Acta Clinica Belgica International Journal of Clinical and Laboratory Medicine
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION L Mazzoleni, S Aydin, M De Meyer, Y Pirson & N Kanaan To cite this article: L Mazzoleni, S Aydin, M De Meyer, Y Pirson & N Kanaan (2013) ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION, Acta Clinica Belgica, 68:5, 389-389 To link to this article: http://dx.doi.org/10.2143/ACB.3331
Published online: 06 May 2014.
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Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [Orta Dogu Teknik Universitesi]
Date: 27 April 2016, At: 17:21
ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION
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ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION Mazzoleni L1, Aydin S2, De Meyer M3, Pirson Y1, Kanaan N1 Division of 1Nephrology, 2Pathology and 3Surgery and Abdominal Transplantation Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
Downloaded by [Orta Dogu Teknik Universitesi] at 17:21 27 April 2016
Correspondence and offprint requests to: Nada Kanaan, E-mail: [email protected]
A 52-year-old man was transplanted with a kidney from a deceased donor for a biopsy-proven renal AA amyloidosis secondary to Crohn’s disease after five years on hemodialysis. His past history included multiple small intestine resections, intermittent diarrhea, and adrenal insufficiency in the context of amyloidosis leading to persistent hypotension. The postoperative period was marked by a delayed graft function initially attributed to acute tubular necrosis secondary to decreased renal perfusion as a consequence of his low blood pressure. Renal function was slow to recover with stagnation of creatinine clearance at 16 ml/ min three weeks after transplantation prompting a kidney graft biopsy. It showed translucent calcium oxalate crystals within renal tubules (Figure 1A), with characteristic birefringence under polarized light microscopy (Figure 1B). Oxaluria was significantly increased taking into account the degree of renal insufficiency (66 mg/g of creatinine (normal: 0-32)). Kidney function did not improve and the patient returned to hemodialysis 5 months later. Acute oxalate nephropathy secondary to enteric hyperoxaluria caused early graft loss in our patient. Enteric hyperoxaluria is due to fat malabsorbtion as encountered in Crohn’s disease, extensive bowel resection, pancreatic insufficiency or bariatric surgery. Non-absorbed bile acids and fatty acids
A
increase intestinal permeability to oxalate. In addition, fatty acids bind calcium in the lumen, decreasing the calcium available for binding oxalate and preventing its intestinal absorption (1). Recognition of enteric hyperoxaluria before transplantation is of importance. Indeed, a large quantity of oxalate accumulated in the body can be rapidly released with a risk of oxalate calcium precipitation in the graft (2). Measures to reduce hyperoxaluria and prevent graft oxalosis must be taken including a low-oxalate and fat diet, oral calcium supplements, high fluid intake, and inhibitors of crystallization such as magnesium and citrate (1). High-efficiency intensive dialysis can also be beneficial to reduce serum oxalate levels (3).
REFERENCES 1. Robijn S, Hoppe B, Vervaet BA, D’Haese PC, Verhukst A. Hyperoxalouria: a gutkidney axis? Kidney international 2011; 80: 1146-1158. 2. Cuvelier C, Goffin E, Cosyns JP, Wauthier M, van Ypersel de Strihou C. Enteric hyperoxaluria: A hidden cause of early renal graft failure in two successive transplants: spontaneous late graft recovery. Am J Kidney Dis 2002; 40: E3. 3. Rankin A.C, Walsh SB, Summers SA, Owen MP, Mansell MA. Acute oxalate nephropathy causing late renal transplant dysfunction due to enteric hypeorxaluria. Am J Transplant 2008: 8: 1755-1758.
B
Figure 1: (A) Intra-tubular translucent crystals with associated tubular injury observed under standard light microscopy (hematoxylin and eosin, original magnification x200). (B) Oxalate crystal deposition with characteristic birefringence under polarized light microscopy (original magnification x100).
doi: 10.2143/ACB.3331
Acta Clinica Belgica, 2013; 68-5
389
ISSN: 1784-3286 (Print) 2295-3337 (Online) Journal homepage: http://www.tandfonline.com/loi/yacb20
ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION L Mazzoleni, S Aydin, M De Meyer, Y Pirson & N Kanaan To cite this article: L Mazzoleni, S Aydin, M De Meyer, Y Pirson & N Kanaan (2013) ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION, Acta Clinica Belgica, 68:5, 389-389 To link to this article: http://dx.doi.org/10.2143/ACB.3331
Published online: 06 May 2014.
Submit your article to this journal
Article views: 8
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=yacb20 Download by: [Orta Dogu Teknik Universitesi]
Date: 27 April 2016, At: 17:21
ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION
Image in Medicine
ACUTE OXALATE NEPHROPATHY AFTER RENAL TRANSPLANTATION Mazzoleni L1, Aydin S2, De Meyer M3, Pirson Y1, Kanaan N1 Division of 1Nephrology, 2Pathology and 3Surgery and Abdominal Transplantation Cliniques Universitaires Saint Luc, Université Catholique de Louvain, Brussels, Belgium
Downloaded by [Orta Dogu Teknik Universitesi] at 17:21 27 April 2016
Correspondence and offprint requests to: Nada Kanaan, E-mail: [email protected]
A 52-year-old man was transplanted with a kidney from a deceased donor for a biopsy-proven renal AA amyloidosis secondary to Crohn’s disease after five years on hemodialysis. His past history included multiple small intestine resections, intermittent diarrhea, and adrenal insufficiency in the context of amyloidosis leading to persistent hypotension. The postoperative period was marked by a delayed graft function initially attributed to acute tubular necrosis secondary to decreased renal perfusion as a consequence of his low blood pressure. Renal function was slow to recover with stagnation of creatinine clearance at 16 ml/ min three weeks after transplantation prompting a kidney graft biopsy. It showed translucent calcium oxalate crystals within renal tubules (Figure 1A), with characteristic birefringence under polarized light microscopy (Figure 1B). Oxaluria was significantly increased taking into account the degree of renal insufficiency (66 mg/g of creatinine (normal: 0-32)). Kidney function did not improve and the patient returned to hemodialysis 5 months later. Acute oxalate nephropathy secondary to enteric hyperoxaluria caused early graft loss in our patient. Enteric hyperoxaluria is due to fat malabsorbtion as encountered in Crohn’s disease, extensive bowel resection, pancreatic insufficiency or bariatric surgery. Non-absorbed bile acids and fatty acids
A
increase intestinal permeability to oxalate. In addition, fatty acids bind calcium in the lumen, decreasing the calcium available for binding oxalate and preventing its intestinal absorption (1). Recognition of enteric hyperoxaluria before transplantation is of importance. Indeed, a large quantity of oxalate accumulated in the body can be rapidly released with a risk of oxalate calcium precipitation in the graft (2). Measures to reduce hyperoxaluria and prevent graft oxalosis must be taken including a low-oxalate and fat diet, oral calcium supplements, high fluid intake, and inhibitors of crystallization such as magnesium and citrate (1). High-efficiency intensive dialysis can also be beneficial to reduce serum oxalate levels (3).
REFERENCES 1. Robijn S, Hoppe B, Vervaet BA, D’Haese PC, Verhukst A. Hyperoxalouria: a gutkidney axis? Kidney international 2011; 80: 1146-1158. 2. Cuvelier C, Goffin E, Cosyns JP, Wauthier M, van Ypersel de Strihou C. Enteric hyperoxaluria: A hidden cause of early renal graft failure in two successive transplants: spontaneous late graft recovery. Am J Kidney Dis 2002; 40: E3. 3. Rankin A.C, Walsh SB, Summers SA, Owen MP, Mansell MA. Acute oxalate nephropathy causing late renal transplant dysfunction due to enteric hypeorxaluria. Am J Transplant 2008: 8: 1755-1758.
B
Figure 1: (A) Intra-tubular translucent crystals with associated tubular injury observed under standard light microscopy (hematoxylin and eosin, original magnification x200). (B) Oxalate crystal deposition with characteristic birefringence under polarized light microscopy (original magnification x100).
doi: 10.2143/ACB.3331
Acta Clinica Belgica, 2013; 68-5
389
