Calcium oxalate crystal related kidney injury in a patient receiving Roux-en Y hepaticojejunostomy due to gall bladder cancer

Tsai, Jun-Li; Tsai, Shih‐Chuan

doi:10.1186/s12882-017-0520-y

Cited by 7 publications

(3 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, none of these reports includes an enteral hyperoxaluria caused by an exocrine pancreatic insufficiency. Instead, in these cases, the enteral hyperoxaluria is caused by short bowel syndrome with chronic diarrhoea,5 a high-output ileostomy6 or a gastric bypass 7. Comparable to our case, all these cases resulted in ESRD.…”

Section: Discussionsupporting

confidence: 40%

Acute oxalate nephropathy due to high vitamin C doses and exocrine pancreatic insufficiency

Fijen

Weijmer

2019

BMJ Case Rep

View full text Add to dashboard Cite

Oxalate kidney injury can manifest as oxalate nephropathy or nephrolithiasis and present as acute kidney injury or even as end-stage renal disease. There are several known causes for acute oxalate nephropathy; however, the combination of exocrine pancreatic insufficiency with overconsumption of vitamin C has not been described before. In this case, a man in his early 80s presented with anorexia and extreme fatigue for 1 week. He had a history of myalgic encephalomyelitis, also known as chronic fatigue syndrome, for which he took several supplements, including high doses of vitamin C. Furthermore, several years ago, he was diagnosed elsewhere with exocrine pancreatic insufficiency. On admission, acute kidney injury was diagnosed. The kidney biopsy showed oxalate nephropathy as the cause. We diagnosed acute oxalate nephropathy due to high vitamin C doses and exocrine pancreatic insufficiency. Within 14 days, his kidney function got worse and he required renal replacement therapy.

show abstract

Section: Discussionsupporting

confidence: 40%

Acute oxalate nephropathy due to high vitamin C doses and exocrine pancreatic insufficiency

Fijen

Weijmer

2019

BMJ Case Rep

View full text Add to dashboard Cite

show abstract

“…1,3,5,6 Post-RYGB renal diseases include calcium oxalate nephrolithiasis and oxalate nephropathy associated with interstitial oxalate deposits. 7 This patient developed oxalate nephropathy manifesting as acute kidney injury on a background of chronic kidney disease approximately 18 months after RYGB.…”

Section: Restriction Of Which One Of the Followingmentioning

confidence: 94%

72-Year-Old Woman With Fatigue, Confusion, and Severe Acute Renal Failure

Zhang

Pawar

Greene

2018

Mayo Clinic Proceedings

View full text Add to dashboard Cite

A 72-year-old woman presented to the hospital with confusion and fatigue accompanied by a 1-month history of declining renal function. Her medical history was notable for type 2 diabetes mellitus, hyperlipidemia, hypertension, obesity, a Roux-en-Y gastric bypass surgical procedure in 2015 (2 years before the current presentation), and a history of diffuse large B-cell lymphoma treated with splenectomy and chemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone). When seeing her primary care physician 2 weeks before the current admission, she had reported several weeks of progressive fatigue. During the primary care evaluation, results of routine complete blood cell count(s) and basic metabolic panel(s) were notable for a hemoglobin level of 10.8 g/dL, mean corpuscular volume of 94 fL, serum urea nitrogen level of 63 mg/dL, and serum creatinine concentration of 5.0 mg/dL (increased from a baseline of 1.6 mg/dL 6 months previously). Outpatient renal ultrasonography and a nephrology clinic consultation were scheduled, but the patient was seen in the emergency department because of acute confusion. Her family reported poor recall of recent events and forgetfulness during conversation. The review of systems was positive for night sweats, chills, and lower extremity edema. She did not have decreased urination, dysuria, hematuria, urinary urgency, increased urinary frequency, and/or urinary retention. At the time of admission, her medication list included acetaminophen, cyanocobalamin injection(s), gabapentin, oxycodone, simvastatin, multivitamin, and venlafaxine. She did not take over-the-counter medication(s) including nonsteroidal anti-inflammatory drugs, COX-2 inhibitors, and/or other supplements. She had no recent travel or illnesses.The patient's vital signs demonstrated normal temperature, heart rate of 78 beats/min, respiratory rate of 13 breaths/min, blood pressure of 147/66 mm Hg, and an oxygen saturation of 98% while breathing room air. Physical examination noted a nondistressed, elderly, white female. Skin examination revealed no petechiae or jaundice. She did not have palpable supraclavicular, infraclavicular, axillary, and/or inguinal lymphadenopathy. Her oral membranes were moist, and the skin turgor was normal. The cardiovascular and pulmonary examinations revealed normal jugular venous pressure(s), absence of murmurs, regular heart rate and rhythm, and clear breath sounds. She did not have costovertebral angle tenderness and/or abdominal bruits. At the time of admission, the patient was oriented to person, place, and time and was able to follow commands appropriately. Neurologic examination revealed intact cranial nerves II through XII without tremors or asterixis.Laboratory studies revealed the following (reference ranges provided parenthetically): hemoglobin, 9.6 g/dL (11.6-15.0 g/dL); mean corpuscular volume, 90 fL; leukocytes, 10.4 Â 10 9 /L; platelet count, 423 Â 10 9 /L; sodium, 134 mmol/L; potassium, 4.7 mmol/L; chloride, 98 mmol/L; bicarbonate, 16 mmol/L; serum urea ...

show abstract

“…In clinical practice, oxalosis can also be found in patients with AKI without kidney transplantation, but its mechanism and participation in the process of acute injury remain unclear. However, researchers still tend to focus on case reports for this disease [4][5][6][7], which lack summaries of relevant ndings. The present study aimed to summarize the clinicopathological features of 23 patients with acute kidney disease (AKD) and renal oxalosis who were diagnosed and followed up in our department, to further understand the characteristics of the disease and their effects on prognosis.…”

Section: Introductionmentioning

confidence: 99%

Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

Zhou¹,

Yu²,

Tao³

et al. 2020

Preprint

View full text Add to dashboard Cite

Backgrounds: This study aimed to summarize and analyze the clinicopathological features of acute kidney disease patients with renal oxalosis, to improve understanding of the disease characteristics. Methods: Data for patients with acute kidney disease (AKD) diagnosed from January 2011 to October 2018 and confirmed by renal biopsy showing oxalate crystal deposition were collected. The underlying diseases, dietary habits before disease onset, pathological characteristics of newly emerging kidney disease, renal oxalosis, and causes of AKD were analyzed. Urine volume, serum creatinine, uric acid, and electrolyte clearance were recorded. The long-term renal prognosis was observed. Results: A total of 23 patients with AKD and renal oxalosis were included. The patients comprised 18 men (78.3%) and 5 women (21.7%) with a mean age of 51.6 ± 15.9 years. The peak serum creatinine was 669.9 ± 299.8 μmol/L, and 95.7% of patients had stage 3 acute kidney injury. Drug-induced AKD was the most common cause (65.2%), followed by severe nephrotic syndrome (17.4%). Other causes included severe glomerulonephritis, and infection. All patients had pathological changes indicating tubulointerstitial disease (TIN), and 11 patients were complicated with newly emerging glomerular disease (GD). Oxalate deposits caused by increased enterogenous oxalate absorption accounted for 26.1%, and most of the causes came from new kidney diseases. Oxalate crystals were located in the renal tubule. The majority (75%) of moderate to severe oxalate crystal deposition occurred in patients without GD. There were no significant differences in the total score for acute tubulointerstitial injury, score for tubular injury (T-IS), and score for interstitial inflammation in patients with different severities of renal oxalosis. Rate of serum creatinine decrease (ΔScr%) was negatively correlated with severity of oxalosis (R = −0.542, P = 0.037), score for acute tubular injury (R = −0.553, P = 0.033), and age (R = −0.736, P = 0.002). ΔScr% at week 4 was correlated with T-IS (R = −0.433, P = 0.050), but was not correlated with severity of oxalosis. Conclusions: The present findings revealed that 95.7% of AKD cases with renal oxalosis occurred in critically ill patients, secondary to kidney injury with tubular injury, and that drug-induced AKD was the most common cause. Severe oxalosis contributed to delayed early recovery of renal function.

show abstract

Calcium oxalate crystal related kidney injury in a patient receiving Roux-en Y hepaticojejunostomy due to gall bladder cancer

Cited by 7 publications

References 13 publications

Acute oxalate nephropathy due to high vitamin C doses and exocrine pancreatic insufficiency

Acute oxalate nephropathy due to high vitamin C doses and exocrine pancreatic insufficiency

72-Year-Old Woman With Fatigue, Confusion, and Severe Acute Renal Failure

Severe Oxalosis Secondary to Acute Kidney Disease Contributes to Delayed Early Recovery of Renal Function

Contact Info

Product

Resources

About