intravenous urography (IVU) as the imaging of choice. Some centres offer ultrasound with plain KUB, although this is somewhat operator dep-endent.
Most modern hospital departments are moving towards a CT KUB rather than the traditional IVU.
The European Society for Urogenital Radiology has issued guidelines for the management of diabetics on metformin who undergo an IVU in either the emergency or elective settings.3
The recently updated American Urological Association/European Association of Urology guidelines for ureteric stones4 discusses choice of imaging in pregnancy: the first-line investigation remains an ultrasound, but states that a limited IVU is safe - particularly from the second trimester onwards - and may be a more practical solution than magnetic resonance urography (MRU).
Key clinical features
- radiates loin to groin
- severe, colicky
- sometimes recognised by patients with previous stones
- Voiding difficulties
- Macroscopic haematuria
- Fever/infection in presence of obstructed renal tract
- Unremitting pain
- Solitary kidney
- Unusual demographics (eg elderly) where alternative significant pathology possible, such as abdominal aortic aneurysm
- Abdominal aortic aneurysm
- Biliary colic
- Bowel obstruction
- Mechanical back pain
- Retroperitoneal mass or lymphadenopathy (for example, RPF)
- Inflammatory bowel disease
- Papillary necrosis
- Ectopic pregnancy
- Pelvic inflammatory disease
- Ovarian cyst
Section 3: Management
Management can be divided into the emergency and elective settings. In acute renal colic, analgesia should be administered early in the form of NSAIDs (such as diclofenac) or opiates as required. The dose and route of administration for diclofenac is 100mg PR, 75mg IM or 50mg PO as tolerated.
If this does not control pain, a morphine injection (IM/IV) may be required, in conjunction with an antiemetic injection.
If paracetamol in conjunction with an NSAID does not control the pain, then the patient should be referred to hospital acutely.
The options for management are then conservative, medical or interventional: lithotripsy or surgery. In the acute setting, it is essential to detect sepsis, as an infected obstructed upper urinary tract can lead to death.
One must establish whether the kidney requires urgent dis-obstruction with the help of imaging. The patient may then proceed to a percutaneous nephrostomy (antegrade) or ureteric stent insertion (retrograde).
Conservative management involves regular analgesia and there is now evidence for the use of medical therapy such as an alpha-blocker (eg tamsulosin) for distal ureteric stones.5
This meta-analysis includes a number of small predominantly European trials that have suggested shorter time to stone clearance with an alpha-blocker. This is currently being assessed in two large multi-centre trials.
With relatively few side-effects, alpha-blockers seem a reasonable adjunct to conservative management.
Lithotripsy is a non-invasive treatment using ultrasound shockwaves that are transmitted through the skin and reach their target up to 15cm beneath the surface. The key features of a lithotripter are that it generates a shockwave that is then focussed (using imaging), coupled with the skin surface, and then fragments the stone, which should pass down the ureter.
Fragments that do not pass, causing a 'steinstrasse' (literally, 'stone-street'), may require ureteric stenting.
Lithotripsy can be offered on an outpatient basis or on an inpatient emergency basis in some centres.
Since their original development, lithotripters have undergone several modifications to allow better tolerability by patients, but patients should be warned that treatment may require more than one session.
The advances in endourological surgery mean that open surgery is a rarity for stone disease in most developed countries.
The two main approaches are through the urethra by ureteroscopy - under general or spinal anaesthesia - or directly into the kidney by percutaneous nephrolithotomy (PCNL).
Generally, PCNL is reserved for stones larger than 2cm or occupying a large part of the kidney such as a 'staghorn' calculus.
After accessing the urinary tract and visualising the stone, different energy sources can be used for fragmentation (for example Holmium laser, electrohydraulic lithotripsy or intracorporeal ultrasound).
Patients may have a ureteric stent inserted and should be made aware of possible side-effects such as pain, urinary frequency, bladder spasm, haematuria or infection.
Metabolic stones can be managed with medication, such as urinary alkalinisation with sodium bicarbonate or potassium citrate for uric acid stones (as well as allopurinol) and chelating agents (eg D-penicillamine) for cystine stones.
Section 4: Prognosis
It is reported that the probability of recurrence of stone disease is 20 per cent within one year and up to 50 per cent within 10 years.
Many patients ask about dietary advice to help prevent recurrence. It is important to emphasise the importance of adequate hydration, with recommendation to drink at least two litres per day.
Delayed IVU showing obstruction of left vesicoureteric junction
Various dietary measures have been debated, including the role of dietary calcium.
Curhan et al highlighted the inverse relationship between dietary calcium intake and risk of stone formation.6 In fact, elimination of calcium from the diet is a risk factor for stone formation as there is no calcium present for dietary oxalate to bind to. Therefore oxalate is not excreted, but will accumulate in the kidney, where it precipitates.
Patients should be told that elimination of dairy products from the diet increases the risk of stones, and that a healthy balanced diet is advisable.
If there is excessive intake of dietary oxalate this should be reduced; foods with a high oxalate content include rhubarb, spinach, cocoa, tea leaves - milky tea is better than black tea as the oxalate is already bound to calcium - and nuts. Again, complete elimination of these products is not necessary, but moderation is advised.
Other evidence for dietary modification supports the restriction of high sodium intake and encourages fruit and vegetable consumption.
Apart from these dietary measures, there are specific metabolic manipulations that can be tried. For example, for stones that are formed in acidic urine (for example, urate or cystine stones), urinary alkalinisation can be performed by the patient titrating their urinary pH to tolerable doses of potassium citrate or sodium bicarbonate.
Citrate is an inhibitor of stone formation, and increasing intake of this (for example, freshly squeezed citrus fruit) may be helpful.
Most patients will not have any obvious underlying metabolic abnormality, however occasionally a biochemical disturbance is detected.
The commonest underlying abnormality is hypercalci-uria, which can be divided into absorptive (increased intestinal absorption), resorptive (for example, with hyperparathyroidism) or renal leak hypercalciuria.
Further evaluation should be performed in a specialist setting, with 24-hour urine collections to measure urine volume and excretion of metabolic consitutents such as calcium, oxalate, urate, citrate and phosphate.
Some stones may be managed conservatively long term, such as a stone in a calyceal diverticulum or lower pole of the kidney, and these patients should undergo surveillance.
1. Scales C D J, Curtis L H, Norris R D et al. Changing gender prevalence of stone disease. J Urol 2007; 177(3): 979-82.
2. Taylor E N, Stampfer M J, Curhan G C. Obesity, weight gain, and the risk of kidney stones. JAMA 2005; 293(4): 455-62.
3. European Society of Urogenital Radiology. ESUR Guidelines on contrast media, Version 6. 2007. www.esur.org/fileadmin/Guidelines/ESUR_2007_Guideline_6_Kern_Ubersicht.p df
4. American Urological Association/European Association of Urology. 2007 Guideline for the Management of Ureteral Calculi. www.uroweb.org/nc/professional-resources/guidelines/online/
5. Hollingsworth J M, Rogers M A, Kaufman S R et al. Medical therapy to facilitate urinary stone passage: a meta-analysis. Lancet 2006; 368 (9542): 1,171-9.
6. Curhan G C, Willett W C, Rimm E B, Stampfer M J. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. N Engl J Med 1993; 328(12): 833-8.
- Delvecchio F C, Preminger G M. Medical management of stone disease. Curr Opin Urol 2003; 13(3): 229-33.
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