In an elderly patient who has had a single episode with one stone, only limited investigation is required. Younger patients and those with recurrent stone formation require detailed investigation.
AN EXCRETION UROGRAM is necessary to define the presence of a primary renal disease predisposing to stone formation.
SIGNIFICANT BACTERIURIA may indicate mixed infective stone formation but relapsing bacteriuria may be a consquence of stone formation rather than the original cause.
CHEMICAL ANALYSIS of any stone passed may be of great value and may be all that is required to make a diagnosis of cystinuria or uric acid stone formation.
SERUM CALCIUM CONCENTRATION should be estimated and corrected for serum albumin concentration.
Hypercalcaemia, if present, should be investigated further.
SERUM URATE CONCENTRATION is often, but not invariably, elevated in uric acid stone-formers.
A SCREENING TEST FOR CYSTINURIA should be carried out by adding sodium nitroprusside to a random unacidified urine sample; a purple colour indicates that cystinuria may be present. Urine chromatography is required to define the diagnosis precisely.
URINARY CALCIUM, OXALATE AND URIC ACID OUTPUT should be measured in two consecutive carefully collected 24-hour urine samples. After withdrawing aliquots for estimation of uric acid, it is necessary 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 results for urinary calcium and oxalate.
PLASMA BICARBONATE is low in renal tubular acidosis . The finding of a urine pH that does not fall below 5.5 in the face of metabolic acidosis is diagnostic of this condition.
The age of the patient and the severity of the problem affect both the need for and the type of prophylaxis. Idiopathic stone-formers Where no metabolic abnormality is present, the mainstay of prevention is maintenance of a high intake of fluid throughout the day and night. The aim should be to ensure a daily urine volume of 2-2.5 litres, which requires a fluid intake in excess of this, substantially so in the case of those who live in hot countries or work in a hot environment. A large glass of water should be drunk before retiring for the night and on waking during the night if this occurs. Special dietary measures are not warranted, although avoidance of excessive consumption of calcium-rich dairy products seems sensible.
Dietary calcium restriction is recommended, although the value of this has recently been questioned. Intake of milk, cheese, and white bread if this is fortified (as it is in the UK) with calcium and vitamin D is reduced. Vitamin D supplements should be avoided. Dietary calcium restriction results in hyperabsorption of oxalate and foods containing large amounts of oxalate should also be limited. The advice of a dietitian is helpful. A high fluid intakeshould be advised as for idiopathic stone-formers. Patients who live in a hard-water area may benefit from drinking softened water.
If hypercalciuria persists and stone formation continues, a thiazide, e.g. bendrofluazide 2.5 or 5 mg each morning is used. Thiazides reduce urinary calcium excretion by a direct effect on the renal tubule. They may occasionally cause hypercalciuria or gout and worsen hypercholesterolaemia. Sodium cellulose phosphate reduces calcium absorption from the gut but increases oxalate absorption, causes diarrhoea and has largely been abandoned. Avoidance of excessive sodium intake is also advisable as sodium and calcium excretion are linked.
Mixed infective stones
Recurrent stones should be prevented by maintenance of a high fluid intake and meticulous control of bacteriuria. This will require long-term follow-up and may demand the use of long-term low-dose prophylactic antibacterial agents.
Uric acid stones
Dietary measures are probably of little value and are difficult to implement. Effective prevention can be achieved by the long-term use of the xanthine oxidase inhibitor allopurinol to maintain the serum urate and urinary uric acid excretion in the normal range. A high fluid intake should also be maintained. Uric acid is more soluble at alkaline pH and long-term sodium bicarbonate supplementation to maintain an alkaline urine is an alternative approach in those few patients unable to take allopurinol. However, alkalinization of the urine facilitates precipitation of calcium oxalate and phosphate.
These can be prevented and indeed will dissolve slowly if there is obsessional attention to maintenance of a high fluid intake-5 litres of water must be drunk each 24 hours, and the patient must wake twice during the night to ingest 500 ml or more of water. Many patients cannot tolerate this regimen. An alternative, though potentially more troublesome, option is the long-term use of the chelating agent penicillamine; this causes cystine to be converted to the more soluble penicillamine-cysteine complex. Side-effects include drug rashes, blood dyscrasias and immune complex-mediated glomerulonephritis and are by no means uncommon. In addition, the drug is expensive. It is, however, especially effective in promoting dissolution of cystine stones already present. Mild hyperoxaluria with calcium oxalate stones A high fluid intake and dietary oxalate restriction are required.
The term nephrocalcinosis means diffuse renal parenchymal calcification that is detectable radiologically. The condition is typically painless. Hypertension and renal impairment commonly occur. The main causes of nephrocalcinosis are listed. Dystrophic calcification occurs following renal corticalnecrosis. In hypercalcaemia and hyperoxaluria, deposition of calci um oxalate results from the high concentration of calcium and oxalate within the kidney. In renal tubular acidosis failure of urinary acidification and a reduction in urinary citrate excretion both favour calcium phosphate and oxalate precipitation, since precipitation occurs more readily in an alkaline medium and the calcium-chelating action of urinary citrate is reduced.
Treatment and prevention of nephrocalcinosis consists of treatment of the cause.