Crescentic Glomerulonephritis and Renal Failure Associated with Malignant Lymphoma ROBERTA. PETZEL, M.D., DAVID C. BROWN, M.D., NANCY A. STALEY, M.D., JAMES J. McMILLEN, M.D. RICHARD K. SIBLEY, M.D. AND CARL M. KJELLSTRAND, M.D.
Petzel, Robert A., Brown, David C , Staley, Nancy A., McMillen, James J., Sibley, Richard K., and Kjellstrand, Carl M.: Crescentic glomerulonephritis and renal failure associated with malignant lymphoma. Am J Clin Pathol 71: 728-732, 1979. Two cases of crescentic glomerulonephritis and renal failure associated with malignant lymphoma are reported. The relationship of the lymphoma to the immunecomplex glomerulonephritis is discussed. (Key words: Crescentic glomerulonephritis; Lymphoma.)
Report of Two Cases Case I: A 57-year-old man was admitted to the University of Minnesota Hospital with a one-week history of pain in the left lower quadrant and hematuria. There was no significant past medical history. Physical examination revealed that the patient was acutely ill and in moderate distress, secondary to abdominal pain. The oral temperature was 40 C, pulse rate 100/min, and blood pressure 140/ 70 mm Hg. The abdomen was distended and diffusely tender, with rebound tenderness in the left lower quadrant and absent bowel sounds. Results of initial laboratory studies were: Hemoglobin 7.2 g/dl, leukocyte count 22,400 cells/cu mm, and urine 2+ for protein and positive for hemoglobin. Microscopic examination of the urine revealed 10-20 erythrocytes/hpf. Serum electrolytes were normal. Blood urea nitrogen was 100 mg/dl, serum creatinine 11 mg/dl, calcium 7.7 mg/dl, phosphorus 10.1 mg/dl, total protein 7.6 g/dl, and albumin 3.5 g/dl. Values for C3 and CH50 were normal. Rheumatoid factor by latex fixation was positive at a titer of 1:2,560. A small amount of mixed cryoglobulin containing IgM and IgG was present on admission in a concentration of 0.13 mg/ml. Quantitative immunoglobulin concentrations were IgG 1,650 mg/dl (normal 3721,356), IgM 81 mg/dl (normal 48-414), IgA 505 mg/dl (normal 40-468), and IgE 3350 IU (normal 12-444). Anti-GBM antibody was not present in the serum. The fluorescent antinuclear antibody test was negative. The patient received hemodialysis once, and then an exploratory laparotomy was performed. Sigmoid diverticulitis Received May 8, 1978; received revised manuscript and accepted for publication June 30, 1978. Address reprint requests to Dr. Petzel: Department of Medicine, Veterans Administration Hospital, 54th Street and 48th Avenue, South, Minneapolis, Minnesota 55417.
was found, and a left hemicolectomy was done. The mesenteric lymph nodes were enlarged, and several were removed for examination. A kidney biopsy was performed. The lymph nodes showed poorly differentiated lymphocytic lymphoma, and examination of the kidney biopsy showed crescentic glomerulonephritis, as described in the Results section. The patient's postoperative course is summarized in Figure 1. Hemodialysis was continued intermittently until the forty-second hospital day. Without further hemodialysis blood urea nitrogen and serum creatinine have remained stable, at 35 mg/dl and 2.5 mg/dl, respectively. The patient was treated with plasma exchange because of the recent report of the successful treatment of crescentic glomerulonephritis with this procedure.12 Prior to beginning the exchange, the patient was given 60 mg prednisone orally and 800 mg cyclophosphamide intravenously. Plasma exchange was begun on the tenth hospital day (1.5 1) and repeated on the fourteenth day (5 1) and the sixteenth day (5 I). On the twenty-fifth hospital day systematic chemotherapy, consisting of nitrogen mustard, vincristine, procarbazine, and prednisone was begun. The cryoglobulin has persisted, and the rheumatoid factor remains positive at a titer of 1:320. Case 2: A 48-year-old man was admitted to the Minneapolis Veterans Administration Hospital for treatment of renal failure. He had been in good health until two months prior to admission, when he had noticed pain and swelling in his left large toe. The diagnosis of acute gouty arthritis was made and treatment with phenylbutazone was begun, with resolution of the symptoms. Subsequent laboratory data obtained included total protein 8.6 g/dl, serum globulin 5.5 g/dl, and serum creatinine 5.4 mg/dl. Serum protein electrophoresis revealed an IgM monoclonal spike. Twenty-four-hour urinary protein was 2.6 g. Serum albumin was 3.1 mg/dl. The patient was admitted to a private hospital, where cystoscopy and bilateral retrograde ureteral catheterizations revealed that the right collecting system was obstructed by an extrinsic mass at the ureteral-pelvic junction. Exploratory laparotomy revealed a retroperitoneal mass obstructing the right ureter. Subsequent histologic examination showed a diffuse, well-differentiated lymphocytic lymphoma. A kidney biopsy taken at that time revealed crescentic glomerulonephritis. Subsequent bone-marrow examination was positive for lymphoma. The postoperative course was complicated by a pulmonary embolus.
0002-9173/79/0600/0728 $00.75 © American Society of Clinical Pathologists
728
Downloaded from http://ajcp.oxfordjournals.org/ by guest on June 7, 2016
ALTHOUGH a wide variety of glomerular diseases, including nil lesion, 19 membranous glomerulonephritis, 7 membranoproliferative glomerulonephritis, 18 and focal glomerulonephritis, 13 have been found in association with malignant lymphoma, crescentic glomerulonephritis has not. We report two cases of patients with the association of crescentic glomerulonephritis with renal failure and lymphoma.
Department of Medicine, Minneapolis Veterans Administration Hospital, University of Minnesota Medical School, Minneapolis, Minnesota: Department of Laboratory Medicine and Pathology, Minneapolis Veterans Administration Hospital, University of Minnesota Medical School; Department of Medicine, University of Minnesota Medical School; Department of Laboratory Medicine and Pathology, University of Minnesota Medical School; and Department of Surgery, University of Minnesota Medical School
CASE REPORTS
Vol. 71 . No. 6
Materials and Methods Light Microscopic, Immunofluorescent Microscopic Studies
and Electron
Kidney tissue (biopsy, Case 1, and autopsy material, one and a half hours postmortem, Case 2) was divided for light-microscopic, immunofluorescent, and electronmicroscopic studies. Tissue was fixed for light microscopy in Zenker's fluid or 10% phosphate-buffered formalin. Serial 2-^m sections were stained with hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome with and without a prior Jones' silver stain. Tissue for immunofluorescence was snap-frozen in isopentane precooled in liquid nitrogen. Sections 2 /xm thick were fixed in acetone, washed in phosphatebuffered saline solution, and incubated at 37 C for 30 minutes with fluorescein-labeled antisera specific for IgG, IgM, IgA, C 3 , fibrinogen, albumin, and IgE (Case 1 only). Sections were examined with a Zeiss
DAYS AFTER ADMISSION FIG. 1. Clinical course of Patient 1. CYT = cyclophosphamide; VCR = vincristine; HN2 = nitrogen mustard; start MOPP = initiation of nitrogen mustard, vincristine, procarbazine, and prednisone regimen.
Universal® microscope equipped with a mercury-vapor light source and appropriate filters. Tissue for electron microscopy was fixed in cold 3% glutaraldehyde in 0.1 M phosphate buffer, postfixed in 1% osmium tetroxide in 0.1 M phosphate buffer, dehydrated in a graded series of ethanol, and embedded in Epon®. Thin sections were stained with uranyl acetate and lead citrate. Results Light Microscopic, Immunofluorescent Microscopic Studies
and Electron
Case 1: The renal biopsy showed a crescentic glomerulonephritis. Thirteen of 18 glomeruli showed segmental or circumferential epithelial crescents with necrosis of capillary tufts, polymorphonuclear leukocytes, and fibrin exudates (Fig. 2, A). Of the five remaining glomeruli, two showed segmental fibrinoid necrosis. Many of the tubules contained erythrocytes. No evidence of vasculitis was present. The interstitial tissue was edematous and contained focal lymphocytic and plasma-cell infiltrates. With immunofluorescent staining, glomeruli showed focal, granular deposition of /3,C (1+) (Fig. 3, A) and IgG (trace) in a mesangial distribution. Two glomeruli were examined by electron microscopy. Both glomeruli had varying degrees of capillary loop collapse, usually paramesangial, with basement membrane wrinkling and thickening. Platelets and fibrin were not present in capillary lumen. A few small, finely granular, electron-dense deposits were found in subendothelial, intramembranous, mesangial, and subepithelial locations (Fig. 4, A). The subepithelial deposits were located on the juxtamesan-
Downloaded from http://ajcp.oxfordjournals.org/ by guest on June 7, 2016
necessitating anticoagulation; fever; hypoxia secondary to a pneumonic process, necessitating antibiotic therapy; and progressive renal failure. On the thirty-third hospital day, the patient was transferred to the Minneapolis Veterans Administration Hospital for further evaluation and treatment. Pertinent physical findings included numerous cutaneous ecchymoses, insignificant peripheral adenopathy, and consolidation in the right chest. Admission laboratory values included hemoglobin 9.5 g/dl, leukocyte count 17,700, with 93% neutrophils, and platelet count 325,000. Serum sodium was 122 mEq/1, serum potassium 8.1 mEq/1, serum chloride 81 mEq/1, serum C02combining power 16.4 miu/l, serum blood urea nitrogen 180 mg/dl, and serum creatinine 17.4 mg/dl. Serum uric acid was 8.4 mg/dl, serum calcium 8.6 mg/dl, serum phosphorus 12.9 mg/dl, total protein 7.3 g/dl, serum albumin 3.1 g/dl, serum globulin 4.2 g/dl, and serum cholesterol 166 mg/dl. Admission urinalysis revealed 4+ proteinuria, numerous erythrocytes, and many erythrocytic casts. The 24-hour urinary protein determination showed 216 mg. The test for Bence Jones protein was negative. Urinary protein electrophoresis revealed numerous serum proteins. C3 and CH50 were normal. Rheumatoid factor by latex fixation was not present. Cryoglobulins were not present. Tests for quantitative immunoglobulins revealed normal levels of IgG, 630 mg/dl, and IgA, 89 mg/dl, and markedly elevated IgM, 2,880 mg/dl. The IgM was found to contain kappa light chains. The fluorescent antinuclear antibody test was negative. A chemotherapeutic regimen consisting of nitrogen mustard, vincristine, prednisone, and procarbazine was begun. Following emergency treatment, the elevated serum potassium returned to normal and cardiac status stabilized. Peritoneal catheters were placed, and over the next two hospital days the patient had 54 peritoneal dialysis runs with only minimal improvement in his blood chemistries, as reflected by a blood urea nitrogen of 115 mg/dl and a serum creatinine of 15.0 mg/dl. On the third hospital day, because of peritonitis, peritoneal dialysis was discontinued and treatment with antibiotics begun. Renal function progressively deteriorated, and signs of fluid overload developed, necessitating the placement of an arteriovenous shunt and the initiation of hemodialysis. In spite of two successful hemodialysis runs, progressive mental obtundation developed, and on the sixth hospital day cardiac arrest occurred and the patient died.
729
PETZEL ETAL.
730
A.J.C.P. • June 1979
•v.
A.'
s~ r-
• i
J*
,
»
'
* '•
'
/ *
/
v
V
gial areas of the basement membrane. There was extensive epithelial foot-process obliteration. Case 2: At autopsy the kidneys showed a crescentic glomerulonephritis. Ninety per cent of the glomeruli showed circumferential epithelial-cell crescents. Extensive fibrin exudates and hemorrhage were present within the crescents (Fig. 2,B). With immunofluorescent staining, all glomeruli showed focal, granular deposition of IgG (3+), IgM (2+), and /3,C (3+) in a mesangial and capillary loop distribution (Fig. 3, B). By electron microscopy, small intramembranous electron-
v
dense deposits were infrequently seen in glomerular capillary loops and mesangium (Fig. 4, B). Discussion Nil lesion,19 membranous glomerulonephritis,7 membranoproliferative glomerulonephritis,18 and focal glomerulonephritis13 have been reported to occur in association with malignant lymphoma.5 Crescentic glomerulonephritis has not, and the only association of this renal lesion with malignancy is that reported by
..»
V
'
'A * * v . *
FIG. 3. Immunofluorescent staining. A, Case 1. B,C antisera. x633. B, Case 2. IgG antisera. x475.
Downloaded from http://ajcp.oxfordjournals.org/ by guest on June 7, 2016
FIG. 2. Light-microscopic study, showing crescentic glomerulonephritis. A, Case 1. Hematoxylin and eosin. x220. B, Case 2. Jones' silver methenamine stain. x!75.
731
CASE REPORTS
Vol. 71 • No. 6
r s*r\.*' M'J •A
:• *^
Petzel, Robert A., Brown, David C , Staley, Nancy A., McMillen, James J., Sibley, Richard K., and Kjellstrand, Carl M.: Crescentic glomerulonephritis and renal failure associated with malignant lymphoma. Am J Clin Pathol 71: 728-732, 1979. Two cases of crescentic glomerulonephritis and renal failure associated with malignant lymphoma are reported. The relationship of the lymphoma to the immunecomplex glomerulonephritis is discussed. (Key words: Crescentic glomerulonephritis; Lymphoma.)
Report of Two Cases Case I: A 57-year-old man was admitted to the University of Minnesota Hospital with a one-week history of pain in the left lower quadrant and hematuria. There was no significant past medical history. Physical examination revealed that the patient was acutely ill and in moderate distress, secondary to abdominal pain. The oral temperature was 40 C, pulse rate 100/min, and blood pressure 140/ 70 mm Hg. The abdomen was distended and diffusely tender, with rebound tenderness in the left lower quadrant and absent bowel sounds. Results of initial laboratory studies were: Hemoglobin 7.2 g/dl, leukocyte count 22,400 cells/cu mm, and urine 2+ for protein and positive for hemoglobin. Microscopic examination of the urine revealed 10-20 erythrocytes/hpf. Serum electrolytes were normal. Blood urea nitrogen was 100 mg/dl, serum creatinine 11 mg/dl, calcium 7.7 mg/dl, phosphorus 10.1 mg/dl, total protein 7.6 g/dl, and albumin 3.5 g/dl. Values for C3 and CH50 were normal. Rheumatoid factor by latex fixation was positive at a titer of 1:2,560. A small amount of mixed cryoglobulin containing IgM and IgG was present on admission in a concentration of 0.13 mg/ml. Quantitative immunoglobulin concentrations were IgG 1,650 mg/dl (normal 3721,356), IgM 81 mg/dl (normal 48-414), IgA 505 mg/dl (normal 40-468), and IgE 3350 IU (normal 12-444). Anti-GBM antibody was not present in the serum. The fluorescent antinuclear antibody test was negative. The patient received hemodialysis once, and then an exploratory laparotomy was performed. Sigmoid diverticulitis Received May 8, 1978; received revised manuscript and accepted for publication June 30, 1978. Address reprint requests to Dr. Petzel: Department of Medicine, Veterans Administration Hospital, 54th Street and 48th Avenue, South, Minneapolis, Minnesota 55417.
was found, and a left hemicolectomy was done. The mesenteric lymph nodes were enlarged, and several were removed for examination. A kidney biopsy was performed. The lymph nodes showed poorly differentiated lymphocytic lymphoma, and examination of the kidney biopsy showed crescentic glomerulonephritis, as described in the Results section. The patient's postoperative course is summarized in Figure 1. Hemodialysis was continued intermittently until the forty-second hospital day. Without further hemodialysis blood urea nitrogen and serum creatinine have remained stable, at 35 mg/dl and 2.5 mg/dl, respectively. The patient was treated with plasma exchange because of the recent report of the successful treatment of crescentic glomerulonephritis with this procedure.12 Prior to beginning the exchange, the patient was given 60 mg prednisone orally and 800 mg cyclophosphamide intravenously. Plasma exchange was begun on the tenth hospital day (1.5 1) and repeated on the fourteenth day (5 1) and the sixteenth day (5 I). On the twenty-fifth hospital day systematic chemotherapy, consisting of nitrogen mustard, vincristine, procarbazine, and prednisone was begun. The cryoglobulin has persisted, and the rheumatoid factor remains positive at a titer of 1:320. Case 2: A 48-year-old man was admitted to the Minneapolis Veterans Administration Hospital for treatment of renal failure. He had been in good health until two months prior to admission, when he had noticed pain and swelling in his left large toe. The diagnosis of acute gouty arthritis was made and treatment with phenylbutazone was begun, with resolution of the symptoms. Subsequent laboratory data obtained included total protein 8.6 g/dl, serum globulin 5.5 g/dl, and serum creatinine 5.4 mg/dl. Serum protein electrophoresis revealed an IgM monoclonal spike. Twenty-four-hour urinary protein was 2.6 g. Serum albumin was 3.1 mg/dl. The patient was admitted to a private hospital, where cystoscopy and bilateral retrograde ureteral catheterizations revealed that the right collecting system was obstructed by an extrinsic mass at the ureteral-pelvic junction. Exploratory laparotomy revealed a retroperitoneal mass obstructing the right ureter. Subsequent histologic examination showed a diffuse, well-differentiated lymphocytic lymphoma. A kidney biopsy taken at that time revealed crescentic glomerulonephritis. Subsequent bone-marrow examination was positive for lymphoma. The postoperative course was complicated by a pulmonary embolus.
0002-9173/79/0600/0728 $00.75 © American Society of Clinical Pathologists
728
Downloaded from http://ajcp.oxfordjournals.org/ by guest on June 7, 2016
ALTHOUGH a wide variety of glomerular diseases, including nil lesion, 19 membranous glomerulonephritis, 7 membranoproliferative glomerulonephritis, 18 and focal glomerulonephritis, 13 have been found in association with malignant lymphoma, crescentic glomerulonephritis has not. We report two cases of patients with the association of crescentic glomerulonephritis with renal failure and lymphoma.
Department of Medicine, Minneapolis Veterans Administration Hospital, University of Minnesota Medical School, Minneapolis, Minnesota: Department of Laboratory Medicine and Pathology, Minneapolis Veterans Administration Hospital, University of Minnesota Medical School; Department of Medicine, University of Minnesota Medical School; Department of Laboratory Medicine and Pathology, University of Minnesota Medical School; and Department of Surgery, University of Minnesota Medical School
CASE REPORTS
Vol. 71 . No. 6
Materials and Methods Light Microscopic, Immunofluorescent Microscopic Studies
and Electron
Kidney tissue (biopsy, Case 1, and autopsy material, one and a half hours postmortem, Case 2) was divided for light-microscopic, immunofluorescent, and electronmicroscopic studies. Tissue was fixed for light microscopy in Zenker's fluid or 10% phosphate-buffered formalin. Serial 2-^m sections were stained with hematoxylin and eosin, periodic acid-Schiff, and Masson's trichrome with and without a prior Jones' silver stain. Tissue for immunofluorescence was snap-frozen in isopentane precooled in liquid nitrogen. Sections 2 /xm thick were fixed in acetone, washed in phosphatebuffered saline solution, and incubated at 37 C for 30 minutes with fluorescein-labeled antisera specific for IgG, IgM, IgA, C 3 , fibrinogen, albumin, and IgE (Case 1 only). Sections were examined with a Zeiss
DAYS AFTER ADMISSION FIG. 1. Clinical course of Patient 1. CYT = cyclophosphamide; VCR = vincristine; HN2 = nitrogen mustard; start MOPP = initiation of nitrogen mustard, vincristine, procarbazine, and prednisone regimen.
Universal® microscope equipped with a mercury-vapor light source and appropriate filters. Tissue for electron microscopy was fixed in cold 3% glutaraldehyde in 0.1 M phosphate buffer, postfixed in 1% osmium tetroxide in 0.1 M phosphate buffer, dehydrated in a graded series of ethanol, and embedded in Epon®. Thin sections were stained with uranyl acetate and lead citrate. Results Light Microscopic, Immunofluorescent Microscopic Studies
and Electron
Case 1: The renal biopsy showed a crescentic glomerulonephritis. Thirteen of 18 glomeruli showed segmental or circumferential epithelial crescents with necrosis of capillary tufts, polymorphonuclear leukocytes, and fibrin exudates (Fig. 2, A). Of the five remaining glomeruli, two showed segmental fibrinoid necrosis. Many of the tubules contained erythrocytes. No evidence of vasculitis was present. The interstitial tissue was edematous and contained focal lymphocytic and plasma-cell infiltrates. With immunofluorescent staining, glomeruli showed focal, granular deposition of /3,C (1+) (Fig. 3, A) and IgG (trace) in a mesangial distribution. Two glomeruli were examined by electron microscopy. Both glomeruli had varying degrees of capillary loop collapse, usually paramesangial, with basement membrane wrinkling and thickening. Platelets and fibrin were not present in capillary lumen. A few small, finely granular, electron-dense deposits were found in subendothelial, intramembranous, mesangial, and subepithelial locations (Fig. 4, A). The subepithelial deposits were located on the juxtamesan-
Downloaded from http://ajcp.oxfordjournals.org/ by guest on June 7, 2016
necessitating anticoagulation; fever; hypoxia secondary to a pneumonic process, necessitating antibiotic therapy; and progressive renal failure. On the thirty-third hospital day, the patient was transferred to the Minneapolis Veterans Administration Hospital for further evaluation and treatment. Pertinent physical findings included numerous cutaneous ecchymoses, insignificant peripheral adenopathy, and consolidation in the right chest. Admission laboratory values included hemoglobin 9.5 g/dl, leukocyte count 17,700, with 93% neutrophils, and platelet count 325,000. Serum sodium was 122 mEq/1, serum potassium 8.1 mEq/1, serum chloride 81 mEq/1, serum C02combining power 16.4 miu/l, serum blood urea nitrogen 180 mg/dl, and serum creatinine 17.4 mg/dl. Serum uric acid was 8.4 mg/dl, serum calcium 8.6 mg/dl, serum phosphorus 12.9 mg/dl, total protein 7.3 g/dl, serum albumin 3.1 g/dl, serum globulin 4.2 g/dl, and serum cholesterol 166 mg/dl. Admission urinalysis revealed 4+ proteinuria, numerous erythrocytes, and many erythrocytic casts. The 24-hour urinary protein determination showed 216 mg. The test for Bence Jones protein was negative. Urinary protein electrophoresis revealed numerous serum proteins. C3 and CH50 were normal. Rheumatoid factor by latex fixation was not present. Cryoglobulins were not present. Tests for quantitative immunoglobulins revealed normal levels of IgG, 630 mg/dl, and IgA, 89 mg/dl, and markedly elevated IgM, 2,880 mg/dl. The IgM was found to contain kappa light chains. The fluorescent antinuclear antibody test was negative. A chemotherapeutic regimen consisting of nitrogen mustard, vincristine, prednisone, and procarbazine was begun. Following emergency treatment, the elevated serum potassium returned to normal and cardiac status stabilized. Peritoneal catheters were placed, and over the next two hospital days the patient had 54 peritoneal dialysis runs with only minimal improvement in his blood chemistries, as reflected by a blood urea nitrogen of 115 mg/dl and a serum creatinine of 15.0 mg/dl. On the third hospital day, because of peritonitis, peritoneal dialysis was discontinued and treatment with antibiotics begun. Renal function progressively deteriorated, and signs of fluid overload developed, necessitating the placement of an arteriovenous shunt and the initiation of hemodialysis. In spite of two successful hemodialysis runs, progressive mental obtundation developed, and on the sixth hospital day cardiac arrest occurred and the patient died.
729
PETZEL ETAL.
730
A.J.C.P. • June 1979
•v.
A.'
s~ r-
• i
J*
,
»
'
* '•
'
/ *
/
v
V
gial areas of the basement membrane. There was extensive epithelial foot-process obliteration. Case 2: At autopsy the kidneys showed a crescentic glomerulonephritis. Ninety per cent of the glomeruli showed circumferential epithelial-cell crescents. Extensive fibrin exudates and hemorrhage were present within the crescents (Fig. 2,B). With immunofluorescent staining, all glomeruli showed focal, granular deposition of IgG (3+), IgM (2+), and /3,C (3+) in a mesangial and capillary loop distribution (Fig. 3, B). By electron microscopy, small intramembranous electron-
v
dense deposits were infrequently seen in glomerular capillary loops and mesangium (Fig. 4, B). Discussion Nil lesion,19 membranous glomerulonephritis,7 membranoproliferative glomerulonephritis,18 and focal glomerulonephritis13 have been reported to occur in association with malignant lymphoma.5 Crescentic glomerulonephritis has not, and the only association of this renal lesion with malignancy is that reported by
..»
V
'
'A * * v . *
FIG. 3. Immunofluorescent staining. A, Case 1. B,C antisera. x633. B, Case 2. IgG antisera. x475.
Downloaded from http://ajcp.oxfordjournals.org/ by guest on June 7, 2016
FIG. 2. Light-microscopic study, showing crescentic glomerulonephritis. A, Case 1. Hematoxylin and eosin. x220. B, Case 2. Jones' silver methenamine stain. x!75.
731
CASE REPORTS
Vol. 71 • No. 6
r s*r\.*' M'J •A
:• *^
