1992, The British Journal of Radiology, 65, 542-545
Case report A 39-year-old man was seen in the emergency department with acute left lower thoracic pain. There was a history of intermittent trauma. Physical examination revealed no obvious abnormality. US examination on admission (Fig. la) showed a subcapsular splenic collection with internal echogenic and peripheral anechoic components. CT (Fig. lb), performed a week later, confirmed the diagnosis of subcapsular haematoma and showed its complex structure of an internal dense area (30 Hounsfield units (HU)) and a low-density, probably liquefied, peripheral zone (15 HU). A US scan performed 1 month after admission again revealed a heterogeneous collection with an alteration in morphology showing a decrease of the echogenicity of the internal part and an increase in volume of the liquefied peripheral component. A CT scan (Fig. lc), performed 5 months after admission, showed a typical, 7 cm, non-enhancing round lesion of liquid density (17 HU) consistent with a subcapsular cyst. This appearance is typical of a "false" cyst of the spleen (Dachmann et al, 1986).
Case reports
The evolution of the false cyst as illustrated by this case includes slow growth (Ross et al, 1977). Rupture, infection and rapid increase in size (Dibble & Weigent, 1965) may lead to acute presentation. The usual treatment is surgical excision of the symptomatic cyst. Percutaneous puncture, laparoscopic cyst puncture and creation of a cyst-peritoneal window have been successfully performed. US demonstration of a splenic cyst at the time of acute abdominal pain may pose a diagnostic dilemma. The major role of imaging following diagnosis is to document the morphological evolution of splenic cysts and haematomas as a complement to clinical evaluation in the determination of the need and timing of surgical and percutaneous drainage procedures. References DACHMANN, A. H. & MAGID, D., 1987. Splenic focal disease. In Radiology of the Liver, Biliary Tract, Pancreas and Spleen, ed. by A. C. Friedman (Williams and Wilkins, Baltimore), pp. 947-984.
Discussion Splenic haematomas would be the main cause of false DACHMANN, A. H., Ros, P. R., MURARI, P. J., OLMSTEDT, W. W. & LICHTENTSTEIN, J. E., 1986. Nonparasitic splenic cyst. The relationship resolving haematoma into splenic cysts: report of 52 cases with radiologic-pathologic cysts was shown in surgical specimens (Economides et correlation. American Journal of Roentgenology, 147, al, 1980) and on US and CT (Dachmann et al, 1986). 537-542. Our case illustrates the transformation of a subcapsular DIBBLE, J. B. & WEIGENT, C. E., 1965. Epidermoid cyst of the collection to a cyst in 5 months. spleen presenting as an abdominal emergency. Journal of the A history of trauma is found in one-quarter to oneAmerican Medical Association, 194, 1144-1146. half of cases of "false" cyst (Garvin & King, 1981), but ECONOMIDES, N. G., BENTON, B. F., FORTNER, T. M. & MILES, R. M., 1980. Splenic pseudocysts: report of two cases and the trauma is often in the distant past and not recalled. review of the literature. American Surgeon, 46, 644-648. More than 50% of false cysts are diagnosed in the 3 years following trauma, and this corresponds with the FOWLER, R. H., 1953. Collective review: nonparasitic benign cystic tumors of the spleen. International Abstracts of delay seen in our case. Surgery, 96, 209-227. Diagnosis of splenic cysts is mainly based on US and GARVIN, D. F. & KING, F. M., 1981. Cysts and nonCT. Once a splenic mass is shown as a large cystic lesion lymphomatous tumours of the spleen. Pathology Annual, 16, with a relatively thin wall, and if echinococcus is 61-80. excluded, a false cyst or true cyst is the likely diagnosis Ross, M. E., ELLWOOD, R., YANG, S. S. & LUCAS, R. J., 1977. (Dachmann & Magid, 1987). Epidermoid splenic cysts. Archives of Surgery, 112, 596-599.
Juxtaglomerular cell tumour of the kidney as cause of hypertension: a case report By Jos C. van den Berg, M D , *Ad R. M. M. Hermus, M D and Gerd R. Rosenbusch, M D Departments of Radiodiagnosis and 'Internal Medicine (Division of Endocrinology), St Radboud Hospital, University of Nijmegen, Geert Grooteplein Zuid 18, 6525 GA Nijmegen, The Netherlands
(Received 3 June 1991 and in final form 28 November 1991, accepted 14 January 1992) Keywords: Hypertension, Kidney neoplasms, Renin, Reninoma
Benign renin-secreting juxtaglomerular cell tumours of the kidney (reninomas) are recognized but rare causes of hypertension. Although 46 well documented cases have been Address reprint requests to Dr J. C. van den Berg. 542
described since the first report by Robertson et al (1967) there has been little emphasis on the radiological aspects of this clinical entity (Conn et al, 1973; Davidson & Clark 1974; Dunnick et al, 1983). The radiodiagnostic criteria and diagnostic investigations will be dealt with in this case report. The British Journal of Radiology, June 1992
Case reports Case report A 33-year-old woman was referred to our hospital because of hypertension (230/130 mmHg) uncontrollable by /^-blocking agents. There were no complaints of increased thirst, polyuria or muscular weakness. On physical examination, no abnormalities except for the hypertension were found. The chest radiograph together with an intravenous urogram were normal. Laboratory examination of the blood showed a lowered serum potassium level, a normal creatinine clearance and no indications of phaeochromocytoma. Plasma-renin activity (PRA) was elevated and there was a markedly increased aldosterone secretion rate. A secondary form of aldosteronism was suspected. Abdominal aortography showed no stenoses of the renal arteries and a barely visible radiolucent area in the lower pole of the right kidney. A subsequent selective study of the renal arteries revealed a hypovascular, smoothly delineated lucent area in the lower pole of the right kidney with a diameter of approximately 3 cm. No calyceal deformity was seen in the excretion phase (Fig. 1). On ultrasound examination this lesion was echogenic (Fig. 2). Computed tomography (CT) was performed and showed an isodense structure in the lower pole of the right kidney, which appeared to be hypodense as compared with the
Figure 2. Renal ultrasound scan showing a homogeneous, well delineated echogenic lesion in the right lower pole.
normal parenchyma after intravenous administration of contrast medium (Fig. 3). Selective renin sampling of the renal veins showed a markedly elevated plasma renin activity on the right side, with a ratio of 24.6 to 16.7 ng/ml/h (for comparison: PRA in the lower inferior caval vein was 11.2 ng/ml/h). Renal radionuclide scanning was not performed. All these findings suggested a renin-secreting tumour in the lower pole of the right kidney and a right lower pole resection was performed, revealing a well encapsulated tumour with a diameter of 2 cm. Histologically it was composed of neoplastic juxtaglomerular cells. Histological and immunocytochemical aspects of this tumour, which are described extensively elsewhere (Hermus et al, 1986), were typical of a benign juxtaglomerular cell tumour. Immediately after extirpation of the tumour, blood pressure fell dramatically to 120/80 mmHg. In the subsequent period the blood pressure stabilized in a range of 130/90 to 160/100 mmHg (this high value is most probably due to essential hypertension) with normal values of PRA. Discussion
Figure 1. Selective right renal arteriography shows sparse vascular structures in the lower pole with a sharply denned radiolucent area (arrows); note the absence of calyceal deformity.
Vol. 65, No. 774
A renin-producing tumour is characterized clinically by a syndrome of (severe) hypertension, hypokalaemia and hyperaldosteronism. Patients may have complaints of headache, polyuria and/or polydipsia or muscle weakness (Robertson et al, 1967; Lam et al, 1982). Patients are usually young, with an age range of 6 to 53 years (mean age 21.5 years) (Corvol et al, 1988). PRA is always elevated (Hirose et al, 1974). These tumours are solitary and are almost always solid on macroscopic examination (only one partly cystic, partly solid tumour has been described; Hanna et al, 1979), with a diameter ranging from 0.2 to 0.8 cm (mean diameter 2.3 cm) (Lam et al, 1982). Juxtaglomerular cell tumours are always located just below the renal capsule and are equally distributed throughout upper and lower pole. Histologically most of the renin-producing tumours originating from the juxtaglomerular apparatus of the kidneys are benign and of the haemangiopericytoma or 543
Case reports
Figure 3. CT scan: the tumour (arrows) appears to be isodense on the native scan (a) and non-enhancing after intravenous administration of contrast medium (b).
hamartoma type (Hirose et al, 1974; Dunnick et al, 1983). Malignant renin-producing tumours of renal origin, such as Wilms tumour, renal cell carcinoma and mesoblastic nephroma (Dunnick et al, 1983; Malone et al, 1989), as well as extrarenal primary tumours {e.g. lung, pancreas and ovary) (Anderson et al, 1989) 544
causing hypertension have also been described, but these are even more rare. Intravenous urography may show stretching or displacement of calices or the mere presence of a mass, (Takahashi et al, 1976; Dunnick et al, 1983; Pedrinelli et al, 1987; Remynse et al, 1989) but in most cases no abnormalities are seen (Robertson et al, 1967; Davidson & Clark, 1974; Lam et al, 1982). With only one cystic (Moss et al, 1982) and only one partly cystic/partly solid mass (Lee, 1971) having been reported in 10 cases, the findings at ultrasound most commonly suggest a solid mass (Dunnick et al, 1983; Pedrinelli et al, 1987). Most of these masses are echogenic, although hypoechoic and isoechoic masses (sometimes surrounded by a hyperechoic rim corresponding to a pseudocapsule) are known (Dunnick et al, 1983). CT scanning may reveal an isodense or hypodense solid tumour (Dunnick et al, 1983; Corvol et al, 1988), which may be surrounded by a small rim of haemorrhage or may show increased density centrally resulting from haemorrhage (Moss et al, 1982; Dunnick et al, 1983). After intravenous administration of contrast medium, the tumour may be non-enhancing owing to hypovascularity (Lee, 1971) or only slightly enhancing (Dunnick et al, 1983; Remynse et al, 1989). Although aortography may be inconclusive or even normal, it is usually able to show a hypovascular mass (Hanna et al, 1979; Lam et al, 1982; Moss et al, 1982; Pedrinelli et al, 1987; Corvol et al, 1988). Despite the presence of well developed vascular spaces microscopically the angiographic features consist of tortuous and sparse, poorly denned vasculature (Conn et al, 1973; Davidson & Clark, 1974; Dunnick et al, 1983; Remynse et al, 1989) with or without abnormal calibre, course or displacement (Takahashi et al, 1976). Cases with an arteriovenous shunt are unknown, but early staining of the renal vein has been described (Takahashi et al, 1976). The renal parenchyma usually shows an area of translucency, sometimes surrounded by a zone of increased density caused by a rim of compressed renal parenchyma (Davidson & Clark, 1974; Takahashi et al, 1976). Selective renin sampling of the renal veins shows lateralization with elevated renin levels on the affected side (Conn et al, 1973; Davidson & Clark, 1974; Pedrinelli et al, 1987). A ratio of more than 1.5 to 1 is considered to be significant and in this way even very small tumours (down to 0.2 cm) can be detected (Hirose et al, 1974). A renal radionuclide scan is usually normal (Hirose et al, 1974; Lam et al, 1982), but a focus of diminished activity may be seen (Takahashi et al, 1976). In establishing the diagnosis of a renin-producing tumour of the kidney, ultrasound and CT together with selective renin sampling of the renal veins is essential. Aortography performed because of suspicion of renal artery stenosis should always look for a mass as described in this case report. Whenever a mass is suspected, selective renal arteriography should be performed in order to confirm and delineate the lesion. Intravenous urography and renal radionuclide scanning The British Journal of Radiology, June 1992
1992, The British Journal of Radiology, 65, 545-547 Case reports have a low sensitivity for the detection of small renal masses such as renin-producing tumours but are usually helpful in excluding other pathological processes.
U. J. & KLOPPENBORG, P. W., 1986. Hypertension and
hypokalaemia due to a renin-secreting kidney tumour. Netherlands Journal of Medicine, 29, 84-91. HIROSE, M., ARAKAWA, K., KIKUCHI, M., KAWASAKI, T., OMOTO, T., KATO, H. & NAGAYAMA, T., 1974. Primary
Acknowledgments The authors would like to thank Miss Mariska Ebbelink and Miss Tineke van IJzendoorn for their secretarial assistance in the preparation of this manuscript.
reninism with renal hamartomatous alteration. Journal of the American Medical Association, 230, 1288-1292. LAM, A. S. C ,
BEDARD, Y. C ,
BUCKSPAN, M. B., LOGAN,
ANDERSON, P. W., MACAULAY, L., D O , Y. S. SHERROD, A., D'ABLAING, G., KOSS, M., SHINAGAWA, T., TRAN, B.,
A. G. & STEINHARDT, M. I., 1982. Surgically curable hypertension associated with reninoma. Journal of Urology, 128, 572-575. LEE, M. R., 1971. Renin-secreting kidney tumors. Lancet, 2, 254-255.
MONTZ, F. J. & HSUEH, W. A., 1989. Extrarenal renin-
MALONE, P. S., DUFFY, P. G., RANSLEY, P. G., RISDON, R. A.,
secreting tumors: insights into hypertension and ovarian renin production. Medicine, 68, 257-268.
COOK, T. & TAYLOR, M., 1989. Congenital mesoblastic
References
CONN,
J. W.,
BOOKSTEIN,
J. J.
&
COHEN,
E. L.,
1973.
Renin-secreting juxtaglomerular cell adenoma. Radiology, 106, 543-544.
nephroma, renin production, and hypertension. Journal of Pediatric Surgey, 24, 599-600. Moss, A. H., PETERSON, L. J., SCOTT, C. W., WINTER,
K.,
OLIN, D. B. & GARBER, R. L., 1982. Delayed diagnosis of
CORVOL, P., PINET, F., GALEN, F. X., PLOUIN, P. F., CHATTELIER, G., PAGNY, J. Y., CORVOL, M. T. & MENARD,
juxtaglomerular cell tumour hypertension. North Carolina Medical Journal, 34, 705-707.
J., 1988. Seven lessons from seven renin-secreting tumours. Kidney International, 34 (Suppl. 25), 3-44.
PEDRINELLI, R., GRAZIADEI, L., TADDEI, S., LENZI, M., MAGAGNA, A., BEVILACQUA, G. & SALVETTI, A., 1987. A
DAVIDSON,
J. K.
& CLARK,
D. C ,
1974.
Renin-secreting
juxtaglomerular-cell tumour. British Journal of Radiology, 47, 594-597. DUNNICK, N. R., HARTMAN, D. S., FORD, K. K., DAVIS, C. J.
& AMIS, E. S., 1983. The radiology of juxtaglomerular tumors. Radiology, 147, 321-326. HANNA, W., TEPPERMAN, B., LOGAN, A. G., ROBINETTE, M. A.,
COLAPINTO, R. & PHILLIPS, M. J., 1979. Juxtaglomerular cell
tumour (reninoma) with paroxysmal hypertension. Canadian Medical Association Journal, 120, 957-959. HERMUS, A. R. M. M., PIETERS, G. F. F. M., LAMERS, A. P. M., SMALS, A. G. H., HANSELAAR, A. G., VAN HAELST,
renin-secreting tumor. Nephron, 46, 380-385. REMYNSE, L. C ,
BEGUN, F. P., JACOBS, S. C. & LAWSON,
R. K., 1989. Juxtaglomerular cell tumor with elevation of serum erythropoietin. Journal of Urology, 142, 1560-1562. ROBERTSON, P. W., KLIDJIAN, A., HARDING, L. K. & WATERS,
G., 1967. Hypertension due to a renin-secreting renal tumour. American Journal of Medicine, 43, 963-976. TAKAHASHI, T., MIURA, T., SUE, A., SAITO, K., SAKANE, M., YAMAGATA, Y., FUKUCHI, S., SATO, Z., HIRAI, T., TERASHIMA, K., OKA, K. & IMAI, Y., 1976. A case of
juxtaglomerular cell tumor Nephron, 17, 483-495.
diagnosed
preoperatively.
Contrast extravasation from a Pulse-Tec graft: a complication of high-dose recombinant tissue-type plasminogen activator therapy By T. M. Buckenham, FRACR, *R. S. Taylor, M S , FRCS, D. Reiff, MRCP and J . E. Page, MRCP, FRCR Departments of Radiology and 'Surgery, St George's Hospital, Blackshaw Road, London SW17 0QT, UK
{Received 1 August 1991 and in revised form 17 October 1991, accepted 20 November 1991) Keywords: Thrombolysis, Extravasation, Recombinant tissue plasminogen activator (rt-PA), Pulse-Tec
Transmural contrast extravasation through both knitted Dacron and Gore-Tex grafts is well documented. Reports have appeared associating this complication with the use of both streptokinase and urokinase (Rabe et al, 1982; Becker et al, 1984; Rosner & Doris, 1984; Perler et al, 1986). We report a case of extravasation through a Pulse-Tec (Newtec Vascular Products Ltd, Address correspondence to Dr T Buckenham, Department of Radiology, St George's Hospital, Blackshaw Road, London SW17 0QT, UK.
Vol. 65, No. 774
UK) graft in association with the use of high-dose recombinant tissue plasminogen activator (rt-PA) therapy. This complication has not previously been reported in this type of graft or with this particular thrombolytic agent. Case report A 75-year-old woman with a long history of peripheral vascular disease presented with an ischaemic ulcerated forefoot. Ankle-brachial indices were 0.4 on the left and 0.6 on the right, which was asymptomatic. A diagnostic arteriogram
545
Case report A 39-year-old man was seen in the emergency department with acute left lower thoracic pain. There was a history of intermittent trauma. Physical examination revealed no obvious abnormality. US examination on admission (Fig. la) showed a subcapsular splenic collection with internal echogenic and peripheral anechoic components. CT (Fig. lb), performed a week later, confirmed the diagnosis of subcapsular haematoma and showed its complex structure of an internal dense area (30 Hounsfield units (HU)) and a low-density, probably liquefied, peripheral zone (15 HU). A US scan performed 1 month after admission again revealed a heterogeneous collection with an alteration in morphology showing a decrease of the echogenicity of the internal part and an increase in volume of the liquefied peripheral component. A CT scan (Fig. lc), performed 5 months after admission, showed a typical, 7 cm, non-enhancing round lesion of liquid density (17 HU) consistent with a subcapsular cyst. This appearance is typical of a "false" cyst of the spleen (Dachmann et al, 1986).
Case reports
The evolution of the false cyst as illustrated by this case includes slow growth (Ross et al, 1977). Rupture, infection and rapid increase in size (Dibble & Weigent, 1965) may lead to acute presentation. The usual treatment is surgical excision of the symptomatic cyst. Percutaneous puncture, laparoscopic cyst puncture and creation of a cyst-peritoneal window have been successfully performed. US demonstration of a splenic cyst at the time of acute abdominal pain may pose a diagnostic dilemma. The major role of imaging following diagnosis is to document the morphological evolution of splenic cysts and haematomas as a complement to clinical evaluation in the determination of the need and timing of surgical and percutaneous drainage procedures. References DACHMANN, A. H. & MAGID, D., 1987. Splenic focal disease. In Radiology of the Liver, Biliary Tract, Pancreas and Spleen, ed. by A. C. Friedman (Williams and Wilkins, Baltimore), pp. 947-984.
Discussion Splenic haematomas would be the main cause of false DACHMANN, A. H., Ros, P. R., MURARI, P. J., OLMSTEDT, W. W. & LICHTENTSTEIN, J. E., 1986. Nonparasitic splenic cyst. The relationship resolving haematoma into splenic cysts: report of 52 cases with radiologic-pathologic cysts was shown in surgical specimens (Economides et correlation. American Journal of Roentgenology, 147, al, 1980) and on US and CT (Dachmann et al, 1986). 537-542. Our case illustrates the transformation of a subcapsular DIBBLE, J. B. & WEIGENT, C. E., 1965. Epidermoid cyst of the collection to a cyst in 5 months. spleen presenting as an abdominal emergency. Journal of the A history of trauma is found in one-quarter to oneAmerican Medical Association, 194, 1144-1146. half of cases of "false" cyst (Garvin & King, 1981), but ECONOMIDES, N. G., BENTON, B. F., FORTNER, T. M. & MILES, R. M., 1980. Splenic pseudocysts: report of two cases and the trauma is often in the distant past and not recalled. review of the literature. American Surgeon, 46, 644-648. More than 50% of false cysts are diagnosed in the 3 years following trauma, and this corresponds with the FOWLER, R. H., 1953. Collective review: nonparasitic benign cystic tumors of the spleen. International Abstracts of delay seen in our case. Surgery, 96, 209-227. Diagnosis of splenic cysts is mainly based on US and GARVIN, D. F. & KING, F. M., 1981. Cysts and nonCT. Once a splenic mass is shown as a large cystic lesion lymphomatous tumours of the spleen. Pathology Annual, 16, with a relatively thin wall, and if echinococcus is 61-80. excluded, a false cyst or true cyst is the likely diagnosis Ross, M. E., ELLWOOD, R., YANG, S. S. & LUCAS, R. J., 1977. (Dachmann & Magid, 1987). Epidermoid splenic cysts. Archives of Surgery, 112, 596-599.
Juxtaglomerular cell tumour of the kidney as cause of hypertension: a case report By Jos C. van den Berg, M D , *Ad R. M. M. Hermus, M D and Gerd R. Rosenbusch, M D Departments of Radiodiagnosis and 'Internal Medicine (Division of Endocrinology), St Radboud Hospital, University of Nijmegen, Geert Grooteplein Zuid 18, 6525 GA Nijmegen, The Netherlands
(Received 3 June 1991 and in final form 28 November 1991, accepted 14 January 1992) Keywords: Hypertension, Kidney neoplasms, Renin, Reninoma
Benign renin-secreting juxtaglomerular cell tumours of the kidney (reninomas) are recognized but rare causes of hypertension. Although 46 well documented cases have been Address reprint requests to Dr J. C. van den Berg. 542
described since the first report by Robertson et al (1967) there has been little emphasis on the radiological aspects of this clinical entity (Conn et al, 1973; Davidson & Clark 1974; Dunnick et al, 1983). The radiodiagnostic criteria and diagnostic investigations will be dealt with in this case report. The British Journal of Radiology, June 1992
Case reports Case report A 33-year-old woman was referred to our hospital because of hypertension (230/130 mmHg) uncontrollable by /^-blocking agents. There were no complaints of increased thirst, polyuria or muscular weakness. On physical examination, no abnormalities except for the hypertension were found. The chest radiograph together with an intravenous urogram were normal. Laboratory examination of the blood showed a lowered serum potassium level, a normal creatinine clearance and no indications of phaeochromocytoma. Plasma-renin activity (PRA) was elevated and there was a markedly increased aldosterone secretion rate. A secondary form of aldosteronism was suspected. Abdominal aortography showed no stenoses of the renal arteries and a barely visible radiolucent area in the lower pole of the right kidney. A subsequent selective study of the renal arteries revealed a hypovascular, smoothly delineated lucent area in the lower pole of the right kidney with a diameter of approximately 3 cm. No calyceal deformity was seen in the excretion phase (Fig. 1). On ultrasound examination this lesion was echogenic (Fig. 2). Computed tomography (CT) was performed and showed an isodense structure in the lower pole of the right kidney, which appeared to be hypodense as compared with the
Figure 2. Renal ultrasound scan showing a homogeneous, well delineated echogenic lesion in the right lower pole.
normal parenchyma after intravenous administration of contrast medium (Fig. 3). Selective renin sampling of the renal veins showed a markedly elevated plasma renin activity on the right side, with a ratio of 24.6 to 16.7 ng/ml/h (for comparison: PRA in the lower inferior caval vein was 11.2 ng/ml/h). Renal radionuclide scanning was not performed. All these findings suggested a renin-secreting tumour in the lower pole of the right kidney and a right lower pole resection was performed, revealing a well encapsulated tumour with a diameter of 2 cm. Histologically it was composed of neoplastic juxtaglomerular cells. Histological and immunocytochemical aspects of this tumour, which are described extensively elsewhere (Hermus et al, 1986), were typical of a benign juxtaglomerular cell tumour. Immediately after extirpation of the tumour, blood pressure fell dramatically to 120/80 mmHg. In the subsequent period the blood pressure stabilized in a range of 130/90 to 160/100 mmHg (this high value is most probably due to essential hypertension) with normal values of PRA. Discussion
Figure 1. Selective right renal arteriography shows sparse vascular structures in the lower pole with a sharply denned radiolucent area (arrows); note the absence of calyceal deformity.
Vol. 65, No. 774
A renin-producing tumour is characterized clinically by a syndrome of (severe) hypertension, hypokalaemia and hyperaldosteronism. Patients may have complaints of headache, polyuria and/or polydipsia or muscle weakness (Robertson et al, 1967; Lam et al, 1982). Patients are usually young, with an age range of 6 to 53 years (mean age 21.5 years) (Corvol et al, 1988). PRA is always elevated (Hirose et al, 1974). These tumours are solitary and are almost always solid on macroscopic examination (only one partly cystic, partly solid tumour has been described; Hanna et al, 1979), with a diameter ranging from 0.2 to 0.8 cm (mean diameter 2.3 cm) (Lam et al, 1982). Juxtaglomerular cell tumours are always located just below the renal capsule and are equally distributed throughout upper and lower pole. Histologically most of the renin-producing tumours originating from the juxtaglomerular apparatus of the kidneys are benign and of the haemangiopericytoma or 543
Case reports
Figure 3. CT scan: the tumour (arrows) appears to be isodense on the native scan (a) and non-enhancing after intravenous administration of contrast medium (b).
hamartoma type (Hirose et al, 1974; Dunnick et al, 1983). Malignant renin-producing tumours of renal origin, such as Wilms tumour, renal cell carcinoma and mesoblastic nephroma (Dunnick et al, 1983; Malone et al, 1989), as well as extrarenal primary tumours {e.g. lung, pancreas and ovary) (Anderson et al, 1989) 544
causing hypertension have also been described, but these are even more rare. Intravenous urography may show stretching or displacement of calices or the mere presence of a mass, (Takahashi et al, 1976; Dunnick et al, 1983; Pedrinelli et al, 1987; Remynse et al, 1989) but in most cases no abnormalities are seen (Robertson et al, 1967; Davidson & Clark, 1974; Lam et al, 1982). With only one cystic (Moss et al, 1982) and only one partly cystic/partly solid mass (Lee, 1971) having been reported in 10 cases, the findings at ultrasound most commonly suggest a solid mass (Dunnick et al, 1983; Pedrinelli et al, 1987). Most of these masses are echogenic, although hypoechoic and isoechoic masses (sometimes surrounded by a hyperechoic rim corresponding to a pseudocapsule) are known (Dunnick et al, 1983). CT scanning may reveal an isodense or hypodense solid tumour (Dunnick et al, 1983; Corvol et al, 1988), which may be surrounded by a small rim of haemorrhage or may show increased density centrally resulting from haemorrhage (Moss et al, 1982; Dunnick et al, 1983). After intravenous administration of contrast medium, the tumour may be non-enhancing owing to hypovascularity (Lee, 1971) or only slightly enhancing (Dunnick et al, 1983; Remynse et al, 1989). Although aortography may be inconclusive or even normal, it is usually able to show a hypovascular mass (Hanna et al, 1979; Lam et al, 1982; Moss et al, 1982; Pedrinelli et al, 1987; Corvol et al, 1988). Despite the presence of well developed vascular spaces microscopically the angiographic features consist of tortuous and sparse, poorly denned vasculature (Conn et al, 1973; Davidson & Clark, 1974; Dunnick et al, 1983; Remynse et al, 1989) with or without abnormal calibre, course or displacement (Takahashi et al, 1976). Cases with an arteriovenous shunt are unknown, but early staining of the renal vein has been described (Takahashi et al, 1976). The renal parenchyma usually shows an area of translucency, sometimes surrounded by a zone of increased density caused by a rim of compressed renal parenchyma (Davidson & Clark, 1974; Takahashi et al, 1976). Selective renin sampling of the renal veins shows lateralization with elevated renin levels on the affected side (Conn et al, 1973; Davidson & Clark, 1974; Pedrinelli et al, 1987). A ratio of more than 1.5 to 1 is considered to be significant and in this way even very small tumours (down to 0.2 cm) can be detected (Hirose et al, 1974). A renal radionuclide scan is usually normal (Hirose et al, 1974; Lam et al, 1982), but a focus of diminished activity may be seen (Takahashi et al, 1976). In establishing the diagnosis of a renin-producing tumour of the kidney, ultrasound and CT together with selective renin sampling of the renal veins is essential. Aortography performed because of suspicion of renal artery stenosis should always look for a mass as described in this case report. Whenever a mass is suspected, selective renal arteriography should be performed in order to confirm and delineate the lesion. Intravenous urography and renal radionuclide scanning The British Journal of Radiology, June 1992
1992, The British Journal of Radiology, 65, 545-547 Case reports have a low sensitivity for the detection of small renal masses such as renin-producing tumours but are usually helpful in excluding other pathological processes.
U. J. & KLOPPENBORG, P. W., 1986. Hypertension and
hypokalaemia due to a renin-secreting kidney tumour. Netherlands Journal of Medicine, 29, 84-91. HIROSE, M., ARAKAWA, K., KIKUCHI, M., KAWASAKI, T., OMOTO, T., KATO, H. & NAGAYAMA, T., 1974. Primary
Acknowledgments The authors would like to thank Miss Mariska Ebbelink and Miss Tineke van IJzendoorn for their secretarial assistance in the preparation of this manuscript.
reninism with renal hamartomatous alteration. Journal of the American Medical Association, 230, 1288-1292. LAM, A. S. C ,
BEDARD, Y. C ,
BUCKSPAN, M. B., LOGAN,
ANDERSON, P. W., MACAULAY, L., D O , Y. S. SHERROD, A., D'ABLAING, G., KOSS, M., SHINAGAWA, T., TRAN, B.,
A. G. & STEINHARDT, M. I., 1982. Surgically curable hypertension associated with reninoma. Journal of Urology, 128, 572-575. LEE, M. R., 1971. Renin-secreting kidney tumors. Lancet, 2, 254-255.
MONTZ, F. J. & HSUEH, W. A., 1989. Extrarenal renin-
MALONE, P. S., DUFFY, P. G., RANSLEY, P. G., RISDON, R. A.,
secreting tumors: insights into hypertension and ovarian renin production. Medicine, 68, 257-268.
COOK, T. & TAYLOR, M., 1989. Congenital mesoblastic
References
CONN,
J. W.,
BOOKSTEIN,
J. J.
&
COHEN,
E. L.,
1973.
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Contrast extravasation from a Pulse-Tec graft: a complication of high-dose recombinant tissue-type plasminogen activator therapy By T. M. Buckenham, FRACR, *R. S. Taylor, M S , FRCS, D. Reiff, MRCP and J . E. Page, MRCP, FRCR Departments of Radiology and 'Surgery, St George's Hospital, Blackshaw Road, London SW17 0QT, UK
{Received 1 August 1991 and in revised form 17 October 1991, accepted 20 November 1991) Keywords: Thrombolysis, Extravasation, Recombinant tissue plasminogen activator (rt-PA), Pulse-Tec
Transmural contrast extravasation through both knitted Dacron and Gore-Tex grafts is well documented. Reports have appeared associating this complication with the use of both streptokinase and urokinase (Rabe et al, 1982; Becker et al, 1984; Rosner & Doris, 1984; Perler et al, 1986). We report a case of extravasation through a Pulse-Tec (Newtec Vascular Products Ltd, Address correspondence to Dr T Buckenham, Department of Radiology, St George's Hospital, Blackshaw Road, London SW17 0QT, UK.
Vol. 65, No. 774
UK) graft in association with the use of high-dose recombinant tissue plasminogen activator (rt-PA) therapy. This complication has not previously been reported in this type of graft or with this particular thrombolytic agent. Case report A 75-year-old woman with a long history of peripheral vascular disease presented with an ischaemic ulcerated forefoot. Ankle-brachial indices were 0.4 on the left and 0.6 on the right, which was asymptomatic. A diagnostic arteriogram
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