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February 2007: Renal stone recurrence can be prevented

What are the common causes of renal stones?

How should renal stones be investigated?

How can recurrence be prevented?

What are the common causes of renal stones?

How should renal stones be investigated?

How can recurrence be prevented?

The incidence of renal stone disease is rising. This increase is linked to dietary changes associated with rising affluence. The overall lifetime risk of renal stones is estimated to be 8-10 per cent. On an average GP list of 1,745 patients, more than 150 patients will have a renal stone during their lifetime. The reported recurrence rate varies with the duration of follow-up, but is estimated to be at least 50 per cent.1

In the UK, about 75 per cent of renal stones are composed of calcium oxalate and/or calcium phosphate.

Magnesium ammonium phosphate stones, also known as struvite stones, account for about 20 per cent of cases. These stones can be very large, occupying more than one renal calyx (staghorn calculus). The remainder are predominantly uric acid stones, with 1 per cent being cystine stones.2

The lifetime risk of symptomatic renal stone disease is at least twice as high for men compared with women. The average age of onset is falling, and is approximately 25 years for men. Struvite stones are more common in women.

White patients have the highest incidence of renal stones. There is no genetic reason, and the increased incidence is possibly because of an historically greater affluence and higher dietary intake of salt and animal protein. Several other important epidemiological factors in renal stone disease are summarised in table 1, attached.

Underlying metabolic disorders that may be associated with renal stones are highlighted in table 2, attached.

Stone formation

When the concentration of ions in a solution reaches a certain point (the saturation product), small amounts begin to associate together (nucleate) and crystallise. These nuclei aggregate together and on epithelial surfaces, with eventual crystal and stone formation.1

All patients have a predisposition to form stones at any time, as urinary supersaturation with calcium oxalate is common in the general population.

Other factors that promote or inhibit nucleation and crystallisation have a role in determining stone formation. Urinary volume and flow rate are important, and urinary pH is crucial as the solubility of many lithogenic ions alters in acid or alkaline conditions.

For example, uric acid can precipitate in persistently acidic urine in the absence of hyperuricaemia or hyperuricosuria, and is more likely to act as a nucleus for calcium oxalate precipitation and aggregation in a low pH environment. Urinary pH is influenced by diet. Meat eaters have a lower urinary pH than vegetarians, caused by the excretion of acids resulting from the breakdown of sulphate and phosphate residues in meat proteins. Other influential ions include sodium, which promotes crystallisation, and magnesium, which inhibits this process.1

Some medical treatments can also cause renal stone development. These include certain antiretroviral drugs for the treatment of HIV and the anti-obesity drug orlistat, which is associated with calcium oxalate stones.3


The classic clinical presentation of renal stone disease is acute onset, loin-to-groin colicky pain, renal angle tenderness and haematuria. This presentation has a reported sensitivity of 84 per cent and specificity of 99 per cent.4 The subsequent passage of grit, gravel or a formed stone is confirmatory.

The differential diagnosis is wide and depends on the presenting features. Acute abdominal conditions have to be considered with a presentation of abdominal pain, nausea and vomiting. Obstetric and gynaecological pathologies may also mimic renal stone disease in presentation. Although there are numerous causes of haematuria, few present acutely. However, renal colic can result from a clot or papillary necrosis rather than a stone. Alternatively the combination of loin pain and haematuria may be caused by a tumour or upper urinary tract infection.


When taking a history, the number, size and frequency of symptomatic episodes, the age at onset and need for urological intervention should be ascertained to gauge disease severity.

A past history of symptoms consistent with hypercalcaemia (‘bones, moans, groans and stones'), malabsorptive conditions, gout, urinary tract abnormalities or genetic disease should be documented. A drug history should also be taken.

The patient should be questioned directly about non-prescription preparations containing calcium or vitamin D.

There is a substantially increased risk of stones in patients with a family history of renal stone disease.5 The patient's occupational history and dietary habits (particularly fluid and salt intake) are helpful in providing advice. The occupational risk relates to reduced fluid intake in jobs where the opportunity for micturition is limited (such as taxi drivers), or insensible fluid losses are high (such as chefs).


In acute presentation the patient is usually writhing in agony unlike the still patient with peritonitis. There is often loin tenderness. The testes may be very painful but will not be tender. Pyrexia may suggest an alternative diagnosis of acute pyelonephritis but could also indicate an infected obstructed urinary system.


The following investigations should be carried out:

• Stone analysis – patients can be asked to pass urine through a sieve and submit stones for analysis. This is particularly helpful for non-calcium based stones, as specific therapies may be able to reduce the risk of recurrence.

• Urine ­– dipstick testing with pH gauge, microscopy and culture.

• Blood – renal function, serum bicarbonate, electrolytes (calcium, phosphate) and uric acid.

• Imaging – plain abdominal X-ray

of the kidneys, ureters and bladder (KUB), and an unenhanced helical

CT are recommended. The latter is reported to have greater sensitivity and specificity than intravenous pyelogram (IVP), the previous gold standard investigation.6 There is increased radiation exposure but no risks from contrast administration.

The local service capacity is likely to determine the choice of imaging modality.

Ultrasound can detect larger stones and is the imaging modality of choice for patients who should avoid radiation (such as pregnant women).

It is not as sensitive or specific as CT or IVP.

Further evaluation

Either the history or initial investigation results will identify patients requiring additional assessment. Triggers for specialist referral include:

• children or young age of onset

• metabolically active stones (increasing in size or number in a year)

• recurrence of large stones

• the need for urological intervention

• associated infection

• non-calcium stones

• hypercalcaemia

• metabolic acidosis

• renal impairment.

Further assessment includes 24-hour urine collection for volume, sodium, creatinine, calcium, uric acid, oxalate and citrate. Ideally these should be carried out when the patient is on their normal diet, about one month after an acute episode. It is worth checking with the receiving laboratory which collection containers are required. Two different collections are usually necessary for full analysis.

Serum parathyroid hormone (PTH) should be investigated if hypercalcaemia is present. A raised level indicates underlying hyperparathyroidism.

Acute management

Initial management can be on an inpatient or urgent outpatient basis in liaison with the local urological/surgical team. Admission for urgent intervention is essential for patients with a suspected infected obstructed renal tract, anuria or renal failure, a solitary kidney or known non-functioning kidney, intractable pain or vomiting. It may also be necessary if there are no facilities for urgent follow-up or if social support is poor.

The majority of stones <5 mm diameter pass spontaneously7 and the chance of spontaneous passage is inversely proportional to stone size. Watchful waiting is therefore reasonable in many cases. However, patients require at least weekly monitoring to assess progression.

Referral for further assessment or intervention should be made when there are signs of infection or obstruction, or failure to achieve adequate analgesia. Ongoing symptoms without stone passage after three or four weeks should also be referred, as spontaneous passage after one to two months is unlikely.8

NSAIDs are established as a good alternative to opioids in providing analgesia, and are associated with less nausea and vomiting than pethidine.9 They must be used judiciously in patients with renal impairment, prescribed renin-angiotensin blocking medication, who are dehydrated or elderly. Ongoing pain unrelieved by apparently adequate analgesia is an indication for referral. However, many patients with recurrent episodes of renal colic prefer to be managed by their GP, as in the majority of patients colicky pain will settle quickly if a small stone passes.

Preventing recurrence

Copious fluid intake reduces the risk and time to recurrence of calcium-based stones. Increasing fluid intake to at least two litres in 24 hours is supported by randomised clinical trial evidence.10

Patients should be advised to make dietary adjustments to lower the quantity of salt and animal protein in their diet. Around 98 per cent of filtered calcium is resorbed; the majority in the proximal tubule, a passive process dependent on an electrochemical gradient set up by tubular sodium resorption. When an increased amount of sodium is ingested there is a greater amount of calcium excreted in the urine. A substantial reduction in dietary salt intake can reduce calcium excretion from the hypercalciuric to the normocalciuric range.11

Animal protein metabolism generates sulphate ions and the resultant acidic urine promotes stone formation.12 There is an increased calcium load filtered, reduced tubular calcium resorption, and less citrate (an important inhibitor of stone formation) excreted. However, most people in the UK do not have an excessively high animal protein intake, and scope for a clinically relevant reduction is rare.

The value of a diet low in animal protein and salt to prevent renal stone disease is supported by epidemiological studies, but there is little evidence from randomised, controlled trials.13,14

A normal calcium intake is recommended. It is now established that less gastrointestinal calcium results in more uncomplexed dietary oxalate, with an increase in intestinal oxalate absorption and a subsequent increase in urinary oxalate, which is lithogenic. Additionally, a low-calcium diet can result in a negative calcium balance and bone demineralisation in patients with idiopathic hypercalciuria.15

The risk-benefit ratio of continuing calcium and vitamin D or loop diuretic medication in patients with calcium-based stones, or thiazide diuretics in those with uric acid stones, should be considered.

Potassium citrate is useful in increasing urinary pH and citrate content, and can be beneficial in the management of calcium-based, uric acid and cystine stones. A summary of therapeutic options is presented in table 3, attached. Complex stone disease is usually managed by a specialist.

The urological management options of upper urinary tract stones that do not pass are, alone or in combination, extracorporeal shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, and open surgery.


Dr Aisling E Courtney
specialist registrar in nephrology

Professor A Peter Maxwell
professor of medicine and consultant nephrologist,
Regional Nephrology Unit, Belfast City Hospital

Table 1: Factors associated with increased risk of renal stone disease Table 2: Metabolic disorders implicated in the pathogenesis of renal stones Table 3: Management strategies that may reduce renal stone formation Key points Useful information

The Edinburgh Renal Unit website provides information for patients and clinicians on kidney stones

The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) NIH, is a US website with good information for patients on all aspects of renal medicine

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