Acute Kidney Disease Due to Excessive Vitamin C Ingestion and Remote Roux-en-Y Gastric Bypass Surgery Superimposed on CKD

Sunkara, Vasu; Pelkowski, Timothy D.; Dreyfus, Darren E.; Satoskar, Anjali A.

doi:10.1053/j.ajkd.2015.06.021

Cited by 25 publications

(22 citation statements)

References 32 publications

(37 reference statements)

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“…Oxalate nephropathy occurs in the setting of hyperoxaluria and can result in excessive renal calcium oxalate deposition. 1 Excessive urinary oxalate excretion can be due to primary endogenous overproduction of oxalate, excess exogenous oxalate intake and/or absorption, or decreased renal clearance. 1,3,10 Serum oxalate levels in adults vary below 1 to 3 mmol/L but can be elevated up to 45 mmol/L in patients undergoing hemodialysis patients.…”

Section: Discussionmentioning

confidence: 99%

“…Vitamin C or ascorbic acid is metabolized to oxalate and accounts for 30% to 50% of endogenously produced oxalate. 1 Ingestion of more than 1000 mg/d of vitamin C has been associated with hyperoxaluria. 2 The remainder of the minerals and vitamins are not known to be associated with elevated serum oxalate levels.…”

Section: Restriction Of Which One Of the Followingmentioning

confidence: 99%

“…Decreased oxalate excretion can be found in patients with chronic kidney disease. 1 Pyridoxine can be used to for treatment in patients with primary hyperoxaluria type 1, which is secondary to mutations in the enzyme alanine glyoxylate aminotransferase (AGT). Pyridoxine is a cofactor for AGT, and its supplementation has been reported to reduce urinary oxalate excretion in 30% of patients in some studies.…”

Section: Restriction Of Which One Of the Followingmentioning

confidence: 99%

“…4 Primary hyperoxaluria is associated with oxalate overproduction as a consequence of genetic disorders associated with rare inborn errors of glyoxylate metabolism. 1,4 In patients with RYGB, hyperoxaluria may develop due to increased enteric absorption of oxalate in the setting of postoperative fat malabsorption and subsequent calcium saponification. 4 Calcium saponification occurs as enteric calcium binds to unabsorbed fat, instead of oxalate.…”

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confidence: 99%

“…Unbound oxalate is more readily absorbed in the remaining small intestine and colon instead of excreted. 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: 99%

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

Zhang

Pawar

Greene

2018

Mayo Clinic Proceedings

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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 ...

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