Updated: Jan 21, 2022
Author: Bijan Shekarriz, MD; Chief Editor: Bradley Fields Schwartz, DO, FACS 

Practice Essentials

Hyperoxaluria—that is, elevated urinary excretion of the metabolic end product oxalate—can contribute to kidney stone formation and other health problems.[1] The normal upper level of urinary oxalate excretion is 40 mg (440 µmol) in 24 hours. Men have a slightly higher normal value (43 mg/d in men vs 32 mg/d in women), but this is primarily due to larger body habitus and larger average meal size rather than to any real intrinsic metabolic difference. Stone formation risk probably depends more on absolute total oxalate excretion and concentration than on arbitrary normal values.

Reflecting these normal values, the usual definition of hyperoxaluria is urinary oxalate excretion that exceeds 40 mg/day. An alternative definition of hyperoxaluria that corrects for size differences is 30 mg of urinary oxalate per 24 hours per gram of excreted creatinine. Still, the relative concentration of oxalate is probably more significant than either of these definitions acknowledges.

Etiologically, the 4 main types of hyperoxaluria are the following[2, 3] :

  • Primary hyperoxaluria (types, I, II and III)
  • Enteric hyperoxaluria
  • Dietary hyperoxaluria
  • Idiopathic or mild hyperoxaluria

Treatment depends to some extent on the underlying etiology and severity of the hyperoxaluria. However, many treatments (eg, dietary measures) can be used in any case of hyperoxaluria, and treatments can be combined for increased efficacy.

For other discussions on nephrolithiasis, see the topics Nephrolithiasis, Pediatric Nephrolithiasis, Imaging Urinary Calculi, Hypercalciuria, and Hypocitraturia.

For patient education resources, see Kidney Stones.


Oxalate Production and Function

Oxalate is an organic salt with the chemical formula of C2O4. At physiological pH levels, oxalate forms a soluble salt with sodium and potassium; however, when combined with calcium, it produces an insoluble product termed calcium oxalate, which is the most common chemical compound found in kidney stones.

Oxalate is absorbed primarily from the colon, but it can be absorbed directly from anywhere in the intestinal tract. In addition, oxalate is created from endogenous sources in the liver as part of glycolate metabolism. In the kidney, oxalate is secreted in the proximal tubule via 2 separate carriers involving sodium and chloride exchange.

Oxalate is normally produced in plants, primarily in their leaves, nuts, fruit, and bark. The amount of oxalate manufactured depends not only on the particular variety of plant but also on the soil and water conditions in which it grows. In general, plants that are grown in fields with a high concentration of ground water calcium have higher concentrations of oxalate. This is one reason why precisely calculating dietary oxalate is difficult.

Oxalate content within the same plant species can vary widely. For example, potatoes contain oxalate levels of 5.5-30 mg per 100 g, broccoli has levels of 0.3-13 mg per 100 g, and wheat bran has levels of 58-524 mg per 100 g.

Plants use oxalate as a calcium sink. Any excess calcium absorbed by the plant from ground water is extracted from the plant’s tissue fluid by the oxalate in the leaves, fruits, nuts, or bark. Eventually, the plant sheds these structures. When humans eat these plant products, they also ingest a variable quantity of oxalate. Food products from animal sources have virtually no oxalate content.

Oxalate is involved in various metabolic and homeostatic mechanisms in fungi and bacteria and may play an important role in various aspects of animal metabolism, including mitochondrial activity regulation, thyroid function, gluconeogenesis, and glycolysis. Interestingly, oxalate was first discovered in animals when sheep became ill after eating vegetation later found to have high oxalate content.

In humans, however, oxalate seems to have no substantially beneficial role and acts as a metabolic end-product, much like uric acid. If not for oxalate’s high affinity for calcium and the low solubility of calcium oxalate, oxalate and oxalate metabolism would be of little interest. Urinary oxalate is the single strongest chemical promoter of kidney stone formation. Ounce for ounce, it is roughly 15-20 times more potent than excess urinary calcium.

Daily oxalate intake in humans is usually 80-120 mg/d; it can range from 44-350 mg/d in individuals who eat a typical Western diet. The solubility of oxalate at body temperature is only approximately 5 mg/L at a pH of 7.0.

Among persons with stones, urinary oxalate levels tend to be significantly higher in summer than in winter. This may be due to the increased consumption of seasonal foods naturally high in oxalate (see the image below). In addition, the average mean urinary oxalate excretion in persons with calcium stones tends to be higher than in individuals without calcium stones.

Oxalate-rich foods. Oxalate-rich foods.

Pathophysiology and Etiology

High levels of oxalate in the system can produce various health problems, particularly kidney stone formation.

The 4 main types of hyperoxaluria—primary hyperoxaluria, enteric hyperoxaluria, dietary hyperoxaluria, and idiopathic or mild hyperoxaluria—are the results of different pathophysiologic processes.

Primary hyperoxaluria

Primary hyperoxaluria is a group of rare disorders due exclusively to genetic defects that cause a loss of specific enzymatic activity. With the normal metabolic pathway blocked, the alternative pathway that leads to oxalate production as an end-product of glyoxylate metabolism becomes extremely active, resulting in extremely high oxalate production.[4]

Three types of primary hyperoxaluria have been identified, each involving a different enzyme. All three types are transmitted as autosomal recessive traits.

Type 1 has been estimated to occur in 1 per 120,000 live births and to account for 70-80% of all diagnosed cases of primary hyperoxaluria, while types 2 and 3 are each estimated to account for approximately 10% of cases.[5] However, a population analysis by Hopp et al suggests that type 3 is underdiagnosed and/or incompletely penetrant, and is in fact as prevalent as type 1 and twice as common as type 2. Furthermore, these researchers propose that primary hyperoxaluria is an order of magnitude more common than determined from clinical cohorts, with a prevalence of approximately 1 per 58,000 and a carrier frequency of approximately 1:70.[6]

Unclassified cases also occur, in patients who present with typical signs and symptoms but lack any identifiable mutation in the genes known to be associated with primary hyperoxaluria.[5, 7]

In type 1 primary hyperoxaluria, the missing enzyme is alanine-glyoxylate aminotransferase (AGT), which is normally found only in the hepatic peroxisomes. This enzyme is necessary to detoxify glyoxylate.[8] When AGT is lacking, oxalate production soars.[2]

Pyridoxine (vitamin B6) is a cofactor in this chemical pathway, which normally converts glyoxylic acid (C2 H2 O3) to glycine.[9] When the pathway is blocked because of a deficiency or absence of AGT, the result is high levels of glycolic and oxalic acid, which readily convert to oxalate.  Oxalate, which is soluble, complexes with calcium to form calcium oxalate, which is insoluble. Calcium oxalate crystallizes and causes nephrocalcinosis and eventually the development of end-stage renal failure, usually in childhood.

A retrospective cohort study by Harambat et al of 155 patients with primary hyperoxaluria type 1 found that in patients who underwent DNA analysis, the p.Gly170Arg AGXT mutation was the most common and was associated with a better prognosis. The median age at end-stage renal disease was 47 years in p.Gly170Arg homozygotes and 35 years in heterozygotes. In patients with other mutations, the median age at end-stage renal disease was 21 years.[10] Phenotype-genotype correlation by Hopp et al, using data from the Rare Kidney Stone Consortium Primary Hyperoxaluria registry, confirmed that the AGXT p.G170R mistargeting allele resulted in milder disease.[6]

In type 2 primary hyperoxaluria the missing enzyme is glyoxylate reductase/hydroxypyruvate reductase (GRHPR), which can be detected in leukocyte preparations. This deficiency promotes the conversion of glyoxylate to oxalate.[8, 11] Type 2 has been considered to have a more favorable prognosis than type 1, a review of the largest cohort of patients (n=101), from the OxalEurope registry, found that median age at first symptom was 3.2 years; aget at diagnosis for index cases was 8.0 years. The majority of patients (82.8%) presented with urolithiasis.[12] Approximately 25-50% of individuals with type 2 progress to kidney failure.[12, 13] Pyridoxine supplementation, which may benefit some patients with type 1 primary hyperoxaluria, is generally not effective in patients with type 2 primary hyperoxaluria.

Type 3 primary hyperoxaluria is due to mutations in the HOGA1 (formerly DHDPSL) gene.[14, 15] Research supports a loss-of-function mechanism, resulting in a build-up of 4-hydroxy-2-oxoglutarate and/or its metabolites in mitochondria with subsequent leakage into the cytosol, where it can be converted to glyoxylate.[16] Type 3 has been reported as a possible cause in patients with idiopathic calcium oxalate stones.[16] Onset of symptoms occurs at a younger age than in types 1 and 2 but decline in kidney function is slower; progression to chronic kidney disease stage 3 or worse has been found in 5.4%-13.9% of patients, with end-stage renal disease rarely reported.[14, 17, 16, 18, 6, 19, 20]

Enteric hyperoxaluria

Enteric hyperoxaluria accounts for approximately 5% of all cases of hyperoxaluria. It is due to a gastrointestinal problem usually associated with chronic diarrhea. Malabsorption from any cause can result in enteric hyperoxaluria. Such causes include intestinal bacterial overgrowth syndromes, fat malabsorption, chronic biliary or pancreatic disease, various intestinal bypass surgical procedures, inflammatory bowel disease, or any medical condition that causes chronic diarrhea.[21]

The basic mechanism is competition for the available ingested calcium, the leading intestinal oxalate-binding agent. Most of the bile acids produced during digestion are reabsorbed in the proximal intestinal tract. When this fails to occur, calcium and magnesium bind to these bile acids through saponification.[22] This leaves very little free calcium available for absorption or binding with oxalate in the lower intestinal tract. Without the calcium necessary to adequately bind oxalate in the intestinal tract, additional oxalate is absorbed and then excreted in the urinary tract.

Increased intestinal membrane oxalate transport and absorption may also occur through direct exposure of the intestinal lining to excess bile salts and fatty acids, which increases the oxalate permeability of the colonic mucosa.[23]

Hyperoxaluria has been reported to be the most common urinary metabolic abnormality in patients with stones who have undergone bariatric surgery.[24, 25] Oxalate absorption by the colon has been shown to increase up to 300-fold following small-bowel bypass surgery; therefore, these individuals must be screened for enteric hyperoxaluria. In some severe cases, the bypass may need to be reversed to control the hyperoxaluria. The recent proliferation of bariatric surgery cases may result in an increased prevalence of enteric hyperoxaluria in the future.[24, 25]

Dietary hyperoxaluria

Previously, dietary oxalate was thought to play a relatively minor role in hyperoxaluria and to account for only 10-20% of the total urinary oxalate produced. Recent evidence suggests that dietary oxalate plays a much more important role and may be responsible for 50% of the total urinary oxalate.[26, 27, 28] In one study, dietary sources were found to be directly responsible for 80% of the total excreted oxalate.

A high intake of oxalate-rich foods (eg, chocolate, nuts, spinach) and a diet rich in animal protein can result in hyperoxaluria. Low dietary calcium intake can also result in hyperoxaluria via decreased intestinal binding of oxalate and the resulting increased absorption. Ascorbic acid can be converted in oxalate, resulting in increased urinary oxalate levels.

Many patients, perhaps as many as 80%, have an abnormal or altered cellular membrane oxalate transport mechanism, which causes abnormally high absorption of dietary oxalate.

Others may have a deficiency of Oxalobacter formigenes, an intestinal facultative anaerobic bacterium that naturally digests oxalate. When this bacterium is lost through prolonged antibiotic use or other reasons, increased intestinal oxalate absorption is likely. Some studies have shown a correlation between decreased activity of this bacterium in the intestine and hyperoxaluria and stone formation.[29, 30, 31]

Oxalobacter is relatively resistant to penicillin and sulfa but sensitive to macrolides, fluoroquinolones, and tetracyclines. Patients with calcium oxalate stones who have lost their natural intestinal Oxalobacter are found to have 40% higher average urinary oxalate levels than patients with calcium oxalate stones who have normal intestinal Oxalobacter colonies. Oxalobacter usually colonizes the intestinal tract at approximately age 3 years. Once lost, recolonizing Oxalobacter in the intestinal tract is very difficult.

Bioavailability of ingested oxalate, dietary calcium and magnesium levels,[32, 22] intestinal transit time, use of sodium cellulose phosphate (which removes calcium and magnesium from the intestine), and lack of intestinal oxalate binders can all affect oxalate absorption. Ethylene glycol ingestion and methoxyflurane exposure can also cause hyperoxaluria through a hepatic metabolic pathway. The rest are thought to be caused by metabolic or hepatic activity.

Idiopathic hyperoxaluria

This is by far the most common variety of hyperoxaluria observed in patients with calcium oxalate stones. It may be due to a simple dietary excess of high-oxalate food sources or to increased endogenous oxalate production. While originally thought to be caused mainly by endogenous oxalate production, more recent evidence suggests that up to 50% or more of urinary oxalate is related to diet.

In 1986, Baggio et al found an enhanced, altered red blood cell membrane oxalate transport mechanism in approximately 80% of patients with idiopathic kidney stones that was not present in the siblings of these patients, who did not have stones.[33] The variable response among patients to a controlled oxalate diet also suggests that a genetic component may play a role in the development of hyperoxaluria by modifying intestinal oxalate absorption.

The problem with oxalate is its strong chemical affinity for calcium and the relatively low solubility of the resulting salt. Most people have a relative supersaturation of calcium oxalate in their urine, which is kept from precipitating by various factors, including dilutional volume and specific inhibitors such as citrate. Optimizing these other risk factors has a beneficial effect on reducing calcium oxalate stone production.



Hyperoxaluria (excessive urinary oxalate) is a common abnormal finding in patients with calcium oxalate kidney stones. Some degree of excessive urinary oxalate is found in 20-30% of all patients with recurrent calcium oxalate stones. Approximately 30 million persons in the United States have kidney stone disease, and 1.2 million new cases are encountered each year. The most common type of kidney stone is calcium oxalate. Although hypercalciuria may be the more common metabolic problem, excess urinary oxalate is a much stronger promotor of urinary stone formation than excess urinary calcium.

Hyperoxaluria seems to be a greater problem in countries that are more highly developed. In Japan, an increasing incidence of calcium oxalate stone disease seems to have accompanied gradual changes in dietary trends. As animal protein and fat intake increases among the Japanese population, oxalate absorption, oxaluria, and calcium oxalate stone disease also increase. Increased dietary fat allows for an increase in calcium complexation, with fatty acids causing a mild form of enteric hyperoxaluria. Primary hyperoxaluria is more common among Muslims.

Kidney stones are more common in whites than in blacks. This is well-established and is thought to be primarily due to the difference in average socioeconomic status and dietary influences.

An intriguing study from South Africa by Lewandowski et al found that urinary oxalate excretion after a controlled oral oxalate load was much higher in whites than in blacks.[34]  This was thought to be due to increased intestinal oxalate transport in the white study group.

A similar study by Rodgers and Lewandowski found that a low-calcium diet caused a statistically significant increase in urinary oxalate only in blacks.[35]  The cause for these racial differences has not been determined, but genetic factors are thought to be involved.

No significant differences in mean urinary oxalate excretion levels or concentration between geriatric and younger cohorts of individuals with calcium oxalate stones have been found.[36, 37]   Primary hyperoxaluria presents primarily as a pediatric disease, but adult onset is also observed. Median age for symptom onset in primary hyperoxaluria is as follows[6] :

  • Type 1: 5.2 years (range, 0.1-53.0 yr)
  • Type 2: 7.4 years (range, 0.6-42.0 yr)
  • Type 3: 2.6 years (range, 0.3-31.0 yr)

Kidney stones are 3 times more common in men than in women, but the reason for this difference is not always clear. Different reference ranges of several urinary metabolites (eg, uric acid, calcium, oxalate) illustrate the difficulties in determining the actual cause of stones in different populations. It is unknown whether the different values are the result of differences in metabolism related to the effects of sex hormones or are incidental to the known differences in dietary intake and body weight.[38]

That kidney stones are equally prevalent among males and females in childhood and in the postmenopausal age group suggests that female sex hormones may play a somewhat protective role. A study involving 4 groups of rats seems to confirm this.[39] Two groups underwent oophorectomy; a third underwent a sham surgery. One of the oophorectomized groups received supplemental estrogen and progesterone. Except for the control group, all groups were given ethylene glycol and vitamin D supplementation to induce calcium oxalate kidney stone formation.

The findings indicated that the urinary oxalate excretion rate was significantly higher in the oophorectomized group than in the groups that retained their ovaries or received supplemental female sex hormones. The renal calcium content, crystal deposition, and osteopontin levels were also higher in the oophorectomized group. The investigators concluded that female sex hormones may protect against calcium oxalate stone formation, with oxalate excretion being a key factor.

A similar study by Fan et al found the same protective benefit from estrogen.[40] Neutered rats given estrogen supplementation had lower levels of urinary and plasma oxalate and did not develop calcium oxalate crystals, even when given ethylene glycol to induce hyperoxaluria. In comparison, 88% of the rats given testosterone produced significant calcium oxalate crystals and had higher serum and urine oxalate levels, which suggests that testosterone plays a significant role in the development of calcium oxalate stones and hyperoxaluria in men.[41]

Another animal study, also by Fan et al, described significantly decreased urinary oxalate levels in both castrated rats and those treated with high-dose finasteride (Proscar), suggesting that dihydrotestosterone may be responsible for some of the differences noted in oxalate excretion between men and women.[42]

Clearly, more research would be helpful in determining the true role of sex hormones in hyperoxaluria and calcium oxalate stone disease.

Some evidence suggests that, for oxalate, the differences are due purely to body weight.[43] When this is considered and corrected with the alternative definition of 30 mg of urinary oxalate per 24 hours per gram of excreted creatinine, the results of one study showed essentially no unexplained differences.

However, a review by Gary Curhan of Harvard based on several very large series found that men have substantially higher mean urinary oxalate and uric acid levels than women in similar weight categories. This suggests that men have higher average urinary oxalate levels than women, even when weight differences are corrected.[44]

Powell et al reviewed the issue of obesity associated with kidney stone formation based on a large national database[43] and found that, in general, women who were obese and had stones tended to be at somewhat higher risk than women who were not obese who had stones. However, little, if any, difference was observed in men.

In both men and women, mean urinary oxalate levels were approximately one third higher in those who were obese and had stones than in those who were not obese and had stones. However, when urinary volume and concentration were considered, the mean average urinary oxalate concentration among men who were obese and had stones was only slightly increased; the same was not true among women who were obese and had stones.

Women have a higher response rate to pyridoxine therapy for mild and moderate hyperoxaluria disorders than men do. The reason for this discrepancy is unclear.

The mean urinary glycosaminoglycans concentration is lower in men with stones than in women with stones; this may play a role in the difference in the stone formation rate between the sexes.



The consequences of hyperoxaluria, like those of all forms of stone disease, are related to stone formation and subsequent damage to the urinary tract. These may include pain, renal obstruction, urosepsis, acute kidney injury, chronic kidney disease, and even death. Primary hyperoxaluria in particular is associated with the most serious health consequences. Approximately half of patients diagnosed with this disorder develop end-stage renal disease, and the mortality rate, particularly in infants, is high (> 50%).[45]

Without treatment, the prognosis for these patients is poor. Chronic kidney disease develops in 50% of patients with primary hyperoxaluria by age 15 years and in 80% by age 30 years. Normal dialysis for uremia cannot remove enough serum oxalate to protect the kidneys and other organs from widespread calcium oxalate deposition (ie, oxalosis) and calcium oxalate stone production.

The prognosis of patients with primary hyperoxaluria depends on early treatment and management of hyperoxaluria and associated renal deterioration. If medical treatment cannot help the patient maintain a normal oxalate level, nephrocalcinosis may develop, with subsequent renal failure. In this situation, combined liver-renal transplantation is necessary for cure.[46, 47]

The prognosis of patients with enteric and mild hyperoxaluria is favorable if medical management and dietary modifications are followed. Periodic retesting using 24-hour urine assessments should be performed regularly to monitor compliance and treatment effectiveness.


Clinical Manifestations

The median age for presentation of initial symptoms related to hyperoxaluria is 5 years. Oxalate deposition can occur in other organs (eg, bones, joints, eyes, heart). In particular, bone tends to be the major repository of excess oxalate in persons with primary hyperoxaluria. Bone oxalate levels are negligible in healthy individuals. Oxalate deposition in the skeleton tends to increase bone resorption and to decrease osteoblast activity.

Because symptoms occur relatively late and are associated with serious complications, all pediatric patients who have stones should be screened for hyperoxaluria. Discovering this condition in siblings may allow earlier testing, detection, diagnosis, and preemptive therapy. Screening for hyperoxaluria is also indicated in adult patients with recurrent kidney stones.[48]

In primary hyperoxaluria, urinary oxalate excretion is typically more than 100 mg/d. Primary hyperoxaluria may result in kidney failure due to nephrocalcinosis. In the past, liver biopsy was typically used to identify the enzyme defect in the different types of primary hyperoxaluria; however,  with the increasingly lower cost and improved sensitivity of molecular genetic testing, the need for liver biopsy has substantially decreased.[5]

Enteric hyperoxaluria is characterized by very high urinary oxalate levels (usually 80 mg/d or more) and hypocalciuria, with urinary calcium excretion usually less than 100 mg/d. Generally, a chronic diarrheal state is present, leading to hypocitraturia and relative dehydration in addition to the hyperoxaluria. It should be considered in any patient with calcium oxalate stone disease and any type of chronic diarrhea.

Other conditions associated with enteric hyperoxaluria include fat malabsorption, steatorrhea, inflammatory bowel disease, pancreatic insufficiency, biliary cirrhosis, and short-bowel syndrome.

Urinary oxalate excretion in idiopathic or mild hyperoxaluria is usually 40-60 mg/d. Most patients with relatively mild hyperoxaluria (approximately 40-60 mg/d) have dietary hyperoxaluria.

Occasionally, oxalate poisoning is reported. Symptoms of oxalate poisoning include local irritation and systemic effects. Patients experience burning of the mouth, pharynx, and esophagus; swallowing difficulties; diarrhea; bradycardia; cardiac arrhythmia; heart failure; and renal failure. In rare cases, convulsions and unconsciousness can develop.

Severe poisoning has been caused by ingestion of the common household plant Dieffenbachia, with symptoms of severe corrosive burns of the mouth, oropharynx, esophagus, and stomach.[49]  See Plant Poisoning from Oxalates.

All forms of hyperoxaluria are associated with recurrent urolithiasis.


Laboratory Studies

Obtain a 24-hour urine collection and include analysis for total creatinine (ie, to determine adequacy of the collection) and other urinary chemistry components that can lead to stone formation, such as oxalate, calcium, uric acid, sodium, phosphate, and total urinary volume. Include an analysis for inhibitors of stone formation, such as potassium, citrate, and magnesium.[44]

Assess total urine volume and pH to determine the contribution of dehydration or pH to the tendency toward crystallization.

All major urinary risk factors (eg, calcium, oxalate, citrate, uric acid, total volume, sodium, phosphate, magnesium) should be periodically reassessed with 24-hour urine collection to monitor treatment efficacy, to identify new kidney stone metabolic risk factors, and to monitor patient compliance.

Repeat testing every 2-3 months while various treatment plans are used until acceptable urinary chemistry levels are reached or maximum therapy has been instituted. Thereafter, retesting every 1-2 years depending on the clinical situation is usually sufficient. The overall success of any stone preventive therapy program depends on the individual patient’s compliance with long-term preventive therapy and the continuous maintenance of an adequate urinary volume.

Obtain serum creatinine levels to evaluate kidney function. Serum calcium levels may be useful in differentiating hypercalcuria from hyperparathyroidism. Tests to measure plasma oxalate levels have become commercially available, so plasma as well as urinary oxalate should be measured now, as blood tests can reveal elevated levels.


Computed Tomography

No specific imaging studies help to identify hyperoxaluria, but calcium oxalate nephrolithiasis can be easily diagnosed. For more information on imaging studies in the evaluation of urolithiasis, please see Nephrolithiasis: Acute Renal Colic.

Computed tomography (CT) scanning, specifically spiral CT scanning without intravenous contrast, is rapidly replacing intravenous pyelography (IVP) (see below) as the preferred method for evaluating patients with acute flank pain who may have a urinary stone.

CT scanning is faster, requires less effort, does not require any potentially hazardous intravenous contrast, and provides useful information on alternatives in the differential diagnosis. Uric acid stones show up clearly on CT scans, but stones made of protease inhibitor medications do not. Intravenous contrast can be used selectively, if needed, to clarify the diagnosis.

Limitations of CT scanning include higher cost, an inability to assess renal function, and an inability to differentiate radiopaque from radiolucent stones. In addition, the precise shape and surgical orientation of a stone can be difficult to determine based on CT scan findings alone. This can be corrected by adding kidney-ureter-bladder (KUB) radiography (see below), which helps not only to determine the size, shape, and location of the stone but also to determine its calcium content based on the degree of radiopacity.

CT scanning cannot be used in pregnant women because it is associated with more significant x-ray exposure. In addition, a small distal ureteral stone in a patient with multiple pelvic calcifications and minimal hydronephrosis may be almost impossible to identify with CT scans alone.


Intravenous Pyelography

IVP images offer the best road map of the upper urinary tract and ureteral anatomy. They can easily reveal the precise location of stones in the urinary tract. They also provide valuable information about relative kidney function that CT scanning and ultrasonography cannot offer. Any anatomical anomalies involving urinary flow can more readily be revealed with IVP, and it often costs less than CT scanning.

Disadvantages of IVP include possible nephrotoxicity and allergy to the injected contrast agent. In general, IVP cannot be safely performed in patients whose serum creatinine level is higher than 2 mg/dL, and more time is required to perform IVP than CT scanning. The IVP provides only very limited information concerning other potential diagnoses that might mimic acute renal colic, such as abdominal aortic aneurysm, which is visualized much more easily on the CT scan.

In pregnant patients, limited IVP studies can be performed but should be minimized as much as possible.


Renal Ultrasound and KUB Radiography

When used in combination, renal ultrasonography and KUB radiography can be useful initial screening tools for hydronephrosis and urolithiasis. Ultrasonography is the primary diagnostic tool in pregnant patients with a suggestive renal or ureteral calculus. KUB radiography can be performed in pregnant patients but should be minimized as much as possible.

For more information on the management of kidney stones during pregnancy, see Pregnancy and Urolithiasis.


Dietary Questionnaire

Dietary excess of oxalate-containing foods (eg, spinach, nuts, rhubarb, cranberry products) can cause hyperoxaluria. Dietary excess of vitamin C can also increase oxalate absorption and excretion, although the degree and importance of vitamin C in the development of calcium oxalate stone disease is somewhat controversial.[9]

Evaluate oral fluid intake to exclude dehydration as a component of hyperoxaluria. Fluid intake should be sufficient to generate 2000 mL or more of urine per day.

High-protein (meat) intake is known to be a significant risk factor for calcium stone disease because of its effect on urinary calcium and uric acid. A 2001 European study by Nguyen et al evaluated the effect of a diet high in meat protein on urinary oxalate in healthy subjects versus patients with idiopathic calcium stones and those with mildly hyperoxaluric calcium stones.[50]

The investigators found that approximately one third of those with idiopathic calcium stones responded to the high meat-protein intake with a significant increase in urinary oxalate excretion, while no effect was noted in healthy subjects. This suggests that, in addition to its effects on urinary calcium and uric acid levels, excessive meat-protein intake may increase urinary oxalate excretion.


General Principles of Treatment

Treatment of hyperoxaluria depends somewhat on the underlying etiology and severity of the hyperoxaluria. Many of the treatments mentioned can be used in any case of hyperoxaluria, and they can be combined for increased efficacy.

Initial first-line therapies include a low-oxalate diet while maintaining adequate calcium intake, pyridoxine (vitamin B6), increased fluids, and optimization of other calcium oxalate nephrolithiasis risk factors. Limit ingestion of vitamin C and cranberry juice products.[9, 51] Calcium supplements are the initial treatment of choice for enteric hyperoxaluria,[52] along with a low-fat diet, antidiarrheal therapy, and sufficient potassium citrate supplementation to maintain optimal urinary citrate levels. Vitamin E can be safely added to any hyperoxaluria treatment regimen.

When initial treatment is insufficient to adequately control excessive urinary oxalate excretion, add orthophosphate supplementation, magnesium supplementation, or both. Both of these therapies can have adverse gastrointestinal effects; therefore, dosages should be titrated to tolerability. Phosphates are preferred in patients with hypophosphatemia or a low level of urinary pyrophosphate, while magnesium therapy is selected in patients with hypomagnesemia or hypomagnesuria.

Oxalate-binding agents such as calcium (preferred) or iron (if hypercalciuria is present) can be used. A higher dose of pyridoxine, up to 400-500 mg/d in divided doses, may also be helpful.[53]

If further treatment is necessary, cholestyramine can be added. Pentosan polysulfate (Elmiron) can be considered, although its actual effectiveness is unclear.[54, 55] Pushing fluids to increase urinary output to 3-4 L/d may be helpful. Other risk factors should be further optimized.

In cases of renal failure, intensive dialysis can be considered. Liver or combined liver-kidney transplantation should be considered in patients with primary hyperoxaluria.[46, 47, 56]


Treatment of Acute Oxalate Poisoning

Treatment for acute oxalate poisoning includes gastric lavage with a calcium solution such as 0.15% calcium hydroxide solution. Brisk diuresis is stimulated with rapid hydration to avoid calcium oxalate crystallization in the kidney. Sodium bicarbonate and sodium hydroxide should not be used because sodium oxalate is readily absorbed, increasing the systemic oxalosis effects.


Treatment of Primary Hyperoxaluria

Patients with primary hyperoxaluria usually present with a urinary oxalate level in excess of 100 mg/d. Early medical treatment is required to decrease the oxalate level and to prevent deterioration of renal function. Early liver-kidney transplantation is often required for definitive cure. However, the survival rates and organ survival rates in patients who undergo treatment for type I hyperoxaluria are inferior to such rates in general transplant patients.[57, 58, 59]

Dietary oxalate restrictions are of no substantial benefit in this type of hyperoxaluric disease. Several medications have been useful.

New and future treatment modalities under investigation include probiotic supplementation,[60] chaperones and hepatocyte cell transplantation, and recombinant gene therapy to replace the enzyme.[61]

High-dose pyridoxine (vitamin B6)

Pyridoxine deficiency is known to increase urinary oxalate excretion. High-dose pyridoxine may reduce the production of oxalate by enhancing the conversion of glyoxylate to glycine, thereby reducing the substrate available for metabolism to oxalate.[8] A daily dose of 150-500 mg may be required to sufficiently reduce the oxalate level. A normal urinary oxalate level (< 40 mg/d) can be achieved in some patients.[53]

Treatment of pyridoxine-resistant primary hyperoxaluria frequently involves combinations of all available therapies and may ultimately entail kidney-liver transplantation.[62]


Orthophosphate, in combination with pyridoxine, has been used effectively in the treatment of primary hyperoxaluria. Milliner et al and others have demonstrated long-term treatment benefits with this combination.[63] The phosphate increases urinary pyrophosphate and complexes with calcium, thus decreasing the urinary calcium level, while pyridoxine reduces urinary oxalate excretion.

Phosphate therapy should not be used in patients with chronic kidney disease.


Supplementation with magnesium in the form of magnesium hydroxide and magnesium oxide has been used. Magnesium can complex with oxalate in the intestinal tract, reducing the level of available free oxalate and urinary calcium oxalate supersaturation. It does not directly affect the increased endogenous production of oxalate.[32, 22]

When used in combination with pyridoxine, significant reductions in urinary oxalate levels have been noted.

Increased urinary volume

Increasing urinary volume is essential. Optimal 24-hour urinary volumes of 3-4 L/d may be needed to ameliorate the effects of severe hyperoxaluria. Increasing urine volume usually requires multiple nightly disruptions of sleep for extra water consumption.

Thiazides have been shown to decrease urinary oxalate excretion somewhat, possibly by decreasing intestinal oxalate transport.

Other factors that can contribute to stone formation, such as urinary citrate and uric acid, need to be optimized.

Glycosaminoglycans (pentosan polysulfate)

Supplementation with glycosaminoglycans may help to reduce calcium oxalate crystallization and stone formation by reducing crystal aggregation. It also may decrease intestinal oxalate transport and urinary oxalate excretion.[64, 54, 55]


Lumasiran (Oxlumo) is an RNA interference (RNAi) agent that targets hydroxyacid oxidase (HAO1), which then reduces levels of the glycolate oxidase (GO) enzyme. Decreased GO levels reduce the amount of available glyoxylate, a substrate of oxalate production.[65]  

In November 2020, the US Food and Drug Administration (FDA) approved lumasiran for treatment of primary hyperoxaluria type 1 (PH1). Approval was based on the ILLUMINATE-A and ILLUMINATE B trial. The randomized, placebo-controlled ILLUMINATE-A trial (n=39; ages 6-61 years), demonstrated a 65% reduction of 24-hr urinary oxalate levels in the lumasiran-treated group compared with an average 12% reduction in the placebo group. By month 6 of the study, 52% of the lumasiran-treated group reached a normal 24-hr urinary oxalate level, compared with no patients in the placebo group. ILLUMINATE-B, which was an open-label study of lumasiran treatment in 16 PH1 patients younger than 6 years, showed an average 71% decrease in urinary oxalate by month 6 of the study.[66]

Intensive dialysis

Intensive dialysis is needed in patients with primary hyperoxaluria and significant kidney failure to minimize serum oxalate levels and to reduce the body stores of oxalate. The standard dialysis regimen for simple uremia is not adequate to remove sufficient oxalate to prevent stone formation or other systemic effects of oxalosis in severe hyperoxaluric states associated with kidney failure. Daily hemodialysis sessions are required that last 6-8 hours per day, which is considerably more dialysis than the typical patient with end-stage kidney disease needs.[67]

Removal of the native kidneys often is recommended at the time of kidney transplantation because the native kidneys often have significant damage and residual stones, which makes them particularly susceptible to recurrent infections and obstruction.


Treatment of Enteric Hyperoxaluria

Several mechanisms have been postulated to help explain the development of hyperoxaluria in patients with intestinal disease. These include increased colonic permeability, reduced free intestinal calcium available to complex with oxalate, and decreased levels of O formigenes in the intestine (which can degrade intestinal oxalate). In any event, the intestinal absorption of oxalate is markedly increased. Based on the pathophysiology, pyridoxine has only a limited beneficial effect in this condition because endogenous oxalate production is not affected.


Calcium supplementation is usually beneficial and is the preferred initial treatment option for most patients with enteric hyperoxaluria.[52] Relatively severe hypocalciuria due to calcium binding to nonabsorbed fatty acids, with eventual loss in feces, usually accompanies enteric hyperoxaluria; therefore, the supplemental calcium is unlikely to cause a hypercalciuric state. In addition, calcium supplementation may be beneficial in sustaining bone mass. Supplemental calcium binds strongly to any free intestinal oxalate, preventing absorption.

The most commonly recommended form is calcium citrate, because the citrate component offers an additional benefit as a natural inhibitor of calcium oxalate urinary crystallization. Calcium citrate without vitamin D should be used because the calcium should remain in the intestinal tract as long as possible to better interact and bind with the available oxalate. Calcium carbonate can also be used but does not have the same beneficial effect as citrate.

Iron or aluminum

Iron can act as a substitute intestinal oxalate-binding agent. Experiments in rats have demonstrated its effectiveness, although calcium is the preferred oxalate-binding agent whenever possible.

Aluminum can also limit oxalate absorption through intestinal binding, but the danger of aluminum toxicity is a concern.


Magnesium also binds free intestinal oxalate and can prevent its absorption; however, magnesium may cause diarrhea in patients with inflammatory bowel disease. This may lead to subsequent stone-promoting effects such as lower urinary pH, decreased urinary volume, and hypocitraturia.[22]

Potassium citrate

Oxalate transport in the proximal renal tubule is indirectly coupled with an Na/H exchanger, which suggests that urinary alkalinization with potassium citrate may reduce urinary oxalate excretion. This has been shown to occur in an animal model, suggesting an additional possible benefit of potassium citrate therapy in patients with calcium oxalate stones.

Potassium citrate in dosages of 40-60 mEq/d in divided doses is beneficial to increase the urinary pH and citrate level. This is particularly helpful in patients with significant diarrhea or hypocitraturia. If the diarrhea can be controlled, the potassium citrate dosage may need to be modified. Control of diarrhea should be a priority whenever possible. Reversal of jejunoileal bypass surgery is sometimes necessary to correct this problem.


Cholestyramine is a nonabsorbable anion exchange resin that selectively binds bile salts, fatty acids, and intestinal oxalate. It can also help reduce the diarrhea associated with enteric hyperoxaluria.

Cholestyramine is available as a dry powder that needs to be mixed with 60-180 mL of water, juice, milk, or other noncarbonated beverages. Preparing the mixture in advance and keeping it refrigerated sometimes helps make it more palatable. Alternatively, crushed pineapple or applesauce can be used as a vehicle for the medication. The usual dosage is 1-4 g 3-4 times daily with meals.

The main adverse effect of cholestyramine is constipation. Dosages larger than 24 g/d are discouraged because they tend to cause steatorrhea. Because chloride is released from the resin, hyperchloremic acidosis is a potential complication. Cholestyramine interferes with the absorption of many other medications, especially thiazide diuretics. If used together, they should be given at widely separated intervals.

Patients on long-term therapy may need fat-absorbable vitamin supplements (vitamin A and folic acid), and cholestyramine use may slightly increase the risk of vitamin K deficiency.

Low-fat, reduced meat-protein, and low-oxalate diets

Diets containing reduced amounts of fat, meat protein, and oxalate are helpful if the patient can tolerate and sustain them.[68] In particular, a low-fat diet helps both the hyperoxaluria and the chronic diarrhea that accompanies enteric hyperoxaluria. The low-fat diet has minimal effect on other types of hyperoxaluria, although it can be recommended for other health reasons.

Increased urinary volume

Increased fluid intake to expand urinary volume is also recommended, not only to restore fluid lost through the digestive tract but also to act as a dilutional inhibitor of crystal and stone formation.

Organic marine hydrocolloid

Organic marine hydrocolloid (OMH) is a high-molecular-weight polymer extracted from plants and seaweed. It was found to be helpful in one study on patients with enteric hyperoxaluria, as reported by Lindsjo and colleagues.[69]

A specially processed OMH charged with calcium and zinc was able to reduce urinary oxalate by an average of more than 20%. Stone production declined, and chronic diarrhea was improved in 70% of patients. While the study had a very limited number of patients, their clinical enteric hyperoxaluria situation was severe.


Treatment of Idiopathic and Mild Hyperoxaluria

Mild hyperoxaluria (40-60 mg/d) occurs in 5-50% of patients with stones who have no other medical conditions. After hypercalciuria, it is the most commonly identified metabolic abnormality found in patients with recurrent stone formation.

Dietary oxalate restriction, pyridoxine treatment, and other measures

This is an important aspect of management in this group. Foods that contain high oxalate levels (eg, spinach, rhubarb, beets, nuts, chocolate, tea, wheat bran, strawberries) should be avoided, while moderate calcium intake in the form of dairy products should be encouraged. Even foods with only a moderate amount of oxalate may need to be limited if large amounts are frequently ingested. Long-term dietary oxalate restriction has not been shown to have any deleterious effects. Increased fluid intake and a low-fat low–meat-protein diet are also suggested.

A lack of response to dietary measures alone may indicate either increased intestinal oxalate transport or inherent endogenous overproduction that may respond to pyridoxine in a manner similar to cases of primary hyperoxaluria.


Pyridoxine has been investigated and found to be helpful in many cases, but dosages up to 400-500 mg/d may be needed. Approximately 50% of patients respond to pyridoxine treatment. For unknown reasons, pyridoxine therapy for hyperoxaluria seems to be more beneficial in women than in men.[53]

Phosphate or magnesium

Other measures, such as phosphate or magnesium supplementation, can also be used. Combination therapy of pyridoxine with magnesium, oral phosphates, or both has been shown to be efficacious in reducing stone recurrences and urinary oxalate excretion.[62, 22, 70]

Vitamins C and E

Excessive vitamin C ingestion should be avoided because of the potential for its conversion into oxalate.[9]

Although it is unclear whether vitamin E has any efficacy in hyperoxaluric humans, adding this therapy to the treatment regimen is of little risk.[71, 72]


Calcium supplementation with calcium citrate to increase intestinal oxalate binding is rarely necessary to control stone production.[52]


Cholestyramine is rarely needed to control nephrolithiasis in these relatively mild cases of hyperoxaluria.

Glycosaminoglycans (pentosan polysulfate)

Glycosaminoglycan supplementation may be of some benefit in preventing calcium oxalate stone formation when other methods are insufficiently effective and stone production continues. Preventing calcium oxalate crystal aggregation is probably the most significant effect of pentosan polysulfate, although it may also have some limited direct beneficial effect on intestinal oxalate transport.[64, 54, 55]

Cranberry (juice and tablets) and other measures

Although often recommended for urinary tract symptoms and urinary tract infections (UTIs), cranberry juice and tablets can increase urinary oxalate by as much as 40% or more because of their relatively high oxalate content and should be avoided.[51]

Low-meat-protein diet

Excessive meat-protein intake should be avoided because it has been shown to significantly increase urinary oxalate excretion in approximately one third of all patients with idiopathic calcium kidney stones.


Dietary Measures

As with other patients with stones, adequate fluid intake and a low-salt and low-protein diet should be encouraged. Ideally, sufficient fluid intake to maintain a urinary output of more than 2 L/d is important, especially in patients with chronic diarrheal states due to intestinal disease. Patients with severe hyperoxaluria may need to achieve a daily urinary output of 3 or even 4 L/d to avoid stone formation.[73]

Patients with enteric and idiopathic hyperoxaluria should avoid oxalate-rich foods such as spinach, tea, chocolate, strawberries, nuts, and peanut butter (see the image below). Furthermore, dietary calcium intake through dairy products should be maintained to decrease urinary oxalate levels. Ascorbic acid may be converted to oxalate in the oxalate metabolic pathway; therefore, the use of ascorbic acid–containing medications should be avoided.

Oxalate-rich foods. Oxalate-rich foods.

Surgical Management

Surgical interventions that may be indicated include lithotripsy and kidney-liver transplantation.


The principles of surgical management in patients with stones who also have hyperoxaluria do not differ from the management principles in other patients with urolithiasis. These patients form calcium oxalate stones that can be monohydrate or dihydrate in nature. Calcium oxalate monohydrate calculi are one of the hardest stone types to fragment with current lithotripsy modalities and may require multiple treatments based on size and location.

Extracorporeal shockwave lithotripsy can be used for renal and ureteral calculi. Intracorporeal lithotripsy using electrohydraulic, pneumatic (Lithoclast), ultrasonic, and holmium laser modalities can all be successful in the management of ureteral and large-burden renal calculi. Ureteroscopic or percutaneous access is required in these cases.

Kidney-liver transplantation

Young patients with primary hyperoxaluria may develop chronic kidney disease due to nephrocalcinosis. Kidney transplantation alone is associated with recurrent stone formation attributable to the persistence of abnormal glyoxylate metabolism in the liver. Therefore, a combined kidney-liver transplantation is necessary and should be performed as early as possible to achieve cure.

In selected patients, early liver transplantation prior to the development of overt renal failure may preserve the native kidneys, thus avoiding kidney transplantation.[47] In general, transplantation is considered when the glomerular filtration rate (GFR) falls to below 25 mL/min/1.73 m2.[74] Kidney transplantation alone is insufficient because the liver defect causing the hyperoxaluria is not corrected.



Consultation with a general surgeon may be required in cases of primary hyperoxaluria if liver transplantation is indicated.[47] Patients with enteric hyperoxaluria also may require a consultation with a general surgeon.

Other consultations with a medical specialist may be indicated for follow-up care in the treatment of patients with bowel disease and primary hyperoxaluria. A pediatrician should be involved in the care of children with primary hyperoxaluria or any serious oxalate problem.

Consultation with a dietitian may help in the diagnosis of dietary excess of oxalate and for counseling patients regarding foods to avoid.


Experimental Therapies

Oxalobacter formigenes administration

O formigenes is a facultative anaerobic bacteria normally found primarily in the colon, and it digests oxalate within the intestinal tract. The intestinal tract is normally colonized with Oxalobacter at approximately age 3 years. Oxalobacter loss is primarily due to prolonged or repeated antibiotic therapy.[31] Fluoroquinolones, cephalosporins, tetracyclines, and macrolide preparations are particularly toxic to Oxalobacter bacteria, while penicillin and sulfa drugs have relatively little effect.[75, 76]

O formigenes is found in 70-80% of all adults but is missing or depleted in more than 60% of patients with hyperoxaluria. Patients with multiple episodes of calcium oxalate stone disease (4 or more separate incidents) are even less likely to have normal Oxalobacter colonies, with 80-90% demonstrating reduced colonization. Urinary oxalate excretion in patients with calcium oxalate stones who have lost their Oxalobacter colonies is typically 40% higher than in their counterparts with normal Oxalobacter levels.

Female patients with stones who have recurrent UTIs and undergo multiple courses of antibiotic therapy tend to be deficient in Oxalobacter and have significantly higher average urinary oxalate levels than similar patients without a history of recurrent urinary tract infections (UTIs).

A study by Siener et al found that average urinary oxalate levels in women with calcium oxalate stones who have recurrent UTIs were almost 18% higher than in women with calcium oxalate stones who did not have a history of UTI.[77] This is most likely due to the effect of repeated courses of antibiotics on intestinal Oxalobacter.

A similar result was found by Sidhu et al in a group of patients with cystic fibrosis (CF), who frequently receive prolonged and repeated courses of antibiotics.[78, 79] In this study, all patients with CF who had active intestinal Oxalobacter colonies had normal urinary oxalate levels, while more than 50% of patients with CF who were found to be deficient in Oxalobacter were hyperoxaluric.

Despite promising preliminary data, there has been no evidence from controlled trials to further support the use of oral O. formigenes therapy in primary hyperoxaluria. In 2017, two controlled trials reported that although the treatment was well tolerated and successfully delivered to the gastrointestinal tract, neither trial could demonstrate a significant reduction in either urinary oxalate excretion or plasma oxalate concentration compared to placebo.[80, 81]  Furthermore, no studies using oral O formigenes in groups of patients with enteric or idiopathic hyperoxaluria have yet appeared in the literature. Thus, the role of pharmacologic use of this bacteria to reduce urinary oxalate excretion, and hence kidney stone risk, remains to be determined.[82]

Plant stem–based therapies

Banana stem juice has been suggested as a possible treatment for hyperoxaluria. While it appeared to be of benefit in animal studies, to date, no human testing has been performed.[83]

Ramakrishnan et al described a plant-based (ie, beet stem) oxalate-digesting enzyme has that may prove to be useful in the treatment of hyperoxaluria in the future.[84]

Lupeol is a pentacyclic triterpene that is extracted from Crataeva nurvala stem bark. It has shown oxalate-reducing activity and is able to significantly reduce the renal excretion of oxalate in an animal model.[85] It also reduces renal tubular damage, presumably through decreased calcium oxalate crystallization.

RNA interference therapy

RNA interference (RNAi) is a naturally occurring cellular mechanism for regulating gene expression mediated by small interfering RNAs (siRNAs). Synthetic siRNAs can be designed to target the endogenous messenger RNA transcript of a given gene, leading to its cleavage and the subsequent suppression of synthesis of the encoded protein.[86, 87, 88, 89]

Nedosiran is an investigational RNAi therapy in development for all three primary hyperoxaluria subtypes. Nedosiran is designed to inhibit the hepatic lactate dehydrogenase (LDH) enzyme and thus, the conversion of glyoxylate to oxalate. In an interim analysis of the ongoing long-term, open-label rollover PHYOX3 trial, all patients with type 1 or 2 primary hyperoxaluria receiving monthly doses of nedosiran achieved normal or near-normal oxalate excretion by month 6. Nedosiran was well-tolerated and no serious safety concerns were identified.[90]

Other experimental therapies

Reloxaliase is a cystalline formulation of the enzyme oxalate decarboxylase that is currently undergoing clinical trials for the treatment of enteric hyperoxaluria. Reloxaliase degrades oxalate in the GI tract, which can decrease the systemic absorption of oxalate into the bloodstream, thus lowering the chances for kidney stones and kidney abnormalities to develop.[91]

The antiepileptic drug stiripentol has been shown to decrease oxalate synthesis by hepatocytes in vitro. The presumed mechanism of action is inhibition of the lactate dehydrogenase–5 (LDH-5) isoenzyme, which transforms glyoxylate to oxalate in the liver. In rat experiments, orally administered stiripentol decreases urine oxalate excretion and protects kidney function and kidney tissue against chronic calcium oxalate crystalline nephropathy.[92] However, case reports of use in patients have yielded conflicting results. Clinical trials of stiripentol in primary hyperoxaluria type 1 are in progress.[93]

L-cysteine has shown some beneficial activity by significantly lowering urinary oxalate and calcium levels while increasing urinary citrate and magnesium levels in an animal model.[94, 32]

Vitamin E supplementation has been suggested to be of some value in reducing calcium oxalate crystallization, but the usefulness of this therapy in humans remains unproven.[71, 72]

Various antioxidant therapies may provide some protection to the delicate proximal renal tubular cells that are very prone to injury from calcium oxalate crystal formation. This may help limit calcium oxalate stone formation.

The manufacturer of Oxadrop, which is a combination of 5 different lactic acid bacteria, has claimed that the product can significantly reduce urinary oxalate excretion. Unfortunately, randomized studies have shown no effect.[95, 82]

These and other experimental therapies will continue to be studied until better and more effective remedies for hyperoxaluria are developed.