Jejuno-ileal bypass, enteric hyperoxaluria, and oxalate nephrosis: a role for polarised light in the renal biopsy

Hicks, Kirsty-Marie; Evans, G B; Rogerson, Mary; Bass, Paul

doi:10.1136/jcp.51.9.700

Cited by 11 publications

(9 citation statements)

References 8 publications

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“…[6,7] Increasing awareness of enteric hyperoxaluria complicating jejunoileal bypass surgery and Roux-en-Y gastric bypass progressing to oxalate nephropa-thy (ON) and renal failure offers reason for pause and concern. [8][9][10][11][12][13][14] An index case of oxalate nephropathy occurring in the transplanted kidney in a recipient that had received jejunoileal gastric bypass (GB) prior to transplantation at our center prompted us to examine outcomes among our post-gastric bypass renal transplant recipients.…”

Section: Introductionmentioning

confidence: 99%

Gastric bypass oxalosis in renal transplant: clinicopathologic correlates

Salazar

Taber

O'Neill

et al. 2016

CRCP

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Background: Reports of oxalate nephropathy after gastric bypass (GB) leading to graft loss of kidneys causes concern for transplant professionals. We examined the clinical phenotype of GB related oxalate nephropathy (ON), its contribution to graft loss and propose a management strategy to mitigate graft loss in renal transplant recipients. Methods: Retrospective case series of patients who had GB surgery prior to renal transplant at a single institution were studied. Oxalate burden in renal transplant biopsies was quantified by intratubular calcium/glomeruli (Ca T/G) ratio and correlated with other clinical covariates. Results: We identified 16 GB patients; the mean BMI pre-GB was 52.5 kg/m 2 (range 42-80), with a follow-up BMI of 30.9 kg/m 2 (range 22-36.5) at transplant evaluation. Among 11 patients who had for cause biopsies, 3 patients had significant intra tubular allograft calcium oxalate deposition with a median time from graft to failure of 9 months. Among patients with functioning grafts, follow up creatinine averaged 1.6 mg/dl (0.9-3.4 mg/dl); median follow up was 4 years (0.5-7 years). Conclusions: The relationship between GB and ON post renal transplant is variable. The expression of ON after acute kidney injury (AKI) suggests that mitigating strategies should be directed at preventing alloimmune and other forms of AKI in addition to managing oxalate intake.

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Section: Introductionmentioning

confidence: 99%

Gastric bypass oxalosis in renal transplant: clinicopathologic correlates

Salazar

Taber

O'Neill

et al. 2016

CRCP

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“…By light microscopy, calcium oxalate crystals are gray-white and spiculated. Most importantly, they are birefringent under polarized light, whereas calcium phosphate crystals do not polarize (5,17,18). In this series, all patients had biopsy-proven AON.…”

Section: Discussionmentioning

confidence: 83%

“…Oxalate precursors incriminated in toxic or drug-induced AON include acute poisoning by ethylene glycol (8) and ascorbic acid (21), respectively. Enteric hyperoxaluria has been described in various malabsorptive intestinal diseases, like jejuno-ileal bypass (17,22), short bowel syndrome (23,24), and chronic inflammatory bowel disease (25)(26)(27). Recently, short series have emphasized the risk of AON after modern bariatric surgery with Roux-en-Y gastric bypass (5,9).…”

Section: Discussionmentioning

confidence: 99%

Oxalate Nephropathy Associated with Chronic Pancreatitis

Cartery¹,

Faguer²,

Karras³

et al. 2011

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives Enteric overabsorption of oxalate may lead to hyperoxaluria and subsequent acute oxalate nephritis (AON). AON related to chronic pancreatitis is a rare and poorly described condition precluding early recognition and treatment.Design, setting, participants, & measurements We collected the clinical characteristics, treatment, and renal outcome of 12 patients with chronic pancreatitis-associated AON followed in four French renal units.Results Before AON, mild to moderate chronic kidney disease was present in all patients, diabetes mellitus in eight (insulin [n ϭ 6]; oral antidiabetic drugs [n ϭ 2]), and known chronic pancreatitis in only eight. At presentation, pancreas imaging showed gland atrophy/heterogeneity, Wirsung duct dilation, calcification, or pseudocyst. Renal findings consisted of rapidly progressive renal failure with tubulointerstitial profile. Acute modification of glomerular filtration preceded the AON (i.e., diarrhea and diuretics). Increase in urinary oxalate excretion was found in all tested patients and hypocalcemia in nine (Ͻ1.5 mmol/L in four patients). Renal biopsy showed diffuse crystal deposits, highly suggestive of oxalate crystals, with tubular necrosis and interstitial inflammatory cell infiltrates. Treatment consisted of pancreatic enzyme supplementation, oral calcium intake, and an oxalate-free diet in all patients and renal replacement therapy in five patients. After a median follow-up of 7 months, three of 12 patients reached end-stage renal disease.Conclusion AON is an under-recognized severe crystal-induced renal disease with features of tubulointerstitial nephritis that may occur in patients with a long history of chronic pancreatitis or reveal the pancreatic disease. Extrinsic triggering factors should be prevented.

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“…In enteric hyperoxaluria, malabsorbed fat reacts with calcium reducing the formation of CaOx-insoluble compounds in the intestinal lumen, hence raising free oxalate absorption [14][15][16][17]. Several authors have reported that increasing dietary fat also leads to increased bile salt synthesis in rats [46][47][48].…”

Section: Discussionmentioning

confidence: 99%

“…The gastrointestinal diseases that have been associated with this entity are those characterized by an absence or nonfunction of the small bowel (enteritis, small bowel resection, or bypass surgery) and those causing defective absorption of fat or bile acids (chronic pancreatitis, biliary cirrhosis, blind loop syndrome, and other diseases) [14][15][16][17]. Unabsorbed bile acids and fatty acids may react with calcium in the intestinal lumen, forming "soaps" that limit the amount of free calcium binding with oxalate, with a consequent increase in intestinal oxalate absorption leading to hyperoxaluria [14,[18][19][20][21][22][23].…”

mentioning

confidence: 99%