There is a really nice article on Medscape [The Role of Diet in the Prevention of Common Kidney Stones by Christy Krieg]. Some of it depends on what type of stone he has (oxalate, etc). In case you can't access it, here are the main points:
Dietary Changes to help prevent kidney stones:
1. Increased fluid intact (to the point of pale urine).
Many patients ask what fluids are recommended, and which are prohibited. The simple answer is that water is best. For those with excessive urinary oxalates, black tea should be eliminated because black tea is a high-oxalate beverage. In summary, stone formers should drink more water and avoid excess caffeine, black tea, and grapefruit and apple juices. Lemonade is often recommended, as it supplies dietary citrate, a stone inhibitor and pH buffer when excreted later in the urine.
2. Consume adequate calcium.
Several recent studies have shown, in fact, that adequate calcium intake is associated with decreased stone formation. Why might increased dietary calcium reduce the risk of calcium stone formation? Calcium and oxalate bind in the gut and in the urine to form a nonabsorbable compound. Low dietary calcium permits greater free oxalate to be absorbed in the gut and excreted in the urine, which may be counterproductive for calcium oxalate stone formers. Restricted calcium intake results in increased urinary oxalates, a risk for stone formation. Low-fat dairy products, green leafy vegetables, broccoli, fortified foods, and almonds are excellent sources. Patients should consume enough dietary calcium to meet (but not exceed) the United States Recommended Daily Allowance (RDA) of calcium, which ranges from 1,000 to 1,200 milligrams daily for adults.
3. Limit dietary oxalates
Oxalate restriction should be attempted. The highest levels of oxalate are found in chocolate, nuts, beans (including soybeans), rhubarb, spinach, beets, and black tea. A thorough oxalate list can be found on the Web site of the Oxalosis and Hyperoxaluria Foundation (http://www.ohf.org/diet.html). This list is exhaustive and may be overwhelming to patients. Vitamin C is a precursor to endogenous production of oxalates, so some clinicians recommend avoiding mega-doses of vitamin C
For a simple list of high-oxalate foods, visit http://www.gicare.com/pated/edtgs29.htm.
4. Limit sodium (salt) intact.
Because calcium and sodium compete for reabsorption in the renal tubules, excess sodium intake and consequent excretion result in loss of calcium in the urine. High-sodium diets are associated with greater calcium excretion in the urine. The goal of therapy should be a "no added salt diet," or the equivalent of 2,000 mg per day or less of dietary sodium. Reduction of dietary sodium is difficult and disappointing to patients. They may believe they have made significant reductions and sacrifices, while their urine sodium remains high. Consultation with a registered dietician may help the patient achieve the specific goal of a sodium intake of 2,000 milligrams or less per day.
5. Limit animal protein
The effect of excess animal protein (purine) is most obvious for the uric acid stone former. Uric acid, a byproduct of purine metabolism, is excreted in large quantities in the urine. Excess protein creates urine with high total urine uric acid, potentially high supersaturation of urine uric acid, and a low pH, necessary for formation of uric acid stones. There is no inhibitor of uric acid crystal formation (Menon & Resnick, 2002), so dietary measures focus on reducing uric acid and increasing urine volume. Reduction of animal protein to 12 ounces per day for adults is recommended.
I hope this will help, though I know it will be tough to get him to make some of the dietary changes. Start small--first with the water intact, less caffeine, etc.