Oxalate Nephropathy: Kidney Damage From Oxalate Crystals

Table of Contents

1. Crystals Inside the Kidney Tissue
2. How It Differs From Kidney Stones
3. Gut Conditions That Raise Oxalate Absorption
4. Juices, Foods and High-Dose Vitamin C
5. Ethylene Glycol and Plant Poisoning
6. The Inherited Form
7. How Often People Recover
8. How It Is Diagnosed
9. Treatments Described in the Literature
10. What Is Not Known
11. Key Research Papers
12. Connections
13. Featured Videos

Crystals Inside the Kidney Tissue

Oxalate is a small waste molecule. Some of it comes from food, and some is made by the body. The body cannot use it or break it down, so it leaves almost entirely in the urine. When there is too much of it, a state called hyperoxaluria (too much oxalate in the urine), it can join with calcium and form calcium oxalate crystals (Demoulin 2022).

Reviews sort the excess into three broad groups (Rosenstock 2022; Demoulin 2022):

• Primary hyperoxaluria — inherited faults in liver enzymes that make the liver overproduce oxalate.
• Enteric hyperoxaluria — gut conditions that let far more oxalate from food be absorbed than normal.
• Ingestion-related hyperoxaluria — very large intakes of oxalate itself, or of substances the body turns into oxalate.

When the crystals lodge inside the kidney, in the tubules and the tissue between them, the biopsy shows more than crystals. In the Mayo Clinic series the crystals came with acute tubular injury (damage to the tubule lining), inflammation, and scarring with shrinking of the tubules (Nasr 2024). A systematic review of 108 published patients found acute tubular injury in 71%, tubular damage and shrinkage in 69% and inflammatory cell infiltration in 72% of biopsies (Lumlertgul 2018).

A pattern runs through the literature. Many people with this injury had a condition that kept their urine oxalate high for a long time, and then something tipped them over. A 2022 review notes that patients with the non-inherited forms frequently have long-standing hyperoxaluria-enabling conditions, which suggests a role for triggers of acute kidney injury such as dehydration (Demoulin 2022). In the Mayo series 53% of patients had diabetes, and 53% had another kidney disease found on the same biopsy, most often diabetic kidney disease (Nasr 2024).

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How It Differs From Kidney Stones

The same crystal, calcium oxalate, is behind the commonest type of kidney stone. The difference is where the crystals end up and what they do there.

• A kidney stone grows in the urine-collecting space of the kidney and the urinary tract. It can block the flow of urine and cause severe pain.
• Oxalate nephropathy means crystals deposited throughout the kidney tubules and the tissue between them, where they injure the cells and set off inflammation and scarring (Rosenstock 2022; Nasr 2024). There may be no stone at all.

The two can share a cause. A Mayo Clinic review of 23 patients who developed enteric hyperoxaluria after Roux-en-Y gastric bypass, the most common type of weight-loss surgery, found 21 with calcium oxalate stones and 2 with oxalate nephropathy. Two patients developed kidney failure and needed long-term hemodialysis (Nelson 2005). In people with enteric hyperoxaluria, higher urine oxalate also predicted more stone events: a population study of 297 patients in Olmsted County, Minnesota, estimated that a 20% fall in urine oxalate went with a 25% fall in the yearly odds of a new stone (D'Costa 2021).

Oxalate nephropathy tends to be quiet. One report describes the clinical picture as non-specific: acute kidney injury with normal results on the blood antibody tests used to look for other kidney diseases (Cossey 2013). Proteinuria (protein in the urine) was reported in 69%, blood in the urine in 32% and crystals in the urine in only 26% of published cases (Lumlertgul 2018). That is part of why the diagnosis is frequently delayed (Demoulin 2022).

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Gut Conditions That Raise Oxalate Absorption

Enteric hyperoxaluria is the cause found most often in the case series. It was the cause in 60% of the 113 Mayo patients, most commonly after Roux-en-Y gastric bypass (Nasr 2024). In the systematic review of 108 published patients, fat malabsorption was the most commonly attributed cause, at 88%, followed by excess oxalate in the diet at 20%; the shares add to more than 100% because many patients had more than one cause (Lumlertgul 2018).

How fat malabsorption frees oxalate

Normally, calcium in the gut binds the oxalate in a meal into insoluble calcium oxalate, which leaves in the stool. When fat is not absorbed, the free fatty acids bind the calcium instead, so less calcium is left to hold the oxalate. Unabsorbed bile salts and fatty acids reaching the colon also make its lining more permeable, and the colon is where the extra oxalate is absorbed (Asplin 2016). Urine oxalate in this condition is frequently above 100 mg a day (1.14 mmol a day), according to the same review.

A 2021 systematic review lists many gut disorders that can do this and notes that the condition has become more common in recent decades, largely because of the wider use of malabsorptive weight-loss surgery (Witting 2021).

After weight-loss surgery

In 2008, a kidney-pathology laboratory at Columbia University reported 11 cases of oxalate nephropathy after Roux-en-Y gastric bypass. Eight had the surgery for severe obesity and three for reconstruction after stomach removal for cancer. All 11 had high blood pressure and 9 had diabetes. They developed acute kidney failure a median of 12 months after surgery, often on top of mild chronic kidney disease (in 7). Eight of the 11 progressed rapidly to end-stage kidney disease and needed hemodialysis at a mean of 3.2 weeks after the biopsy; the other three were left with significant chronic kidney disease. The authors called it an under-recognized complication of the operation (Nasr 2008).

The time from surgery varies widely. In the 2005 Mayo review, enteric hyperoxaluria was recognized at a mean of 29 months after the bypass, with a range of 2 to 85 months, after a mean weight loss of 46 kg (Nelson 2005).

A weight-loss medicine that blocks fat absorption

Orlistat, a medicine that blocks the gut enzyme that digests fat, works by causing fat malabsorption, and case reports describe oxalate nephropathy with it. The first report, in 2007, was a woman with existing chronic kidney disease whose kidney injury followed an increase in her orlistat dose and more frequent loose, oily stools. The urine contained abundant calcium oxalate crystals and 24-hour urine oxalate was raised. Orlistat was stopped and her fluid intake was increased; a second biopsy a month later showed no crystals, kidney function improved steadily, and a repeat 24-hour urine oxalate three weeks later was within normal limits (Singh 2007).

A 2016 report described a 76-year-old woman with chronic kidney disease who had started orlistat 120 mg three times a day six weeks before admission. Her biopsy showed massive calcium oxalate deposits. After five dialysis sessions she gradually returned to her earlier baseline kidney function (Humayun 2016).

Pancreatic insufficiency

When the pancreas does not make enough digestive enzymes, fat is poorly absorbed. A 2021 report described a 68-year-old man with type 2 diabetes and an unrecognized exocrine pancreatic insufficiency whose dialysis-dependent kidney injury turned out to be oxalate nephropathy; he made a complete recovery after a multi-part treatment described below (Tilia 2021).

Antibiotics come up repeatedly as a possible contributor. One review discusses the possibility that antibiotic use predisposes to oxalate nephropathy (Rosenstock 2022), and the green-smoothie case described in the next section had a recent prolonged antibiotic course on top of an old gastric bypass (Makkapati 2018).

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Juices, Foods and High-Dose Vitamin C

Excessive intake of foods high in oxalate, or of substances the body turns into oxalate, was the cause in 23% of the Mayo patients, most commonly vitamin C. Patients in this group most often arrived with acute kidney injury (Nasr 2024). The individual case reports describe a range of foods.

Juicing and green-smoothie cleanses

A 2013 Mayo Clinic report described a patient with chronic kidney disease whose acute kidney failure was attributed to heavy drinking of oxalate-rich fruit and vegetable juices made at home. The same paper reviewed 65 Mayo patients seen from 1985 to 2010 with kidney failure and biopsy-proven calcium oxalate crystals. A cause was identified in every one: a single cause in 36 and at least two in 29. Only three, including the index patient, had presumed diet-induced oxalate nephropathy, and all three had chronic kidney disease (Getting 2013).

A 2018 report described a 65-year-old woman with normal kidney function before a green-smoothie juice cleanse made from oxalate-rich leafy vegetables and fruits. She developed acute kidney injury that progressed to end-stage kidney disease. Her predisposing factors were a gastric bypass long before and a recent prolonged course of antibiotics (Makkapati 2018).

A 2023 report described a man with diabetes and normal kidney function who was put on a juice diet for a week because of bleeding in the upper gut. He developed biopsy-proven oxalate nephropathy that needed dialysis. The authors list age, diabetes, dehydration and underlying chronic kidney disease as likely risk factors (Raja 2023).

Spinach and sorrel are among the highest-oxalate leaves people eat, and juicing removes the bulk that would otherwise limit how much leaf a person can take in at once; the measured oxalate contents are set out on Sorrel Safety: Oxalates and Kidney Risk and Spinach: Iron Absorption and Oxalates.

Star fruit

The first two cases tied to star fruit (carambola) were reported from Taiwan in 2001. Within hours of drinking large amounts of sour star-fruit juice, both people had nausea, vomiting, abdominal pain and backache, followed by acute kidney failure with very little urine. Both needed hemodialysis. Their kidney function recovered four weeks later without specific treatment. The authors noted that the commercial juice is usually pickled and diluted, which markedly lowers its oxalate, whereas the pure fresh juice or mildly diluted pickled juice used as a traditional remedy in these cases is high in oxalate. They suggested that an empty stomach and dehydration may add to the risk (Chen 2001).

Rhubarb, nuts and seeds

A 2012 report from Munich described acute kidney failure after excessive rhubarb intake in a person with type 1 diabetes and previously normal kidney function. The biopsy showed mild diabetic changes but prominent oxalate crystals in the tubules, and blood oxalate was raised (Albersmeyer 2012). More on the plant is on the Rhubarb page.

A 2008 report from Japan described a 65-year-old man who had eaten about 100 to 200 g of peanuts and drunk 750 to 1,000 mL of beer every day for two or three months; his biopsy showed oxalate crystals under polarized light, and the authors strongly suspected the peanuts (Sasaki 2008). A 2020 report described a 59-year-old woman who ate six tablespoons of chia seeds and five handfuls of almonds a day to manage irritable bowel syndrome. Her 24-hour urine showed high oxalate and low citrate, her biopsy showed calcium oxalate deposits, and her laboratory results improved after she switched to a low-oxalate diet (Garland 2020).

High-dose vitamin C

The body turns part of the vitamin C it takes in into oxalate (Raja 2023). Vitamin C was the commonest cause in the ingestion group of the Mayo series (Nasr 2024). A 2013 report described acute oxalate nephropathy in a patient with lupus who had recently received intravenous vitamin C (Cossey 2013). These reports concern large supplemental or intravenous doses. The cohort data on vitamin C from food and from ordinary supplements and kidney stones are on Vitamin C Toxicity: Kidney Stones.

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Ethylene Glycol and Plant Poisoning

Ethylene glycol is a sweet-tasting, odorless solvent found in products such as antifreeze. The body breaks it down into glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid. These breakdown products are toxic to cells and can cause heart and lung failure, life-threatening metabolic acidosis (too much acid in the blood), depression of the nervous system and kidney injury. The oxalic acid can precipitate as calcium oxalate monohydrate crystals inside the tubules (Seo 2012).

A 2026 report described a 35-year-old man brought to an emergency department unconscious after a suspected ethylene glycol ingestion. Tests showed severe metabolic acidosis with a raised anion gap (a blood calculation that points to an unmeasured acid), acute kidney injury and high potassium. The biopsy showed acute tubular necrosis with many oxalate crystals. He was treated with intravenous fluids, bicarbonate, ethyl alcohol and hemodialysis. He regained consciousness, the acidosis improved, and he did not need further dialysis (Xu 2026).

Swallowing ethylene glycol is a poisoning that hospitals treat as an emergency; unconsciousness and severe acidosis are among the signs in the reports above.

Poisoning by oxalate-containing plants is a separate, older story. A 1992 forensic review describes poisoning by plants such as raw rhubarb as infrequent and deaths as rare, and reviews the clinical and pathological findings in fatal cases (Sanz 1992).

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The Inherited Form

In primary hyperoxaluria, an inherited fault in a liver enzyme makes the liver overproduce oxalate (Demoulin 2022). Diet is not the main source, so the same crystals can build up in the kidneys of children and young adults with no gut disease and no unusual diet. The Primary Hyperoxaluria page covers the three genetic types, how the disease progresses and how it is confirmed.

Lumasiran, an injected RNA-interference medicine that lowers the liver's oxalate production by reducing the enzyme glycolate oxidase, was tested in a placebo-controlled trial in 39 people aged 6 and older with primary hyperoxaluria type 1. Over six months, 24-hour urine oxalate fell by 65.4% on lumasiran, 53.5 percentage points more than on placebo, and 84% of those on lumasiran reached normal or near-normal urine oxalate (no more than 1.5 times the upper limit of normal), against 0% on placebo. Mild, short-lived injection-site reactions were reported in 38% (Garrelfs 2021). The trial was funded by the manufacturer. The drug's mechanism and the longer follow-up are on the Lumasiran page.

The trial enrolled only people with the inherited type 1 disease. It does not tell us anything about the non-inherited forms of oxalate nephropathy that make up most of the case series on this page.

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How Often People Recover

The case series are small, mostly from single centers, and look back at patients sick enough to have a kidney biopsy. With that limit in mind, the numbers run in both directions.

The larger series

• Mayo Clinic, 113 patients, 2001–2023. After a median follow-up of 36 months, 27% (30 of 112) had recovered kidney function, 19% (21 of 112) had lasting kidney dysfunction, 54% (61 of 112) had reached kidney failure, and 29% (32 of 112) had died. Mean kidney survival was 30 months in patients with another kidney disease on the biopsy against 96 months in those without one (Nasr 2024).
• Systematic review, 108 published patients, 1950–2018. 55% needed dialysis. Of those, none recovered completely, 42% recovered partly and 58% stayed on dialysis. A third of all patients died. Mean 24-hour urine oxalate was 85.4 mg a day (Lumlertgul 2018).
• Columbia University, 11 patients after gastric bypass. Eight reached end-stage kidney disease; the other three were left with significant chronic kidney disease (Nasr 2008).

What predicted the outcome

In the Mayo series, the independent predictors of kidney failure were the amount of scarring and tubular shrinkage on the biopsy and the lowest estimated glomerular filtration rate (the standard calculated measure of kidney filtering) reached during the illness. The amount of crystal on the biopsy did not predict it (Nasr 2024).

The reports of recovery

• Both star-fruit patients, who had needed hemodialysis, recovered kidney function four weeks later (Chen 2001).
• Kidney function improved steadily after orlistat was stopped in the 2007 case, and the 2016 orlistat patient returned to her earlier baseline (Singh 2007; Humayun 2016).
• The patient with pancreatic insufficiency made a complete recovery from dialysis-dependent injury (Tilia 2021). The authors note that complete recovery is extremely rare even with early treatment.
• The ethylene glycol patient needed no further dialysis (Xu 2026).

Single case reports are more likely to be published when the story is striking, so they cannot give a recovery rate.

After a kidney transplant

Among 23 Mayo patients who received a kidney transplant, followed for a median of 58 months, 4 lost the graft, 3 of them because oxalate nephropathy recurred in the new kidney. Graft survival was 90% at 2 years, 79% at 5 years and 50% at 10 years. The authors conclude that recurrence and graft loss may occur if hyperoxaluria is not controlled (Nasr 2024).

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How It Is Diagnosed

Kidney biopsy and polarized light

The diagnosis rests on a kidney biopsy. Reports describe abundant polarizable calcium oxalate crystals in the lining cells and the open channel of the tubules (Makkapati 2018), alongside acute tubular injury (Cossey 2013). "Polarizable" means the crystals stand out when the tissue slide is viewed under polarized light; the 2008 peanut report, for example, describes oxalate crystals seen this way (Sasaki 2008).

The case definition in the reviews is a fall in kidney function together with crystal deposition in the tubules (Rosenstock 2022). In the Mayo series the amount of crystal did not predict how the kidneys fared (Nasr 2024).

Urine and blood oxalate

A 24-hour urine collection measures how much oxalate the kidneys are passing. It was raised in the orlistat cases (54 to 96 mg in 24 hours in the 2016 report), and in the nut-and-seed case it showed high oxalate together with low citrate (Singh 2007; Humayun 2016; Garland 2020). In the gastric-bypass review, 20 of 23 patients tested had increased oxalate excretion (Nelson 2005). Blood oxalate was raised in the rhubarb and 2016 orlistat cases (Albersmeyer 2012; Humayun 2016).

Searching for the cause

A crystal on a biopsy is a finding, not a cause. The 2013 Mayo review concluded that calcium oxalate crystals on a kidney biopsy should prompt a search for the cause of the oxalate excess, including a detailed dietary history (Getting 2013). The 2020 nut-and-seed report adds that an earlier dietary history could have raised the question before the biopsy (Garland 2020). The 2021 pancreatic case describes a wide diagnostic search that turned up an exocrine pancreatic insufficiency nobody had known about (Tilia 2021). In a young person with no gut disease and no unusual diet, the inherited form is part of the search; the Primary Hyperoxaluria page describes genetic testing.

For ethylene glycol, the clues in the 2026 report were a suspected history of ingestion and a metabolic acidosis with a raised anion gap, confirmed by the biopsy (Xu 2026).

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Treatments Described in the Literature

For the non-inherited forms, the evidence here is reviews, case series and single case reports, and a 2021 systematic review found evidence on clinically significant outcomes lacking (Witting 2021). What follows is what reviews describe as standard care and what individual reports say was done.

Removing the cause

A 2022 review lists the current standard of care in the non-inherited forms as managing the underlying cause, high fluid intake and calcium supplements (Demoulin 2022). In the case reports, removing the cause meant stopping orlistat (Singh 2007), treating the pancreatic insufficiency and fat malabsorption (Tilia 2021), or switching to a low-oxalate diet (Garland 2020). In the gastric-bypass setting, the 2021 systematic review lists the current options as correcting the underlying gut disorder, intensive dietary changes and calcium salts to bind oxalate in the gut (Witting 2021).

Calcium with meals

Calcium taken with food binds oxalate in the gut so that it leaves in the stool rather than the urine. Reviews describe oral calcium salts as the primary medical step in enteric hyperoxaluria (Asplin 2016; Witting 2021). The 2021 pancreatic case used calcium supplements with meals (Tilia 2021). In the 2016 orlistat case, the patient was also on a stomach-acid-lowering medicine, and the authors report that only calcium citrate bound the oxalate effectively (Humayun 2016). The same principle, that calcium eaten with food lowers oxalate absorption, is why the kidney-stone research finds a normal-calcium diet linked to fewer calcium oxalate stones than a low-calcium one; that evidence is on the Kidney Stones page.

Fluids and citrate

High fluid intake is part of the standard care listed in the 2022 review (Demoulin 2022), and dehydration appears in several reports as a likely trigger (Chen 2001; Raja 2023). The 2021 pancreatic case used potassium citrate and sodium bicarbonate (Tilia 2021), and the 2020 nut-and-seed case had low urine citrate (Garland 2020).

Other measures in reviews and reports

• Diet in enteric hyperoxaluria. A 2016 review describes the dietary side as limiting oxalate and fat intake, since in this condition unabsorbed fat is what frees the oxalate (Asplin 2016).
• Bile acid binders. The same review describes bile acid sequestrants as useful in patients who have had part of the ileum (the last section of the small intestine) removed and who malabsorb bile acids (Asplin 2016).
• Oxalate-degrading bacteria. Probiotics containing bacteria that break down oxalate are being studied, but no definite benefit has been shown with the preparations available so far (Asplin 2016).
• Steroids. The 2021 pancreatic case also received methylprednisolone, as part of a multi-part plan (Tilia 2021). One case cannot show which part helped.
• Dialysis. Dialysis was used as support in many reports, and in the ethylene glycol case alongside fluids, bicarbonate and ethyl alcohol (Xu 2026).
• Lumasiran in the inherited type 1 form. Tested in a placebo-controlled trial, described in the section on the inherited form above (Garrelfs 2021).

Decisions about medicines, supplements and diet in kidney disease belong with the person's clinicians.

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What Is Not Known

• Whether the standard treatments change outcomes. The 2021 systematic review states that evidence for the effect of the treatments for enteric hyperoxaluria on stone events or chronic kidney disease is currently lacking (Witting 2021). The 2018 systematic review calls for studies of prevention and treatment in high-risk patients (Lumlertgul 2018).
• Why only some people are hit. Many people live for years with gut conditions that raise oxalate absorption. Why a few develop sudden kidney injury is not settled; reviews point to triggers such as dehydration on top of long-standing hyperoxaluria (Demoulin 2022).
• How much is too much. The food reports describe large, sustained intakes, often in people with diabetes, chronic kidney disease, a gastric bypass or recent antibiotics. No study sets a safe oxalate or vitamin C threshold for any one person.
• Unexplained cases. In 17% of the Mayo patients no cause was found (Nasr 2024).
• How common it really is. The figures come from people who had a biopsy. A 2022 review notes that diagnosis is frequently delayed (Demoulin 2022), so milder or missed cases are not counted.
• The role of antibiotics and gut bacteria. Antibiotic use is discussed as a possible predisposing factor (Rosenstock 2022), and oxalate-degrading probiotics have not shown a definite benefit (Asplin 2016).

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Key Research Papers

1. Nasr SH, Valeri AM, Said SM, Sethi S, Nath KA, Lieske JC, Bu L. Clinicopathologic Characteristics, Etiologies, and Outcome of Secondary Oxalate Nephropathy. Mayo Clin Proc. 2024;99(4):593-606. PubMed PMID: 38310502
2. Lumlertgul N, Siribamrungwong M, Jaber BL, Susantitaphong P. Secondary Oxalate Nephropathy: A Systematic Review. Kidney Int Rep. 2018;3(6):1363-1372. PubMed PMID: 30450463
3. Rosenstock JL, Joab TMJ, DeVita MV, Yang Y, Sharma PD, Bijol V. Oxalate nephropathy: a review. Clin Kidney J. 2022;15(2):194-204. PubMed PMID: 35145635
4. Demoulin N, Aydin S, Gillion V, Morelle J, Jadoul M. Pathophysiology and Management of Hyperoxaluria and Oxalate Nephropathy: A Review. Am J Kidney Dis. 2022;79(5):717-727. PubMed PMID: 34508834
5. Nasr SH, D'Agati VD, Said SM, Stokes MB, Largoza MV, Radhakrishnan J, Markowitz GS. Oxalate nephropathy complicating Roux-en-Y Gastric Bypass: an underrecognized cause of irreversible renal failure. Clin J Am Soc Nephrol. 2008;3(6):1676-83. PubMed PMID: 18701613
6. Nelson WK, Houghton SG, Milliner DS, Lieske JC, Sarr MG. Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy: potentially serious and unappreciated complications of Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2005;1(5):481-5. PubMed PMID: 16925274
7. Witting C, Langman CB, Assimos D, Baum MA, Kausz A, Milliner D, Tasian G, Worcester E, Allain M, West M, Knauf F, Lieske JC. Pathophysiology and Treatment of Enteric Hyperoxaluria. Clin J Am Soc Nephrol. 2021;16(3):487-495. PubMed PMID: 32900691
8. Asplin JR. The management of patients with enteric hyperoxaluria. Urolithiasis. 2016;44(1):33-43. PubMed PMID: 26645872
9. D'Costa MR, Kausz AT, Carroll KJ, Ingimarsson JP, Enders FT, Mara KC, Mehta RA, Lieske JC. Subsequent urinary stone events are predicted by the magnitude of urinary oxalate excretion in enteric hyperoxaluria. Nephrol Dial Transplant. 2021;36(12):2208-2215. PubMed PMID: 33367720
10. Singh A, Sarkar SR, Gaber LW, Perazella MA. Acute oxalate nephropathy associated with orlistat, a gastrointestinal lipase inhibitor. Am J Kidney Dis. 2007;49(1):153-7. PubMed PMID: 17185156
11. Humayun Y, Ball KC, Lewin JR, Lerant AA, Fülöp T. Acute oxalate nephropathy associated with orlistat. J Nephropathol. 2016;5(2):79-83. PubMed PMID: 27152294
12. Tilia R, Kojc N, Škoberne A. Secondary oxalate nephropathy in a patient with exocrine pancreatic insufficiency successfully treated, with complete kidney recovery. Clin Nephrol. 2021;96(1):62-67. PubMed PMID: 34643493
13. Getting JE, Gregoire JR, Phul A, Kasten MJ. Oxalate nephropathy due to 'juicing': case report and review. Am J Med. 2013;126(9):768-72. PubMed PMID: 23830537
14. Makkapati S, D'Agati VD, Balsam L. "Green Smoothie Cleanse" Causing Acute Oxalate Nephropathy. Am J Kidney Dis. 2018;71(2):281-286. PubMed PMID: 29203127
15. Raja N, Radhakrishnan H, Masilamani S. Oxalate Nephropathy: A Case Report of Acute Kidney Injury Due to Juice Diet. Cureus. 2023;15(12):e51226. PubMed PMID: 38283477
16. Chen CL, Fang HC, Chou KJ, Wang JS, Chung HM. Acute oxalate nephropathy after ingestion of star fruit. Am J Kidney Dis. 2001;37(2):418-22. PubMed PMID: 11157385
17. Albersmeyer M, Hilge R, Schröttle A, Weiss M, Sitter T, Vielhauer V. Acute kidney injury after ingestion of rhubarb: secondary oxalate nephropathy in a patient with type 1 diabetes. BMC Nephrol. 2012;13:141. PubMed PMID: 23110375
18. Sasaki M, Murakami M, Matsuo K, Matsuo Y, Tanaka S, Ono T, Mori N. Oxalate nephropathy with a granulomatous lesion due to excessive intake of peanuts. Clin Exp Nephrol. 2008;12(4):305-308. PubMed PMID: 18335167
19. Garland V, Herlitz L, Regunathan-Shenk R. Diet-induced oxalate nephropathy from excessive nut and seed consumption. BMJ Case Rep. 2020;13(11):e237212. PubMed PMID: 33257378
20. Cossey LN, Rahim F, Larsen CP. Oxalate nephropathy and intravenous vitamin C. Am J Kidney Dis. 2013;61(6):1032-5. PubMed PMID: 23548555
21. Seo JW, Lee JH, Son IS, Kim YJ, Kim DY, Hwang Y, Chung HA, Choi HS, Lim SD. Acute oxalate nephropathy caused by ethylene glycol poisoning. Kidney Res Clin Pract. 2012;31(4):249-52. PubMed PMID: 26889430
22. Xu Z, Dai Y, You Y, Huang Y, Chen H, Ye H, Yue S, Yang Q. Ethylene Glycol Poisoning With Oxalate Nephropathy and Acute Kidney Injury: A Case Report and Review of the Literature. Clin Case Rep. 2026;14(1):e71774. PubMed PMID: 41509084
23. Sanz P, Reig R. Clinical and pathological findings in fatal plant oxalosis. A review. Am J Forensic Med Pathol. 1992;13(4):342-5. PubMed PMID: 1288268
24. Garrelfs SF, Frishberg Y, Hulton SA, Koren MJ, O'Riordan WD, Cochat P, Deschênes G, Shasha-Lavsky H, Saland JM, Van't Hoff WG, Fuster DG, Magen D, Moochhala SH, Schalk G, Simkova E, Groothoff JW, Sas DJ, Meliambro KA, Lu J, Sweetser MT, Garg PP, Vaishnaw AK, Gansner JM, McGregor TL, Lieske JC; ILLUMINATE-A Collaborators. Lumasiran, an RNAi Therapeutic for Primary Hyperoxaluria Type 1. N Engl J Med. 2021;384(13):1216-1226. PubMed PMID: 33789010

PubMed Topic Searches

1. PubMed: oxalate nephropathy
2. PubMed: enteric hyperoxaluria after gastric bypass
3. PubMed: oxalate nephropathy and vitamin C
4. PubMed: oxalate nephropathy and juices
5. PubMed: ethylene glycol and oxalate nephropathy

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Connections

• Nephrology & Hepatology — the kidney and liver section
• Primary Hyperoxaluria — the inherited form of oxalate overload
• Lumasiran — the RNA medicine for primary hyperoxaluria type 1
• Kidney Stones — the same crystal in the urinary tract
• Acute Kidney Injury — the way oxalate nephropathy usually presents
• Sorrel Safety: Oxalates and Kidney Risk — oxalate in food, measured
• Spinach: Iron Absorption and Oxalates — the best-known high-oxalate leaf
• Vitamin C Toxicity: Kidney Stones — vitamin C as an oxalate source
• Rhubarb — a high-oxalate plant in the case reports
• Kidney Disease — chronic kidney disease, the commonest backdrop

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