Nephrology: 1. Investigation and treatment of recurrent kidney stones

A 60-year-old man is discharged from hospital after his second bout of renal colic in 2 years. Both times, he passed a stone without any need for surgical intervention. There is no other relevant history. The stones were analyzed biochemically and found to be composed of pure calcium oxalate. Imaging studies do not suggest the presence of residual calculi in the renal tract. The patient is, understandably, reluctant to pass any more kidney stones. The results of relevant laboratory investigations are as follows: serum biochemistry normal, urine volume 1.75 L over 24 hours, urinary calcium excretion 2.9 mmol/day, urinary phosphate excretion 24 mmol/day, urinary uric acid excretion 5.5 mmol/day, urinary oxalate excretion 270 pmol/day and urinary citrate excretion 0.6 mmol/day. The patient asks you what the probable cause is of his recurrent nephrolithiasis. What medication could be prescribed to help him and what side effects could he anticipate? What other measures could the patient take to reduce his risk of stone recurrence? Kidney stones are rarely, if ever, fatal. The main impact of nephrolithiasis is felt by young, otherwise healthy adults in the form of acute renal colic, causing symptoms of pain, nausea, vomiting and hematuria. The estimated cost of this condition in the United States for 1993 was US$1.83 billion.1 The lifetime risk of passing a kidney stone is about 8%-10% among North American males, and the peak age of incidence is 30 years. The rate of kidney stone formation in women is about half that in men, with 2 peaks, the first among women aged 35 years and the second among those aged 55 years.: Among patients who have passed one kidney stone, the lifetime recurrence rate is 60%-80%.2 There is significant geographic and seasonal variation in rates of stone formation. The reasons for this variation are not entirely clear, but they may relate to climate and the mineral content of drinking water. The frequency of kidney stones (notably calcium oxalate stones) has increased with improved standards of living.2 Citrate is derived from both endogenous (tricarboxylic acid cycle) and exogenous sources (citrus fruits such as oranges and grapefruit), however, the bulk of urinary citrate is the result of renal tubular cell excretion. In the presence of intracellular acidosis and hypokalemia, renal tubular citrate excretion is decreased. Hypocitraturia is a common, correctable cause of recurrent stone formation (pure calcium phosphate [brushite] stones).