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

      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 × 109/L; platelet count, 423 × 109/L; sodium, 134 mmol/L; potassium, 4.7 mmol/L; chloride, 98 mmol/L; bicarbonate, 16 mmol/L; serum urea nitrogen, 92 mg/dL; creatinine, 8.0 mg/dL; uric acid, 6.2 mg/dL; phosphorus, 9.1 mg/dL; total calcium, 7.4 mg/dL; and albumin, 4.0 g/dL. Midstream urinalysis demonstrated urine osmolality of 223 mOsm/kg, protein to osmolality ratio of 0.40 (<0.42 ratio), hemoglobin and red blood cells not present, 1 to 3 white blood cells, and normal microscopic findings. Renal ultrasonography demonstrated bilateral kidneys approximately 10 cm in size and accompanied by an echogenic echotexture. Results were negative for kidney stones and evidence of obstruction, including hydronephrosis. Computed tomography (CT) of the chest, abdomen, and pelvis without contrast medium revealed no evidence of infection, masses, kidney stones, and/or adenopathy. Other laboratory data including serum and urine protein electrophoresis and immunofixation studies yielded negative results.
      • 1.
        With the aforementioned history, physical examination findings, and laboratory data, which one of the following is the most likely cause of this patient's renal dysfunction?
        • a.
          Rapidly progressive glomerulonephritis
        • b.
          Oxalate nephropathy
        • c.
          Acute interstitial nephritis (AIN)
        • d.
          Light chain deposition disease
        • e.
          Nephrolithiasis
      Rapidly progressive glomerulonephritis is in the differential diagnosis, but it is unlikely in the absence of an active urinary sediment (hematuria, proteinuria, red blood cell casts, or dysmorphic red blood cells). The possibility of oxalate nephropathy as a cause for acute renal dysfunction should be considered in patients with a history of prior Roux-en-Y gastric bypass (RYGB) surgery. Studies have found that hyperoxaluria is common after RYGB surgery and can lead to a spectrum of kidney diseases, including calcium oxalate nephrolithiasis, acute renal failure, chronic kidney disease, and ultimately end-stage renal disease in patients with unrecognized hyperoxaluria.
      Acute interstitial nephritis is unlikely in this patient. It is usually associated with medications such as antibiotics, proton pump inhibitors, infections, autoimmune and/or allergic diseases, and malignancies. Major risk factors for AIN were not present in this patient. The microscopic urinalysis was also negative for white blood cell casts and eosinphils, which may be present in patients with AIN. Although the patient is at risk for light chain deposition disease because of her medical history of lymphoma, it is less likely in the current absence of serum and urine free light chains. Nephrolithiasis, while possible, is less likely to lead to progressive renal failure unless the stones result in bilateral ureteral obstruction. Furthermore, CT revealed no evidence of kidney stones. When presenting with nephrolithiasis, patients usually report abdominal or flank pain, nausea, vomiting, and/or hematuria.
      Measurement of the patient's plasma oxalate concentration revealed an elevated level of 88.9 μmol/L (<1.6 μmol/L). In the setting of worsening renal function and because of the patient's confusion and generalized malaise (attributable to uremia), intermittent hemodialysis was initiated to reduce symptoms. A renal biopsy was performed to establish a tissue diagnosis.
      • 2.
        Restriction of which one of the following dietary elements should be considered in this patient?
        • a.
          Vitamin C
        • b.
          Iron
        • c.
          Magnesium
        • d.
          Folic acid
        • e.
          Calcium
      Vitamin C or ascorbic acid is metabolized to oxalate and accounts for 30% to 50% of endogenously produced oxalate.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      Ingestion of more than 1000 mg/d of vitamin C has been associated with hyperoxaluria.
      • Agrawal V.
      • Wilfong J.B.
      • Rich C.E.
      • Gibson P.C.
      Reversal of gastric bypass resolves hyperoxaluria and improves oxalate nephropathy secondary to Roux-en-Y gastric bypass.
      The remainder of the minerals and vitamins are not known to be associated with elevated serum oxalate levels. Magnesium and calcium supplementation have found to decrease gastrointestinal oxalate absorption by binding to intestinal oxalate.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      Our patient met with the hospital nutrition service regarding education for a low-oxalate diet and appropriate nutrition in the setting of acute and chronic kidney disease. In general, patients with hyperoxaluria are advised to avoid foods containing high levels of oxalate, for example, pomegranate, rhubarb, star fruit, spinach, almonds, and soy products.
      The patient's renal biopsy revealed acute tubular necrosis on a background of chronic tubulointerstitial injury and contained numerous calcium oxalate crystals. The crystals appeared birefringent under polarized light. Approximately 70% to 80% of the renal tubules demonstrated evidence of tubular atrophy consistent with chronic injury. Immunofluorescence studies were negative for IgA, IgG, IgM, C1q, C3, albumin, fibrinogen, and κ or λ light chains. Electron microscopy revealed evidence of mild mesangial matrix expansion in the glomeruli, global thickening of capillary loops, and mild effacement of visceral epithelial cell foot processes. No immunoelectron-dense deposits or tubuloreticular inclusion bodies were identified. The final pathologic diagnosis was acute renal injury on the background of chronic oxalate nephropathy.
      • 3.
        Which one of the following underlying processes/mechanisms occurring after RYGB surgery led to hyperoxaluria in this patient?
        • a.
          Excess dietary intake
        • b.
          Decreased oxalate excretion
        • c.
          Pyridoxine deficiency
        • d.
          Endogenous oxalate overproduction
        • e.
          Steatorrhea
      Although patients with a history of RYGB surgery should be counseled to avoid high-oxalate foods, excessive oxalate intake is not the primary reason for hyperoxaluria in these patients. Decreased oxalate excretion can be found in patients with chronic kidney disease.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      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.
      • Bhasin B.
      • Ürekli H.M.
      • Atta M.G.
      Primary and secondary hyperoxaluria: understanding the enigma.
      Primary hyperoxaluria is associated with oxalate overproduction as a consequence of genetic disorders associated with rare inborn errors of glyoxylate metabolism.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      • Bhasin B.
      • Ürekli H.M.
      • Atta M.G.
      Primary and secondary hyperoxaluria: understanding the enigma.
      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.
      • Bhasin B.
      • Ürekli H.M.
      • Atta M.G.
      Primary and secondary hyperoxaluria: understanding the enigma.
      Calcium saponification occurs as enteric calcium binds to unabsorbed fat, instead of oxalate. Unbound oxalate is more readily absorbed in the remaining small intestine and colon instead of excreted.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      • Nasr S.H.
      • D'Agati V.D.
      • Said S.M.
      • et al.
      Oxalate nephropathy complicating Roux-en-Y gastric bypass: an underrecognized cause of irreversible renal failure.
      • Moreland A.M.
      • Santa Ana C.A.
      • Asplin J.R.
      • et al.
      Steatorrhea and hyperoxaluria in severely obese patients before and after Roux-en-Y gastric bypass.
      Post-RYGB renal diseases include calcium oxalate nephrolithiasis and oxalate nephropathy associated with interstitial oxalate deposits.
      • Tsai J.L.
      • Tsai S.F.
      Calcium oxalate crystal related kidney injury in a patient receiving Roux-en Y hepaticojejunostomy due to gall bladder cancer.
      This patient developed oxalate nephropathy manifesting as acute kidney injury on a background of chronic kidney disease approximately 18 months after RYGB.
      • 4.
        Which one of the following treatments can be considered for this patient?
        • a.
          Orlistat
        • b.
          Prednisone
        • c.
          Hydrochlorothiazide
        • d.
          Calcium carbonate
        • e.
          Spironolactone
      Orlistat is a lipase inhibitor that is commonly used for weight loss. Because it causes fat malabsorption, it can lead to hyperoxaluria and should not be considered for this patient.
      • Humayun Y.
      • Ball K.C.
      • Lewin J.R.
      • Lerant A.A.
      • Fülöp T.
      Acute oxalate nephropathy associated with orlistat.
      Corticosteroids are used to treat many causes of acute kidney injury including acute interstitial nephritis and glomerulonephritis, but they have not been shown to be beneficial in oxalate nephropathy. Thiazide diuretics increase calcium reabsorption in the distal tubule and are used to treat recurrent kidney stones in patients with idiopathic hypercalciuria. They have not been shown to be of benefit in hyperoxaluria. Meal time calcium carbonate can be used to bind enteric oxalate.
      • Agrawal V.
      • Wilfong J.B.
      • Rich C.E.
      • Gibson P.C.
      Reversal of gastric bypass resolves hyperoxaluria and improves oxalate nephropathy secondary to Roux-en-Y gastric bypass.
      Patients are carefully monitored for hypercalcemia, which is unlikely due to calcium saponification. Spironolactone is not known to affect serum oxalate concentration or urinary oxalate excretion.
      The patient was discharged from the hospital with recommendations to follow a low-oxalate and low-fat diet and to continue intermittent in-center hemodialysis. A follow-up appointment with a nephrologist was scheduled.
      • 5.
        Which one of the following diseases could also be considered in this patient given the diagnosis of hyperoxaluria?
        • a.
          Cirrhosis
        • b.
          Inflammatory bowel disease
        • c.
          Amyloidosis
        • d.
          Human immunodeficiency virus
        • e.
          Systematic lupus erythematosus
      Cirrhosis is not associated with hyperoxaluria, although liver transplant is curative for primary hyperoxaluria type 1 because it corrects the underlying AGT enzymatic defect.
      Inflammatory bowel disease can cause hyperoxaluria through a similar mechanism of fat malabsorption.
      • Bhasin B.
      • Ürekli H.M.
      • Atta M.G.
      Primary and secondary hyperoxaluria: understanding the enigma.
      • Nasr S.H.
      • D'Agati V.D.
      • Said S.M.
      • et al.
      Oxalate nephropathy complicating Roux-en-Y gastric bypass: an underrecognized cause of irreversible renal failure.
      • Kumar R.
      • Lieske J.C.
      • Collazo-Clavell M.L.
      • et al.
      Fat malabsorption and increased intestinal oxalate absorption are common after Roux-en-Y gastric bypass surgery.
      Although amyloidosis can involve the kidneys because of immunoglobulin or amyloid deposits, it does not directly cause hyperoxaluria and or oxalate nephropathy.
      Human immunodeficiency virus infection can lead to associated nephropathy, and antiretroviral therapy can also be associated with drug-induced nephropathy. Systematic lupus erythematosus is associated with several types of kidney disease including immune complex–mediated glomerulonephritis but not with hyperoxaluria.
      In patients presenting with hyperoxaluria, it is important to consider and treat the underlying cause. For our patient, the history of RYGB surgery was the most likely underlying etiology. Moreover, her kidney biopsy did not demonstrate evidence of other systemic illnesses such as systematic lupus erythematosus or amyloidosis. With dietary restrictions and hemodialysis, the patient's plasma oxalate level decreased to 42.9 μmol/L at 12 days and 15.6 μmol/L at 20 days after hospital admission. Unfortunately, she continued to require intermittent hemodialysis 3 months after initial presentation. She is currently undergoing living donor kidney transplant evaluation.

      Discussion

      Oxalate nephropathy occurs in the setting of hyperoxaluria and can result in excessive renal calcium oxalate deposition.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      Excessive urinary oxalate excretion can be due to primary endogenous overproduction of oxalate, excess exogenous oxalate intake and/or absorption, or decreased renal clearance.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      • Sun Y.
      • Horowitz B.L.
      • Servilla K.S.
      • et al.
      Chronic nephropathy from dietary hyperoxaluria: sustained improvement of renal function after dietary intervention.
      Serum oxalate levels in adults vary below 1 to 3 μmol/L but can be elevated up to 45 μmol/L in patients undergoing hemodialysis patients.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      Malabsorptive bariatric surgeries, such as RYGB, can cause secondary oxalate nephropathy due to intestinal oxalate absorption. The incidence of hyperoxaluria after RYGB has been reported to be as high as 42% to 67% at 1 to 3.5 years postoperatively.
      • Agrawal V.
      • Wilfong J.B.
      • Rich C.E.
      • Gibson P.C.
      Reversal of gastric bypass resolves hyperoxaluria and improves oxalate nephropathy secondary to Roux-en-Y gastric bypass.
      The RYGB procedure results in fat malabsorption and accompanying increased fat excretion in the stool.
      • Nasr S.H.
      • D'Agati V.D.
      • Said S.M.
      • et al.
      Oxalate nephropathy complicating Roux-en-Y gastric bypass: an underrecognized cause of irreversible renal failure.
      • Kumar R.
      • Lieske J.C.
      • Collazo-Clavell M.L.
      • et al.
      Fat malabsorption and increased intestinal oxalate absorption are common after Roux-en-Y gastric bypass surgery.
      Fat malabsorption subsequently leads to calcium saponification, decreased available free intestinal calcium, and increased free and unbound intestinal oxalate. Because the intestinal oxalate is not bound to calcium, oxalate is more readily absorbed in the small and large intestine rather than being excreted in the stool as in the normal physiologic state.
      • Sunkara V.
      • Pelkowski T.D.
      • Dreyfus D.
      • Satoskar A.
      Acute kidney disease due to excessive vitamin C ingestion and remote Roux-en-Y gastric bypass surgery superimposed on CKD.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      • Nasr S.H.
      • D'Agati V.D.
      • Said S.M.
      • et al.
      Oxalate nephropathy complicating Roux-en-Y gastric bypass: an underrecognized cause of irreversible renal failure.
      • Moreland A.M.
      • Santa Ana C.A.
      • Asplin J.R.
      • et al.
      Steatorrhea and hyperoxaluria in severely obese patients before and after Roux-en-Y gastric bypass.
      Increased serum oxalate levels can cause nephrotoxicity because most oxalate is excreted by the kidneys by glomerular filtration and proximal tubule secretion.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      A minority of oxalate (5%-7%), as shown in a study utilizing a rat model, is excreted in the stool.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      Much of this data is supported by a study that found that obese patients undergoing RYGB surgery have higher urinary oxalate excretion compared to nonobese individuals.
      • Moreland A.M.
      • Santa Ana C.A.
      • Asplin J.R.
      • et al.
      Steatorrhea and hyperoxaluria in severely obese patients before and after Roux-en-Y gastric bypass.
      Patients with previous RYGB surgery also have an increased incidence of calcium oxalate nephrolithiasis and can have development of both acute and chronic kidney disease secondary to oxalosis.
      • Agrawal V.
      • Liu X.J.
      • Campfield T.
      • Romanelli J.
      • Enrique Silva J.
      • Braden G.L.
      Calcium oxalate supersaturation increases early after Roux-en-Y gastric bypass.
      In one study, RYGB patients were found to have approximately 70% greater chance of developing nephrolithiasis but, interestingly, did not have significantly increased risk of developing chronic kidney disease.
      • Lieske J.C.
      • Mehta R.A.
      • Milliner D.S.
      • Rule A.D.
      • Bergstralh E.J.
      • Sarr M.G.
      Kidney stones are common after bariatric surgery.
      Oxalate nephropathy is characterized by calcium oxalate crystals ultimately resulting in progressive tubulointerstitial injury and fibrosis.
      • Nasr S.H.
      • D'Agati V.D.
      • Said S.M.
      • et al.
      Oxalate nephropathy complicating Roux-en-Y gastric bypass: an underrecognized cause of irreversible renal failure.
      Studies in animal models have demonstrated the involvement of oxalate in inflammatory pathways as a potential underlying mechanism for oxalate nephropathy. Oxalate crystals are reported to cause inflammasome activation and the release of cytokines such as interleukin 1β and interleukin 18 that can contribute to tubular injury.
      • Ermer T.
      • Eckardt K.U.
      • Aronson P.S.
      • Knauf F.
      Oxalate, inflammasome, and progression of kidney disease.
      In patients diagnosed with oxalate nephropathy after RYGB surgery, one study reported that as many as 73% of patient had progression to end-stage renal disease within 3 months of diagnosis.
      • Nasr S.H.
      • D'Agati V.D.
      • Said S.M.
      • et al.
      Oxalate nephropathy complicating Roux-en-Y gastric bypass: an underrecognized cause of irreversible renal failure.
      Medical management for these patients includes low-fat and low-oxalate diet, enteric oxalate-binding agents (eg, calcium carbonate), and bile acid sequestrants (eg, cholestyramine) with the goal of achieving normal urinary oxalate levels.
      • Agrawal V.
      • Wilfong J.B.
      • Rich C.E.
      • Gibson P.C.
      Reversal of gastric bypass resolves hyperoxaluria and improves oxalate nephropathy secondary to Roux-en-Y gastric bypass.
      Dialysis and kidney transplant may be considered in patients with advanced renal disease. A recent case report suggested that both hyperoxaluria and acute kidney injury resolved in a patient after reversal of RYGB, but definitive evidence for this therapy is currently limited.
      • Agrawal V.
      • Wilfong J.B.
      • Rich C.E.
      • Gibson P.C.
      Reversal of gastric bypass resolves hyperoxaluria and improves oxalate nephropathy secondary to Roux-en-Y gastric bypass.

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