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Diet-induced oxalate nephropathy from excessive nut and seed consumption

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Abstract

Oxalate is a metabolite consumed in nuts, beans and leaves, and excreted in urine. Oxalosis can cause nephropathy. We describe a rare case of a high-oxalate diet intended for irritable bowel syndrome (IBS) treatment causing oxalate nephropathy. A 59-year-old woman with a history of controlled hypertension presented with creatinine 1.8 mg/dL, increased from baseline 1.3 mg/dL. She denied recent illness, urinary stones, medication adjustments, herbal supplements and non-steroidal anti-inflammatory drugs use. Diet included six tablespoons of chia seeds and five handfuls of almonds daily to manage IBS symptoms. Her electrolytes, urinalysis and renal ultrasound were unremarkable. Her 24-hour urine output revealed increased oxalate and low citrate. Renal biopsy showed glomerulosclerosis, fibrosis and calcium oxalate deposition. She switched to a low-oxalate diet, with improvement in laboratory markers. An earlier dietary history could have raised concern for oxalosis prior to renal biopsy. Providers should be trained to identify at-risk patients and provide appropriate dietary counselling.
1
GarlandV, etal. BMJ Case Rep 2020;13:e237212. doi:10.1136/bcr-2020-237212
Diet- induced oxalate nephropathy from excessive nut
and seedconsumption
Victoria Garland,1 Leal Herlitz,2 Renu Regunathan- Shenk3
Case report
To cite: GarlandV, HerlitzL,
Regunathan- ShenkR. BMJ
Case Rep 2020;13:e237212.
doi:10.1136/bcr-2020-
237212
1Medicine, George Washington
University School of Medicine
and Health Sciences,
Washington, DC, USA
2Anatomic Pathology, Cleveland
Clinic, Cleveland, Ohio, USA
3Division of Kidney Disease and
Hypertension, Department of
Medicine, George Washington
University School of Medicine
and Health Sciences,
Washington, DC, USA
Correspondence to
Dr Victoria Garland;
vgarland01@ gwu. edu
Accepted 26 October 2020
© BMJ Publishing Group
Limited 2020. Re- use
permitted under CC BY- NC. No
commercial re- use. See rights
and permissions. Published
by BMJ.
SUMMARY
Oxalate is a metabolite consumed in nuts, beans
and leaves, and excreted in urine. Oxalosis can cause
nephropathy. We describe a rare case of a high- oxalate
diet intended for irritable bowel syndrome (IBS)
treatment causing oxalate nephropathy. A 59- year-
old woman with a history of controlled hypertension
presented with creatinine 1.8 mg/dL, increased from
baseline 1.3 mg/dL. She denied recent illness, urinary
stones, medication adjustments, herbal supplements and
non- steroidal anti- inflammatory drugs use. Diet included
six tablespoons of chia seeds and five handfuls of
almonds daily to manage IBS symptoms. Her electrolytes,
urinalysis and renal ultrasound were unremarkable. Her
24- hour urine output revealed increased oxalate and low
citrate. Renal biopsy showed glomerulosclerosis, fibrosis
and calcium oxalate deposition. She switched to a low-
oxalate diet, with improvement in laboratory markers.
An earlier dietary history could have raised concern for
oxalosis prior to renal biopsy. Providers should be trained
to identify at- risk patients and provide appropriate
dietary counselling.
BACKGROUND
Oxalate is an organic acid and end product of
ascorbic acid metabolism in humans and plants.
In humans, dietary free oxalate is absorbed in the
stomach, distal small intestine and colon; oxalate
bound to calcium, iron and magnesium is excreted
in faeces.1 Serum oxalate is excreted in urine and
excessive filtration can cause calcium oxalate stones
or nephropathy. Oxalate nephropathy (ON), is a
rare form of kidney injury from calcium oxalate
crystal deposition in the kidney parenchyma. It can
lead to tubular damage, interstitial inflammation
and fibrosis that can cause acute or chronic renal
failure, and may progress to end- stage renal disease.
Oxalosis is most commonly caused by fat malab-
sorption, but other factors include mineral defi-
ciencies, fasting states, loss of oxalate, degrading
microbes, genetic defects in metabolism and
diet.2 3 We describe a rare case of a high- oxalate
diet, recommended for irritable bowel syndrome
(IBS) treatment, causing ON.
CASE PRESENTATION
A 59- year- old Caucasian woman with chronic
kidney disease stage 3bA1 of unknown aetiology,
IBS, osteoporosis, controlled hypertension and
hyperthyroidism was found to have acute- on-
chronic kidney injury during routine follow- up
with her nephrologist. She denied recent illnesses,
change in urine, lower extremity edema and history
of urinary stones. She denied non- steroidal anti-
inflammatory drugs, vitamin, antibiotic and herbal
supplement use. Medications included amlodipine
and methimazole. She was a non- smoker, drank
alcohol occasionally and denied illicit drug use.
INVESTIGATIONS
Her laboratory workup was significant for an
increase in creatinine to 1.8 mg/dL from 1.34 mg/
dL, 6 months earlier. Electrolytes were in normal
range. Urinalysis was negative for proteinuria or
haematuria. Renal ultrasound showed normal
kidneys without stones, masses, hydronephrosis
or increased echogenicity. She underwent renal
biopsy which showed diffuse global glomeruloscle-
rosis with prominent subcapsular fibrosis, tubular
atrophy, severe interstitial fibrosis involving 60% of
the cortex (figure 1) and calcium oxalate deposi-
tion (figure 2) on light microscopy. Her immuno-
fluorescence and electron microscopy results were
unremarkable. She completed a 24- hour urine
collection, revealing adequate urine output (3.18
L/day), high oxalate (101 mg/day, normal (nl)
20–40 mg/day), normal calcium level (55 mg/day,
nl 51–262 mg/day), low urine pH (5.35, nl 5.8–6.2)
and low citrate (496 mg/day, nl >550 mg/day).
After the investigation, a diet history was
obtained. She reported following the ‘virgin diet’
to treat her IBS symptoms for the past 6 years,
which comprised avoiding gluten, dairy, eggs,
soy, peanuts, corn and sugar/artificial sweeteners.
Finding digestive relief from chia seeds, in the past
year, she ingested six tablespoons of chia seeds and
five handful of almonds daily, with an estimated
intake of 1 g of soluble oxalate daily compared with
the normal western diet of <200 mg/day.1
TREATMENT
Based on the high oxalate content of her urine
collection and calcium oxalate deposition on
kidney biopsy, she was counselled to switch to a
low- oxalate diet with high fluid intake. She started
calcium carbonate with meals and worked with a
nutritionist.
OUTCOME AND FOLLOW-UP
Follow- up labs 2 months later showed improved
creatinine to 1.57 mg/dL, and it has remained at
her baseline 1.3–1.6 mg/dL. Repeat 24- hour urine
testing showed normalised oxalate (33 mg/day) and
citrate (624 mg/day) excretion, with pH 7.2 (nl
5.8–6.2). Since cutting down on nuts and changing
her diet, she has lost weight. She exercises daily and
her blood pressures have remained with systolics at
2GarlandV, etal. BMJ Case Rep 2020;13:e237212. doi:10.1136/bcr-2020-237212
Case report
110–120 mm Hg. She also started denosumab injections every 6
months for osteoporosis.
DISCUSSION
This case demonstrates diet- induced oxalosis causing calcium
oxalate deposition in the kidneys. It exposes the unintended
consequences of consuming large quantities of almonds and
seeds for suspected health benefits of improving IBS symptoms
and highlights the close relationship between nutrition, the
gastrointestinal tract and kidney health.
Oxalosis can be either primary from genetic enzyme deficien-
cies or secondary from increase in oxalate absorption from the
gastrointestinal tract.4 Normally, small amounts of free oxalate
are absorbed by the stomach, distal small intestines and colon
in humans.2 5 Oxalate also binds calcium, iron and magnesium,
and in the gut this gets excreted with faeces. Any host or dietary
factor that alters the amount of free oxalate influences absorp-
tion.2 The most common cause of secondary oxalosis is from
fat malabsorption, responsible for 88% of cases in a systematic
review by Lumlertgul et al.6 Conditions that cause fat malab-
sorption, such as gastric bypass surgery, Crohn’s disease, coeliac
sprue, pancreatic deficiency and medications leave more free
oxalate available for absorption. This is because fat has a greater
affinity for calcium than oxalate. Calcium, iron and magnesium
deficiencies as well as fasting states can also increase oxalate
absorption. The microbiome, including Oxalobacter formi-
genes and Lactobacillus acidophilus, plays an important role in
degrading oxalate.3 The diversity and extent of these gut bacteria
fluctuates in response to dietary oxalate and antibiotics, further
influencing oxalosis.3 Diets high in free oxalate also result in
increased absorption.5
Dietary oxalate comes primarily from plants. It is found in
higher concentrations in the leaves and seeds. Foods known
to have high levels of oxalate include nuts, beans, tea, spinach
and kale, rhubarb, beets, potato skins, soy and cocoa. Vitamin
C is also a potent source of oxalate as it is an end product of
metabolism,.2 Absorption rates vary between foods depending
on the content of soluble oxalate, which is more bioavailable,2 7
Tea has a significantly higher percentage of oxalate absorption
compared with spinach and rhubarb.2 Almonds, Brazil and pine
nuts contain nearly twice as much soluble oxalate, compared
with peanuts, pistachios and chestnuts.8
Our patient consumed a high- oxalate diet as a result of
following a popular diet for digestive health. The virgin diet,
promoted to alleviate food intolerances and IBS, advocates
elimination of certain foods and consumption of greens, nuts
and seeds. In response, our patient consumed an estimated
five times the typical quantity of oxalate daily. She ingested
approximately 150 g of almonds daily (147–250 mg of gastric
soluble oxalate/100 g and 216–305 mg of intestinal insoluble
oxalate/100 g) and six tablespoons (1/8 cup) of chia seeds
(380 mg oxalate/one- quarter cup), which ultimately caused
kidney injury.1 While high- oxalate foods are nutritional, oxalosis
can be harmful. Case reports have documented diet- induced ON
secondary to spinach, kale, berries, nuts and nut milk, cocoa
powder, wheat germ, green smoothies, chagas mushrooms and
vitamin C supplements.9–14 The majority followed this diet for
presumed health benefits and had partial recovery with restric-
tion of oxalate consumption, increased oral hydration and
calcium acetate supplementation to bind gut oxalate.
This case proves the importance of taking a thorough dietary
history. In our case, a dietary history could have raised a concern
for oxalosis earlier. While hypertension may have also contrib-
uted to the development of interstitial fibrosis, the patient’s
blood pressure was controlled at the time of biopsy, thus the
major intervention after completing the biopsy and urine collec-
tion was dietary counselling. At- risk patients with pre- existing
gastrointestinal disease, kidney disease or mineral deficiencies
should be counselled on the effect of high- oxalate diets on
the kidneys. Vegetarians, who may consume greater quantities
of foods rich in oxalate may also be vulnerable. Education on
Figure 1 Trichrome taken at 40× magnification showing the
background fibrosis and glomerulosclerosis.
Figure 2 H&E stain taken at 600× magnification with polarisation
showing a couple of calcium oxalate deposits within renal tubules.
Learning points
While oxalate nephropathy is a less common cause of kidney
disease, it should be considered when patients present
with chronic kidney disease or acute- on- chronic kidney
injury, particularly in patients with history of pre- existing
gastrointestinal, kidney or mineral disease.
A thorough dietary history is extremely important in disease
prevention, intervention and management.
Curriculum in physician training should include nutrition
education so that providers are comfortable discussing diet
and can provide appropriate counselling.
3
GarlandV, etal. BMJ Case Rep 2020;13:e237212. doi:10.1136/bcr-2020-237212
Case report
cooking techniques, such as soaking and cooking plants to help
leach oxalate, fluid hydration, balancing high- oxalate diets with
foods rich in free calcium, magnesium and iron, and limiting
consumption of tea and nuts is important.2
Given the popularity of fad diets, the curriculum in physi-
cian training should include nutrition education. Providers must
learn to take a dietary history and be prepared to provide appro-
priate counselling.
Contributors VG is the corresponding and first author. She is a third- year Internal
Medicine resident (PGY3) at the George Washington University. She performed the
literature review, wrote and revised the manuscript under consideration. LH was the
pathologist on the case and prepared the slides. The senior author, RR is the patient’s
current nephrologist. She gave guidance for the paper, and helped with editing and
revising the manuscript. All authors have accountability and responsibility for the
work and have approved of the final product.
Funding The authors have not declared a specific grant for this research from any
funding agency in the public, commercial or not- for- profit sectors.
Competing interests None declared.
Patient consent for publication Obtained.
Provenance and peer review Not commissioned; externally peer- reviewed.
Open access This is an open access article distributed in accordance with the
Creative Commons Attribution Non Commercial (CC BY- NC 4.0) license, which
permits others to distribute, remix, adapt, build upon this work non- commercially,
and license their derivative works on different terms, provided the original work
is properly cited and the use is non- commercial. See:http:// creativecommons. org/
licenses/ by- nc/ 4. 0/.
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3 Miller AW, Oakeson KF, Dale C, etal. Effect of dietary oxalate on the gut
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Hyperoxaluria can cause not only nephrolithiasis and nephrocalcinosis, but also renal parenchymal disease histologically characterized by deposition of calcium oxalate crystals throughout the renal parenchyma, profound tubular damage and interstitial inflammation and fibrosis. Hyperoxaluric nephropathy presents clinically as acute or chronic renal failure that may progress to end-stage renal disease (ESRD). This sequence of events, well recognized in the past in primary and enteric hyperoxalurias, has also been documented in a few cases of dietary hyperoxaluria. Estimates of oxalate intake in patients with chronic dietary hyperoxaluria who developed chronic kidney disease or ESRD were comparable to the reported average oxalate content of the diets of certain populations worldwide, thus raising the question whether dietary hyperoxaluria is a primary cause of ESRD in these regions. Studies addressing this question have the potential of improving population health and should be undertaken, alongside ongoing studies which are yielding fresh insights into the mechanisms of intestinal absorption and renal excretion of oxalate, and into the mechanisms of development of oxalate-induced renal parenchymal disease. Novel preventive and therapeutic strategies for treating all types of hyperoxaluria are expected to develop from these studies.
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