Update in Diagnosis and Management
Urinary citrate levels are largely determined at the level of the proximal tubule. Filtered citrate can be reabsorbed there, enter the citric acid cycle, and be broken down to generate bicarbonate ions. Control of these events is driven largely by systemic acid base status, which in turn affects intracellular pH. This makes sense, since the net result is to regenerate bicarbonate and help correct the acidosis.
Control of Citrate
Jump to section:
- 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