RENAL PLASMACYTOMA: MAYO CLINIC EXPERIENCE AND REVIEW OF THE LITERATURE TODD C. IGEL, M.D. DONALD E. ENGEN, M.D. PETER M. BANKS, M.D. GARY L. KEENEY, M.D. From the Department of Urology and the Section of Surgical Pathology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota
Extramedullary plasmacytoma arising in the kidney is rare. Only 8 cases have been ~ntly, we noted the ninth case, the second case seen at the Mayo Clinic. Clinically, the a renal cell carcinoma or a transitional cell carcinoma of the renal pelvis.
~lasmacytoma is a rare presencell dyscrasia. Most such tuupper aerodigestive tract. We such case of this process apa the kidney. 1-4Diagnosis of an renal plasmaeytoma histori~d on pathologic evaluation of men.
eal standpoint, the preoperaplasmaeytoma from renal cell :ransitional cell carcinoma of is difficult, yet appropriate magement and interventional I different for each of these ff neoplasia. Case Report man was referred with ~S ~y'four-year-old ~ p t o m s of prostatism and the diagnosis ii i6State nodule. Six weeks before evalua!; 16mffered an acute anterior subendocar~Ocardial infarction During the six ~k! Since the infarction, lae had been relat~ ~symptomatic On physical examination, [0i iinal masses were not palpable. Rectal exlni lion revealed a moderately enlarged,
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APRIL 1991
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VOLUME XXXVII, NUMBER 4
slightly asymmetric, mobile prostate with a firm nodular right base. Serum electrolyte levels were within normal limits, serum calcium level was 10.4 mg/dL (normal, 8.9 to 10.1), and the alkaline phosphatase level was 426 U/L (normal, 90 to 239). Fractionation of the serum alkaline phosphatase identified the increased level to be of liver origin only. The sedimentation rate was 56 mm in one hour. Hemoglobin was 12.7 mg/dL, with a hematocrit of 37.2 percent. Urinalysis revealed more than 100 leukocytes and was negative for protein. The acid phosphatase level was 4.8 U/L (normal, 3 to 7), with a tartrate inhibition of 10.7 percent (normal, < 26%). A bone scan revealed no areas of increased activity. Subsequent transrectal needle biopsy of the prostate revealed a grade 2 acinar adenocarcinoma of the prostate. Because of the recent myocardial infarction and angiographic findings of triple-vessel disease with a significant akinetic wall segment, the decision was made to administer radiation therapy with curative intent. Before the initiation of localized prostatic radiation, a routine diagnostic computed tomographic scan of the abdomen and pelvis revealed a large soft-tissue
385
FIGURE 1.
Computed tomographic scan shows large mass in left renal pelvis extending into perirenal area.
FIGURE2. Excretory urogram ]ailed to reveal caliceal distortion. mass emanating from the region of the left renal pelvis (Fig. 1). The mass seemed to extend into the perirenal fat and involved the left renal vein. Additionally, the patient's known prostate carcinoma showed gross extension to the seminal vesicles bilaterally. Subsequent excretory urography revealed a mass in the left upper pole medially, without apparent caliceal distortion (Fig. 2). Ultrasound of the left kidney and vena cava revealed a solid mass involving the upper pole of the left kidney, contiguous with a 386
soft-tissue process that surrou~ the renal pelvis. The left dist not visualized, but the proxii and vena cava were free of 2). The differential diagnosis includedl tional cell carcinoma of the renal pelvi!~i ~'~ cal presentation of renal cortical car~~ and malignant lymphoma. In spite of high risk of reinfarction an~ quent mortality, the patient opted for~ exploration and concomitant bilateral:ii tomy for hormonal treatment of his! cancer. A radical nephrector through a left subcostal proach. There was a con edema involving perirenal large yet did not invol Enlarged, firm para-aorti removed along with the lc Pathologic examinatior medullary plasmacytoma ing in the hilar and supel (Fig. 3). The tumor su pelvis, upper ureter, and direct luminal involvemeJ riaortic lymph node invc fled. Two cortical adenor were recognized microsco
UROLOGY
/
APRIL 1991
/
VOl
Hhtologieally, the neoplasm was composed uOiformly well-differentiated plasma cells. a~l fallicular structures, also predominantly piasma cells, were noted (Fig. 4). Immunostochemical studies for identification of tu0~:immunoglobulin light chain types and • ~y chain classes were done, both on paraffin ti0ns and on frozen sectxons from tumor tls~'snap-frozen in liquid nitrogen. With both eth0ds utilizing peroxidase-conjugated reents, monotypic immunoglobulin x light din production was demonstrated, almost exam@elyin paraffin section preparations, somehai Obscured by background plasma immunoc~hl:in in frozen sections Dense polyclonal imunoglobulin-stained dendritic reticular ills:werepresent in frozen sections in the follie~i zones and, together with small intermixed l~stersof polyelonal plasma cells, suggested ~epossibility of a preexistent benign inflam}~ry lymphoid proliferation. e postoperative surgical course was un~nplicated. Hematologic workup included rual protein electrophoresis, which revealed a i~l rnonoelonal IgM ~ paraprotein of 845
l
!:i~LOCY
/ APRIL 1991
/
VOLUME XXXVII, NUMBER 4
mg/dL. Urine protein eleetrophoresis failed to identify a monoclonal protein. The plasma cell labeling index using a monoclonal antibody technique for bromodeoxyuridine marking of cells in S phase was 1.3 pereent (1% upper limits of normal). Bone marrow aspirate revealed only 3 percent plasma cells without cytologic atypia. The metastatic bone survey was negative. The patient received 5,580 rad to the left renal bed. At two-month follow-up, serum protein electrophoresis revealed only a diminished monoclonal IgM ~ protein spike of 302 mg/dL. At sixmonth follow-up, the IgM x protein spike had decreased to a low-normal range of 109 mg/dL. Plans for future management were to initiate low-dose melphalan and prednisone for presumed systemic disease, if an inerease in the serum paraprotein was detected. Summary of Previously Reported Case An earlier case reported from the Mayo Clinic by Farrow and associates 6 involved a fifty-three-year-old man with a six-week history 387
of a large mass in his left flank. On examination, a large mass and varicocele were identified. As in our recent case, protein was not identified in the urine. However, excretory urography revealed a nonfunetioning left kidney. The left kidney was removed without difficulty. The kidney was 21 x 14 x 12 cm and had evidence of pelvis and capsule invasion. The renal vein and hilar lymph nodes were free of involvement. Microscopically, pure sheets of well-differentiated plasma cells with abundant cytoplasm were identified. The patient received two courses of adjunctive radiation therapy directed to the operative site and lived symptom-free for sixteen years, when he died suddenly of an acute myocardial infarction. Comment Plasma cell dyscrasias have been grouped according to clinical and histologic patterns of presentations into three categories: myelomatosis (multiple myeloma), solitary myeloma of bone (plasmacytoma of bone), and plasma cell leukemia. ~,'7 Myelomatosis (multiple myeloma) consists of a group of tumors with multiple areas of bone rarefaction or evidence of diffuse osteoporosis. Bone marrow aspirate will identify plasma cell infiltration with concomitant morphologic abnormalities. In addition, there is usually monoclonal immunoglobulin in the serum or urine (or both). Solitary myeloma of bone (plasmacytoma of bone) is diagnosed when there is a single osteolytic lesion along with biopsy-proved evidence of a plasma cell tumor at the site. Routine bone marrow aspiration is negative. The differentiation of solitary myeloma of bone from multiple myeloma is not easy. In plasma cell leukemia, many abnormal plasma cells are seen in the peripheral blood at presentation. Whereas myelomatosis and plasma cell leukemias denote diffuse systemic disease and solitary myeloma of bone is a localized lesion of bone, extramedullary plasmacytoma is a tumor localized to an extramedullary site in the soft tissue. Extramedullary plasmacytoma also differs from solitary myeloma of bone by its pattern of spread. Unlike myelomatosis and solit a r y m y e l o m a of b o n e , e x t r a m e d u l l a r y plasmacytoma tends to spread as additional extramedullary tumors. As a group, extramedullary plasmaeytomas may constitute 7 percent of all plasma cell dyscrasias. 8 As many as 85 per-
388
cent of these tumors aris tory tract, with the high nasopharynx, nasal c~ sinuses. The incidence c maeytoma is three tim~ date, 8 males and 1 fema as having extramedullar kidney). Usually, the les tients who are between seventy years. 8,9,1° Spe diagnosis of extramed vary. ~-8,1° These include proved by biopsy at one normal findings on serur gression of monoelonal (3) lack of Benee Jones p (4) normal bone marrov cent plasma cells identit creasing or persistently i in the serum or of elevat protein in the urine is e diffuse disease. Extramedullary plasn distinguished histologiea tory process denoted a~ granuloma. Extramed consists of pure sheets oi with an associated al: network, whereas plasn sists of an edematous with production of gran~ erogeneous cellular app, Grossly, extramedui smooth and yellow-gra confined to the primary with lymph node involv tumors with systemic Sl~ We now have data on have extramedullary pl~ ney. Several of these I concomitant evidence c disease, Benee Jones F bone marrow b i o p s y myelomatosis. At presentation, 4 of dominal mass, and 2 ha al. n reported a patient had lost 9 kg (20 lb) an tion in the feet. As previ presented with sympto the extramedullary rene incidental finding at diagnostic CT scan. To date, CT scan, ex arteriography have bee
UROLOGY
/
APRIL 1991
/
tl plasmacytoma from a reor a transitional cell earMvis. Solomito and Grise 12 :aphic findings in a ease of which revealed neovaseustinguishable from a large ' evaluation in the ease real. n and in our ease sugcinoma as the most proba~tory urography was also aough it has revealed a idney in most cases. In our 'aphy showed prompt func~aliceal distortion but evi~diatly placed mass. Thus, ge of radiographic appear-
missions than in multiple myeloma or solitary plasmacytoma of bone. 6 Commenting on the high rate of progression to disseminated disease, Catalona and Biles ~a believed that primary therapy should consist of chemotherapy with attention paid to preserving all remaining functional renal tissue. Evidence suggests, however, that the proper classification of patients with extramedullary plasmacytoma using the criteria outlined here may result in cure or longterm survival in patients with low-stage disease. 6,7,1° At present, surgical excision of the tumor is the treatment of choice. High-dose radiation therapy is added if the primary tumor is inoperable or if Stage II disease is identified.
ed pathologic diagnosis of maeytoma of the kidney is c evaluation is necessary to ,elomatosis. Sedimentation ne protein electrophoreses, ophoresis should be obould be analyzed for Bence ~statie skeletal survey and ;y are required to exclude ause 85 percent of patients ,ma have anemia at presenof anemia strengthens the sis of a solitary renal plasously mentioned, persistent ~tein peaks indicate recurttion of diffuse myelomato-
Mayo Clinic 200 First Street S.W. Rochester, Minnesota 55905 (DR. ENGEN)
xamedullary renal plasmaa normal-appearing eontraudes radical nephreetomy terilization of the operative herapy. Corwin and Lind4,000 to 6,000 rad provide ntrol. Evolution of the dislomatosis or to persistently pikes requires consideration prednisone-based adjuvant results of chemotherapy [ity seems to give longer re-
P'~ii2Oey / APRIL 1991
/
VOLUME XXXVII, NUMBER 4
References 1. Dolin S, and Dewar ~P: Extramedullary plasmacytoma, Am J Pathol 32:83 (1956). 2. Knudsen O: Case of plasmacytoma of kidney, Nord Med 14: 1493 (1937). 3. Siemers PT, and Coel MN: Solitary renal plasmacytoma with palisading tumor vaseularity, Radiology 123:597 (1977). 4. Morris SA, Vaughan ED Jr, and Makoui C: Renal plasrnacytoma with palisading tumor vascularity, Urology 9:303 (1977). 5. Farrow GM, Harrison EG Jr, and Utz DC; Sarcomas and sarcomatoid and mixed malignant tumors of the kidney in adults, part II, Cancer 22:551 (1968). 6. Wiltshaw E: The natural history of extramedullary plasmacytoma and its relation to solitary myeloma of hone and myelomatosis, Medicine (Baltimore) 55:217 (1976). 7. Barat M, and Seiubba JJ: Pathologic quiz case 2, Arch Otolaryngol 110:820 (1984). 8. Conklin 1t, and Alexanian R: Clinical classification of plasma cell myeloma, Arch Intern Med 135" I39 (1975). 9. Poole AG, and Marchetta FC'. Extramedullary plasmacytoma of the head andneck, Cancer g2:14 (1968). 10. Corwin ], and Lindberg RD: Solitary plasmacytoma 0f bone vs. extramedullary plasmacytoma and their relationship to multiple myeloma, Cancer 43:1007 (1979). 11. Kandei LB, et al: Renal plasmaeytoma: a ease report and summary of reported cases, ] Urol 132:1167 (1984). 12. Solomito VL, and Grise ]: Angiographic findings in renal (extramedullary) plasmacytoma: ease report, Radiology 102:559 (1972). 13. Catalona WJ, and Biles ]DIII: Therapeutic considerations in renal ptasmacytoma, J Urol 111:582 (1974).
389
Extramedullary plasmacytoma arising in the kidney is rare. Only 8 cases have been ~ntly, we noted the ninth case, the second case seen at the Mayo Clinic. Clinically, the a renal cell carcinoma or a transitional cell carcinoma of the renal pelvis.
~lasmacytoma is a rare presencell dyscrasia. Most such tuupper aerodigestive tract. We such case of this process apa the kidney. 1-4Diagnosis of an renal plasmaeytoma histori~d on pathologic evaluation of men.
eal standpoint, the preoperaplasmaeytoma from renal cell :ransitional cell carcinoma of is difficult, yet appropriate magement and interventional I different for each of these ff neoplasia. Case Report man was referred with ~S ~y'four-year-old ~ p t o m s of prostatism and the diagnosis ii i6State nodule. Six weeks before evalua!; 16mffered an acute anterior subendocar~Ocardial infarction During the six ~k! Since the infarction, lae had been relat~ ~symptomatic On physical examination, [0i iinal masses were not palpable. Rectal exlni lion revealed a moderately enlarged,
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APRIL 1991
/
VOLUME XXXVII, NUMBER 4
slightly asymmetric, mobile prostate with a firm nodular right base. Serum electrolyte levels were within normal limits, serum calcium level was 10.4 mg/dL (normal, 8.9 to 10.1), and the alkaline phosphatase level was 426 U/L (normal, 90 to 239). Fractionation of the serum alkaline phosphatase identified the increased level to be of liver origin only. The sedimentation rate was 56 mm in one hour. Hemoglobin was 12.7 mg/dL, with a hematocrit of 37.2 percent. Urinalysis revealed more than 100 leukocytes and was negative for protein. The acid phosphatase level was 4.8 U/L (normal, 3 to 7), with a tartrate inhibition of 10.7 percent (normal, < 26%). A bone scan revealed no areas of increased activity. Subsequent transrectal needle biopsy of the prostate revealed a grade 2 acinar adenocarcinoma of the prostate. Because of the recent myocardial infarction and angiographic findings of triple-vessel disease with a significant akinetic wall segment, the decision was made to administer radiation therapy with curative intent. Before the initiation of localized prostatic radiation, a routine diagnostic computed tomographic scan of the abdomen and pelvis revealed a large soft-tissue
385
FIGURE 1.
Computed tomographic scan shows large mass in left renal pelvis extending into perirenal area.
FIGURE2. Excretory urogram ]ailed to reveal caliceal distortion. mass emanating from the region of the left renal pelvis (Fig. 1). The mass seemed to extend into the perirenal fat and involved the left renal vein. Additionally, the patient's known prostate carcinoma showed gross extension to the seminal vesicles bilaterally. Subsequent excretory urography revealed a mass in the left upper pole medially, without apparent caliceal distortion (Fig. 2). Ultrasound of the left kidney and vena cava revealed a solid mass involving the upper pole of the left kidney, contiguous with a 386
soft-tissue process that surrou~ the renal pelvis. The left dist not visualized, but the proxii and vena cava were free of 2). The differential diagnosis includedl tional cell carcinoma of the renal pelvi!~i ~'~ cal presentation of renal cortical car~~ and malignant lymphoma. In spite of high risk of reinfarction an~ quent mortality, the patient opted for~ exploration and concomitant bilateral:ii tomy for hormonal treatment of his! cancer. A radical nephrector through a left subcostal proach. There was a con edema involving perirenal large yet did not invol Enlarged, firm para-aorti removed along with the lc Pathologic examinatior medullary plasmacytoma ing in the hilar and supel (Fig. 3). The tumor su pelvis, upper ureter, and direct luminal involvemeJ riaortic lymph node invc fled. Two cortical adenor were recognized microsco
UROLOGY
/
APRIL 1991
/
VOl
Hhtologieally, the neoplasm was composed uOiformly well-differentiated plasma cells. a~l fallicular structures, also predominantly piasma cells, were noted (Fig. 4). Immunostochemical studies for identification of tu0~:immunoglobulin light chain types and • ~y chain classes were done, both on paraffin ti0ns and on frozen sectxons from tumor tls~'snap-frozen in liquid nitrogen. With both eth0ds utilizing peroxidase-conjugated reents, monotypic immunoglobulin x light din production was demonstrated, almost exam@elyin paraffin section preparations, somehai Obscured by background plasma immunoc~hl:in in frozen sections Dense polyclonal imunoglobulin-stained dendritic reticular ills:werepresent in frozen sections in the follie~i zones and, together with small intermixed l~stersof polyelonal plasma cells, suggested ~epossibility of a preexistent benign inflam}~ry lymphoid proliferation. e postoperative surgical course was un~nplicated. Hematologic workup included rual protein electrophoresis, which revealed a i~l rnonoelonal IgM ~ paraprotein of 845
l
!:i~LOCY
/ APRIL 1991
/
VOLUME XXXVII, NUMBER 4
mg/dL. Urine protein eleetrophoresis failed to identify a monoclonal protein. The plasma cell labeling index using a monoclonal antibody technique for bromodeoxyuridine marking of cells in S phase was 1.3 pereent (1% upper limits of normal). Bone marrow aspirate revealed only 3 percent plasma cells without cytologic atypia. The metastatic bone survey was negative. The patient received 5,580 rad to the left renal bed. At two-month follow-up, serum protein electrophoresis revealed only a diminished monoclonal IgM ~ protein spike of 302 mg/dL. At sixmonth follow-up, the IgM x protein spike had decreased to a low-normal range of 109 mg/dL. Plans for future management were to initiate low-dose melphalan and prednisone for presumed systemic disease, if an inerease in the serum paraprotein was detected. Summary of Previously Reported Case An earlier case reported from the Mayo Clinic by Farrow and associates 6 involved a fifty-three-year-old man with a six-week history 387
of a large mass in his left flank. On examination, a large mass and varicocele were identified. As in our recent case, protein was not identified in the urine. However, excretory urography revealed a nonfunetioning left kidney. The left kidney was removed without difficulty. The kidney was 21 x 14 x 12 cm and had evidence of pelvis and capsule invasion. The renal vein and hilar lymph nodes were free of involvement. Microscopically, pure sheets of well-differentiated plasma cells with abundant cytoplasm were identified. The patient received two courses of adjunctive radiation therapy directed to the operative site and lived symptom-free for sixteen years, when he died suddenly of an acute myocardial infarction. Comment Plasma cell dyscrasias have been grouped according to clinical and histologic patterns of presentations into three categories: myelomatosis (multiple myeloma), solitary myeloma of bone (plasmacytoma of bone), and plasma cell leukemia. ~,'7 Myelomatosis (multiple myeloma) consists of a group of tumors with multiple areas of bone rarefaction or evidence of diffuse osteoporosis. Bone marrow aspirate will identify plasma cell infiltration with concomitant morphologic abnormalities. In addition, there is usually monoclonal immunoglobulin in the serum or urine (or both). Solitary myeloma of bone (plasmacytoma of bone) is diagnosed when there is a single osteolytic lesion along with biopsy-proved evidence of a plasma cell tumor at the site. Routine bone marrow aspiration is negative. The differentiation of solitary myeloma of bone from multiple myeloma is not easy. In plasma cell leukemia, many abnormal plasma cells are seen in the peripheral blood at presentation. Whereas myelomatosis and plasma cell leukemias denote diffuse systemic disease and solitary myeloma of bone is a localized lesion of bone, extramedullary plasmacytoma is a tumor localized to an extramedullary site in the soft tissue. Extramedullary plasmacytoma also differs from solitary myeloma of bone by its pattern of spread. Unlike myelomatosis and solit a r y m y e l o m a of b o n e , e x t r a m e d u l l a r y plasmacytoma tends to spread as additional extramedullary tumors. As a group, extramedullary plasmaeytomas may constitute 7 percent of all plasma cell dyscrasias. 8 As many as 85 per-
388
cent of these tumors aris tory tract, with the high nasopharynx, nasal c~ sinuses. The incidence c maeytoma is three tim~ date, 8 males and 1 fema as having extramedullar kidney). Usually, the les tients who are between seventy years. 8,9,1° Spe diagnosis of extramed vary. ~-8,1° These include proved by biopsy at one normal findings on serur gression of monoelonal (3) lack of Benee Jones p (4) normal bone marrov cent plasma cells identit creasing or persistently i in the serum or of elevat protein in the urine is e diffuse disease. Extramedullary plasn distinguished histologiea tory process denoted a~ granuloma. Extramed consists of pure sheets oi with an associated al: network, whereas plasn sists of an edematous with production of gran~ erogeneous cellular app, Grossly, extramedui smooth and yellow-gra confined to the primary with lymph node involv tumors with systemic Sl~ We now have data on have extramedullary pl~ ney. Several of these I concomitant evidence c disease, Benee Jones F bone marrow b i o p s y myelomatosis. At presentation, 4 of dominal mass, and 2 ha al. n reported a patient had lost 9 kg (20 lb) an tion in the feet. As previ presented with sympto the extramedullary rene incidental finding at diagnostic CT scan. To date, CT scan, ex arteriography have bee
UROLOGY
/
APRIL 1991
/
tl plasmacytoma from a reor a transitional cell earMvis. Solomito and Grise 12 :aphic findings in a ease of which revealed neovaseustinguishable from a large ' evaluation in the ease real. n and in our ease sugcinoma as the most proba~tory urography was also aough it has revealed a idney in most cases. In our 'aphy showed prompt func~aliceal distortion but evi~diatly placed mass. Thus, ge of radiographic appear-
missions than in multiple myeloma or solitary plasmacytoma of bone. 6 Commenting on the high rate of progression to disseminated disease, Catalona and Biles ~a believed that primary therapy should consist of chemotherapy with attention paid to preserving all remaining functional renal tissue. Evidence suggests, however, that the proper classification of patients with extramedullary plasmacytoma using the criteria outlined here may result in cure or longterm survival in patients with low-stage disease. 6,7,1° At present, surgical excision of the tumor is the treatment of choice. High-dose radiation therapy is added if the primary tumor is inoperable or if Stage II disease is identified.
ed pathologic diagnosis of maeytoma of the kidney is c evaluation is necessary to ,elomatosis. Sedimentation ne protein electrophoreses, ophoresis should be obould be analyzed for Bence ~statie skeletal survey and ;y are required to exclude ause 85 percent of patients ,ma have anemia at presenof anemia strengthens the sis of a solitary renal plasously mentioned, persistent ~tein peaks indicate recurttion of diffuse myelomato-
Mayo Clinic 200 First Street S.W. Rochester, Minnesota 55905 (DR. ENGEN)
xamedullary renal plasmaa normal-appearing eontraudes radical nephreetomy terilization of the operative herapy. Corwin and Lind4,000 to 6,000 rad provide ntrol. Evolution of the dislomatosis or to persistently pikes requires consideration prednisone-based adjuvant results of chemotherapy [ity seems to give longer re-
P'~ii2Oey / APRIL 1991
/
VOLUME XXXVII, NUMBER 4
References 1. Dolin S, and Dewar ~P: Extramedullary plasmacytoma, Am J Pathol 32:83 (1956). 2. Knudsen O: Case of plasmacytoma of kidney, Nord Med 14: 1493 (1937). 3. Siemers PT, and Coel MN: Solitary renal plasmacytoma with palisading tumor vaseularity, Radiology 123:597 (1977). 4. Morris SA, Vaughan ED Jr, and Makoui C: Renal plasrnacytoma with palisading tumor vascularity, Urology 9:303 (1977). 5. Farrow GM, Harrison EG Jr, and Utz DC; Sarcomas and sarcomatoid and mixed malignant tumors of the kidney in adults, part II, Cancer 22:551 (1968). 6. Wiltshaw E: The natural history of extramedullary plasmacytoma and its relation to solitary myeloma of hone and myelomatosis, Medicine (Baltimore) 55:217 (1976). 7. Barat M, and Seiubba JJ: Pathologic quiz case 2, Arch Otolaryngol 110:820 (1984). 8. Conklin 1t, and Alexanian R: Clinical classification of plasma cell myeloma, Arch Intern Med 135" I39 (1975). 9. Poole AG, and Marchetta FC'. Extramedullary plasmacytoma of the head andneck, Cancer g2:14 (1968). 10. Corwin ], and Lindberg RD: Solitary plasmacytoma 0f bone vs. extramedullary plasmacytoma and their relationship to multiple myeloma, Cancer 43:1007 (1979). 11. Kandei LB, et al: Renal plasmaeytoma: a ease report and summary of reported cases, ] Urol 132:1167 (1984). 12. Solomito VL, and Grise ]: Angiographic findings in renal (extramedullary) plasmacytoma: ease report, Radiology 102:559 (1972). 13. Catalona WJ, and Biles ]DIII: Therapeutic considerations in renal ptasmacytoma, J Urol 111:582 (1974).
389
