Update in Diagnosis and Management
Much of the oxalate in foods is not readily absorbed, most likely because it is complexed with calcium. An average value for net oxalate absorption might be 10%, as shown on this slide. The remainder comes from liver production of oxalate, which is an end product of metabolism that must be renally eliminated. Liver production increases markedly in patients with the genetic disorders primary hyperoxaluria.
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- Kidney Stones
- Why do Kidney Stones Form?
- Genetics and Environment
- Not All Stones are Created Equal: Stone Analysis is Very Helpful
- Laboratory Evaluation
- Supersaturation Index
- Components of the Urinary Supersaturation Profile
- Uses of Urinary Supersaturation
- Common Features Increase Urinary Supersaturation in Patients with Idiopathic Calcium Oxalate Nephrolithiasis
- "Conservative" Dietary Recommendations for Calcium Oxalate Stone Formers
- Causes of Hypercalciuria
- Genetic Hypercalciuria
- Genetic Hypercalciuria: Treatment
- What is Oxalate?
- Hyperoxaluria: What is the Relevant Concentration?
- Oxalate Balance on a Typical Western Diet
- Enteric Hyperoxaluria is Caused by Fat Malabsorption
- Control of Urinary Citrate: Largely Due to Systemic Acid Base Balance
- Treatments for Enteric Hyperoxaluria
- Low Urinary Citrate
- Hyperuricosuria is a Risk Factor for Calcium Oxalate Stones
- Uric Acid is Very Insoluble at Low pH
- Calcium Phosphate is Very Insoluble at High pH!
- Cystine Stones
- Struvite stones