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Surgical treatment of renal cell carcinoma associated with Budd–Chiari syndrome: report of four cases and review of the literature
European Journal of Surgical Oncology 1999; 25: 71–75
Surgical treatment of renal cell carcinoma associated with Budd–Chiari syndrome: report of four cases and review of the literature H. Kume, S. Kameyama, Y. Kasuya, A. Tajima and K. Kawabe Department of Urology, Faculty of Medicine, University of Tokyo, Japan
Aims: Renal cell carcinoma is sometimes associated with inferior vena caval tumour thrombus, but occlusion of hepatic veins by the tumour thrombus causing liver dysfunction, the so-called Budd–Chiari syndrome, is relatively uncommon. There are only a few reports in the literature which discuss this condition. Methods: Four cases admitted to our hospital over a 7-year period and eight cases reported in detail in the English and the Japanese literature were included in this study. They are classified into two groups: mild/silent, without liver failure, and severe, with liver failure. Results: Five patients were classified as mild/silent and seven as severe. Clinical manifestations were mild in the former cases and acute in the latter. Surgery was performed in four of the former cases but only in one case of the latter cases. Conclusions: In mild cases, surgical treatment seems to avoid imminent hepatic failure effectively and should be performed as soon as possible. In such cases Budd–Chiari syndrome in itself does not affect the prognosis. In severe cases, however, surgical treatment is very difficult and risky due to the existing hepatic failure. Key words: renal cell carcinoma; Budd–Chiari syndrome; surgical treatment; tumour thrombus.
Introduction Renal cell carcinoma is often associated with a tumour thrombus, which sometimes extends into the inferior vena cava (IVC). However, hepatic venous obstruction by a tumour thrombus, which causes Budd–Chiari syndrome, is relatively uncommon.1–8 Due to the lack of detailed reports in the literature, little is known of the clinical course of unusual condition. In this study, we analysed 12 cases, including eight cases reported in the English1–4 and the Japanese5–8 literature. The indications for and efficacy of thrombectomy are discussed.
Methods Between January 1990 and December 1997, four patients with renal cell carcinoma associated with Budd–Chiari syndrome were admitted to our hospital (Fig. 1). The diagnosis was confirmed by signs, symptoms and laboratory tests. In three of the four cases, Doppler ultrasonography showed decreased or reversed flow of hepatic veins. In all
Correspondence to H. Kume, Department of Urology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan. Fax: 81-3-5800-8917. 0748–7983/99/010071+05 $12.00/0
our surgical cases, diagnosis was confirmed by enlarged and congested liver, which rapidly returned to normal size, colour and consistency after removal of the tumour thrombi. In each case, histological examination revealed renal cell carcinoma. In addition to these four cases, we extracted eight well-documented cases from the literature.1–8 We classified the 12 cases into two groups, mild/silent and severe. Mild/silent is characterized by the absence of liver failure and severe by the presence of liver failure. We compared clinical signs and symptoms, laboratory parameters, treatment and prognosis between these two groups.
Results Five cases were classified as mild/silent and seven as severe. Age and sex were similar between the two groups, except for age in case 3, who had been diagnosed as having von Hippel–Lindau disease in addition to Budd–Chiari syndrome. The side, size and site of the renal tumours were also similar between the two groups. Clinical characteristics of the patients are summarized in Tables 1 and 2. The onset of Budd–Chiari syndrome was gradual in mild/ silent cases, whereas it was sudden and acute in severe cases. Hepatomegaly and ascites were present in both groups, 1999 W.B. Saunders Company Limited
Rt, L Rt, U Lt, U Lt Lt, L
Lt, L Rt Rt, M Rt Rt Rt Rt
63/M 67/M 51/M 59/M 68/M 63/M 62/M
Site
61/M 54/M 29/F 60/M 60/M
Age/sex
10 20 5 N/A 7 N/A N/A
5 11 8 N/A 5
Size (cm) atrium atrium atrium atrium atrium
Right ventricle N/A Right ventricle Hepatic vein Right atrium Hepatic vein Right atrium
Right Right Right Right Right
Tumour thrombus
None N/A Lung, lymph nodes N/A N/A N/A N/A
None Lung None N/A Liver
Metastasis
Sudden N/A Sudden Sudden Sudden Sudden N/A
Gradual Gradual Gradual Gradual Gradual
Onset
− − − − − + − + N/A + + N/A
+ + + + + + +
DIC or DIC-like status
− − − − −
Liver failure
∗ Time from surgery or presentation. M, male; F, female; Rt, right; Lt, left; L, lower; U, upper; Mid, middle; N/A, not available.
Mild/silent Case 1 Case 2 Case 3 Case 41 Case 52 Severe Case 6 Case 73 Case 84 Case 95 Case 106 Case 117 Case 128
Type of disease
Renal cell carcinoma
Table 1. Patient characteristics
− − − − − − −
+ + + + −
Surgery
Died (1 month) Died (3 days) Died (1 month) N/A Died (2 weeks) Died (1.5 months) Died (1 month)
Died (10 months) Died (8 months) Alive (37 months) Died (N/A) Died (N/A)
Outcome∗
72 H. Kume et al.
73
Renal cell carcinoma in Budd–Chiari syndrome Case 1
Case 2
Case 3
Case 6
Right lower, φ5 cm. pT3bpN0M0. RCC, CC and GC, Grade 1 > 2
Right upper, φ11 cm pT3bpN0M1 (pulmonary metastasis: rt. middle lobe) RCC, CC, Grade 3 >> 2
Left upper, φ8 cm Right upper, φ4 cm Bilateral, several tumours, φ1–2 cm pT3bpN0M0. RCC, CC, Grade 2 Pheochromocytoma of rt. adrenal.
Left lower, φ10 cm pT3bpN0M0 RCC, CC, Grade 3
Fig. 1. Localization, size, staging and histology of our four cases. Cases 1–3; surgically proved staging. Case 6; autopsy findings. Lt, left; rt, right; RCC, renal cell carcinoma; CC, clear cell; GC, granular cell.
Table 2. Clinical manifestations
Hepatomegaly Ascites Jaundice Encephalopathy Leg oedema
Mild/silent cases (n/total)
Severe cases (n/total)
5/5 5/5 0/4 0/3 2/5
7/7 6/6 5/5 5/5 4/6
other causes, including metastatic disease or local recurrence of the IVC tumour thrombus. In the severe cases, surgery was performed only in case 8, who died from liver failure, renal failure and septicaemia 1 month after surgery.4 The other six severe cases were inoperable and died from liver failure within 1 month.
Discussion
while jaundice and encephalopathy were more frequently seen in severe cases. Moreover, at least four of the seven cases with severe Budd–Chiari syndrome had disseminated intravascular coagulation (DIC) or a DIC-like status, whereas none of five mild/silent cases had such a manifestation. Figure 2 shows the results of the liver function tests in our four cases. In the three mild/silent cases the results were abnormal, but the degree of abnormality was greater in case 6, who had severe disease. These values normalized after surgery in our three surgical cases. Results of liver function tests were not well-documented in the eight cases taken from the literature. In four of five mild/silent type cases surgery was performed. Surgery could not be performed in the other case, reported by Smith et al.,2 because of the extent of the carcinoma. Of the five mild/silent cases, cases 1, 2 and 3 survived for a relatively long period. Case 3 is currently alive, 3 years after surgery, with no evidence of recurrent disease. At least three cases, numbers 1, 2 and 4, died from
Budd–Chiari syndrome is a relatively uncommon disorder, in which occlusion of the hepatic veins and/or the inferior vena cava causes hepatic congestion and liver dysfunction.9, 10 It may sometimes result from malignant tumours, such as primary hepatocellular carcinoma, sarcoma arising from the IVC, adrenal carcinoma, Wilms’ tumour and renal cell carcinoma.9,10 In patients with renal cell carcinoma, Budd–Chiari syndrome is caused by an existing IVC thrombus occluding the hepatic veins. We classified the cases studied into two groups, mild/ silent (without liver failure) and severe (with liver failure). Patients with mild/silent disease had a gradual onset and slight liver dysfunction, probably due to incomplete and/or gradual obstruction, which may allow a collateral circulation to develop and may minimize the liver damage. Patients with severe disease had an acute onset with serious liver damage and subsequent DIC or DIC-like status, which may result from sudden and complete obstruction of the hepatic veins. In some patients, mild/silent manifestations may become severe during the clinical course. We have shown here that in cases with mild/silent
74
H. Kume et al. (a)
(b)
600
(c)
4.0
100
3.0
75
100
50
0
µg/dl
mg/dl
IU/l
150
2.0
1.0
Before
After
0
50
25
Before
After
0
Before After
Fig. 2. Changes in clinical parameters of liver function. (a) Transaminases; (b) total bilirubin; (c) ammonia. Μ: GOT, severe case, Α: GOT, mild/silent case, Ν: GPT, severe case, Κ: GPT, mild/silent case, Ο: total bilirubin, severe case, Η: bilirubin, mild/silent case, Χ: NH3, severe case, Β: NH3, mild/silent case.
Fig. 3. Enhanced abdominal CT scan of case 6. (a) Hepatomegaly and ascites are present. The liver is enhanced heterogeniously. Arrow heads indicate the IVC tumour thrombus. (b) The renal cancer, left lower pole, about 10 cm in diameter.
Fig. 4. Post-mortem examination of case 6. (a) Histology of the renal tumour was renal cell carcinoma, clear cell type. (b) The liver. Marked congestion with necrosis and loss of hepatocytes in the perivenular area (c). G shows periportal area.
Budd–Chiari syndrome, thrombectomy seems effectively to avoid imminent hepatic failure and therefore surgery should be performed as soon as possible to minimize the risk of
disease progression. In retrospect, nephrectomy and thrombectomy should have been performed earlier in case 6, before Budd–Chiari syndrome developed.
Renal cell carcinoma in Budd–Chiari syndrome Budd–Chiari syndrome in itself does not effect prognosis. No mild/silent cases died from existing Budd–Chiari syndrome and their outcome was similar to that of cases with IVC thrombus but without Budd–Chiari syndrome.11,12 Moreover, long-term survival has recently been reported11–13 in some patients with renal cell carcinoma associated with IVC thrombi who underwent extensive surgical procedures. In some patients with mild/silent Budd–Chiari syndrome, therefore, long-term survival can be expected after surgery, as seen in our case 3. In cases with severe disease, complete or incomplete thrombectomy is difficult and risky due to the hepatic failure and the poor general condition of the patients. However, it may be applicable in some cases, as several cases with Budd–Chiari syndrome, although without renal cell carcinoma, and showing liver failure have been reported as being successfully treated with thrombectomy.14,15 Thus, if surgical treatment is applicable, it will resolve the existing hepatic failure and in such cases long-term survival can be expected.
5. 6. 7. 8. 9. 10.
11.
12.
References 1. Okulski TA, Soulen RL. Renal cell carcinoma presenting as the Budd–Chiari syndrome. AJR 1977; 128: 140–2. 2. Smith KC, Birmingham CL, Murphy KC, Grymaloski MR. Renal cell carcinoma presenting as Budd–Chiari syndrome. Can Med Assoc J 1984; 130: 12–3. 3. Spapen HDM, Volckaert A, Bourgain C, Braeckman J, vanBelle SJP. Acute Budd–Chiari syndrome with portosystemic encephalopathy as first sign of renal carcinoma. Br J Urol 1988; 62: 274–5. 4. Nakajima Y, Baba S, Nagahama T, Tazaki H. Renal cell
13.
14. 15.
75
carcinoma presenting as Budd–Chiari syndrome. Urol Int 1989; 44: 173–6. Yano Y, Watanbe T, Mimura N, Ishimi Z. A case of renal cell carcinoma presenting as Budd–Chiari syndrome. Jpn J Int Med 1966; 55: 84. Hayashida M, Nishino K, Hayashi T, et al. A case of renal cell carcinoma associated with inferior vena caval tumor thrombus extending to the right atrium. Jpn J Int Med 1978; 67: 220. Aoki K, Matsuo S, Kodama J, et al. A case of renal cell carcinoma presenting as Budd–Chiari syndrome producing erythropoietin. Jpn J Int Med 1978; 67: 103. Ueno Y, Takeda H, Inudou K. A case of Grawitz tumor presenting as Budd–Chiari syndrome due to the tumor thrombus. Jpn J Int Med 1972; 61: 1363. Reynolds TB. Budd–Chiari syndrome. In: Schiff L, Schiff ER (eds). Diseases of the Liver (7th edn). Philadelphia: J.B. Lippincott, 1993: 1091–8. Wanless IR. Vascular disorders. In: MacSween RNM, Anthony PP, Scheuer PJ, Burt AD, Portmann BC (eds). Pathology of the Liver (3rd edn). Edinburgh: Churchill Livingstone, 1994: 535–62. Marshall FF, Dietrick DD, Baumgartner WA, Reitz BA. Surgical management of renal cell carcinoma with intracaval neoplastic extension above the hepatic veins. J Urol 1988; 139: 1166–72. Hatcher PA, Anderson EE, Paulson DF, Carson CC, Robertson JE. Surgical management and prognosis of renal cell carcinoma invading the vena cava. J Urol 1991; 145: 20–4. Okada Y, Kumada K, Terachi T, Nishimura K, Tomoyoshi T, Yoshida O. Long-term follow up of patients with tumor thrombi from renal cell carcinoma and total replacement of the inferior vena cava using an expanded polytetrafluoroethylene tubular graft. J Urol 1996; 155: 444–7. Kinmond S, Carter R, Skeoch CH, Morton NS. Nephroblastoma presenting with acute hepatic encephlopathy. Arch Dis Child 1990; 65: 542–3. Schraut WH, Chilcote RR. Metastatic Wilms’ tumor causing acute hepatic-vein occlusion (Budd–Chiari syndrome). Gastroenterology 1985; 88: 576–9.
Accepted for publication 14 October 1998
Surgical treatment of renal cell carcinoma associated with Budd–Chiari syndrome: report of four cases and review of the literature H. Kume, S. Kameyama, Y. Kasuya, A. Tajima and K. Kawabe Department of Urology, Faculty of Medicine, University of Tokyo, Japan
Aims: Renal cell carcinoma is sometimes associated with inferior vena caval tumour thrombus, but occlusion of hepatic veins by the tumour thrombus causing liver dysfunction, the so-called Budd–Chiari syndrome, is relatively uncommon. There are only a few reports in the literature which discuss this condition. Methods: Four cases admitted to our hospital over a 7-year period and eight cases reported in detail in the English and the Japanese literature were included in this study. They are classified into two groups: mild/silent, without liver failure, and severe, with liver failure. Results: Five patients were classified as mild/silent and seven as severe. Clinical manifestations were mild in the former cases and acute in the latter. Surgery was performed in four of the former cases but only in one case of the latter cases. Conclusions: In mild cases, surgical treatment seems to avoid imminent hepatic failure effectively and should be performed as soon as possible. In such cases Budd–Chiari syndrome in itself does not affect the prognosis. In severe cases, however, surgical treatment is very difficult and risky due to the existing hepatic failure. Key words: renal cell carcinoma; Budd–Chiari syndrome; surgical treatment; tumour thrombus.
Introduction Renal cell carcinoma is often associated with a tumour thrombus, which sometimes extends into the inferior vena cava (IVC). However, hepatic venous obstruction by a tumour thrombus, which causes Budd–Chiari syndrome, is relatively uncommon.1–8 Due to the lack of detailed reports in the literature, little is known of the clinical course of unusual condition. In this study, we analysed 12 cases, including eight cases reported in the English1–4 and the Japanese5–8 literature. The indications for and efficacy of thrombectomy are discussed.
Methods Between January 1990 and December 1997, four patients with renal cell carcinoma associated with Budd–Chiari syndrome were admitted to our hospital (Fig. 1). The diagnosis was confirmed by signs, symptoms and laboratory tests. In three of the four cases, Doppler ultrasonography showed decreased or reversed flow of hepatic veins. In all
Correspondence to H. Kume, Department of Urology, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan. Fax: 81-3-5800-8917. 0748–7983/99/010071+05 $12.00/0
our surgical cases, diagnosis was confirmed by enlarged and congested liver, which rapidly returned to normal size, colour and consistency after removal of the tumour thrombi. In each case, histological examination revealed renal cell carcinoma. In addition to these four cases, we extracted eight well-documented cases from the literature.1–8 We classified the 12 cases into two groups, mild/silent and severe. Mild/silent is characterized by the absence of liver failure and severe by the presence of liver failure. We compared clinical signs and symptoms, laboratory parameters, treatment and prognosis between these two groups.
Results Five cases were classified as mild/silent and seven as severe. Age and sex were similar between the two groups, except for age in case 3, who had been diagnosed as having von Hippel–Lindau disease in addition to Budd–Chiari syndrome. The side, size and site of the renal tumours were also similar between the two groups. Clinical characteristics of the patients are summarized in Tables 1 and 2. The onset of Budd–Chiari syndrome was gradual in mild/ silent cases, whereas it was sudden and acute in severe cases. Hepatomegaly and ascites were present in both groups, 1999 W.B. Saunders Company Limited
Rt, L Rt, U Lt, U Lt Lt, L
Lt, L Rt Rt, M Rt Rt Rt Rt
63/M 67/M 51/M 59/M 68/M 63/M 62/M
Site
61/M 54/M 29/F 60/M 60/M
Age/sex
10 20 5 N/A 7 N/A N/A
5 11 8 N/A 5
Size (cm) atrium atrium atrium atrium atrium
Right ventricle N/A Right ventricle Hepatic vein Right atrium Hepatic vein Right atrium
Right Right Right Right Right
Tumour thrombus
None N/A Lung, lymph nodes N/A N/A N/A N/A
None Lung None N/A Liver
Metastasis
Sudden N/A Sudden Sudden Sudden Sudden N/A
Gradual Gradual Gradual Gradual Gradual
Onset
− − − − − + − + N/A + + N/A
+ + + + + + +
DIC or DIC-like status
− − − − −
Liver failure
∗ Time from surgery or presentation. M, male; F, female; Rt, right; Lt, left; L, lower; U, upper; Mid, middle; N/A, not available.
Mild/silent Case 1 Case 2 Case 3 Case 41 Case 52 Severe Case 6 Case 73 Case 84 Case 95 Case 106 Case 117 Case 128
Type of disease
Renal cell carcinoma
Table 1. Patient characteristics
− − − − − − −
+ + + + −
Surgery
Died (1 month) Died (3 days) Died (1 month) N/A Died (2 weeks) Died (1.5 months) Died (1 month)
Died (10 months) Died (8 months) Alive (37 months) Died (N/A) Died (N/A)
Outcome∗
72 H. Kume et al.
73
Renal cell carcinoma in Budd–Chiari syndrome Case 1
Case 2
Case 3
Case 6
Right lower, φ5 cm. pT3bpN0M0. RCC, CC and GC, Grade 1 > 2
Right upper, φ11 cm pT3bpN0M1 (pulmonary metastasis: rt. middle lobe) RCC, CC, Grade 3 >> 2
Left upper, φ8 cm Right upper, φ4 cm Bilateral, several tumours, φ1–2 cm pT3bpN0M0. RCC, CC, Grade 2 Pheochromocytoma of rt. adrenal.
Left lower, φ10 cm pT3bpN0M0 RCC, CC, Grade 3
Fig. 1. Localization, size, staging and histology of our four cases. Cases 1–3; surgically proved staging. Case 6; autopsy findings. Lt, left; rt, right; RCC, renal cell carcinoma; CC, clear cell; GC, granular cell.
Table 2. Clinical manifestations
Hepatomegaly Ascites Jaundice Encephalopathy Leg oedema
Mild/silent cases (n/total)
Severe cases (n/total)
5/5 5/5 0/4 0/3 2/5
7/7 6/6 5/5 5/5 4/6
other causes, including metastatic disease or local recurrence of the IVC tumour thrombus. In the severe cases, surgery was performed only in case 8, who died from liver failure, renal failure and septicaemia 1 month after surgery.4 The other six severe cases were inoperable and died from liver failure within 1 month.
Discussion
while jaundice and encephalopathy were more frequently seen in severe cases. Moreover, at least four of the seven cases with severe Budd–Chiari syndrome had disseminated intravascular coagulation (DIC) or a DIC-like status, whereas none of five mild/silent cases had such a manifestation. Figure 2 shows the results of the liver function tests in our four cases. In the three mild/silent cases the results were abnormal, but the degree of abnormality was greater in case 6, who had severe disease. These values normalized after surgery in our three surgical cases. Results of liver function tests were not well-documented in the eight cases taken from the literature. In four of five mild/silent type cases surgery was performed. Surgery could not be performed in the other case, reported by Smith et al.,2 because of the extent of the carcinoma. Of the five mild/silent cases, cases 1, 2 and 3 survived for a relatively long period. Case 3 is currently alive, 3 years after surgery, with no evidence of recurrent disease. At least three cases, numbers 1, 2 and 4, died from
Budd–Chiari syndrome is a relatively uncommon disorder, in which occlusion of the hepatic veins and/or the inferior vena cava causes hepatic congestion and liver dysfunction.9, 10 It may sometimes result from malignant tumours, such as primary hepatocellular carcinoma, sarcoma arising from the IVC, adrenal carcinoma, Wilms’ tumour and renal cell carcinoma.9,10 In patients with renal cell carcinoma, Budd–Chiari syndrome is caused by an existing IVC thrombus occluding the hepatic veins. We classified the cases studied into two groups, mild/ silent (without liver failure) and severe (with liver failure). Patients with mild/silent disease had a gradual onset and slight liver dysfunction, probably due to incomplete and/or gradual obstruction, which may allow a collateral circulation to develop and may minimize the liver damage. Patients with severe disease had an acute onset with serious liver damage and subsequent DIC or DIC-like status, which may result from sudden and complete obstruction of the hepatic veins. In some patients, mild/silent manifestations may become severe during the clinical course. We have shown here that in cases with mild/silent
74
H. Kume et al. (a)
(b)
600
(c)
4.0
100
3.0
75
100
50
0
µg/dl
mg/dl
IU/l
150
2.0
1.0
Before
After
0
50
25
Before
After
0
Before After
Fig. 2. Changes in clinical parameters of liver function. (a) Transaminases; (b) total bilirubin; (c) ammonia. Μ: GOT, severe case, Α: GOT, mild/silent case, Ν: GPT, severe case, Κ: GPT, mild/silent case, Ο: total bilirubin, severe case, Η: bilirubin, mild/silent case, Χ: NH3, severe case, Β: NH3, mild/silent case.
Fig. 3. Enhanced abdominal CT scan of case 6. (a) Hepatomegaly and ascites are present. The liver is enhanced heterogeniously. Arrow heads indicate the IVC tumour thrombus. (b) The renal cancer, left lower pole, about 10 cm in diameter.
Fig. 4. Post-mortem examination of case 6. (a) Histology of the renal tumour was renal cell carcinoma, clear cell type. (b) The liver. Marked congestion with necrosis and loss of hepatocytes in the perivenular area (c). G shows periportal area.
Budd–Chiari syndrome, thrombectomy seems effectively to avoid imminent hepatic failure and therefore surgery should be performed as soon as possible to minimize the risk of
disease progression. In retrospect, nephrectomy and thrombectomy should have been performed earlier in case 6, before Budd–Chiari syndrome developed.
Renal cell carcinoma in Budd–Chiari syndrome Budd–Chiari syndrome in itself does not effect prognosis. No mild/silent cases died from existing Budd–Chiari syndrome and their outcome was similar to that of cases with IVC thrombus but without Budd–Chiari syndrome.11,12 Moreover, long-term survival has recently been reported11–13 in some patients with renal cell carcinoma associated with IVC thrombi who underwent extensive surgical procedures. In some patients with mild/silent Budd–Chiari syndrome, therefore, long-term survival can be expected after surgery, as seen in our case 3. In cases with severe disease, complete or incomplete thrombectomy is difficult and risky due to the hepatic failure and the poor general condition of the patients. However, it may be applicable in some cases, as several cases with Budd–Chiari syndrome, although without renal cell carcinoma, and showing liver failure have been reported as being successfully treated with thrombectomy.14,15 Thus, if surgical treatment is applicable, it will resolve the existing hepatic failure and in such cases long-term survival can be expected.
5. 6. 7. 8. 9. 10.
11.
12.
References 1. Okulski TA, Soulen RL. Renal cell carcinoma presenting as the Budd–Chiari syndrome. AJR 1977; 128: 140–2. 2. Smith KC, Birmingham CL, Murphy KC, Grymaloski MR. Renal cell carcinoma presenting as Budd–Chiari syndrome. Can Med Assoc J 1984; 130: 12–3. 3. Spapen HDM, Volckaert A, Bourgain C, Braeckman J, vanBelle SJP. Acute Budd–Chiari syndrome with portosystemic encephalopathy as first sign of renal carcinoma. Br J Urol 1988; 62: 274–5. 4. Nakajima Y, Baba S, Nagahama T, Tazaki H. Renal cell
13.
14. 15.
75
carcinoma presenting as Budd–Chiari syndrome. Urol Int 1989; 44: 173–6. Yano Y, Watanbe T, Mimura N, Ishimi Z. A case of renal cell carcinoma presenting as Budd–Chiari syndrome. Jpn J Int Med 1966; 55: 84. Hayashida M, Nishino K, Hayashi T, et al. A case of renal cell carcinoma associated with inferior vena caval tumor thrombus extending to the right atrium. Jpn J Int Med 1978; 67: 220. Aoki K, Matsuo S, Kodama J, et al. A case of renal cell carcinoma presenting as Budd–Chiari syndrome producing erythropoietin. Jpn J Int Med 1978; 67: 103. Ueno Y, Takeda H, Inudou K. A case of Grawitz tumor presenting as Budd–Chiari syndrome due to the tumor thrombus. Jpn J Int Med 1972; 61: 1363. Reynolds TB. Budd–Chiari syndrome. In: Schiff L, Schiff ER (eds). Diseases of the Liver (7th edn). Philadelphia: J.B. Lippincott, 1993: 1091–8. Wanless IR. Vascular disorders. In: MacSween RNM, Anthony PP, Scheuer PJ, Burt AD, Portmann BC (eds). Pathology of the Liver (3rd edn). Edinburgh: Churchill Livingstone, 1994: 535–62. Marshall FF, Dietrick DD, Baumgartner WA, Reitz BA. Surgical management of renal cell carcinoma with intracaval neoplastic extension above the hepatic veins. J Urol 1988; 139: 1166–72. Hatcher PA, Anderson EE, Paulson DF, Carson CC, Robertson JE. Surgical management and prognosis of renal cell carcinoma invading the vena cava. J Urol 1991; 145: 20–4. Okada Y, Kumada K, Terachi T, Nishimura K, Tomoyoshi T, Yoshida O. Long-term follow up of patients with tumor thrombi from renal cell carcinoma and total replacement of the inferior vena cava using an expanded polytetrafluoroethylene tubular graft. J Urol 1996; 155: 444–7. Kinmond S, Carter R, Skeoch CH, Morton NS. Nephroblastoma presenting with acute hepatic encephlopathy. Arch Dis Child 1990; 65: 542–3. Schraut WH, Chilcote RR. Metastatic Wilms’ tumor causing acute hepatic-vein occlusion (Budd–Chiari syndrome). Gastroenterology 1985; 88: 576–9.
Accepted for publication 14 October 1998