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Nonocclusive Mesenteric Ischemia in a Dialysis Patient With Extensive Vascular Calcification
Imaging Teaching Case Nonocclusive Mesenteric Ischemia in a Dialysis Patient With Extensive Vascular Calcification Umberto G. Rossi, MD, Francesco Petrocelli, MD, Sara Seitun, MD, and Carlo Ferro, MD We describe a case of nonocclusive mesenteric ischemia in a 37-year-old man with hemodialysis-dependent chronic kidney disease due to diabetes who was admitted to our hospital with abdominal pain. A plain radiograph of the abdomen showed distended loops of small bowel and gas in the hepatic portal vein. Multidetector computed tomography showed massive wall calcification of the superior mesenteric artery and its collaterals, pneumatosis intestinalis of a segment of the jejunum, and porto-mesenteric vein gas. Urgent laparotomy confirmed segmental necrosis of the jejunum, which was resected. Pathologic examination showed whole-layer necrosis of the resected bowel without arterial or venous thrombosis. Nonocclusive mesenteric ischemia is an increasingly recognized and potentially lethal complication in hemodialysis patients. In the present case, critical factors for the development of nonocclusive mesenteric ischemia may have included prolonged hypotension during hemodialysis treatments that reduced blood flow to the small bowel and massive vascular calcification that negatively affected compliance of the superior mesenteric artery and its branches. Am J Kidney Dis. 60(5):843-846. © 2012 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved. INDEX WORDS: Mesenteric ischemia; pneumatosis intestinalis; hepatic portal venous gas; arterial calcifications; hemodialysis.
INTRODUCTION Nonocclusive mesenteric ischemia is a rare complication in dialysis patients, with potentially fatal consequences if not recognized and managed promptly.1 Although both the diagnosis and perioperative management of nonocclusive mesenteric ischemia have improved, mortality remains high.1-3 Porto-mesenteric vein gas is a rare condition, and its pathogenesis is still not well understood. Generally, it is associated with extensive bowel necrosis and death.4 Vascular calcification is common in patients with hemodialysisdependent chronic kidney disease (CKD) due to diabetes, and it is correlated strongly with coronary artery disease and future cardiovascular events.5 We describe a diabetic patient with hemodialysis-dependent CKD who developed nonocclusive mesenteric ischemia with pneumatosis intestinalis and portomesenteric vein gas in the context of massive calcification of the superior mesenteric artery (SMA) and its collaterals. CASE REPORT Clinical History and Initial Laboratory Data A 37-year-old man with a 3-year history of hemodialysisdependent CKD due to diabetes mellitus was admitted to our hospital for progressive abdominal pain. He had no fever, vomiting, hematemesis, or melena. The patient underwent hemodialysis 9 hours before acute presentation and reported an episode of prolonged hypotension (blood pressure, 85/42 mm Hg) during the treatment that resolved without medication. Physical examination showed blood pressure of 105/45 mm Hg and heart rate of 68 beats/min. His abdomen was slightly distended but nontender, with hypoactive bowel sounds in all 4 quadrants. Blood work showed Am J Kidney Dis. 2012;60(5):843-846
elevation of alanine aminotransferase (231 U/L), aspartate aminotransferase (132 U/L), lactate dehydrogenase (381 U/L), white blood cell count (12.45 ⫻ 103/L [12.45 ⫻ 109/L]), and C-reactive protein (83.4 mg/L) levels.
Imaging Studies A plain radiograph of the abdomen showed air-filled dilated loops of small bowel (jejunum) in the mid-left abdomen and gas was noted in the hepatic portal vein (Fig 1). Non–contrastenhanced and contrast-enhanced multidetector computed tomography (CT) showed massive mold-like wall calcification of the celiac trunk, SMA, and its collaterals. Air distension of small-bowel loops, pneumatosis intestinalis of a segment of the jejunum in the left upper quadrant, and gas in the main trunk of the superior mesenteric vein and its collaterals extending into the portal vein also were seen (Fig 2A-D). Despite extensive calcification of the SMA and its branches, neither occlusive thrombosis nor significant luminal narrowing was detected.
From the Department of Radiology and Interventional Radiology, IRCCS San Martino University Hospital, IST–National Institute for Cancer Research, Genova, Italy. Received March 22, 2012. Accepted in revised form May 30, 2012. Originally published online July 17, 2012. Address correspondence to Umberto G. Rossi, MD, Department of Radiology and Interventional Radiology, IRCCS San Martino University Hospital, IST–National Institute for Cancer Research, Largo Rosanna Benzi 10, 16132 Genova, Italy. E-mail: urossi76@ hotmail.com © 2012 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved. 0272-6386/$36.00 http://dx.doi.org/10.1053/j.ajkd.2012.05.020 843
Rossi et al
Figure 1. Abdominal radiograph on admission shows airfilled dilated loops of small bowel (jejunum) in the mid-left abdomen and hepatic portal venous gas in the right lower lobe (arrow).
Diagnosis Nonocclusive mesenteric ischemia with porto-mesenteric vein gas due to massive calcification of the SMA vasculature was suspected.
Clinical Follow-up The patient underwent urgent laparotomy that confirmed the ischemic changes in 120 mm of jejunum. This bowel had a remarkably thin wall. The SMA and its collaterals were very heavily calcified. The segment with ischemic change in the jejunum was excised, and end-to-end bowel anastomosis was performed. Pathologic examination showed whole-layer necrosis of the resected bowel without arterial or venous thrombosis. The patient recovered without incident and left the hospital on postoperative day 18. A regimen of careful monitoring of blood pressure was instituted for dialysis sessions, and the patient’s condition has been stable during the 9 months of follow-up.
DISCUSSION Recently, nonocclusive mesenteric ischemia has been seen increasingly as a serious complication in hemodialysis patients.6,7 Delay in a correct diagnosis culminates in a high mortality rate (up to 85%).1 Hypotension during or at the end of the hemodialysis treatment is the most significant and directly linked precipitating factor for nonocclusive mesenteric ischemia in these patients.1 When hypotension is coupled with intravascular depletion due to the ultrafiltration during hemodialysis, a low-flow state in the SMA develops.6 As demonstrated by other authors,1,6,7 all patients who developed nonocclusive mesenteric ischemia report severe hypotension prior to the onset of abdominal pain. However, intradialytic hypotensive episodes are common and far outnumber the fre844
quency of nonocclusive mesenteric ischemia events in these patients. Other risk factors that leave an individual dialysis patient vulnerable to the development of nonocclusive mesenteric ischemia include vascular calcification, diabetes mellitus, advanced age, and increased time on dialysis.1,6,7 In our patient, only massive vascular calcification and diabetes mellitus were present. Over the last 2 decades, evidence has accumulated that vascular calcification is an active and regulated process that has significant consequences for hemodialysis-dependent patients with CKD.5,8-10 Two patterns of vascular calcification have been identified. In the process of atherosclerotic plaque formation, lipidladen foam cells at the base of the plaque located in the intima are associated with the occurrence of calcification. This calcification is focused, and nearby vessel wall regions appear normal.10 The other form of vascular calcification, Monckeberg sclerosis, involves mineral deposits diffused throughout the vascular tree. It occurs primarily in the media of the vessel; the internal elastic lamina is the most common location. There is no connection to the process of atheromatous plaque formation.10,11 This second form of vascular calcification is typical in patients with CKD and diabetes mellitus.11,12 The presence of medial calcification in medium- to small-sized mesenteric arteries contributes to stiffening of these vessel walls and a reduction in vascular compliance, particularly in hypotensive states. Porto-mesenteric vein gas is not a disease, but a radiologic sign of an underlying pathologic state within the gastrointestinal tract.13 Porto-mesenteric vein gas can be observed in a number of clinical settings, including bowel necrosis, inflammatory bowel disease, diverticulitis, gastrointestinal dilatation, intraabdominal abscesses, sepsis, trauma, and iatrogenic complications.14 The most common and serious cause is necrotic bowel. There are 3 mechanisms of gas formation in the mesenteric-portal vein system13,14: (1) intestinal wall alteration, in which the endothelial barriers between the small mesenteric veins and gas in the enteric lumen break down; (2) bowel loop overdistension, with elevated intramural pressure leading to mucosal disruption and passage of intraluminal gas into the vasculature; and (3) intra-abdominal sepsis, with anaerobic gas-forming bacteria gaining access to the mesenteric veins through the bowel wall. Patients with CKD have much higher numbers of microbial flora in the small intestine, consisting of both anaerobes and aerobes.14 This clinical setting explains a possible contributory cause in the mechanism of portomesenteric vein gas in patients with CKD. Imaging findings of porto-mesenteric vein gas are visualized with conventional radiography and multideAm J Kidney Dis. 2012;60(5):843-846
Bowel Ischemia for Mesenteric Artery Ca⫹⫹
Figure 2. (A) Non– contrast-enhanced phase multidetector computed tomographic (CT) coronal images show massive calcification of the celiac trunk (arrow) and the superior mesenteric artery and its collaterals (arrowhead). (B) Non– contrast-enhanced phase multidetector CT axial image with lung window shows gas in the jejunal veins (black arrows) and intramural bowel gas in the jejunum (arrowheads). (C) Contrast-enhanced phase multidetector CT axial image shows gas in the main trunk of the superior mesenteric vein (arrowhead), its branches (white arrows), and intrahepatic portal veins (black arrow) as multiple areas of low attenuation. (D) Contrast-enhanced phase multidetector CT axial image confirming gas in the jejunal veins (white arrows) and intramural bowel gas in the jejunum (arrowheads).
tector CT. The radiographic criterion for portomesenteric vein gas is a branching area of low attenuation extending to within 2 cm of the liver capsule.15 With multidetector CT, porto-mesenteric vein gas appears as tubular areas of decreased attenuation in the periphery of the liver and in the porto-mesenteric venous system.4 Porto-mesenteric vein gas is distinguished from biliary gas in both location and character. Portomesenteric vein gas is peripheral, extending near or out of the hepatic capsule. The collections appear smaller and more numerous. Biliary gas is more central due to the centripetal flow of bile.4 Portomesenteric vein gas often is associated with pneumatosis intestinalis (mural necrosis), posing a grave prognosis. On multidetector CT, pneumatosis intestinalis is evidenced by distended bowel loops and gas in the bowel wall.4 Am J Kidney Dis. 2012;60(5):843-846
In our patient, the clinical and pathologic setting can be explained by the profound and prolonged hypotension during the hemodialysis session that reduced blood flow to the small bowel and massive vascular calcification that disrupted the autoregulatory capacity (vascular compliance) of the peripheral superior mesenteric arterioles. Consequently, local ischemia led to paralytic ileus with bowel distension that was worsened by the fermentation of bacteria usually found in patients with CKD. These processes caused mucosal injury that allowed the passage of intraluminal gas into the bowel wall (pneumatosis) and consequently into the porto-mesenteric venous system. In conclusion, hemodialysis patients, particularly those with massive vascular calcification, have to be considered at high risk of developing severe nonocclusive mesenteric ischemia. 845
Rossi et al
ACKNOWLEDGEMENTS The authors thank Stefano Di Domenico, MD, of the Department of Abdominal Surgery and Department of Nephrology for his contribution to the manuscript. Support: None. Financial Disclosure: The authors declare that they have no relevant financial interest.
REFERENCES 1. Ori Y, Chagnac A, Schwartz A, et al. Non-occlusive mesenteric ischemia in chronically dialyzed patients: a disease with multiple risk factors. Nephron Clin Pract. 2005;101(2):c87-c93. 2. Duron JJ, Peyrard P, Boukhtouche S, Farah A, Suc B. Acute mesenteric ischemia: changes in 1985–1995. Surgical Research Associations. Chirurgie. 1998;123(4):335-342. 3. Lagana S, Barras JP. Surgical therapy of mesenteric infarct. Zentralbl Chir. 1998;123(12):1405-1410. 4. Sebastià C, Quiroga S, Espin E, Boye R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):12131224; discussion 1224-1226. 5. Reslerova M, Moe SM. Vascular calcification in dialysis patients: pethogenesis and consequences. Am J Kidney Dis. 2003; 41(3)(suppl 1):S96-S99. 6. John AS, Tuerff SD, Kerstein MD. Nonocclusive mesenteric infarction in hemodialysis patients. Am J Coll Surg. 2000;190(1): 84-88.
846
7. Bassilion N, Menoyo V, Berger A, et al. Mesenteric ischemia in haemodialysis patients: a case/control study. Nephrol Dial Transplant. 2003;18(5):911-917. 8. Goldsmith DJA, Covic A, Sambrook PA, Ackrill P. Vascular calcification in long-term haemodialysis patients in a single unit: a retrospective study. Nephron. 1997;77(1):37-43. 9. Guerin AP, London GM, Marchais SJ, Metivier F. Arterial stiffening and vascular calcifications in end-stage renal disease. Nephrol Dial Transplant. 2000;15(7):1014-1021. 10. Davies MR, Hruska KA. Pathophysiological mechanisms of vascular calcification in end-stage renal disease. Kidney Int. 2001;60(2):472-479. 11. Ibel LS, Alfrey AC, Huffer WE, Craswell PW, Anderson JT, Weil R III. Arterial calcification and pathology in uremic patients undergoing dialysis. Am J Med. 1979;66(5):790-796. 12. Edmonds ME. Medial arterial calcification and diabetes mellitus. Z Kardiol. 2000;89(suppl 2):101-104. 13. Monneuse O, Pilleul F, Barth X, et al. Portal venous gas detected on computed tomography in emergency situations: surgery is still necessary. World J Surg. 2007;31(5):10651071. 14. Morimoto Y, Yamakawa T, Tanaka Y, Hiranaka T, Kim M. Recurrent hepatic portal venous gas in a patient with hemodialysisdependent chronic renal failure. J Hepatobiliary Pancreat Surg. 2001;8(3):274-278. 15. Liebman PR, Patten MT, Manny J, Benfield JR, Hechtman HB. Hepatic-portal venous gas in adults: etiology, pathophysiology and clinical significance. Ann Surg. 1978;3:281-287.
Am J Kidney Dis. 2012;60(5):843-846
INTRODUCTION Nonocclusive mesenteric ischemia is a rare complication in dialysis patients, with potentially fatal consequences if not recognized and managed promptly.1 Although both the diagnosis and perioperative management of nonocclusive mesenteric ischemia have improved, mortality remains high.1-3 Porto-mesenteric vein gas is a rare condition, and its pathogenesis is still not well understood. Generally, it is associated with extensive bowel necrosis and death.4 Vascular calcification is common in patients with hemodialysisdependent chronic kidney disease (CKD) due to diabetes, and it is correlated strongly with coronary artery disease and future cardiovascular events.5 We describe a diabetic patient with hemodialysis-dependent CKD who developed nonocclusive mesenteric ischemia with pneumatosis intestinalis and portomesenteric vein gas in the context of massive calcification of the superior mesenteric artery (SMA) and its collaterals. CASE REPORT Clinical History and Initial Laboratory Data A 37-year-old man with a 3-year history of hemodialysisdependent CKD due to diabetes mellitus was admitted to our hospital for progressive abdominal pain. He had no fever, vomiting, hematemesis, or melena. The patient underwent hemodialysis 9 hours before acute presentation and reported an episode of prolonged hypotension (blood pressure, 85/42 mm Hg) during the treatment that resolved without medication. Physical examination showed blood pressure of 105/45 mm Hg and heart rate of 68 beats/min. His abdomen was slightly distended but nontender, with hypoactive bowel sounds in all 4 quadrants. Blood work showed Am J Kidney Dis. 2012;60(5):843-846
elevation of alanine aminotransferase (231 U/L), aspartate aminotransferase (132 U/L), lactate dehydrogenase (381 U/L), white blood cell count (12.45 ⫻ 103/L [12.45 ⫻ 109/L]), and C-reactive protein (83.4 mg/L) levels.
Imaging Studies A plain radiograph of the abdomen showed air-filled dilated loops of small bowel (jejunum) in the mid-left abdomen and gas was noted in the hepatic portal vein (Fig 1). Non–contrastenhanced and contrast-enhanced multidetector computed tomography (CT) showed massive mold-like wall calcification of the celiac trunk, SMA, and its collaterals. Air distension of small-bowel loops, pneumatosis intestinalis of a segment of the jejunum in the left upper quadrant, and gas in the main trunk of the superior mesenteric vein and its collaterals extending into the portal vein also were seen (Fig 2A-D). Despite extensive calcification of the SMA and its branches, neither occlusive thrombosis nor significant luminal narrowing was detected.
From the Department of Radiology and Interventional Radiology, IRCCS San Martino University Hospital, IST–National Institute for Cancer Research, Genova, Italy. Received March 22, 2012. Accepted in revised form May 30, 2012. Originally published online July 17, 2012. Address correspondence to Umberto G. Rossi, MD, Department of Radiology and Interventional Radiology, IRCCS San Martino University Hospital, IST–National Institute for Cancer Research, Largo Rosanna Benzi 10, 16132 Genova, Italy. E-mail: urossi76@ hotmail.com © 2012 by the National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved. 0272-6386/$36.00 http://dx.doi.org/10.1053/j.ajkd.2012.05.020 843
Rossi et al
Figure 1. Abdominal radiograph on admission shows airfilled dilated loops of small bowel (jejunum) in the mid-left abdomen and hepatic portal venous gas in the right lower lobe (arrow).
Diagnosis Nonocclusive mesenteric ischemia with porto-mesenteric vein gas due to massive calcification of the SMA vasculature was suspected.
Clinical Follow-up The patient underwent urgent laparotomy that confirmed the ischemic changes in 120 mm of jejunum. This bowel had a remarkably thin wall. The SMA and its collaterals were very heavily calcified. The segment with ischemic change in the jejunum was excised, and end-to-end bowel anastomosis was performed. Pathologic examination showed whole-layer necrosis of the resected bowel without arterial or venous thrombosis. The patient recovered without incident and left the hospital on postoperative day 18. A regimen of careful monitoring of blood pressure was instituted for dialysis sessions, and the patient’s condition has been stable during the 9 months of follow-up.
DISCUSSION Recently, nonocclusive mesenteric ischemia has been seen increasingly as a serious complication in hemodialysis patients.6,7 Delay in a correct diagnosis culminates in a high mortality rate (up to 85%).1 Hypotension during or at the end of the hemodialysis treatment is the most significant and directly linked precipitating factor for nonocclusive mesenteric ischemia in these patients.1 When hypotension is coupled with intravascular depletion due to the ultrafiltration during hemodialysis, a low-flow state in the SMA develops.6 As demonstrated by other authors,1,6,7 all patients who developed nonocclusive mesenteric ischemia report severe hypotension prior to the onset of abdominal pain. However, intradialytic hypotensive episodes are common and far outnumber the fre844
quency of nonocclusive mesenteric ischemia events in these patients. Other risk factors that leave an individual dialysis patient vulnerable to the development of nonocclusive mesenteric ischemia include vascular calcification, diabetes mellitus, advanced age, and increased time on dialysis.1,6,7 In our patient, only massive vascular calcification and diabetes mellitus were present. Over the last 2 decades, evidence has accumulated that vascular calcification is an active and regulated process that has significant consequences for hemodialysis-dependent patients with CKD.5,8-10 Two patterns of vascular calcification have been identified. In the process of atherosclerotic plaque formation, lipidladen foam cells at the base of the plaque located in the intima are associated with the occurrence of calcification. This calcification is focused, and nearby vessel wall regions appear normal.10 The other form of vascular calcification, Monckeberg sclerosis, involves mineral deposits diffused throughout the vascular tree. It occurs primarily in the media of the vessel; the internal elastic lamina is the most common location. There is no connection to the process of atheromatous plaque formation.10,11 This second form of vascular calcification is typical in patients with CKD and diabetes mellitus.11,12 The presence of medial calcification in medium- to small-sized mesenteric arteries contributes to stiffening of these vessel walls and a reduction in vascular compliance, particularly in hypotensive states. Porto-mesenteric vein gas is not a disease, but a radiologic sign of an underlying pathologic state within the gastrointestinal tract.13 Porto-mesenteric vein gas can be observed in a number of clinical settings, including bowel necrosis, inflammatory bowel disease, diverticulitis, gastrointestinal dilatation, intraabdominal abscesses, sepsis, trauma, and iatrogenic complications.14 The most common and serious cause is necrotic bowel. There are 3 mechanisms of gas formation in the mesenteric-portal vein system13,14: (1) intestinal wall alteration, in which the endothelial barriers between the small mesenteric veins and gas in the enteric lumen break down; (2) bowel loop overdistension, with elevated intramural pressure leading to mucosal disruption and passage of intraluminal gas into the vasculature; and (3) intra-abdominal sepsis, with anaerobic gas-forming bacteria gaining access to the mesenteric veins through the bowel wall. Patients with CKD have much higher numbers of microbial flora in the small intestine, consisting of both anaerobes and aerobes.14 This clinical setting explains a possible contributory cause in the mechanism of portomesenteric vein gas in patients with CKD. Imaging findings of porto-mesenteric vein gas are visualized with conventional radiography and multideAm J Kidney Dis. 2012;60(5):843-846
Bowel Ischemia for Mesenteric Artery Ca⫹⫹
Figure 2. (A) Non– contrast-enhanced phase multidetector computed tomographic (CT) coronal images show massive calcification of the celiac trunk (arrow) and the superior mesenteric artery and its collaterals (arrowhead). (B) Non– contrast-enhanced phase multidetector CT axial image with lung window shows gas in the jejunal veins (black arrows) and intramural bowel gas in the jejunum (arrowheads). (C) Contrast-enhanced phase multidetector CT axial image shows gas in the main trunk of the superior mesenteric vein (arrowhead), its branches (white arrows), and intrahepatic portal veins (black arrow) as multiple areas of low attenuation. (D) Contrast-enhanced phase multidetector CT axial image confirming gas in the jejunal veins (white arrows) and intramural bowel gas in the jejunum (arrowheads).
tector CT. The radiographic criterion for portomesenteric vein gas is a branching area of low attenuation extending to within 2 cm of the liver capsule.15 With multidetector CT, porto-mesenteric vein gas appears as tubular areas of decreased attenuation in the periphery of the liver and in the porto-mesenteric venous system.4 Porto-mesenteric vein gas is distinguished from biliary gas in both location and character. Portomesenteric vein gas is peripheral, extending near or out of the hepatic capsule. The collections appear smaller and more numerous. Biliary gas is more central due to the centripetal flow of bile.4 Portomesenteric vein gas often is associated with pneumatosis intestinalis (mural necrosis), posing a grave prognosis. On multidetector CT, pneumatosis intestinalis is evidenced by distended bowel loops and gas in the bowel wall.4 Am J Kidney Dis. 2012;60(5):843-846
In our patient, the clinical and pathologic setting can be explained by the profound and prolonged hypotension during the hemodialysis session that reduced blood flow to the small bowel and massive vascular calcification that disrupted the autoregulatory capacity (vascular compliance) of the peripheral superior mesenteric arterioles. Consequently, local ischemia led to paralytic ileus with bowel distension that was worsened by the fermentation of bacteria usually found in patients with CKD. These processes caused mucosal injury that allowed the passage of intraluminal gas into the bowel wall (pneumatosis) and consequently into the porto-mesenteric venous system. In conclusion, hemodialysis patients, particularly those with massive vascular calcification, have to be considered at high risk of developing severe nonocclusive mesenteric ischemia. 845
Rossi et al
ACKNOWLEDGEMENTS The authors thank Stefano Di Domenico, MD, of the Department of Abdominal Surgery and Department of Nephrology for his contribution to the manuscript. Support: None. Financial Disclosure: The authors declare that they have no relevant financial interest.
REFERENCES 1. Ori Y, Chagnac A, Schwartz A, et al. Non-occlusive mesenteric ischemia in chronically dialyzed patients: a disease with multiple risk factors. Nephron Clin Pract. 2005;101(2):c87-c93. 2. Duron JJ, Peyrard P, Boukhtouche S, Farah A, Suc B. Acute mesenteric ischemia: changes in 1985–1995. Surgical Research Associations. Chirurgie. 1998;123(4):335-342. 3. Lagana S, Barras JP. Surgical therapy of mesenteric infarct. Zentralbl Chir. 1998;123(12):1405-1410. 4. Sebastià C, Quiroga S, Espin E, Boye R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):12131224; discussion 1224-1226. 5. Reslerova M, Moe SM. Vascular calcification in dialysis patients: pethogenesis and consequences. Am J Kidney Dis. 2003; 41(3)(suppl 1):S96-S99. 6. John AS, Tuerff SD, Kerstein MD. Nonocclusive mesenteric infarction in hemodialysis patients. Am J Coll Surg. 2000;190(1): 84-88.
846
7. Bassilion N, Menoyo V, Berger A, et al. Mesenteric ischemia in haemodialysis patients: a case/control study. Nephrol Dial Transplant. 2003;18(5):911-917. 8. Goldsmith DJA, Covic A, Sambrook PA, Ackrill P. Vascular calcification in long-term haemodialysis patients in a single unit: a retrospective study. Nephron. 1997;77(1):37-43. 9. Guerin AP, London GM, Marchais SJ, Metivier F. Arterial stiffening and vascular calcifications in end-stage renal disease. Nephrol Dial Transplant. 2000;15(7):1014-1021. 10. Davies MR, Hruska KA. Pathophysiological mechanisms of vascular calcification in end-stage renal disease. Kidney Int. 2001;60(2):472-479. 11. Ibel LS, Alfrey AC, Huffer WE, Craswell PW, Anderson JT, Weil R III. Arterial calcification and pathology in uremic patients undergoing dialysis. Am J Med. 1979;66(5):790-796. 12. Edmonds ME. Medial arterial calcification and diabetes mellitus. Z Kardiol. 2000;89(suppl 2):101-104. 13. Monneuse O, Pilleul F, Barth X, et al. Portal venous gas detected on computed tomography in emergency situations: surgery is still necessary. World J Surg. 2007;31(5):10651071. 14. Morimoto Y, Yamakawa T, Tanaka Y, Hiranaka T, Kim M. Recurrent hepatic portal venous gas in a patient with hemodialysisdependent chronic renal failure. J Hepatobiliary Pancreat Surg. 2001;8(3):274-278. 15. Liebman PR, Patten MT, Manny J, Benfield JR, Hechtman HB. Hepatic-portal venous gas in adults: etiology, pathophysiology and clinical significance. Ann Surg. 1978;3:281-287.
Am J Kidney Dis. 2012;60(5):843-846