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CASE REPORT Open Access
Calcium oxalate crystal related kidney
injury in a patient receiving Roux-en Y
hepaticojejunostomy due to gall bladder
cancer
Jun-Li Tsai1 and Shang-Feng Tsai2,3,4*
Abstract
Background: Calcium oxalate nephropathy is rare in current practice. It was a common complication during
jejunoileal bypass, but much less seen in modern gastric bypass surgery for morbid obesity. The major cause of
it is enteric hyperoxaluria.
Case presentation: We report on a patient here with acute kidney disease due to calcium oxalate nephropathy,
rather than the conditions mentioned above. The male patient received a Roux-en Y hepaticojejunostomy and
common bile duct drainage. In addition to enteric hyperoxaluria, chronic kidney disease related metabolic acidosis,
chronic diarrhea related volume depletion, a high oxalate and low potassium diet, long term ascorbic acid intake
and long term exposure to antibiotics, all predisposed him to having oxalate nephropathy.
Conclusion: This is the first case with such conditions and we recommend that similarly diagnosed patients avoid
all these predisposing factors, in order to avoid this rare disease and its undesired outcome.
Keywords: Calcium oxalate, Acute kidney injury, Roux-en Y hepaticojejunostomy
Background
Oxalate nephropathy is a rare disease, and most cases
are due to enteric hyperoxalauria. Calcium oxalate
crystal related renal injury in the past was mostly due to
a jejunoileal bypass (JIB) performed for the treatment of
obesity. Owing to too many complications, modern
surgery for morbid obesity today is through Roux-en-Y
gastric bypass (RYGB) surgery. Much less oxalate
nephropathy will be seen in the currently performed sur-
gery for morbid obesity. Herein, we report the first case
of oxalate nephropathy related acute kidney injury
receiving a Roux-en Y hepaticojejunostomy due to gall
bladder carcinoma, not previously reported in the litera-
ture. We also did literature reviews for calcium oxalate
nephropathy and held discussions regarding the charac-
teristics of this patient.
Case presentation
A 67-year-old man was experiencing gallbladder carcin-
oma with common bile duct (CBD) invasion related
jaundice and cholangitis s/p cholecystectomy, hilar
lymph node dissection and Roux-en Y hepaticojejunost-
omy three years ago. However, six months after diagno-
sis, the carcinoma reoccurred, so he received a partial
hepatectomy along with chemotherapy (Cisplatin and
5-FU over six cycles). After chemotherapy, the serum
creatinine was 4.7 mg/dl (13 mL/min/1.73 m2 of GFR).
Due to obstructive jaundice, a CBD drainage tube was
inserted. He also experienced frequent cholangitis and
his bile cultures yielded Klebsiella pneumoniae,
Citrobacter freundiim, Enterococcus sp., Group D strepto-
coccus not enterococcus, and Escherichia coli. Due to
these conditions, he received Cefoperazone for an exten-
sive period of time (6 months). Afterward, he suffered
* Correspondence: s881056@gmail.com
2Division of Nephrology, Department of Internal Medicine, Taichung Veterans
General Hospital, 1650 Taiwan Boulevard Sect. 4, Taichung, Taiwan 40705,
Taiwan, Republic of China
3Department of Life Science, Tunghai University, Taichung, Taiwan
Full list of author information is available at the end of the article
© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Tsai and Tsai BMC Nephrology  (2017) 18:106 
DOI 10.1186/s12882-017-0520-y
from chronic diarrhea for two years, five times per day.
The renal function was stable even the above conditions.
This time (three years after RYGB), he was admitted to
hospital due to kidney injury (4.7 to 14.7 mg/dl of serum
creatinine), which is less likely pre-renal azotemia. A
renal biopsy disclosed mild interstitial inflammation,
moderate interstitial fibrosis and tubular atrophy with
intratubular crystal deposition (Fig. 1a). Under polarized
light, the deposits appeared strongly birefringent, which
formed fan-like, sheaf-like, or irregular shapes consistent
with calcium oxalate crystals (Fig. 1b). Under a low
power field with polarized light, almost all tubular
lumens were filled with crystals (Fig. 1c). The patient’s
24-h urinary oxalate level was found to be significantly
elevated, at 60 mg/day (normal range is up to 40 mg/
day). Serum calcium, thyroid function, and uric acid
were all within normal limits. Calcium oxalate crystal
related acute kidney injury was confirmed, and the pa-
tient was placed on a low oxalate diet. However, soon
after the diagnosis, he went into end-stage renal disease
and was placed on hemodialysis. Before this admission,
he had been on a low potassium diet because of long-
term renal dysfunction. The patient himself had
approved the course of treatment, and had given signed
consent.
Discussion
Endogenous oxalate is primarily derived from the metab-
olism of glycine and ascorbic acid [1]. Calcium oxalate
crystal related renal injury in the past was mostly due to
JIB, which was a surgical weight-loss procedure per-
formed for the relief of morbid obesity during the 1950s
through the 1970s. However, there remained too many
complications, including mineral and electrolyte imbal-
ance, protein calorie malnutrition, enteric complications,
and renal disease (hyperoxaluria, with oxalate stones or
interstitial oxalate deposits). The multiple complications
which were associated with JIB, led to a search for alter-
native procedures. In 1979 [2], one type of modern
bariatric surgery was gastric bypass. Full procedure
gastric bypass included RYGB surgery, biliopancreatic
diversion with duodenal switch, vertical banded gastro-
plasty, and laparoscopic adjustable gastric banding. A
study by Asplin et al. revealed a mean oxalate excretion
of 83 mg/day in patients who underwent RYGB [3]. This
was significantly higher than that found in routine kid-
ney stone formers or normal subjects (39 and 34 mg/
day, respectively), but lower when compared to patients
who had undergone JJIB (103 mg/day). To the best of
our knowledge, our patient is the first case of a calcium
oxalate related renal injury due to having received a
Fig. 1 a Mild interstitial inflammation, moderate interstitial fibrosis and tubular atrophy with intratubular crystal deposition. (400X, PAS staining).
b The deposits appeared strongly birefringent, forming fan-like, sheaf-like, or irregular shapes consistent with calcium oxalate crystals (400X,
polarized light). c Almost all tubular lumens were filled with crystals (100X, polarized light)
Tsai and Tsai BMC Nephrology  (2017) 18:106 Page 2 of 4
Roux-en-Y hepaticojejunostomy, in order to treat gall-
bladder carcinoma rather cancer obesity.
The cause of hyperoxaluria related calcium oxalate
crystals could be multifactorial in nature. Firstly, malab-
sorption leading to steatorrhea plays a central role in all
forms of enteric hyperoxaluria [4, 5]. Under normal cir-
cumstances, calcium will bind to oxalate within the in-
testinal lumen to form insoluble calcium oxalate, that is
excreted in feces. If with fat malabsorption, excessive
intraluminal free fatty acids bind to and saponify cal-
cium, which inhibits the formation of calcium oxalate.
Bile plays an important role in fat digestion, emulsifying
fat as the first stage in its digestion. There was only a
50% bile level for this patient to help digest fat because a
CBD drainage was performed to avoid obstructive jaun-
dice (about 500 ml per day, according to the medical re-
cords). Therefore, because fat malabsorption was
anticipated in this patient, more soluble free oxalate was
absorbed by the colonic mucosa. In addition, the other
50% nonabsorbed bile salts were drained into the colon,
causing increased colonic permeability to small mole-
cules such as oxalate [6, 7]. Both soluble free oxalate in
the lumen, and higher permeability to oxalate cause en-
teric hyperoxaluria. Secondly, the patient also experi-
enced diarrhea without enough fluid supplements to
enable him to avoid chronic kidney injury related edema.
The diarrheal fluid losses can lead to a reduction in
urine volume, along with intratubular concentrations of
oxalate and calcium.
In addition to the risk factors associated with the sur-
gery or bile salt, the patient also had other predisposing
factors. One is that he had renal dysfunction related
metabolic acidosis, which led to a low urine pH (5.0).
Since acidemia enhances proximal citrate reabsorption
[8] and urinary citrate is a potent inhibitor of calcium
stone formation, these factors promote calcium oxalate
precipitation. Secondly, the patient changed his dietary
intake habits due to long-term diarrhea. He consumed
food with high oxalate levels each day, including beans,
beets, cranberries and nuts. He also thoroughly enjoyed
both coffee and black tea. Therefore, his diet contained
high oxalate levels. Thirdly, prolonged administration of
antibiotics will cause loss of Oxalobacter formigenes,
which can lead to a decreased degradation of oxalate,
and thus, increasing the risk of hyperoxaluria [9].
Fourthly, as a patient with chronic kidney disease, he
maintained a low potassium diet. However, it is a higher
potassium intake that may reduce the risk of stone for-
mation by reducing urinary calcium excretion [10], and
may also increase urinary citrate excretion, because
potassium-rich foods tend to have a high alkali content.
Thus, his low potassium diet further made the patient
more susceptible to calcium oxalate nephropathy.
Fifthly, the patient had been taking ascorbic acid for two
years to assist in the healing of a scar, which was due to
earlier surgery and a CBD drainage catheter. A high dos-
age of vitamin C could cause an increase in oxalate gen-
eration [11]. Last but not the least, Cisplatin may
enhance calcium oxalate crystal adherence to inner me-
dullary collecting duct cells [12] even though the contri-
bution of Cisplatin to oxalate nephropathy is more
speculative than other causes.
In a series of 132 patients with nephrolithiasis who
had undergone gastric bypass surgery, the average time
for the formation of the first stone was 3.6 years [3],
which is compatible with our case. Even though his urin-
ary oxaluria was much less than patients undergoing
gastric bypass (60 mg/day vs. 83 mg/day), this patient
still had other risk factors involved, including metabolic
acidosis, chronic diarrhea related volume depletion, high
oxalate and low potassium diet, long-term ascorbic acid
intake, along with long-term exposure to antibiotics.
The prognosis of oxalate nephropathy after RYGB
would be considered dismal, with the progression to
end-stage renal disease coming within three months in
72.7% of the patients in this study [13]. In our case, the
prognosis of oxalate nephropathy after Roux-en Y hepa-
ticojejunostomy was also poor. The patient required
long-term hemodialysis after this episode of acute kidney
injury, even while maintaining a low oxalate diet.
This is a limitation to this report because we did not
have the report of citrate, calcium, and uric acid of 24-h
urine study.
Conclusion
In patients receiving Roux-en Y hepaticojejunostomy, it
is necessary to keep in mind the possibility of oxalate
nephropathy occurring. Avoiding volume depletion,
renal dysfunction, long-term antibiotics, Vitamin C and
a low potassium intake are all mandatory guidelines in
order to help prevent this rare disease and its undesired
outcome.
Abbreviations
CBD: Common bile duct; JIB: Jejunoileal bypass; RYGB: Roux-en-Y gastric bypass
Acknowledgements
The authors declare that they have no acknowledgments.
Availability of data and materials
All available data supporting this care report has been included in this publication.
Authors’ contributions
JLT and SFT both cared this patient in clinical practice. JLT wrote the draft
and SFT revised this manuscript. JLT and SFT both did literatures review. JLT
and SFT conceived of the study, and participated in its design and
coordination. Both authors read and approved the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Consent for publication
Consent to publish was obtained from this case's child.
Tsai and Tsai BMC Nephrology  (2017) 18:106 Page 3 of 4
Ethics and consent to participate
Ethical approval was not required, but the patient consented to the
treatment administered.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.
Author details
1Department of Family Medicine, Cheng Ching General Hospital, Taichung,
Taiwan. 2Division of Nephrology, Department of Internal Medicine, Taichung
Veterans General Hospital, 1650 Taiwan Boulevard Sect. 4, Taichung, Taiwan
40705, Taiwan, Republic of China. 3Department of Life Science, Tunghai
University, Taichung, Taiwan. 4School of Medicine, National Yang-Ming
University, Taipei, Taiwan.
Received: 7 July 2016 Accepted: 22 March 2017
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Tsai and Tsai BMC Nephrology  (2017) 18:106 Page 4 of 4


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