scholarly journals Recurrence of Hyperoxaluria and Kidney Disease after Combined Intestine-Kidney Transplantation for Enteric Hyperoxaluria

2016 ◽  
Vol 44 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Burcin Ekser ◽  
Richard S. Mangus ◽  
Chandrashekhar A. Kubal ◽  
Jonathan A. Fridell ◽  
John A. Powelson ◽  
...  

Background: Enteric hyperoxaluria (EH) occurs with a rate of 5-24% in patients with inflammatory bowel disease, ileal resection and modern bariatric surgery. The excessive absorption of calcium oxalate causes chronic kidney disease (CKD) in patients with EH. In the literature, a single experience was reported in combined intestine-kidney transplantation (CIKTx) in patients with CKD due to EH. Methods: After a report of 2 successful cases of CIKTx in patients with EH and CKD, one was performed at our center in a 59-year-old Caucasian female who developed intestinal failure with total parenteral nutrition (TPN) dependence after a complication post-bariatric surgery. Before CIKTx, she underwent kidney transplantation alone (KTA) twice, which failed due to oxalate nephropathy. Results: In July 2014, the patient underwent CIKTx and bilateral allograft nephrectomy to avoid EH and oxalate stone burden. The postoperative course was complicated with acute tubular necrosis due to the use of high pressors related to perioperative bleeding. The patient was discharged 79 days after CIKTx with a serum creatinine (sCr) of 1.2 mg/dl and free of TPN. Her sCr increased at 7 months and a renal biopsy showed oxalate nephropathy. SLC26A6 (oxalate transporter) staining was significantly diminished in native duodenum/rectum as well as in intestinal allograft compared to control. Conclusions: KTA in patients with CKD secondary to EH should not be recommended due to high risk of recurrence. Although other centers showed good long-term outcomes in CIKTx, our patient experienced recurrence of EH due to oxalate transporter defect, early kidney allograft dysfunction and prolonged antibiotic use.

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Francesca Santarsia ◽  
Ilaria Gandolfini ◽  
Marco Delsante ◽  
Alessandra Palmisano ◽  
Francesco Peyronel ◽  
...  

Abstract Background and Aims Despite the obvious efficacy in achieving weight loss, traditional malabsorptive procedures (intestinal by-pass) used for the treatment of obesity, may be associated with enteric oxaluria. Enteric oxaluria, by causing calcium-oxalate stones and nephrocalcinosis, represents an under-recognized cause of end-stage kidney disease in patients with history of intestinal by-pass. Herein, we describe a patient with a long-standing history of intestinal by-pass who developed a devastating acute oxalate nephropathy first diagnosed after kidney transplantation. Method A white female aged 50, who started hemodialysis one year earlier because of tubule-interstitial nephritis on a kidney biopsy, and who had history of recurrent kidney stones (calcium oxalate), underwent urgent deceased-donor kidney transplantation because of exhausted vascular access for hemodialysis (tunneled CVC right giugular vein as the last resort). She had received intestinal by-pass surgery 20 yrs earlier, and had a pacemaker implantation in the left sublavian vein for AV block two years earlier. She was highly sensitized because of blood transfusions at the time of surgery. Results After transplantation, graft function had immediate recovery, serum creatinine decreasing to 2.0mg/dL (117 mmol/L) on post-operative day (POD) 3. Shortly after, serum creatinine started rising until it reached 4.0mg/dL (354mmol/L) on POD 5. Three graft biopsies (performed on POD 6, 9 and 15 post-transplant) revealed acute oxalate nephropathy ( Figure1-2 large oxalate crystals on fresh unfixed core of kidney tissue analyzed under bright field microscope using polarized light) with no sign of rejection. Serial monitoring of Luminex SAB did not reveal circulating anti-HLA donor specific antibodies. Fundus examination revealed two tiny mono-lateral retinal oxalate deposits, whereas bone biopsy did not reveal oxalate accumulation. Plasma oxalate levels were 43 mmol/L on POD 10 were urinary oxalate excretion was 29mg /day on POD 14. The patient slowly progressed to end-stage kidney disease 2-month post-transplantation despite daily high flux dialysis since POD 7, fat-free and oxalate-free diet, oral potassium and high dose pyridoxine supplements. Conclusion Patients on chronic dialysis with a previous history of bariatric surgery via intestinal by-pass may have oxalate nephropathy caused by enteric oxaluria as unknown primary renal disease. The disease may recur shortly after transplantation despite the adoption of prompt aggressive treatment for oxalate removal.


2018 ◽  
Vol 14 (11) ◽  
pp. S53-S55
Author(s):  
Colleen Tewksbury ◽  
Jordana Cohen ◽  
Samuel Torres Landa ◽  
Octavia Pickett-Blakely ◽  
Noel N Williams ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Ravi Parasuraman ◽  
Ping L. Zhang ◽  
Dilip Samarapungavan ◽  
Krishna Pothugunta ◽  
Gampala Reddy ◽  
...  

Primary nonfunction (PNF) accounts for 0.6 to 8% of renal allograft failure, and the focus on causes of PNF has changed from rejection to other causes. Calcium oxalate (CaOx) deposition is common in early allograft biopsies, and it contributes in moderate intensity to higher incidence of acute tubular necrosis and poor graft survival. A-49-year old male with ESRD secondary to polycystic kidney disease underwent extended criteria donor kidney transplantation. Posttransplant, patient developed delayed graft function (DGF), and the biopsy showed moderately intense CaOx deposition that persisted on subsequent biopsies for 16 weeks, eventually resulting in PNF. The serum oxalate level was 3 times more than normal at 85 μmol/L (normal <27 μmol/L). Allograft nephrectomy showed massive aggregates of CaOx crystal deposition in renal collecting system. In conclusion, acute oxalate nephropathy should be considered in the differential diagnosis of DGF since optimal management could change the outcome of the allograft.


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