This is the third and last in a series of articles about research studies concerning kidney stones. My goal hasn’t been to merely describe the latest research about the prevention and treatment of kidney stones, but to show how researchers and doctors try to simplify their management considerations by asking, then answering, a series of simple questions.

Here is the question presented in the research study I will discuss today: can recurrent kidney stones be prevented by diet modification? The study, authored by the late Professor Loris Borghi from the University of Parma in Italy, isn’t as recent as the other studies I had described–it was published in the New England Journal of Medicine in January 2002. Twenty-two years later, Dr. Borghi’s findings still reverberate in the minds of doctors and clinicians, affecting the guidelines doctors follow and the advice they give their patients.

The study was performed on patients with high levels of calcium in their urine (the medical term is idiopathic hypercalciuria; ‘idiopathic’ means ‘of unknown cause’; and ‘hypercalciuria’ means ‘excessive calcium levels in the urine’). Until the publication of Borghi’s study, the prevailing way of thinking went something like this: most kidney stones are made of calcium oxalate which is a compound made of calcium ions and oxalate ions. The more calcium patients consume in their diet, the more calcium they are likely to excrete in their urine. And the more calcium they excrete in their urine, the more likely they are to form calcium oxalate stones. For decades, doctors followed this concept and recommended that recurrent stone formers will go on a low calcium diet.

This way of thinking is so logical that it must be true. Right? Well, not so fast.

For 5 years, Prof. Borghi and his colleagues examined the effect of two different diets on 120 men with recurrent calcium oxalate stones and hypercalciuria. Half of the men were assigned to a low calcium diet. The other half were advised to go on a diet with a normal amount of calcium, reduced amounts of animal proteins, and reduced intake of salt.

The results were unexpected, counterintuitive, some would even say shocking! The group on the low calcium diet didn’t do better, they did much worse. Indeed, they were about twice as likely to form new, recurrent stones.

The researchers also noted that despite their different diets, the urine of both groups contained approximately the same amounts of calcium. However, the amount of oxalate in the urine of patients who consumed the low calcium diet was higher.

Remember the theory doctors used to explain their support of a low calcium diet? Based on Borghi’s study, that theory had to be changed. It would take into account not only what is happening in the kidneys, but what takes place in the gut first: when patients consume less calcium in their diet, there is less calcium in their guts. Oxalate ions that would otherwise bind to calcium and be excreted in the stool roam free in the gut. They are more readily absorbed into the blood and more likely to be excreted into the urine. There, in the urine, more urinary oxalate ions bind to calcium ions and form kidney stones.

This other theory, the one based on Prof. Borghi’s research, makes as much sense as the theory that came before it. The difference is that the second theory is probably closer to the truth. So far, it’s the second theory that prevailed. It is a concept upon which new guidelines were formulated, and it was accepted as a valid theory for 22 years.

As I had discussed in my previous columns, with each study new questions arise: would the results hold true for women? Would the same diet work for kidney stones of different chemical composition? Which part of the interventional diet was most important for stone prevention–was it the normal amount of calcium, reduced amounts of animal proteins, or reduced intake of salt? Perhaps sticking to only one of the restrictions would suffice?

For now the American Urological Association recommends the following diet modifications for stone formers (ask your primary care provider or a urologist for optimal recommendations in your specific case): increase fluid intake to produce at least 2.5 liters of urine a day; maintain normal dietary calcium (1,000-1200 mg of dietary calcium per day); limit sodium intake to less than 2,300 mg/day; limit high oxalate foods; limit animal protein; and increase citrate-rich foods like lemons, limes, and oranges.

We tell ourselves stories in order to understand the world. Often, two or more contradictory stories compete on our attention. Scientific research may be challenging and at time controversial, but it is the most promising path to pursue the truth.

EDITOR’S NOTE: Shahar Madjar, MD, MBA, is a urologist and an author. He practices in Michigan, at Schoolcraft Memorial Hospital in Manistique, and in Baraga County Memorial Hospital in L’Anse. Find his books on Amazon or contact him at smadjar@yahoo.com.