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13. Rabinowitz JG, Tweresky J, Guttadauria M: Similar bone manifestations of scleroderma and rheumatoid arthritis. Radiology 121:35-44, 1974 14. Seifert MH, Steigerwald JC, Clif MM: Bone resorption of the mandible in progressive systemic sclerosis. Arthritis Rheum 18:507-512, 1975 15. Steigerwald JC, Seifert MH, Cliff MM, Neff TA: Bone resorption of ribs and pulmonary function in progressive systemic sclerosis. Chest 68:838-840, 1975

16. Leonard DG, O'Duffy JD, Rogers RS 111: Prospective analysis of psoriatic arthritis in patients hospitalized for psoriasis. Mayo Clin Proc 535 I 1-5 18, 1978 17. Sasazuki T, McDevitt HO, Grumet FC: The association between genes in the major histocompatibility complex and disease susceptibility. Ann Rev Med 28~425452,1977 18. Whyte MP, Murphy WA, Kleerekoper M, Teitelbaum SL, Avioli LV: Idiopathic multicentric osteolysis. Arthritis Rheum 21:367-376, 1978

GLOMERULONEPHRITIS IN RHEUMATOID ARTHRITIS JAMES A. DAVIS, ARTHUR H. COHEN, RICHARD WEISBART, and HAROLD E. PAULUS

Glomerulonephritis is rarely a complication of rheumatoid arthritis (RA) despite the observation of significant amounts of circulating immune complexes in both glomerulonephritis and RA (1). Among 5,232 patients with a diagnosis of RA, hospitalized at the UCLA Center for the Health Sciences from 1955 to 1977, glomerulonephritis was diagnosed in only 4 patients, all of whom also met diagnostic criteria for systemic lupus erythematosus or mixed connective tissue disease. We present a well documented case of proliferative glomerulonephritis in association with RA in the absence of another immunologically mediated disease.

CASE REPORT A 57-year-old white male customs inspector first developed RA in 1969. The RA was well controlled with nonsteroidal antiinflammatory drugs until August 1974, when he was admitted to a community hospital with a flare of RA associated with fever, marked malaise, minimal proteinuria, and microscopic hematuria. Laboratory results (Table 1) revealed no source for fever other than RA. He started prednisone 40 From the Department of Medicine, UCLA School of Medicine, Los Angeles, California, and Department of Pathology, Harbor General Hospital, Torrance, California. Supported in part by the Thomas and Dorothy Leavey Trust. James A. Davis, MD; Arthur H. Cohen, MD; Richard Weisbart, MD; Harold E. Paulus, MD. Address reprint requests to James A. Davis, MD, loo0 Veteran Avenue, Los Angeles, California 90024. Submitted for publication February 23, 1979; accepted May 9, 1979. Arthritis and Rheumatism, Vol. 22, No. 9 (September 1979)

mg daily and received 200 mg of aurothiomalate with no change in clinical status and was then admitted to Sepulveda Veterans Administration Hospital in October 1974. Physical examination revealed temperature 101.4'F, generalized moderately active RA, nodules over both elbows, small left pleural effusion, and mild hepatomegaly without splenomegaly. Examination included a liver-spleen scan that showed mild hepatomegaly, normal liver biopsy, and a bone marrow examination that showed mild granulocytic hyperplasia. He was treated with prednisone 15 mg per day and aspirin 5.4 gm per day, with improvement of the RA and resolution of the hematuna and proteinuria. Aurothiomalate was resumed in November 1974. From November 1974 to November 1976 he received 1985 mg of aurothiomalate but then was again noted to have hematuria and proteinuria which were attributed to gold induced nephropathy. An IVP and cystography showed normal results. In November 1976 he was first noted to have the murmur of aortic insufficiency. Numerous blood cultures revealed negative results and the murmur was attributed to RA. Although gold therapy was stopped, hematuria and proteinuria persisted during the next year and serum creatinine increased from 1.3 to 2.1 mg/dl. Therefore, he was admitted to Sepulveda Veterans Administration Hospital in January 1978 for a kidney biopsy. The patient had no signs or symptoms of Sjogren's syndrome, cutaneous vasculitis, butterfly rash, alopecia, photosensitivity, or Raynaud's phenomenon. Physical examination. Temperature was 97.8'F, blood pressure 130/55, pulse 90. No rash was evident; numerous rheumatoid nodules were found over the extensor surface of the elbows, achilles tendons, and fingers. Swan neck deformities of several fingers were observed and there was decreased range of motion of the wrists, elbows, shoulders, cervical spine, and ankles. Minimal swelling was present in almost all the small joints of the hands and feet, wrists, el-

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Table 1. Laboratory parameters Urinalysis Leuko- Hemocytes, globin, Date cells/mm3 gm/dl 9/74 10/74 11/75 12/76 2/77 5/77 11/77 1/78

17,000 24,000 5,400 5,000

4,500 4,900 4,800 5,100

10.I 10.3 11.2 9.8 9.8 10.0 10.1 7.6

BUN, mg/dl 28 27 17 35 32 43 46 41

Creatinine, mg/dl

I .o I .o 1.3 1.8 1.8 I .9 2. I

Urine protein mg/24 hr (M+)

(I+) 650 (0) I24 3+ (0) (3+) 2,160

Cells/high power field RBC

WBC

15-20 1-3 0 8-12 2C30 0 15-25 20-30

2-5 2-3 0 0 1-3 0 cL2 0-2

Rheumatoid factor ANA Anti-DNA ESR, (latex titer) titer antibody. CH5Ot mm/hr+ 1:1280 70 I10

63 52

1:40

Neg

I:1280 1:10,240

Neg

< I pg

38

56

1:20,480 1:2,560

1:120 1:80

< I pg

58

58

* pg DNA bound per ml by radioimmunoassay.Normal less than 1.

*

t Normal 30-84.

Wintrobe method.

bows, and knees. Fundi and conjunctiva were normal; lungs were clear. The heart had a regular rate; grades II/VI systolic murmur and I/VI early diastolic murmur were heard best at the left lower sternal border. Liver span was 13 cm; the liver was nontender, and no splenomegaly was evident, although there was trace pedal edema. Results of neurologic tests were normal. Laboratory data (Table 1). The white blood cell count was 5,100 cells/mm3; neutrophils, 85%; lymphocytes, 14%; eosinophils, 1%; hematocrit, 28%; hemoglobin, 7.6 gm/dl. Blood smear showed normochromic normocytic erythrocytes. Wintrobe erythrocyte sedimentation rate was 58 mm/hour; creatinine, 2.1 mg/dl; BUN, 41 mg/dl; total protein, 6.1 gm/dl; albumin, 2.6 gm/dl. Quantitative immunoglobulins were IgG, 1,760; IgA, 230; IgM, 282 mg/dl. Latex fixation test for rheumatoid factor was positive at a titer of 1 :2,560; antinuclear antibody was positive at a titer of I :80. DNA binding was 5% by the Farr technique (normal less than 2Wo); anti-DNA antibody, less than I pg DNA bound per ml (radioimmunoassay, normal less than 1.0); C3, 172 mg/dl (normal 70-176). AntiENA antibody titers were RNP,

Glomerulonephritis in rheumatoid arthritis.

ALARCON-SEGOVIA AND URIBE-URIBE 1018 13. Rabinowitz JG, Tweresky J, Guttadauria M: Similar bone manifestations of scleroderma and rheumatoid arthrit...
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