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Amyloidosis of renal pelvis and urinary bladder
AMYLOIDOSIS
OF RENAL PELVIS
AND URINARY BLADDER
RICHARD
DIAS,
M.D.
MANUEL
FERNANDES,
RAJENDRAPRASAD JEAN-JACQUES RUSSELL
DE
M.D.
C. PATEL,
M.D.
SHADAREVIAN,
W. LAVENGOOD,
M.D.
M.D.
From the Urology Service, St. Luke’s Hospital Center, New York, New York
- We ahcribe a patient with amyloidosis of renal pelvis and 2 patients with urinary bladder amyloidosis. Clinical presentation in all of the cases mimicked cancer of the respective sites. Clinical diagnosis of amyloidosis is not possible, making biopsy mandatory. Immunology of amyloid formation and treatment of amyloidosis are discussed. ABSTRACT
Amyloidosis, a disease resulting from the infiltration of organs by a proteinaceous material, has been recognized as a clinical pathologic entity for the past one hundred thirty years. It can involve urogenital tract in either a primary or secondary form. Primary amyloidosis occurs in the absence of chronic disease. It is subdivided into systemic form when it involves multiple organs, and localized f&-m when only one organ is involved. The secondary form is found in association with chronic inflammatory disease and familial Mediterranean fever. We report 3 cases of primary amyloidosis of the urinary tract. The renal pelvis was involved in 1 case, and 2 patients presented with bladder lesions, one was localized and the other systemic.
junction obstruction to the left kidney. Cystoscopy disclosed hemorrhagic areas in the bladder mucosa, which on biopsy were found to be inflammatory. Bladder urine was examined on repeated occasions by the Papanicolaou technique, and a barium enema was found to be unremarkable. Hematuria ceased, and the patient was discharged home only to be readmitted two months later with gross hematuria. Repeat intravenous pyelogram and left retrograde
Case Reports Case 1 A sixty-seven-year-old woman was admitted to this Center on March 9, 1974, with her first episode of painless gross hematuria. The patient had undergone a left hemicolectomy for carcinoma of the sigmoid colon in 1971. On admission, her hemoglobin was 8 Gm./ 100 ml., with a hematocrit of 25. An intravenous urogram revealed a grossly normal right kidney and ureter with partial ureteropelvic
UROLOGY
I
OCTOBER
1979
/
VOLUME
XIV
NUMBER4
FIGURE 1. Excretory urogram showing ureteropelvic junction obstruction.
partial left
401
FIGURE 2. Renal medulla and pelvis revealing nodular infiltrate in tunica propia. Remainder of kidney proper entirely normal. Hematoxylin-eosin, original magni$cation X 160.
FIGURE 3. Characteristic vasocentric deposition of amyloid. Urothelium is thrown into nodular elevax tion. Hematoxylin-eosin, original magnijcation 160.
pyelogram revealed partial ureteropelvic junction obstruction with a questionable filling defect in the left renal pelvis (Fig. 1). Selective renal arteriography failed to reveal any renal tumor or abnormal vessels in the region of the renal pelvis. Urine for cytology from the bladder and the renal pelvis showed no evidence of malignancy. Surgical exploration was performed on July 3, 1974. There was marked inflammatory reaction around the left renal pelvis and ureter; no lesion was seen. Frozen section biopsies were taken from the renal pelvis, parapelvis, and paraureteral tissues, all of which were &ee of tumor. Attempted pyeloplasty failed because of the marked inflammatory reaction in the renal pelvis and ureter. A nephrectomy and partial ureterectomy were performed. On microscopic examination, the renal pelvis and calyces were involved with amyloidosis (Fig. 2). No amyloidosis was seen in the kidney. The patient did well postoperatively. She was readmitted six months later with alcoholic cirrhosis of the liver. Celiac arteriogram showed no evidence of metastatic disease. The patient died at home on March 1, 1977.
Case 2
402
An eighty-one-year-old woman was admitted in June, 1977, with a history of intermittent, painless, gross hematuria of two months’ duration. There was no history of chronic disease. Physical examination was unremarkable. Complete blood cell count, urinalysis (except for red cells), urine cytology, and intravenous urogram were normal. Cystoscopy revealed a velvety lesion on the left lateral bladder wall, biopsy of which revealed amyloidosis. Fulguration of the lesion was performed, and the hematuria ceased postoperatively. Complete investigation failed to detect any systemic disease. Serum protein electrophoresis revealed normal serum albumin. Serum immunoglobulin G (IgG) was slightly elevated. Case 3
A sixty-three-year-old woman, with documented amyloidosis of the gastrointestinal tract and bone marrow, was admitted in June, 1977, with gross hematuria and urinary incontinence. Intravenous pyelogram revealed normal upper tracts. Cystoscopy showed a raised hemorrhagic lesion on the posterior bladder wall,
UROLOGY
/ OCTOBER
1979 / VOLUME
XIV
NUMBER4
FIGURE 4. (A) Technique of corroborating amyloid. Congo red stain - not specify stain but based on metachromusia. Amybid appears as mahogany color. Polarization of amyloid stained with congo red gives apple green birefiigence. (B) Demonstrates more speci$c stain by SAB (sulphonated aniline blue); note bluish green coloration of oasocentric amyloid.
biopsy of which revealed amyloidosis (Fig. 3). Hematuria ceased fallowing fulguration of the area. Serum protein electrophoresis revealed low albumin and decreased serum IgA and IgG. Comment Amyloidosis of the renal pelvis has been reported previously in 6 cases1m5 Ureteral amyloidosis has been reported in 30 cases. Treatment has consisted of nephroureterectomy and resection of distal ureter with ureteroneocystostomy. r Primary amyloidosis of the bladder is rare, 38 cases being reported in the English literature. Nearly all cases presented with intermittent gross hematuria.8-10 A few of the cases presented with flank pain, fever, chills, and acute urinary retention. Cystoscopic appearance resembles infiltrating carcinoma. It is often described as “a solid, circumscribed, elevated mass with a hemorrhagic irregular surface of yellowish tint frequently oozing blood.” Differential diagnosis on gross examination includes tumor, endometriosis, hemangioma, and cystitis glandularis. A correct diagnosis prior to histologic examination has never been made. Various modalities of treatment have been employed in bladder amyloidosis, including transurethral biopsy and resection, partial cystectomy, radium implantation, and even urinary diversion by ileal conduit for severe
UROLOGY
/ OCTOBER
1979 / VOLUMEXIV
NUMBER4
irritative bladder symptoms12,13 and bilateral ureteric obstruction. 12-14 Differentiation from secondary amyloidosis is by exclusion of recognizable predisposing causes. I5 Where secondary amyloidosis develops, it usually does so after many years (seven to fifteen) of continued inflammatory stimulus. In a number of reported cases, treatment of the underlying inflammatory disease has brought about a decrease in the progression of the disease. l6 Renal involvement occurs in most cases of secondary amyloidosis, and in one half of the patients with myeloma and related amyloidosis. ” Once the renal involvement progresses to the point of renal failure, death usually occurs within approximately one year. l7 Primary amyloidosis carries a much more hopeful prognosis. The incidence of amyloid deposition in the prostate ranges from 1.5 to 10 per cent in prostatectomy specimens. ‘* The testis was involved in 10 to 20 per cent of the men known to have systemic amyloidosis who underwent autopsy. ls Involvement of seminal vesicles, penis, and urethra have also been reported.18,20 The main amyloid protein is a microfiber which possesses properties distinct from those of any other known mammalian protein. Grossly it stains black with iodine. It has a fibrillar appearance by electron microscopy. Figure 4 shows the appearance of amyloid by congo red stain and sulphonated aniline blue (SAB) stain, respectively.
403
TWO observations have been made about the relationship between amyloid and immune system. l8 Apitz*r demonstrated that many patients with primary amyloidosis had abnormal plasma cells and plasmacytosis of bone marrow. The secondary form of amyloidosis has been associated with chronic antigenic stimulation. Glenner and his associates**-24 by analyzing the amino acid sequencing of amyloid have shown tissue deposition of the variable portion of the immunoglobulin light chains. Although abnormalities of serum proteins or immunoglobulins could be expected in amyloidosis because of immunologic basis, it has not been found to be true in all cases. ‘*s Amyloid fibrils have been demonstrated in the urinary sediment of patients with renal amyloidosis. 26 At the present time there is no known effective treatment for amyloidosis other than elimination of the antigenic stimulus in those cases associated with an infectious process or other known antigenic source. Renal transplantation has been reported in cases of renal amyloidosis. *’ Treatment using immunosuppressive or cytotoxic agents is suggested to reduce the synthesis of monoclonal protein in those cases of amyloidosis in which the major protein of the fibrils is of immunoglobulin origin.23j24,27 Those cases of amyloidosis in which the major protein of the fibrils is not of immunoglobulin origin have to await knowledge of the cellular origin of this protein.24 New York, New York 10025 (DR. LAVENGOOD) References 1. Gardner KD, Jr, et al: Primary amyloidosis of renal pelvis, N. Engl. J. Med. 284: 1196 (1971). 2. Ullman AS: Primary amyloidosis of the renal pelvis, a case report and review of literature, Mich. Med. 72: 29 (1973). 3. Chisholm GD, Cooter, NBE, and Dawson JM: Primary amyloidosis of the renal pelvis, Br. Med. J. 1: 736 (1967).
404
4. Sato S: Primary amyloidosis of renal pelvis and ureter: report of a case, Acta Med. Biol. 5: 15 (1957). 5. Gilbert LW, and McDonald JR: Primary amyloidosis of renal pelvis and ureter, J. Urol. 68: 137 (1952). 6. Klotz PG: Primary amyloidosis of the ureter, Br. J, Urol. 47: 578 (1975). 7. Johnson HW, and Ankenman GJ: Bilateral ureteral primary amyloidosis, J. Urol. 92: 275 (1964). 8. Strong GH, Kelsey D, and Hoch W: Primary amyloid disease of the bladder, ibid. 112: 463 (1974). 9. Grace DA, and Walton KN: Primary localized amyloidosis of the bladder, ibid. 92: 655 (1964). 10. Au KK, and Cilbaugh JH, Jr: Primary amyloidosis of the bladder, ibid. 114: 786 (1975). 11. MacDonald JH, and Heckel NJ: Primary amyloidosis of lower genitourinary tract, ibid. 75: 122 (1956). 12. Kinzel RC, Harrison EG, and Utz DC: Primary localized amyloidosis of the bladder, ibid. 85: 785 (1961). 13. Blath AB, and Bucy JG: Localized primary amyloidosis of the bladder, Br. J. Urol. 48: 219 (1976). 14. Hudson HC, and Tingley JO: Primary amyloidosis of the bladder, J. Med. Assoc. Alabama 35: 353 (1965). 15. Symmers WSC: Primary amyloidosis: a review, J. Clin. Pathol. 9: 187 (1956). 16. Lowenstein J, and Gallo A: Remission of the nephrotic syndrome in renal amyloidosis, N. Engl. J. Med. 282: 128 (1976). 17. Catkins E: Amyloidosis, in: Harrison’s Principles of Internal Medicine, 8th ed., New York, McGraw-Hill, 1976. 18. Carris CK, McLaughlin AP, III, and Gittes RF: Amyloidosis of the lower genitourinary tract, J. Urol. 115: 423 (1976). 19. Mostofi FK: Lecture notes, Armed Forces Institute of Pathology, Bethesda, Maryland, Feb., 1978. 20. Nagel R: Localized amyloidosis of the bladder, J. Urol. 88: 56 (1962). 21. Apitz K: Quoted by Carris, C. K., et al., op ci1.i’ 22. Glenner GG, Terry W, Iserky C, and Page D: Amyloid fibril proteins: proof of homology with immunoglobulin light chains by sequence analysis, Science 172: 1150 (1971). 23. Glenner GG, Ein D, and Tierry WD: The immunoglobulin origin of amyloid, Am. J. Med. 52: 141 (1972). 24. Glenner GG: The nature and pathogenesis of systemic amyloidosis, Adv. Nephrol. 4: 291 (1974). 25. Barth WF, Willerson JT, Waldman TA, and Decker JL: immunochemical and immunoPrimary amyloidosis, clinical, glo bu 1’ m metabolism studies in 15 patients, Am. J. Med. 47: 259 (1969). 26. Derosena R, Koss MN, and Pirani CL: Demonstration of amyloid fibrils in urinary sediment, N. Engl. J. Med. 293: 1131 (1975). 27. Cohen AS, Bricetti AB, Harrington JT, and Mannick JA: Renal transplantation in 2 cases of amyloidosis, Lancet 2: 531 (1971). 28. Jones NF, Hilton PJ, Tighe JR, and Hobbs JR: Treatment of primary renal amyloidosis with melphalan, ibid. 2: 616 (1972).
UROLOGY
/
OCTOBER
1979
/
VOLUME
XIV
NUMBER4
OF RENAL PELVIS
AND URINARY BLADDER
RICHARD
DIAS,
M.D.
MANUEL
FERNANDES,
RAJENDRAPRASAD JEAN-JACQUES RUSSELL
DE
M.D.
C. PATEL,
M.D.
SHADAREVIAN,
W. LAVENGOOD,
M.D.
M.D.
From the Urology Service, St. Luke’s Hospital Center, New York, New York
- We ahcribe a patient with amyloidosis of renal pelvis and 2 patients with urinary bladder amyloidosis. Clinical presentation in all of the cases mimicked cancer of the respective sites. Clinical diagnosis of amyloidosis is not possible, making biopsy mandatory. Immunology of amyloid formation and treatment of amyloidosis are discussed. ABSTRACT
Amyloidosis, a disease resulting from the infiltration of organs by a proteinaceous material, has been recognized as a clinical pathologic entity for the past one hundred thirty years. It can involve urogenital tract in either a primary or secondary form. Primary amyloidosis occurs in the absence of chronic disease. It is subdivided into systemic form when it involves multiple organs, and localized f&-m when only one organ is involved. The secondary form is found in association with chronic inflammatory disease and familial Mediterranean fever. We report 3 cases of primary amyloidosis of the urinary tract. The renal pelvis was involved in 1 case, and 2 patients presented with bladder lesions, one was localized and the other systemic.
junction obstruction to the left kidney. Cystoscopy disclosed hemorrhagic areas in the bladder mucosa, which on biopsy were found to be inflammatory. Bladder urine was examined on repeated occasions by the Papanicolaou technique, and a barium enema was found to be unremarkable. Hematuria ceased, and the patient was discharged home only to be readmitted two months later with gross hematuria. Repeat intravenous pyelogram and left retrograde
Case Reports Case 1 A sixty-seven-year-old woman was admitted to this Center on March 9, 1974, with her first episode of painless gross hematuria. The patient had undergone a left hemicolectomy for carcinoma of the sigmoid colon in 1971. On admission, her hemoglobin was 8 Gm./ 100 ml., with a hematocrit of 25. An intravenous urogram revealed a grossly normal right kidney and ureter with partial ureteropelvic
UROLOGY
I
OCTOBER
1979
/
VOLUME
XIV
NUMBER4
FIGURE 1. Excretory urogram showing ureteropelvic junction obstruction.
partial left
401
FIGURE 2. Renal medulla and pelvis revealing nodular infiltrate in tunica propia. Remainder of kidney proper entirely normal. Hematoxylin-eosin, original magni$cation X 160.
FIGURE 3. Characteristic vasocentric deposition of amyloid. Urothelium is thrown into nodular elevax tion. Hematoxylin-eosin, original magnijcation 160.
pyelogram revealed partial ureteropelvic junction obstruction with a questionable filling defect in the left renal pelvis (Fig. 1). Selective renal arteriography failed to reveal any renal tumor or abnormal vessels in the region of the renal pelvis. Urine for cytology from the bladder and the renal pelvis showed no evidence of malignancy. Surgical exploration was performed on July 3, 1974. There was marked inflammatory reaction around the left renal pelvis and ureter; no lesion was seen. Frozen section biopsies were taken from the renal pelvis, parapelvis, and paraureteral tissues, all of which were &ee of tumor. Attempted pyeloplasty failed because of the marked inflammatory reaction in the renal pelvis and ureter. A nephrectomy and partial ureterectomy were performed. On microscopic examination, the renal pelvis and calyces were involved with amyloidosis (Fig. 2). No amyloidosis was seen in the kidney. The patient did well postoperatively. She was readmitted six months later with alcoholic cirrhosis of the liver. Celiac arteriogram showed no evidence of metastatic disease. The patient died at home on March 1, 1977.
Case 2
402
An eighty-one-year-old woman was admitted in June, 1977, with a history of intermittent, painless, gross hematuria of two months’ duration. There was no history of chronic disease. Physical examination was unremarkable. Complete blood cell count, urinalysis (except for red cells), urine cytology, and intravenous urogram were normal. Cystoscopy revealed a velvety lesion on the left lateral bladder wall, biopsy of which revealed amyloidosis. Fulguration of the lesion was performed, and the hematuria ceased postoperatively. Complete investigation failed to detect any systemic disease. Serum protein electrophoresis revealed normal serum albumin. Serum immunoglobulin G (IgG) was slightly elevated. Case 3
A sixty-three-year-old woman, with documented amyloidosis of the gastrointestinal tract and bone marrow, was admitted in June, 1977, with gross hematuria and urinary incontinence. Intravenous pyelogram revealed normal upper tracts. Cystoscopy showed a raised hemorrhagic lesion on the posterior bladder wall,
UROLOGY
/ OCTOBER
1979 / VOLUME
XIV
NUMBER4
FIGURE 4. (A) Technique of corroborating amyloid. Congo red stain - not specify stain but based on metachromusia. Amybid appears as mahogany color. Polarization of amyloid stained with congo red gives apple green birefiigence. (B) Demonstrates more speci$c stain by SAB (sulphonated aniline blue); note bluish green coloration of oasocentric amyloid.
biopsy of which revealed amyloidosis (Fig. 3). Hematuria ceased fallowing fulguration of the area. Serum protein electrophoresis revealed low albumin and decreased serum IgA and IgG. Comment Amyloidosis of the renal pelvis has been reported previously in 6 cases1m5 Ureteral amyloidosis has been reported in 30 cases. Treatment has consisted of nephroureterectomy and resection of distal ureter with ureteroneocystostomy. r Primary amyloidosis of the bladder is rare, 38 cases being reported in the English literature. Nearly all cases presented with intermittent gross hematuria.8-10 A few of the cases presented with flank pain, fever, chills, and acute urinary retention. Cystoscopic appearance resembles infiltrating carcinoma. It is often described as “a solid, circumscribed, elevated mass with a hemorrhagic irregular surface of yellowish tint frequently oozing blood.” Differential diagnosis on gross examination includes tumor, endometriosis, hemangioma, and cystitis glandularis. A correct diagnosis prior to histologic examination has never been made. Various modalities of treatment have been employed in bladder amyloidosis, including transurethral biopsy and resection, partial cystectomy, radium implantation, and even urinary diversion by ileal conduit for severe
UROLOGY
/ OCTOBER
1979 / VOLUMEXIV
NUMBER4
irritative bladder symptoms12,13 and bilateral ureteric obstruction. 12-14 Differentiation from secondary amyloidosis is by exclusion of recognizable predisposing causes. I5 Where secondary amyloidosis develops, it usually does so after many years (seven to fifteen) of continued inflammatory stimulus. In a number of reported cases, treatment of the underlying inflammatory disease has brought about a decrease in the progression of the disease. l6 Renal involvement occurs in most cases of secondary amyloidosis, and in one half of the patients with myeloma and related amyloidosis. ” Once the renal involvement progresses to the point of renal failure, death usually occurs within approximately one year. l7 Primary amyloidosis carries a much more hopeful prognosis. The incidence of amyloid deposition in the prostate ranges from 1.5 to 10 per cent in prostatectomy specimens. ‘* The testis was involved in 10 to 20 per cent of the men known to have systemic amyloidosis who underwent autopsy. ls Involvement of seminal vesicles, penis, and urethra have also been reported.18,20 The main amyloid protein is a microfiber which possesses properties distinct from those of any other known mammalian protein. Grossly it stains black with iodine. It has a fibrillar appearance by electron microscopy. Figure 4 shows the appearance of amyloid by congo red stain and sulphonated aniline blue (SAB) stain, respectively.
403
TWO observations have been made about the relationship between amyloid and immune system. l8 Apitz*r demonstrated that many patients with primary amyloidosis had abnormal plasma cells and plasmacytosis of bone marrow. The secondary form of amyloidosis has been associated with chronic antigenic stimulation. Glenner and his associates**-24 by analyzing the amino acid sequencing of amyloid have shown tissue deposition of the variable portion of the immunoglobulin light chains. Although abnormalities of serum proteins or immunoglobulins could be expected in amyloidosis because of immunologic basis, it has not been found to be true in all cases. ‘*s Amyloid fibrils have been demonstrated in the urinary sediment of patients with renal amyloidosis. 26 At the present time there is no known effective treatment for amyloidosis other than elimination of the antigenic stimulus in those cases associated with an infectious process or other known antigenic source. Renal transplantation has been reported in cases of renal amyloidosis. *’ Treatment using immunosuppressive or cytotoxic agents is suggested to reduce the synthesis of monoclonal protein in those cases of amyloidosis in which the major protein of the fibrils is of immunoglobulin origin.23j24,27 Those cases of amyloidosis in which the major protein of the fibrils is not of immunoglobulin origin have to await knowledge of the cellular origin of this protein.24 New York, New York 10025 (DR. LAVENGOOD) References 1. Gardner KD, Jr, et al: Primary amyloidosis of renal pelvis, N. Engl. J. Med. 284: 1196 (1971). 2. Ullman AS: Primary amyloidosis of the renal pelvis, a case report and review of literature, Mich. Med. 72: 29 (1973). 3. Chisholm GD, Cooter, NBE, and Dawson JM: Primary amyloidosis of the renal pelvis, Br. Med. J. 1: 736 (1967).
404
4. Sato S: Primary amyloidosis of renal pelvis and ureter: report of a case, Acta Med. Biol. 5: 15 (1957). 5. Gilbert LW, and McDonald JR: Primary amyloidosis of renal pelvis and ureter, J. Urol. 68: 137 (1952). 6. Klotz PG: Primary amyloidosis of the ureter, Br. J, Urol. 47: 578 (1975). 7. Johnson HW, and Ankenman GJ: Bilateral ureteral primary amyloidosis, J. Urol. 92: 275 (1964). 8. Strong GH, Kelsey D, and Hoch W: Primary amyloid disease of the bladder, ibid. 112: 463 (1974). 9. Grace DA, and Walton KN: Primary localized amyloidosis of the bladder, ibid. 92: 655 (1964). 10. Au KK, and Cilbaugh JH, Jr: Primary amyloidosis of the bladder, ibid. 114: 786 (1975). 11. MacDonald JH, and Heckel NJ: Primary amyloidosis of lower genitourinary tract, ibid. 75: 122 (1956). 12. Kinzel RC, Harrison EG, and Utz DC: Primary localized amyloidosis of the bladder, ibid. 85: 785 (1961). 13. Blath AB, and Bucy JG: Localized primary amyloidosis of the bladder, Br. J. Urol. 48: 219 (1976). 14. Hudson HC, and Tingley JO: Primary amyloidosis of the bladder, J. Med. Assoc. Alabama 35: 353 (1965). 15. Symmers WSC: Primary amyloidosis: a review, J. Clin. Pathol. 9: 187 (1956). 16. Lowenstein J, and Gallo A: Remission of the nephrotic syndrome in renal amyloidosis, N. Engl. J. Med. 282: 128 (1976). 17. Catkins E: Amyloidosis, in: Harrison’s Principles of Internal Medicine, 8th ed., New York, McGraw-Hill, 1976. 18. Carris CK, McLaughlin AP, III, and Gittes RF: Amyloidosis of the lower genitourinary tract, J. Urol. 115: 423 (1976). 19. Mostofi FK: Lecture notes, Armed Forces Institute of Pathology, Bethesda, Maryland, Feb., 1978. 20. Nagel R: Localized amyloidosis of the bladder, J. Urol. 88: 56 (1962). 21. Apitz K: Quoted by Carris, C. K., et al., op ci1.i’ 22. Glenner GG, Terry W, Iserky C, and Page D: Amyloid fibril proteins: proof of homology with immunoglobulin light chains by sequence analysis, Science 172: 1150 (1971). 23. Glenner GG, Ein D, and Tierry WD: The immunoglobulin origin of amyloid, Am. J. Med. 52: 141 (1972). 24. Glenner GG: The nature and pathogenesis of systemic amyloidosis, Adv. Nephrol. 4: 291 (1974). 25. Barth WF, Willerson JT, Waldman TA, and Decker JL: immunochemical and immunoPrimary amyloidosis, clinical, glo bu 1’ m metabolism studies in 15 patients, Am. J. Med. 47: 259 (1969). 26. Derosena R, Koss MN, and Pirani CL: Demonstration of amyloid fibrils in urinary sediment, N. Engl. J. Med. 293: 1131 (1975). 27. Cohen AS, Bricetti AB, Harrington JT, and Mannick JA: Renal transplantation in 2 cases of amyloidosis, Lancet 2: 531 (1971). 28. Jones NF, Hilton PJ, Tighe JR, and Hobbs JR: Treatment of primary renal amyloidosis with melphalan, ibid. 2: 616 (1972).
UROLOGY
/
OCTOBER
1979
/
VOLUME
XIV
NUMBER4