How to prevent urinary stone formation

The age of the patient and the severity of the problem affect both the need for and the kind of prophylaxis.

Idiopathic stone-formers

Where no metabolic abnormality is detected, the basis of prevention is continuation of a high intake of fluid all through the day and night. The aim should be to make sure a daily urine volume of 2-2.5 L, which requires a fluid intake in surplus of this, considerably so in the case of those who live in hot countries or work in a hot surroundings.

Idiopathic hypercalciuria

Severe dietary calcium restriction is unsuitable. Patients should be encouraged to eat a normal-calcium (30 mmol/day) diet. Dietary calcium limit results in hyper absorption of oxalate, and so foods containing excessive amounts of oxalate should also be restricted. A high fluid drinking is recommended as for idiopathic stone-formers. Patients who reside in a hard water region may benefit from intake of softened water. If hypercalciuria persists and stone formation continues, a thiazide diuretic is used (e.g. bendroflumethiazide 2.5 or 5 mg every morning). Thiazides decrease urinary calcium excretion by a direct action on the renal tubule. Thiazides may precipitate diabetes mellitus or gout and worsen their hyper cholesterolaemia. Decrease the intake of animal proteins to 50 g/day and sodium intake to 50 mmol/day is also advisable, as a randomized controlled trial has found that a diet restricted in animal protein and salt but with normal calcium was more effective in the prevention of calcium and particularly oxalate stones than a diet restricted in calcium.


Mixed infective stones

Recurrent stones of these kinds should be prevented by continuance of a high fluid drinking and scrupulous control of bacteriuria. This will need long-term follow-up and frequently the use of long-term low-dose prophylactic antibacterial drugs.

Uric acid stones

Dietary measures are probably of negligible value and are hard to put into practice. Successful prevention can be achieved by the long-term use of allopurinol to preserve the serum urate and urinary uric acid excretion in the physilogical range. A high fluid drinking should also be continued. Uric acid is more soluble at alkaline pH, and long term sodium bicarbonate supplementation to preserve an
alkaline urine is an substitute approach in those few patients, who are not capable to take allopurinol. However, alkalinization of the urine favors precipitation of
calcium oxalate and phosphate.

Cystine stones

These can be prevented and indeed will dissolve slowly with a high fluid intake. Five litres of water has to be drunk each 24 hours, and the patient must wake twice in the night to drink 500 ml or more of water. Many patients cannot accept this regimen. An alternative, though in fact more bothersome, option is the long-term intake of the chelating agent penicillamine; this helps cystine to be transformed to the more soluble penicillamine-cysteine complex. Side-effects of penicillamine are drug rashes, blood dyscrasias and immune complex-mediated glomerulonephritis. However, it is especially effective fo the dissolution of the existing cystine stones.

Mild hyperoxaluria with calcium oxalate stones

A high fluid ingestion and dietary oxalate constraint are necessary. Dietary advice as in hypercalciuria is to be followed.

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Investigations to detect the causes of urinary stone formation

In an elderly patient who has had a single incident with one stone, only restricted investigation is necessary. Younger patients and those with recurring stone formation necessitate detailed investigation.

Following are the investigations done to find out the causes urinary stone formation.

Renal imaging is required to define the presence of a primary renal disease predisposing to stone formation.

Urine culture to detect significant bacteriuria may point to mixed infective stone development, but relapsing bacteriuria may be an effect of stone formation rather than the original source.


Chemical analysis of any stone passed may be of immense value and all that is necessary in the diagnosis of cystinuria or uric acid stone formation.

Serum calcium concentration should be measured and corrected for serum albumin concentration. Hypercalcaemia (High blood calcium level), if present, should be investigated further for hyperparathyroidism.

Serum urate concentration is usually, but not always, elevated in uric acid stone-formers.

A screening test for cystinuria should be done by adding sodium nitroprusside to a random unacidified urine sample; a purple color indicates that cystinuria may be present. Urine chromatography is necessary to identify the diagnosis precisely.

Urinary calcium, oxalate and uric acid output should be measured in two successive cautiously collected 24- hour urine samples. After withdrawing aliquots for measurement of uric acid, it is required to add acid to the urine in order to prevent crystallization of calcium salts upon the walls of the collection vessel, which would give falsely low reports for urinary calcium and oxalate.

Plasma bicarbonate is low in renal tubular acidosis. The report of a urine pH that does not dip below 5.5 in the face of metabolic acidosis is diagnostic of this condition.

Related articles:

Stones in kidneys, ureter and urinary bladder
Symptoms of urinary stones
Investigations and treatment of urinary stones
Investigation to detect the causes of urinary stones
How to prevent urinary stone formation

Symptoms of urinary stones

Most people with urinary tract calculi are asymptomatic. Pain is the most common symptom and may be sharp or dull, constant, intermittent or colicky. When urinary tract obstruction is present, measures that increase urine volume, such as copious fluid intake or diuretics, including alcohol, make the pain worse.

Clinical features of urinary tract stones

Physical exertion may cause mobile calculi to move, precipitating pain and, occasionally, haematuria (blood in the urine) . Ureteric colic occurs when a stone enters the ureter and either obstructs it or causes spasm during its passage down the ureter. This is one of the most severe pains known. Radiation from the flank to the to the lower abdomen and testis or labium in the distribution of the first lumbar nerve root is common. Pallor, sweating and vomiting often occur and the patient is restless, tending to assume a variety of positions in an unsuccessful attempt to obtain relief from the pain. Haematuria often occurs. Untreated, the pain of ureteric colic typically subsides after a few hours. When urinary tract obstruction and infection are present, the features of acute pyelonephritis or of a Gram negative septicaemia may dominate the clinical picture.


Vesical calculi associated with bladder bacteriuria may present with frequency, dysuria and haematuria; severe introital or perineal pain may occur. A calculus at the bladder neck or an obstruction in the urethra may cause bladder outflow obstruction, resulting in anuria (complete stoppage of urine) and painful bladder distension.

History of the following is often present:

-occupation and residence in hot countries likely to be associated with dehydration
-a history of vitamin D consumption
-gouty arthritis.

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