Collagen in meat supplies the amino acid hydroxyproline, which is metabolized to oxalate.
The role of meat consumption in the development of kidney stones remains controversial. Most of the recent research on this topic has focused on the effect of dietary protein on acid-base metabolism, calcium excretion, and uric acid production. Stone-formation risk varies with relative saturation of calcium oxalate, which is directed related to urinary oxalate. Although dietary oxalate accounts for about one half of urinary oxalate, the other half comes from endogenous synthesis. The daily turnover of collagen in humans is a major source of the amino acid hydroxyproline, which is metabolized to oxalate via glycolate. Overall, collagen turnover may account for 5%-20% of urinary oxalate daily.
A little-studied aspect of meat consumption is the role of its hy-droxyproline content on urinary oxalate. John Knight, PhD, of Wake Forest University School of Medicine in Winston-Salem, N.C., and his colleagues (Kidney Int. 2006;70:1929-1934) compared 24-hour urinary oxalate on the third day of 30-gram loads of gelatin versus whey protein in 10 subjects with no history of nephrolithiasis. Urinary oxalate after whey protein consumption was not different from self-selected diet (17.2 vs. 17.6 mg/g creatinine) but increased significantly to 24.4 mg/g after gelatin. As a follow-up study, they fed the same volunteers 10 grams of gelatin (a more likely intake from food), and observed the kinetics of plasma hy-droxyproline and glycolate, urinary glycolate, and oxalate for 24 hours. Plasma hydroxyproline increased, peaking at 1-7 hours after consumption, whereas plasma glycolate did not differ. Plasma oxalate peaked at 3-7 hours while urinary oxalate was increased over the entire 24-hour collection period. A comparison of gelatin load sizes from 1-10 grams demonstrated that either a 5- or 10-gram load significantly raised urinary oxalate for at least six hours.

All meat tissues contain some collagen, but various meat forms have different amounts. Samples of lean beef, bovine liver, chicken, fish, lean lamb, and sausage contained from 2.5%-4.9% collagen by weight, according to a study published in Food Chemistry (1995;53:209-210). A Canadian researcher with Agriculture Canada reported that composite meats, e.g., wieners and sausages, had collagen contents that varied from 4.1%-19.0% of weight (J Agric Food Chem. 1992;40:790-800). In another study published in the Journal of Food Science (1999;64:377-383), investigators reported that samples of ground beef had a collagen content ranging from 0.7%-7.1% of weight, depending on the cuts of beef used.

Meat that contains 7% collagen will have 7 grams per 100 gram serving (3.5 ounces) and 10 grams per 140 gram serving (5 ounces or about one third of a pound). Gelatin is a protein resulting
from cooking or processing of collagen, so it, too, has the potential to increase urinary oxalate. Knox gelatin has 7 grams per package, as does a 3-ounce box of Jello. Several dietary supplements promoted for skin, bone, and joint health contain gelatin at 10 grams per recommended dose.
Research to date hasn’t looked at whether the collagen content of meat consumed can affect the outcome of dietary studies looking at the relationship of protein to calcium oxalate kidney stone risk. In studies where subjects self-selected their diets, there could be considerable variability in collagen/
gelatin intake, even if protein in-take was constant. In addition, genetic abnormalities that lead
to variations in enzymes that metabolize hydroxyproline can contribute to stone risk. For ex-ample, polymorphisms in hepattic alanine:glyoxylate aminotransferase (AGT1) lead to primary hyperoxaluria I.

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In a previously published study, researchers at University Hospital in Berne, Switzerland, noted that only seven of 20 male recurrent idiopathic stone-formers had increased urinary oxalate after increasing protein intake from 160 grams of lean meat or fish protein to 700 grams daily (Kidney Int. 2001;59:2273-2281). Interestingly, nine of 13 controls had mild metabolic hyperoxaluria on the lower “moderate” protein diet, even though all had normal oxalate levels on three days of self-selected diet. These controls, however, showed no statistically significant mean increase in urinary oxalate when they ate the very high protein diet. There was only a significant difference in mean response in the 12 stone-formers with mild metabolic hyperoxaluria (MMH). The group increase in oxalate in the eight stone-formers without MMH was not statistically significant, although three of these subjects had large increases that raised their urinary oxalate into the level defined as MMH.

Additional studies need to be done on the genetic variability of urinary oxalate response to dietary gelatin/collagen, especially with regard to polymorphisms of AGT1. Meanwhile, stone-formers should be advised of the possible risk of consuming gelatin and to avoid composite meats such as wieners and sausages, gelatin salads and desserts, and supplements containing collagen hydrolysates or gelatin.