Saudi Journal of Kidney Diseases and Transplantation

: 2015  |  Volume : 26  |  Issue : 5  |  Page : 1026--1027

Oxalate nephropathy after Jejuno-Ileal bypass surgery

Diana Taheri1, Tannaz Sarmadi2, Shahrzad Shahidi3, Shahram Taheri3, Mojgan Mortazavi3, Abdolamir Atapour3, Shahaboddin Dolatkhah4, Reza Moayednia2,  
1 Department of Pathology, Isfahan Kidney Diseases Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
2 Department of Pathology, Isfahan University of Medical Sciences, Isfahan, Iran
3 Department of Nephrology, Isfahan University of Medical Sciences, Isfahan, Iran
4 Isfahan Kidney Diseases Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence Address:
Dr. Diana Taheri
Department of Pathology, Isfahan Kidney Diseases Research Center, Isfahan University of Medical Sciences, Isfahan

How to cite this article:
Taheri D, Sarmadi T, Shahidi S, Taheri S, Mortazavi M, Atapour A, Dolatkhah S, Moayednia R. Oxalate nephropathy after Jejuno-Ileal bypass surgery.Saudi J Kidney Dis Transpl 2015;26:1026-1027

How to cite this URL:
Taheri D, Sarmadi T, Shahidi S, Taheri S, Mortazavi M, Atapour A, Dolatkhah S, Moayednia R. Oxalate nephropathy after Jejuno-Ileal bypass surgery. Saudi J Kidney Dis Transpl [serial online] 2015 [cited 2022 Aug 19 ];26:1026-1027
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Full Text

To the Editor,

Oxalate nephropathy causes include primary or hereditary hyperoxalosis or secondary to enteric hyperoxaluria due to fat malabsorption, vitamin B deficiency, vitamin C excessive ingestion, anesthetic agent exposure, ethanol intoxication or dietary foods such as nuts and cocoa with a lot of oxalic acid. [1]

Physiologically, calcium and oxalate combine together to form calcium oxalate along the lumen of the intestine. This complex is insoluble and excreted with feces.

In patients with fat malabsorption, fat combines with calcium and great quantities of soluble oxalate remain free and reabsorbed through the colonic mucosa and induce hyperoxaluria. In the recent century, there is a tendency for bariatric surgeries as a treatment for morbid obesity and may be complicated by fat malabsorption and hyperoxaluria. [2],[3]

We report three cases of secondary hyperoxaluria. Patient 1 was a 49-year-old male with rising creatinine up to 2.6 mg/dL and hematuria 2+. Patient 2 was a 54-year-old female with rising creatinine of 1.1 up to 4.2 mg/dL, proteinuria 2+ and trace hematuria. Patient 3 was a 45-year-old male with rising creatinine up to 10 mg/dL. Serologic tests were negative in all the three patients. They underwent renal biopsy that revealed moderate to severe interstitial fibrosis and tubular atrophy with an accompanying patchy mild to moderate mononuclear and polymorphous cells infiltration. Some tubules show mild dilatation with marked degenerative changes. The prominent finding in all the biopsies was the birefringent deposits of calcium oxalate in the renal tubules [Figure 1].{Figure 1}

Immunoflorescent staining for C3, C4, C1q, IgG, IgA, IgM and fibrinogen was negative in all the patients.

A retrospective review of the medical history revealed that all three patients underwent jejuno-ileal (JI) bypass surgery for obesity treatment about four to five years ago.

To the best of our knowledge, this is the first report on oxalate nephropathy due to secondary oxalosis after bariatric surgery in Iran.

JI bypass was the first procedure of bariatric surgery. In this operation, the proximal 35 cm of the jejunom is anastomosed to the ileum 10 cm from the ileocecal valve. [4] Through this short intestinal lumen, surface for absorption is little; specially, fatty acids cannot be absorbed and excreted in the feces. [4]

John R. Asplin in Litholink Corporation and the University of Chicago studied 132 patients having a history of bariatric surgery to measure urine oxalate excretion. Patients with JI bypass had high urine oxalate excretion >100 mg/dL. The results support the hypothesis of renal failure as a complication of bariatric surgery. [3]

Mole et al reported 18 patients on follow-up after JI bypass to explore the association between JI bypass and hyperoxaluria. Between 4% and 29% of these patients had hyperoxaluria and renal stones; the average time from bypass to renal failure was 18-20 months. Kidney biopsies revealed interstitial nephritis in 11 cases and calcium oxalate crystals were seen in all the biopsies. Oxalate nephropathy appeared in four patients and resulted in kidney failure. [5]

A retrospective study by Nasr et al. on 11 patients with renal insufficiency and rising creatinine and a history of Roux-en-y gastric bypass showed that kidney biopsy of all the patients revealed calcium oxalate crystal deposits within the renal tubules and interstitium as a cause of renal failure.

A retrospective review of a woman with renal insufficiency due to AA amyloidosis revealedhyperoxaluria following JI bypass surgery for obesity treatment. In this case, chronic inflammation disease, including oxalate arthritis and vasculitis, caused AA amyloidosis. Increased oxalate serum level following JI bypass was the main cause of this condition. [6]

In conclusion, the incidence of oxalate nephropathy will likely increase because of enteric fat malabsorption due to surgical obesity treatments. On the basis of our data, patients who undergo bariatric surgery should have long-term follow-up of renal function and metabolic parameters with dietary modification or even surgical reversal at an early time point at which this intervention may be beneficial.

Conflict of interest: None declared.


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