Abstract: TH-PO0005
Dietary Calcium Supplementation Reduces Urinary Oxalate Excretion and Attenuates Kidney Injury in a Novel Murine Model of Enteric Hyperoxaluria
Session Information
- Mineral Balance: Physiology and Pathophysiology
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Bone and Mineral Metabolism
- 501 Bone and Mineral Metabolism: Basic
Authors
- Jaber, Karim, NYU Langone Health, New York, New York, United States
- Mishra, Rashmi, NYU Langone Health, New York, New York, United States
- Merritts, Kyle, NYU Langone Health, New York, New York, United States
- Xiong, Xiaozhong, NYU Langone Health, New York, New York, United States
- Nazzal, Lama, NYU Langone Health, New York, New York, United States
Background
Enteric hyperoxaluria (EH) is a complication of inflammatory bowel disease and results from fatty acid malabsorption that sequesters calcium increasing oxalate bioavailability, leading to hyperoxaluria, nephrolithiasis, and oxalate nephropathy. Dietary calcium can bind oxalate within the intestinal lumen, reducing its absorption and subsequent urinary excretion. Although calcium supplementation is a mainstay of therapy in patients with EH, its efficacy has not been tested in our recently established SAMP1 mouse model of EH. This study investigated whether calcium supplementation reduces urinary oxalate excretion and kidney injury in this model.
Methods
20 12-week-old SAMP1/YitFc mice (M/F=1) were placed on a 45% fat diet supplemented with 1% sodium oxalate and randomized 1:1 to either a standard calcium diet (0.5%, SCD) or a high calcium diet (1.5%, HCD). After 4 weeks, 24-h urine samples were collected for measurement of oxalate (UOx), creatinine (UCr) and calcium (UCa), and fecal pellets were collected. After 6 weeks, mice were euthanized. Plasma creatinine (PCr) and blood urea nitrogen (BUN) were measured to assess kidney function. Kidney histology, fibrosis and crystal formation were evaluated using hematoxylin and eosin (H&E), Masson's trichrome staining (MTS) and Pizzolato staining.
Results
Mice receiving HCD had significantly lower UOx/UCr (0.22 ± 0.1 mg/mg vs. 0.91 ± 0.4 mg/mg, p<0.05). Fecal oxalate excretion was significantly higher in the HCD group (0.14 ± 0.1 mg/mg of stool vs. 0.02 ± 0.0 mg/mg of stool, p<0.01), suggesting reduced intestinal oxalate absorption. Kidney function was better preserved in HCD mice, with lower PCr (0.62 ± 0.2 vs. 0.91 ± 0.2 mg/dL, p<0.05) and BUN (14.22 ± 7.2 vs. 21.12 ± 6.0 mg/dL, p=0.06). Renal fibrosis was reduced in HCD mice on MTS (3.36 ± 0.8% vs. 6.48 ± 2.0%, p<0.05). Both groups had similar levels of UCa/UCr (1.38 ± 0.8 vs. 1.29 ± 0.7 mg/mg, p=0.83) and crystal deposition (62 ± 22 in HCD mice vs. 44 ± 38 crystals/slide in SCD mice, p=0.40).
Conclusion
Dietary calcium supplementation reduced urinary oxalate excretion and attenuated kidney injury in this murine model of EH, validating it as a platform for testing therapeutic interventions in EH. Further studies are needed to evaluate optimal dosing, potential side effects, underlying mechanisms and explore interactions with the gut microbiome.
Funding
- NIDDK Support