Work-up for calcium-containing kidney stones

I am surprised at how often I see a new patient for an endocrine disorder who nonchalantly reports a past medical history of kidney stone. Even more surprising is that these patients do not recall having an evaluation of the etiology of the stone nor any advice about limiting the possible recurrence of stones. Most of these patients have not had any recurrence of stones and report no family history of stones. I am in two minds about proceeding to a “stone” workup because their clinic visit is for an entirely unrelated endocrinopathy, which clearly has precedence.

Calcium-containing kidney stones are usually calcium oxalate stones, and much less frequently calcium phosphate stones. Hypercalciuria without attendant hypercalcemia (i.e. not primary hyperparathyroidism) is common, but there is confusion about making a diagnosis of hypercalciuria. Most labs report an upper limit of 24-hour urine calcium as 250 mg in women and 300 mg in men. More correctly, the upper limit should be 4 mg/kg body weight in both women and men. It is worthwhile to mention here that the same should apply to measurement of 24-hour urine calcium when evaluating a patient with osteoporosis. Another contributor to hypercalciuria is dietary sodium — the salt intake today is excreted in the urine tomorrow and takes calcium with it. My work-up for patients with calcium-containing kidney stones or with osteoporosis always includes 24-hour urine calcium, sodium and creatinine — this latter as a “measure” of the completeness of the collection.

The work-up should also include a measurement of urinary citrate since citrate is an inhibitor of calcium oxalate stone formation. In these patients, urine calcium excretion may not be elevated and the management may focus more on dietary citrate, or potassium citrate, rather than dietary calcium. Keep this in mind when considering a low-calcium diet in stone formers. This may upset the balance between urine calcium, oxalate and citrate in the development of calcium oxalate stones.

A high urine oxalate can clearly contribute to the formation of calcium oxalate stones, although most patients in whom the etiology is hyperoxaluria are recurrent stone formers. A markedly increased urine oxalate should alert you to the possibility of inflammatory bowel disease.

Don’t forget that some patients may have mixed calcium and urate stones.

I haven’t yet addressed my initial quandary: Should a patient with a remote history of kidney stones have a stone work up when they present for another medical condition? My sense is no, at least not until the reason for the initial visit has been adequately addressed. That said, it would be appropriate to discuss daily fluid intake with the patient, emphasizing the importance of adequate fluid intake throughout the entire 24-hour day. I would not ask these patients to get up in the middle of the night to take in some additional fluid, but if they do get up a glass of water before getting back in bed is potentially of benefit and unlikely to do harm.

Better still: Develop the habit of identifying the etiology of the stone disease after the first occurrence. Passing a kidney stone is particularly painful and unpleasant, and after that first stone your patient is most likely to adhere to your recommendation.