Patients with calcium oxalate kidney stones and enteric hyperoxaluria due to malabsorptive bowel conditions exhibit significantly higher urinary oxalate excretion (median 14.8% intestinal absorption) and lower estimated glomerular filtration rate (median 75.7 mL/min/1.73 m²) compared to idiopathic stone formers (median 8.9% intestinal absorption, eGFR 90.7 mL/min/1.73 m²).

When the gut cannot absorb fat properly, bile acids are lost, which prevents calcium from binding to oxalate in the intestine. This leaves more oxalate free to be absorbed into the blood, which the kidneys then filter out in large amounts. At the same time, the gut loses bicarbonate, making the blood more acidic. The kidneys respond by working harder to remove acid, which damages their filtering tubes over time. The combination of too much oxalate and chronic acid stress causes the kidneys to lose filtering capacity.