That is a mouthful of a title! Phew! I recently received this question. Thanks so much for reaching out! Though before we get to the answer, lets take a minute and check in – what even is oxalate nephropathy? Is that even a thing?
What is oxalate nephropathy?
According to this 2022 article, oxalate nephropathy is: “defined as a syndrome of decreased renal function associated with deposition of calcium oxalate crystals in kidney tubules”.
The three different causes of oxalate nephropathy are:
- Primary hyperoxaluria
- Enteric hyperoxaluria
- Ingestion-related hyperoxaluria
Most cases of oxalate nephropathy are diagnosed with a 24 hour urine oxalate >40-45mg/day.
What is Primary Hyperoxaluria?
Primary hyperoxaluria is the most common type of oxalate nephropathy. 1-2% of ESRD in pediatric patients is causes by primary hyperoxaluria. The average age at diagnosis is 5.5 years old. But, adults can also be diagnosed.
Primary hyperoxaluria is an autosomal recessive disorder. Genetic testing is recommended to make the diagnosis. It causes overproduction of oxalates in the liver. Primary hyperoxaluria tends to have a worse prognosis than other causes of oxalate nephropathy and you tend to see higher levels of urine oxalates (>88mg/day).
What is Enteric Hyperoxaluria?
Occurs in the setting of fat malabsorption. Normally calcium binds to oxalates in the gut and calcium oxalates are excreted in the feces. In syndromes of fat malabsorption, calcium binds to fatty acids and is unable to bind to oxalates. This increases the intestinal reabsorption of oxalates.
The most common causes of enteric hyperoxaluria are gastric bypass surgeries (including the roux-en-y). Orlistat is also associated with enteric hyperoxaluria.
What is Ingested Hyperoxaluria?
As the name suggests, this is related to high intakes of oxalates or oxalate pre-cursors, most notably Vitamin C. Most case reports link ingested hyperoxaluria to mega-doses of either high oxalate foods or Vitamin C supplements. Ethylene glycol (anti-freeze) ingestion is also with ingestion hyperoxaluria. There is also a more clear link with liquid sources (e.g. Star Fruit juice or high intakes of juiced spinach) than from whole foods.
The authors report that foods that have higher oxalate bioavailability are more likely to cause ingested hyperoxaluria. Calcium lowers the bioavailability of oxalates.
What nutrition interventions are indicated for oxalate nephropathy?
For Primary Hyperoxaluria:
| Treatment | Mechanism | Notes |
| High Fluid Intake | Lowers urine calcium oxalate concentration | High fluid intake with urine alkalization can slow progression. In this guideline, the recommendation is 3.5-4L per day for adults and 2-3L/m2 BSA in children for those with preserved kidney function. |
| Citrate | Inhibits calcium oxalate crystallization | May stabilize or improve renal function. This guidelines recommends dosing of potassium citrate of 0.1-0.15g/kg for those with preserved kidney function. |
In 2023 guideline on Primary Hyperoxaluria, the nutrition recommendations are:
- Hyperhydration aiming for 3.5–4 L/day in adults; 2–3 L/m2 BSA in children, in all patients with suspected PH and preserved kidney function
- Potassium citrate supplementation (0.1–0.15 g/kg) in patients with preserved kidney function
- Consume a balanced diet, avoiding only foods that contain extremely high levels of oxalate
For Enteric Hyperoxaluria:
| Treatment | Mechanism | Notes |
| Increased calcium and reduced fat intake | Calcium binds oxalate in the gut | Can lower urinary oxalates |
| Lower oxalate intake | Decreases gut oxalates | Not all studies have shown this to be beneficial |
| Citrate | Inhibits calcium oxalate crystallization | Only data is in stone patients with low urine citrate |
| Probiotics (O. formigenes) | Increase oxalate degradation in the gut | Has not been effective in clinical trials |
For Ingestion Hyperoxaluria:
Identify and remove offending agents from the diet. Case studies have reported biopsy proven oxalate nephropathy from:
- Star fruit, 200-3000mL juice OR 6-12 fruits in 1 sitting
- Vitamin C Supplements, 2-6.5g daily
- Irumban Puli, 150-400mL juice
- Peanuts, 100-243g daily for 2-3 months
- Cashews, 1kg per week for 4 weeks
- Almonds and marzipan, 150-200g almond + 50-100g marzipan daily
- Rhubarb, >500g fresh rhubarb daily for >4 weeks
- Chaga Mushroom Powder, 4-5 teaspoons per day for 6 months
- Black Iced Tea, 16 * 8oz glasses daily
- Juicing celery, carrots, parsley, beets with greens, spinach (estimated oxalate intake ~1300mg)
What about dialysis?
The 2023 Primary Hyperoxaluria guidelines note that in primary hyperoxaluria the liver produces 4-7mmol of oxalate daily. Average oxalate removal on HD is 1.0-1.4mmol daily. Clearly not enough! The weekly oxalate removal for 3 HD sessions per week and daily PD is similar.
The recommendation is to increase the frequency of dialysis sessions. Increased frequency vs longer time is preferable as oxalate removal decreases during the HD session. In one study, patients needed 6 * 4.5 hours HD sessions per week to match oxalate removal with their body’s oxalate production. That’s a lot of dialysis!
What about transplant?
There is a risk for recurrent or new onset of oxalate nephropathy post kidney transplant. Consider work up for oxalate nephropathy in cases of spontaneous graft dysfunction.
The 2023 Primary Hyperoxaluria guidelines highlight that liver transplantation is the only cure for primary hyperoxaluria. Combined kidney/liver transplantation results in better kidney graft survival that kidney transplant alone.
So back to our original questions – should we recommend low oxalate diets for adults on HD prior to transplant?
Well, according to both articles, while there are plenty of nutrition interventions that we should talk about, but low oxalate diets isn’t making our top priority list.
If it were my patient, these would be my first steps:
- Ensure they are not consuming any mega doses of oxalates or Vitamin C (I would refer to the doses listed above under interventions of ingested hyperoxaluria)
- Consider increasing calcium intake (depending on their serum calcium values)
- Increased fluid intake may not be appropriate for HD patients. To determine if high fluid intake would be reasonable for your patient, I would recommend 24 hour urine collection and reviewing their intra-dialytic weight gains. 24 hour urine volumes >2L and minimal IDWG <2kg suggest that patients have preserved volume handling.
