Nutrition and Kidney Stones, Part I
G. Douglas Andersen, DC, DACBSP, CCN
Vol. 22, number 23, 11/4/04, page 30
Recently an excellent review on kidney stones came across my desk.1 The highlights of this article are the basis of this two-part series.
Ask anyone who has passed a kidney stone what it felt like, and even the most laid-back person will suddenly become animated. Ask them if they look forward to having the experience again, and the answer is almost universal; that is, they would not wish the experience on their worst enemy. Kidney stones (nephrolithiasis) occur in a little over 10% of North Americans. When a patient informs you he or she has or has had kidney stones and wants nutritional advice, the first step is a record request from the physician who managed their problem. This is because your advice will vary depending on the pathophysiology of the kidney stone. You need to determine the casue - hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, hypomagnesuria, or renal tubular acidosis.
Other types of hypercalciuria include resorpt and renal. Resorptive hypercalciuria accounts for 5% of all cases. It is caused by subclinical hyperparathyroidism and has the classic finding of bone demineralization and elevated fasting urinary calcium levels. Renal hypercalciuria is due to the kidneys' decreased ability to reabsorb calcium. This causes the body to increase vitamin D synthesis. Fasting urinary calcium levels are normal.
Dietary treatment for hypercalciuria*
*Please note: These are general guidelines only and will very depending on a patient's specific need.
A recent paper showed that keeping dietary calcium at normal RDA levels and lowering sodium, protein, and oxalates with high levels of fluid and citrus consumption was superior to a low calcium diet in reducing the risk of recurrent stones.3 All patients with hypercalciuria should be referred to rule out hyperparathyroidism.1
Next month in part 2 we will review the other metabolic defects that promote stone formation including hyperoxaluria, hyperuricosuria, hypocitraturia, hypomagnesuria, and renal tubular acidosis.
E. Imperial Hwy.
2004, G. Douglas Andersen, DC, DACBSP, CCN, 916 E. Imperial Hwy, Brea,
CA 92821, (714) 990-0824