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Renal vein thrombosis presenting as renal mass
RENAL VEIN THROMBOSIS PRESENTING AS RENAL MASS LEONARD
G. GOMELLA,
M.D.
THOMAS H. WAID, M.D. STEVEN
P PETROU,
ROBERT
C. FLANIGAN,
J. WILLIAM
M.D.
McROBERTS,
M.D. M.D.
From the Division of Urology/Department of Surgery and the Division of Nephrology/Department of Medicine, VA. Medical Center, Lexington, Kentucky
ABSTRACTThe excretory urogram of patients with acute renal vein thrombosis typically demonstrates symmetric enlargement of the involved kidney. We report a case of renal vein thrombosis that presented as a discrete renal mass on excretory urography and abdominal computerized tomography. The entity of renal vein thrombosis is briefly reviewed along with the computerized tomography findings seen in this setting.
Acute thrombosis of the renal vein classically presents with flank pain and gross hematuria. Usually, a characteristic excretory urogram is seen showing symmetrical enlargement of the kidney, with a decreased and prolonged nephrogram. We report on a case of renal vein thrombosis with radiographic evidence of a discrete renal mass. Renal vein thrombosis, with particular attention to the computerized tomographic (CT) findings seen in this setting, is reviewed. Case Report A sixty-two-year-old black man presented with acute onset of right flank pain radiating to the groin. The pain was consistent with renal colic and was accompanied by nausea and vomiting. He had no previous urologic problems, and significant past medical history was of gout and mild hypertension. Physical examination was remarkable for mild right costovertebral angle tenderness. His admission laboratory data included a normal hemogram;
164
blood urea nitrogen of 20 mg/dL and creatinine of 1.6 mg/dL; normal electrolytes, and a urinalysis with large occult blood, protein (3 + ), greater than 100 red blood cells per high-powered field, and 0 to 5 white cells per high-powered field. Urine culture was negative. Excretory urography showed a normal left kidney and ureter. The right kidney had a delayed faint but persistent nephrogram, with essentially nonvisualization of the collecting system at two and twelve hours. The right kidney was slightly enlarged, and there was a distinct mass effect on a lateral aspect of the kidney (Fig. 1). Cystoscopy and right retrograde pyelography done to rule out obstruction were unremarkable. The working diagnosis at this time was a right renal mass. Enhanced CT scan of the abdomen showed a filling defect from the right renal vein extending to the infrahepatic vena cava (Fig. 2A). A hyperdense nephrogram was seen on the right, with a mass effect on the anterior and lateral aspects of the kidney. The mass enhanced to the
UROLOGY
/
SEPTEMBER
1989
/
VOLUME XXXIV, NUMBER 3
the right renal vein. A diagnosis of renal vein thrombosis was made. The patient was given hepa.rin, followed by oral warfarin (Coumadin) anticoagulant therapy. Adequate hydration was maintained during the workup, and creatinine did not rise above 1.8 mg/dL. Creatinine clearance was 55 mL/min and a twenty-four-hour-urine protein was 3.5 g. The patient was free of symptoms at the time of discharge, but returned three days later with symptoms suggestive of and a pulmonary perfusion scan consistent with a pulmonary embolism. He was reheparinized and continued on warfarin on discharge. Follow-up CT scan six weeks later revealed complete resolution of the right renal mass, except for some residual thickening of the Gerota fascia (Fig. 2B). Laboratory studies revealed a serum creatinine of 1.1, a t.wenty-four-hour creatinine clearance of 62 mlimin, and 1.1 g of protein in the twenty-four-hour urine specimen. One-year follow-up excretory urography was normal and serum creatinine was 1.3 mgl dL. Proteinuria, greater than 5 g per day, has developed, and a percutaneous needle biopsy of the kidney confirmed the diagnosis of membranous glomerulonephritis. FIGURE 1.
Nephrotomogram ten-minute excretory wokram ejject on lateral aspect.
of right kidney on dimo&trating mass
same degree as the rest of the right renal parenchyma. The mass combined with presence of a thrombus raised the possibility of a neoplasm in the involved kidney. A renal arteriogram was normal, and an inferior venacavogram confirmed a partial filling defect at the origin of
Comment Keating and Althauser’ recently divided the etiologies of renal vein thrombosis into four basic categories: (1) alteration of renal blood flow (volume loss, dehydration), most common in neonates and infants; (2) thromboembolic states, either as direct extension of leg venous or pelvic venous thrombosis or as results of hypercoagulable states (malignancy, oral contraceptives, congestive heart disease); (3) involvement
FIGURE 2. (A) Enhanced CT scan of kidneys at level of renal arteries. Mass seen on lateral and anterior aspect of right kidney with filling de-
fect in inferior vena cava (arrow). (B) CT .scan at same level as (A) aft er six weeks of anticoagulant therapy. Complete clearing of caval thrombus and alm,ost complete re.yolution of mass except for .some residual thirkening of Gerota f ascia .
UROI,O<:Y
i
SEPTEMBER
1989 I
VOLUME
XXXIV.
NUMBER
3
165
of the vascular pedicles, seen with retroperitoneal fibrosis, abscess, or lymphoma; and (4) nephropathic conditions and tumors, including renal cell carcinoma, membranous and membranoproliferative glomerulonephritis, amyloidosis, collagen vascular diseases, and diabetic glomerulosclerosis. Whether the nephrotic proteinuria syndrome, such as that seen with membranous glomerulonephritis, is a cause or effect of renal vein thrombosis has been debated. Ample evidence has now accumulated indicating that renal vein thrombosis is most likely to be a consequence of nephrotic proteinuria, rather than its cause.2 Clinically, renal vein thrombosis is often subacute. The presenting symptoms are usually of a chronic nature consisting of nausea, apathy, weakness, and edema. Less often, renal vein thrombosis presents acutely with sudden flank pain, with or without hematuria or hypertension.3 Laboratory findings may include azotemia, hematuria, proteinuria, hypoalbuminemia, hypoproteinemia, and decreased platelet count and fibrinogen levels. Red blood cell casts are found in a high percentage of patients.3 Excretory urography findings suggestive of renal vein thrombosis include faint excretion of the contrast material, a diminished nephrogram, enlargement of one or both kidneys, and ureteral notching due to collateral circulation. The definitive diagnosis of renal vein thrombosis usually is made by an inferior venacavogram. The thrombus can usually be seen in the renal vein or extending into the cava. Collateral vessels may be seen with chronic occlusion of the renal vein. However, recent advances in CT scanning, particularly when it is used in conjunction with contrast injection into the femoral vein or pedal veins, improves the diagnostic accuracy of the CT scan.4 Much of the early radiologic literature concerning the usefulness of the CT scan in the diagnosis of renal vein thrombosis centered on the identification of the intraluminal thrombus. Few authors commented on the CT contrast enhancement of the involved kidney. Glazer et al. 5 have described prolonged cortical enhancement relative to medullary enhancement on CT scan. In our patient, a hyperdense nephrogram was seen on CT scan. This finding can be attributed to the prolonged “corticopelvic junction time” that occasionally may be seen in renal diseases such as renal vein thrombosis.6
166
Perirenal subcapsular fluid collections7 and perirenal “cobwebs” (serpiginous densities in the perinephric space caused by enlarged veins and lymphatics)s have also been described on CT scans. The CT findings of renal vein thrombosis may be summarized as follows: (1) demonstration of low attenuation clot in the renal veins, inferior vena cava or both, along with associated enlargement of the renal veins; (2) enlargement of the involved kidney; (3) thickening of the Gerota fascia with perirenal “whiskering” due to edema or hemorrhage; (4) perirenal collateral vessels; and (5) abnormal renal opacification pattern consisting of either prolonged corticomedullary discrimination or prolonged and/or persistent parenchymal opacification, delayed or absent pyelocaliceal opacifications and attenuation of the collecting system.g Ultrasound may also be used as a diagnostic modality, lo and magnetic resonance imaging has not been widely used in this disease but is currently under study. l1 The localized mass effect associated with a thrombus in the renal vein is a unique finding. The typical setting for this is a renal cell carcinoma with an associated tumor thrombus. Arteriography was performed to help exclude the presence of a neoplasm. The anatomy of the right kidney on the initial CT scan resembled the so-called anterior renal hilar lip as described by Kolbenstvedt and Lien.12 This normal renal anatomic varient is diagnosed by its typical appearance and contrast enhancement to the same degree as the rest of the kidney. However, this should be a constant finding and not disappear with the resolution of the renal vein thrombus, as was the case in our patient. Unlike the segmental intrarenal arterial supply, the venous system is freely anastomosing. A localized thrombus of the intrarenal system would be unlikely to explain the mass. The mass effect on the right kidney most probably represented an asymmetric swelling of that kidney. The mainstay of the treatment of renal vein thrombosis is now conservative with rehydration and systemic anticoagulation replacing the aggressive surgical approach of thrombectomy used in the past. Several authors report success with the use of thrombolytic therapy including streptokinase or urokinase. 13.14Renal biopsy is often recommended to determine any covert renal pathology and was essential to the followup of our patient.
UROLOGY
/ SEPTEMBER1989
i VOLUMEXXXIV.
NUMBER3
All patients treated for renal vein thrombosis must have long-term follow-up so that the return of renal function may be monitored, and the development of heavy proteinuria associated with nephrotic syndrome may be detected. Jefferson Medical College Department of Urology Suite 1112, 1025 Walnut Street Philadelphia, Pennsylvania 19107) (DR. GOMELLA) References 1. Krating MA. and Althausen AF: The clinical spectrum of renal vein thrombosis, J Urol 133: 938 (1985). 2. Chugh KS, et al: Renal vein thrombosis in nephrotic syndrome: a prospective study and review, Fellowsh Postgrad Med 57: 566 (1981). 3. O’Dea MJ, Malek RS, Tucker RM, and Fulton RE: Renal vein thrombosis, J Ural 116: 110 (1976). 4. Zerhouni EA. Bartu KM, and Siegelman SS: Demonstration
UROLOGY
i
SEPTEMBER
1989
/
VOLUME
of venous thrombosis by computerized tomography, Am J Roentgen01 134: 753 (1980). 5. Glazer GM, Francis IR, Gross BM.. and Amendola MA: Computed tomography of renal vein thrombosis. J Comput Assist Tomogr 8: 288 (1984). 6. Ishikawa 1, et al: Renal cortex visualization and analysis of dynamic CT curves of the kidney. J Comput Assist Tomogr 5: 695 (1981). 7. Orofino L, rt al: Perirenal subcapsular fluid collection in a patient with membranous nephropathy and renal vein thrombosis, J Urol 136: 1287 (1986). 8. Winfield A, Gerlock AJ, and Schaff MI: Perirenal cobwebs: a CT sign of renal vein thrombosis, J Comput Assist Tomogr 5: 705 (1981). in patients 9. Gatewood OMB, rt al: Renal vein thrombosis with nephrotic syndrome: CT diagnosis, Radiology 159: 117 (1986). 10. Braun B, Weileman LS, and Weigand M’: Ultrasonographic diagnosis of renal vein thrombosis. Am J Radio1 138: 157 (1980). 11. Rapoport S, et al: Venous clots: evaluation with MR imaging, Radi&& 162: 527 (1987). 12. Kolbenstvedt A. and Lien H: Isolated renal hilar liu on computed tomography; Radiology 143: 150 (1982). I 13. Burrow CR, Walker WG, Bell WA., and Gatemond OB: Streptokinase salvage of renal function after renal vein thrombosis, Ann Intern Med 100: 237 (1984). 14. Rowe JM, et al: Successful thrombolytic therapy in two patients with renal vein thrombosis, Am J Med 77: 1111 (1984).
XXXIV, NUMBER
3
167
G. GOMELLA,
M.D.
THOMAS H. WAID, M.D. STEVEN
P PETROU,
ROBERT
C. FLANIGAN,
J. WILLIAM
M.D.
McROBERTS,
M.D. M.D.
From the Division of Urology/Department of Surgery and the Division of Nephrology/Department of Medicine, VA. Medical Center, Lexington, Kentucky
ABSTRACTThe excretory urogram of patients with acute renal vein thrombosis typically demonstrates symmetric enlargement of the involved kidney. We report a case of renal vein thrombosis that presented as a discrete renal mass on excretory urography and abdominal computerized tomography. The entity of renal vein thrombosis is briefly reviewed along with the computerized tomography findings seen in this setting.
Acute thrombosis of the renal vein classically presents with flank pain and gross hematuria. Usually, a characteristic excretory urogram is seen showing symmetrical enlargement of the kidney, with a decreased and prolonged nephrogram. We report on a case of renal vein thrombosis with radiographic evidence of a discrete renal mass. Renal vein thrombosis, with particular attention to the computerized tomographic (CT) findings seen in this setting, is reviewed. Case Report A sixty-two-year-old black man presented with acute onset of right flank pain radiating to the groin. The pain was consistent with renal colic and was accompanied by nausea and vomiting. He had no previous urologic problems, and significant past medical history was of gout and mild hypertension. Physical examination was remarkable for mild right costovertebral angle tenderness. His admission laboratory data included a normal hemogram;
164
blood urea nitrogen of 20 mg/dL and creatinine of 1.6 mg/dL; normal electrolytes, and a urinalysis with large occult blood, protein (3 + ), greater than 100 red blood cells per high-powered field, and 0 to 5 white cells per high-powered field. Urine culture was negative. Excretory urography showed a normal left kidney and ureter. The right kidney had a delayed faint but persistent nephrogram, with essentially nonvisualization of the collecting system at two and twelve hours. The right kidney was slightly enlarged, and there was a distinct mass effect on a lateral aspect of the kidney (Fig. 1). Cystoscopy and right retrograde pyelography done to rule out obstruction were unremarkable. The working diagnosis at this time was a right renal mass. Enhanced CT scan of the abdomen showed a filling defect from the right renal vein extending to the infrahepatic vena cava (Fig. 2A). A hyperdense nephrogram was seen on the right, with a mass effect on the anterior and lateral aspects of the kidney. The mass enhanced to the
UROLOGY
/
SEPTEMBER
1989
/
VOLUME XXXIV, NUMBER 3
the right renal vein. A diagnosis of renal vein thrombosis was made. The patient was given hepa.rin, followed by oral warfarin (Coumadin) anticoagulant therapy. Adequate hydration was maintained during the workup, and creatinine did not rise above 1.8 mg/dL. Creatinine clearance was 55 mL/min and a twenty-four-hour-urine protein was 3.5 g. The patient was free of symptoms at the time of discharge, but returned three days later with symptoms suggestive of and a pulmonary perfusion scan consistent with a pulmonary embolism. He was reheparinized and continued on warfarin on discharge. Follow-up CT scan six weeks later revealed complete resolution of the right renal mass, except for some residual thickening of the Gerota fascia (Fig. 2B). Laboratory studies revealed a serum creatinine of 1.1, a t.wenty-four-hour creatinine clearance of 62 mlimin, and 1.1 g of protein in the twenty-four-hour urine specimen. One-year follow-up excretory urography was normal and serum creatinine was 1.3 mgl dL. Proteinuria, greater than 5 g per day, has developed, and a percutaneous needle biopsy of the kidney confirmed the diagnosis of membranous glomerulonephritis. FIGURE 1.
Nephrotomogram ten-minute excretory wokram ejject on lateral aspect.
of right kidney on dimo&trating mass
same degree as the rest of the right renal parenchyma. The mass combined with presence of a thrombus raised the possibility of a neoplasm in the involved kidney. A renal arteriogram was normal, and an inferior venacavogram confirmed a partial filling defect at the origin of
Comment Keating and Althauser’ recently divided the etiologies of renal vein thrombosis into four basic categories: (1) alteration of renal blood flow (volume loss, dehydration), most common in neonates and infants; (2) thromboembolic states, either as direct extension of leg venous or pelvic venous thrombosis or as results of hypercoagulable states (malignancy, oral contraceptives, congestive heart disease); (3) involvement
FIGURE 2. (A) Enhanced CT scan of kidneys at level of renal arteries. Mass seen on lateral and anterior aspect of right kidney with filling de-
fect in inferior vena cava (arrow). (B) CT .scan at same level as (A) aft er six weeks of anticoagulant therapy. Complete clearing of caval thrombus and alm,ost complete re.yolution of mass except for .some residual thirkening of Gerota f ascia .
UROI,O<:Y
i
SEPTEMBER
1989 I
VOLUME
XXXIV.
NUMBER
3
165
of the vascular pedicles, seen with retroperitoneal fibrosis, abscess, or lymphoma; and (4) nephropathic conditions and tumors, including renal cell carcinoma, membranous and membranoproliferative glomerulonephritis, amyloidosis, collagen vascular diseases, and diabetic glomerulosclerosis. Whether the nephrotic proteinuria syndrome, such as that seen with membranous glomerulonephritis, is a cause or effect of renal vein thrombosis has been debated. Ample evidence has now accumulated indicating that renal vein thrombosis is most likely to be a consequence of nephrotic proteinuria, rather than its cause.2 Clinically, renal vein thrombosis is often subacute. The presenting symptoms are usually of a chronic nature consisting of nausea, apathy, weakness, and edema. Less often, renal vein thrombosis presents acutely with sudden flank pain, with or without hematuria or hypertension.3 Laboratory findings may include azotemia, hematuria, proteinuria, hypoalbuminemia, hypoproteinemia, and decreased platelet count and fibrinogen levels. Red blood cell casts are found in a high percentage of patients.3 Excretory urography findings suggestive of renal vein thrombosis include faint excretion of the contrast material, a diminished nephrogram, enlargement of one or both kidneys, and ureteral notching due to collateral circulation. The definitive diagnosis of renal vein thrombosis usually is made by an inferior venacavogram. The thrombus can usually be seen in the renal vein or extending into the cava. Collateral vessels may be seen with chronic occlusion of the renal vein. However, recent advances in CT scanning, particularly when it is used in conjunction with contrast injection into the femoral vein or pedal veins, improves the diagnostic accuracy of the CT scan.4 Much of the early radiologic literature concerning the usefulness of the CT scan in the diagnosis of renal vein thrombosis centered on the identification of the intraluminal thrombus. Few authors commented on the CT contrast enhancement of the involved kidney. Glazer et al. 5 have described prolonged cortical enhancement relative to medullary enhancement on CT scan. In our patient, a hyperdense nephrogram was seen on CT scan. This finding can be attributed to the prolonged “corticopelvic junction time” that occasionally may be seen in renal diseases such as renal vein thrombosis.6
166
Perirenal subcapsular fluid collections7 and perirenal “cobwebs” (serpiginous densities in the perinephric space caused by enlarged veins and lymphatics)s have also been described on CT scans. The CT findings of renal vein thrombosis may be summarized as follows: (1) demonstration of low attenuation clot in the renal veins, inferior vena cava or both, along with associated enlargement of the renal veins; (2) enlargement of the involved kidney; (3) thickening of the Gerota fascia with perirenal “whiskering” due to edema or hemorrhage; (4) perirenal collateral vessels; and (5) abnormal renal opacification pattern consisting of either prolonged corticomedullary discrimination or prolonged and/or persistent parenchymal opacification, delayed or absent pyelocaliceal opacifications and attenuation of the collecting system.g Ultrasound may also be used as a diagnostic modality, lo and magnetic resonance imaging has not been widely used in this disease but is currently under study. l1 The localized mass effect associated with a thrombus in the renal vein is a unique finding. The typical setting for this is a renal cell carcinoma with an associated tumor thrombus. Arteriography was performed to help exclude the presence of a neoplasm. The anatomy of the right kidney on the initial CT scan resembled the so-called anterior renal hilar lip as described by Kolbenstvedt and Lien.12 This normal renal anatomic varient is diagnosed by its typical appearance and contrast enhancement to the same degree as the rest of the kidney. However, this should be a constant finding and not disappear with the resolution of the renal vein thrombus, as was the case in our patient. Unlike the segmental intrarenal arterial supply, the venous system is freely anastomosing. A localized thrombus of the intrarenal system would be unlikely to explain the mass. The mass effect on the right kidney most probably represented an asymmetric swelling of that kidney. The mainstay of the treatment of renal vein thrombosis is now conservative with rehydration and systemic anticoagulation replacing the aggressive surgical approach of thrombectomy used in the past. Several authors report success with the use of thrombolytic therapy including streptokinase or urokinase. 13.14Renal biopsy is often recommended to determine any covert renal pathology and was essential to the followup of our patient.
UROLOGY
/ SEPTEMBER1989
i VOLUMEXXXIV.
NUMBER3
All patients treated for renal vein thrombosis must have long-term follow-up so that the return of renal function may be monitored, and the development of heavy proteinuria associated with nephrotic syndrome may be detected. Jefferson Medical College Department of Urology Suite 1112, 1025 Walnut Street Philadelphia, Pennsylvania 19107) (DR. GOMELLA) References 1. Krating MA. and Althausen AF: The clinical spectrum of renal vein thrombosis, J Urol 133: 938 (1985). 2. Chugh KS, et al: Renal vein thrombosis in nephrotic syndrome: a prospective study and review, Fellowsh Postgrad Med 57: 566 (1981). 3. O’Dea MJ, Malek RS, Tucker RM, and Fulton RE: Renal vein thrombosis, J Ural 116: 110 (1976). 4. Zerhouni EA. Bartu KM, and Siegelman SS: Demonstration
UROLOGY
i
SEPTEMBER
1989
/
VOLUME
of venous thrombosis by computerized tomography, Am J Roentgen01 134: 753 (1980). 5. Glazer GM, Francis IR, Gross BM.. and Amendola MA: Computed tomography of renal vein thrombosis. J Comput Assist Tomogr 8: 288 (1984). 6. Ishikawa 1, et al: Renal cortex visualization and analysis of dynamic CT curves of the kidney. J Comput Assist Tomogr 5: 695 (1981). 7. Orofino L, rt al: Perirenal subcapsular fluid collection in a patient with membranous nephropathy and renal vein thrombosis, J Urol 136: 1287 (1986). 8. Winfield A, Gerlock AJ, and Schaff MI: Perirenal cobwebs: a CT sign of renal vein thrombosis, J Comput Assist Tomogr 5: 705 (1981). in patients 9. Gatewood OMB, rt al: Renal vein thrombosis with nephrotic syndrome: CT diagnosis, Radiology 159: 117 (1986). 10. Braun B, Weileman LS, and Weigand M’: Ultrasonographic diagnosis of renal vein thrombosis. Am J Radio1 138: 157 (1980). 11. Rapoport S, et al: Venous clots: evaluation with MR imaging, Radi&& 162: 527 (1987). 12. Kolbenstvedt A. and Lien H: Isolated renal hilar liu on computed tomography; Radiology 143: 150 (1982). I 13. Burrow CR, Walker WG, Bell WA., and Gatemond OB: Streptokinase salvage of renal function after renal vein thrombosis, Ann Intern Med 100: 237 (1984). 14. Rowe JM, et al: Successful thrombolytic therapy in two patients with renal vein thrombosis, Am J Med 77: 1111 (1984).
XXXIV, NUMBER
3
167