Investigation and Management of Renal Stone Disease

Holly R. Mabillard; Charles R. V. Tomson


Nephrol Dial Transplant. 2017;32(12):1984-1986. 

In This Article


Find out What the Stones are Made of

Knowledge of the chemical make-up of the stone hugely influences management. Wherever possible, stones (either caught by the patient—ask them to pass urine through a tea strainer during colic episodes—or retrieved ureteroscopically or percutaneously) should be analysed.

Microscope the Urine

Recognition of the crystal type, e.g. cystine, can make the diagnosis.

Review Radiology

If stone chemistry is not available, radiology can provide some clues. The distinction between 'radiolucent' stones (urate, cystine) and 'radio-opaque' stones (calcium oxalate, calcium phosphate and struvite) is not absolute; if the stone is big enough, stone density measurement (Hounsfield units) on computed tomography of the kidneys, ureters and bladder can help distinguish the stone type.

Look for medullary sponge kidney and for marked anatomical abnormalities that might lead to urinary stasis, including evidence of reflux nephropathy with associated struvite stones. Do not assume that all 'staghorn' calculi are infection related; cystine and calcium stones can form staghorns.

Stone monitoring and removal decisions should be undertaken by an endourologist.[1]

Review Serum Biochemistry

Look for evidence of renal tubular acidosis and hypophosphataemia. Check for hypercalcaemia and investigate fully if found: primary hyperparathyroidism is a treatable cause of hypercalciuria and calcium kidney stones. Hyperuricaemia is relevant if it is due to increased production but not due to reduced renal excretion.

Check Urine Chemistry

Cystinuria can be diagnosed using 'spot urine' cystine, but the severity and response to intervention is best assessed by a 24-h urine cystine divided into daytime and nighttime aliquots (lower fluid intake often causes higher nighttime concentration). Measure creatinine and sodium on every urine collection: 24-h creatinine excretion should be very similar for each collection if complete; high Urinary Sodium is linked to higher calcium and cystine excretion. For initial assessment and monitoring of calcium oxalate stone formers, measure calcium, oxalate, citrate, urate and magnesium as well as sodium and creatinine (Table 1). Calcium phosphate crystallization is highly dependent on the degree of ionization of phosphate (not phosphate concentration), which is very pH dependent.

Measure pre-meal urine pH, ideally with a pH meter, in patients with uric acid stones. The 24-h urine uric acid excretion is nearly irrelevant since uric acid solubility is so pH dependent.[4]

The distinction between 'absorptive type 1', 'absorptive type 2' and 'renal' hypercalciuria gives clues on stone formation pathophysiology, but there is no current evidence that management should vary between subtypes.

Formulas and algorithms exist to estimate stone formation probability from urine biochemistry, but their utility in clinical management remains unproven.

Think About Rare Genetic Conditions

The earlier the onset and the worse the phenotype, the more justified it is to look for rare conditions that would require a different management approach and/or genetic counselling. Measure urine retinol-binding protein (or a different tubular protein, depending on local laboratory practices) if Dent's disease is suspected. Testing for known causative mutations is now preferred for differentiating Types 1, 2 and 3 hyperoxaluria. Plasma oxalate is normal or near normal in these conditions unless glomerular filtration rate is reduced.