- Email: [email protected]
Chronic myelogenous leukemia and glomerulonephritis: report of a new case
LETTERS TO THE EDITOR
4. 5.
6.
7.
8.
Wintrobe MM: Clinical hematology, 8th ed. Philadelphia: Lea and Febiger, 1981; 1655. Festa M, Machiodi F, Palmisano L: Considerazzioni un case di morbo di Hodgkin a primitiva localizzazione splenica. Minerva Med 1980; 71: 3005-3009. Silberman AW, Deterling RA, Gembarowicz RM: Staging laparotomy for Hodgkin’s disease. Surg Gynecol Obstet 1982; 154: 545547. Safran C, Desforges JF, Tsichlis PN, Bluming AZ: Decision analysis to evaluate lymphangiography in the management of patients with Hodgkin’s disease. N Engl J Med 1977; 296: 1088. Safran C, Tsichlis PN, Bluming AZ, Desforges JF: Diagnostic planning using computer assisted decision making for patients with Hodgkin’s disease. Cancer 1977; 39: 2426. Submitted
August
8,1986,
and accepted
August
CHRONIC MYELOGENOUS LEUKEMIA AND GLOMERULONEPHRITlS: REPORT OF A NEW
Figure 2. mor.
Macroscopic
-...
picture
of the spleen and the tct
--
Figure 3. Light photomicrograph showing Hodgkin’s disease of spleen (hematoxylin and eosin stain; original magnk fication X 500, reduced by 25 percent).
1. 2. 3.
Kaplan HS: Contiguity and progression in Hodgkin’s disease. Cancer 1971; 31: 1811-1819. Teillet F: A reappraisal of clinical and biological signs in staging of Hodgkin’s disease. Cancer Res 1971; 31: 1723-1728. Martinazzi M, Palatini M: A causal finding of primary splenic Hodgkin’s disease in a case of traumatic rupture of the spleen. Tumori 1978; 64: 639-643.
December
18, 1986.
CASE
To the Editor: We have read with interest a report by Dabbs et al (Am J Med 1986; 80: 63-70) in which it was stressed how uncommon the association is between glomerular lesions and chronic myelogenous leukemia. There are only two reported cases of patients with myelogenous leukemia, one acute and one chronic, presenting with nephrotic syndrome and renal biopsy findings [ 1,2]. We thus believe it of interest to report a new case of chronic myelogenous leukemia associated with nephrotic-range proteinuria, as studied in our hospital. Chronic myelogenous leukemia was diagnosed in a previously healthy 49-year-old man in July 1981. The spleen was palpable at 6 cm below the rib border. The full blood count was as follows: white blood cell count 5.2 X 10g/liter; hemoglobin 16.1 g/dl; platelet count 945 X 1Og/liter; leukocyte alkaline phosphatase 2 percent; karyotype: 46, XY, t(9;22) in the 16 metaphases analyzed (Figure 1). The findings on bone marrow aspiration biopsy were suggestive of a chronic myeloproliferative disorder without fibrosis. Results of urinalysis were normal. Specific chemotherapy was begun with 4 mg/kg per day of busulfan. One month later, the full blood count had normalized, and the spleen was no longer palpable. Eight months later, he presented with edema of the ankles, and proteinuria of 4 g per day. Creatinine clearance was 97 ml per minute. Total serum protein level was 6.6 g/dl, with albumin level of 3.6 g. The full blood count and levels of serum complement and immunoglobulins were normal, and cryocrit was not detectable. Single-needle renal biopsy was performed, with a pathologic diagnosis of minimal-change glomerulonephritis. Immunofluorescent studies did not reveal deposits, and there was no interstitial myeloid cell infiltration. Oral prednisone therapy was initiated and maintained at a dosage of 1.5 mg/kg per day for eight weeks. The proteinuria and the edema disappeared and the medication was gradually withdrawn. As of April 1986, proteinuria continues to be absent, renal function is normal, and the myelogenous disorder remains in a chronic stable phase. Although the appearance of glomerular nephropathies in lymphoproliferative syndromes has been described with certain frequency [3-51, to the best of our knowledge there has been only one reported case of a nephrotic syndrome in 1986
The American
Journal
of Medicine
Volume
81
1121
LETTERS TO THE EDITOR
Figure 1. Metaphase and katyotype showing 9;22 transbcation: Ph,.
patients with chronic myelogenous leukemia [2]. Various pathogenic theories have been invoked to explain this association: immunocomplex deposits, viral antigens, nonspecific antibodies, and lymphocyte T disorders 13-51, although a cause-and-effect relationship has not been definitively established between the two [I]. The favorable resolution of the proteinuria in the present case and in that described by Sudholt and Heironimus [2] following treatment with steroids, without modifications in the course of the hematologic disease (whereas these usually run parallel in lymphoproliferative syndromes [4,5]), and the low number of described cases, lead us to conclude that the association is a chance one. Continued screening of the kidneys of patients such’ as those described should yield more information regarding the association between the nephrotic syndrome and myelogenous leukemia. EMILIO S. GAGO, ELlSA Luik, Luls QUI~ONES, FERMIN JONTE, JAIME ALVAREZ,
M.D. M.D. M.D.
M.D. M.D. Divisions of Nephrology and Hematology Department of Medicine Hospital “Ntra.Sra. Covadonga” Oviedo, Spain 1.
2. 3.
1122
Dosa S, Phillips TM, Antovych TT, Segal A, Guba A, Thompson AM: Acute myelomonocytic leukemia associated with nephrotic syndrome. Nephron 1983; 43: 125-129. Sudholt BA, Heironimus JD: Chronic myelogenous leukemia with nephrotic syndrome. Arch Intern Med 1983; 143: 168-169. Eagen JW, Lewis EJ: Glomerulopathies of neoplasia. Kidney Int 1977; 11: 297-306.
December
1986
The
American
Journal
of Medicine
4.
5.
Fer MF, McKinney TD, Richardson RL, Hande KR, Oldham RK, Greco FA: Cancer and the kidney: renal complications of neoplasms. Am J Med 1981; 71: 704-718. Zimmerman SW, Moorthy AV, Burkholder PM, Jenkins PG: Glomerulopathies associated with neoplastic disease. In: Rieselbath RE, Garnick MB, eds. Cancer and the kidney. Philadelphia: Lea and Febiger, 1982; 306-378. Submitted
ACUTE
AIDS
July 31, 1986,
VIRAL
and accepted
August
18, 1986.
INFECTlObJ
To the Editor: We read with interest the article by Kreiss et al (Am J Med 1986; 80: 345-350) on the early results of their prospective study of hemophiliac subjects and the acquired immune deficiency syndrome (AIDS). We find it interesting that no acute syndromes from primary infection with the human lmmunodeficiency virus (HIV) were reported. Our prospective seroepidemiologic study of 1,034 men randomly selected from an area with a high prevalance of AIDS (San Francisco Men’s Health Study) [I] has revealed one such case so far. A 35year-old man was seen for his third routine sixmonth clinic visit in October 1985. He had been well until about two weeks before his visit, when he began experiencing fevers to 103’F, night sweats, loss of appetite, and a 1Zpound weight loss. He also noted swollen inguinal nodes, nonproductive cough, shortness of breath, and a nonpruritic truncal rash. These symptoms lasted IO days and all resolved prior to his clinic visit except for the rash. He also reported one episode of receptive anal intercourse with ejaculation two weeks before the onset of symptoms. Physical examination revealed partially confluent, dif-
Volume
81
4. 5.
6.
7.
8.
Wintrobe MM: Clinical hematology, 8th ed. Philadelphia: Lea and Febiger, 1981; 1655. Festa M, Machiodi F, Palmisano L: Considerazzioni un case di morbo di Hodgkin a primitiva localizzazione splenica. Minerva Med 1980; 71: 3005-3009. Silberman AW, Deterling RA, Gembarowicz RM: Staging laparotomy for Hodgkin’s disease. Surg Gynecol Obstet 1982; 154: 545547. Safran C, Desforges JF, Tsichlis PN, Bluming AZ: Decision analysis to evaluate lymphangiography in the management of patients with Hodgkin’s disease. N Engl J Med 1977; 296: 1088. Safran C, Tsichlis PN, Bluming AZ, Desforges JF: Diagnostic planning using computer assisted decision making for patients with Hodgkin’s disease. Cancer 1977; 39: 2426. Submitted
August
8,1986,
and accepted
August
CHRONIC MYELOGENOUS LEUKEMIA AND GLOMERULONEPHRITlS: REPORT OF A NEW
Figure 2. mor.
Macroscopic
-...
picture
of the spleen and the tct
--
Figure 3. Light photomicrograph showing Hodgkin’s disease of spleen (hematoxylin and eosin stain; original magnk fication X 500, reduced by 25 percent).
1. 2. 3.
Kaplan HS: Contiguity and progression in Hodgkin’s disease. Cancer 1971; 31: 1811-1819. Teillet F: A reappraisal of clinical and biological signs in staging of Hodgkin’s disease. Cancer Res 1971; 31: 1723-1728. Martinazzi M, Palatini M: A causal finding of primary splenic Hodgkin’s disease in a case of traumatic rupture of the spleen. Tumori 1978; 64: 639-643.
December
18, 1986.
CASE
To the Editor: We have read with interest a report by Dabbs et al (Am J Med 1986; 80: 63-70) in which it was stressed how uncommon the association is between glomerular lesions and chronic myelogenous leukemia. There are only two reported cases of patients with myelogenous leukemia, one acute and one chronic, presenting with nephrotic syndrome and renal biopsy findings [ 1,2]. We thus believe it of interest to report a new case of chronic myelogenous leukemia associated with nephrotic-range proteinuria, as studied in our hospital. Chronic myelogenous leukemia was diagnosed in a previously healthy 49-year-old man in July 1981. The spleen was palpable at 6 cm below the rib border. The full blood count was as follows: white blood cell count 5.2 X 10g/liter; hemoglobin 16.1 g/dl; platelet count 945 X 1Og/liter; leukocyte alkaline phosphatase 2 percent; karyotype: 46, XY, t(9;22) in the 16 metaphases analyzed (Figure 1). The findings on bone marrow aspiration biopsy were suggestive of a chronic myeloproliferative disorder without fibrosis. Results of urinalysis were normal. Specific chemotherapy was begun with 4 mg/kg per day of busulfan. One month later, the full blood count had normalized, and the spleen was no longer palpable. Eight months later, he presented with edema of the ankles, and proteinuria of 4 g per day. Creatinine clearance was 97 ml per minute. Total serum protein level was 6.6 g/dl, with albumin level of 3.6 g. The full blood count and levels of serum complement and immunoglobulins were normal, and cryocrit was not detectable. Single-needle renal biopsy was performed, with a pathologic diagnosis of minimal-change glomerulonephritis. Immunofluorescent studies did not reveal deposits, and there was no interstitial myeloid cell infiltration. Oral prednisone therapy was initiated and maintained at a dosage of 1.5 mg/kg per day for eight weeks. The proteinuria and the edema disappeared and the medication was gradually withdrawn. As of April 1986, proteinuria continues to be absent, renal function is normal, and the myelogenous disorder remains in a chronic stable phase. Although the appearance of glomerular nephropathies in lymphoproliferative syndromes has been described with certain frequency [3-51, to the best of our knowledge there has been only one reported case of a nephrotic syndrome in 1986
The American
Journal
of Medicine
Volume
81
1121
LETTERS TO THE EDITOR
Figure 1. Metaphase and katyotype showing 9;22 transbcation: Ph,.
patients with chronic myelogenous leukemia [2]. Various pathogenic theories have been invoked to explain this association: immunocomplex deposits, viral antigens, nonspecific antibodies, and lymphocyte T disorders 13-51, although a cause-and-effect relationship has not been definitively established between the two [I]. The favorable resolution of the proteinuria in the present case and in that described by Sudholt and Heironimus [2] following treatment with steroids, without modifications in the course of the hematologic disease (whereas these usually run parallel in lymphoproliferative syndromes [4,5]), and the low number of described cases, lead us to conclude that the association is a chance one. Continued screening of the kidneys of patients such’ as those described should yield more information regarding the association between the nephrotic syndrome and myelogenous leukemia. EMILIO S. GAGO, ELlSA Luik, Luls QUI~ONES, FERMIN JONTE, JAIME ALVAREZ,
M.D. M.D. M.D.
M.D. M.D. Divisions of Nephrology and Hematology Department of Medicine Hospital “Ntra.Sra. Covadonga” Oviedo, Spain 1.
2. 3.
1122
Dosa S, Phillips TM, Antovych TT, Segal A, Guba A, Thompson AM: Acute myelomonocytic leukemia associated with nephrotic syndrome. Nephron 1983; 43: 125-129. Sudholt BA, Heironimus JD: Chronic myelogenous leukemia with nephrotic syndrome. Arch Intern Med 1983; 143: 168-169. Eagen JW, Lewis EJ: Glomerulopathies of neoplasia. Kidney Int 1977; 11: 297-306.
December
1986
The
American
Journal
of Medicine
4.
5.
Fer MF, McKinney TD, Richardson RL, Hande KR, Oldham RK, Greco FA: Cancer and the kidney: renal complications of neoplasms. Am J Med 1981; 71: 704-718. Zimmerman SW, Moorthy AV, Burkholder PM, Jenkins PG: Glomerulopathies associated with neoplastic disease. In: Rieselbath RE, Garnick MB, eds. Cancer and the kidney. Philadelphia: Lea and Febiger, 1982; 306-378. Submitted
ACUTE
AIDS
July 31, 1986,
VIRAL
and accepted
August
18, 1986.
INFECTlObJ
To the Editor: We read with interest the article by Kreiss et al (Am J Med 1986; 80: 345-350) on the early results of their prospective study of hemophiliac subjects and the acquired immune deficiency syndrome (AIDS). We find it interesting that no acute syndromes from primary infection with the human lmmunodeficiency virus (HIV) were reported. Our prospective seroepidemiologic study of 1,034 men randomly selected from an area with a high prevalance of AIDS (San Francisco Men’s Health Study) [I] has revealed one such case so far. A 35year-old man was seen for his third routine sixmonth clinic visit in October 1985. He had been well until about two weeks before his visit, when he began experiencing fevers to 103’F, night sweats, loss of appetite, and a 1Zpound weight loss. He also noted swollen inguinal nodes, nonproductive cough, shortness of breath, and a nonpruritic truncal rash. These symptoms lasted IO days and all resolved prior to his clinic visit except for the rash. He also reported one episode of receptive anal intercourse with ejaculation two weeks before the onset of symptoms. Physical examination revealed partially confluent, dif-
Volume
81