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Nephrotic syndrome induced by tioproninAssociation with the HLA-DR3 antigen.

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LETTERS
1. Ferrante FM, Myerson GE, Goldman JA: Subclavian artery
thrombosis mimicking the aortic arch syndrome in systemic
lupus erythernatosus. Arthritis Rheum 25:1501-1504, 1982
2 . Lessof MH, Glynn L E : The pulseless syndrome. Lancet i:799801, 1959
3 . Harris E N , Loizou S. Englert H , Derue G , Chan JK, Gharavi
A E , Hughes GRV: Anticardiolipin antibodies and lupus anticoagulant (letter). Lancet ii:1099, 1984
4. Harris E N , Gharavi A E , Boey ML, Patel BM, MackworthYoung C G , Loizou S . Hughes GRV: Anticardiolipin antibodies:
detection by radioirnmunoassay and association with thrombosis, in systemic lupus erythematosus. Lancet ii:1211-1214, 1983
5 . Boey ML. Colaco CB, Gharavi AE, Elkon KB, Loizou S,
Hughes GRV: Thrombosis in systemic lupus erythematosus:
striking association with the presence of circulating lupus anticoagulant. Br Med J 287:1021-1023, 1984
6. Harris E N , Gharavi A E , Asherson RA, Boey ML. Hughes
GRV: Cerebral infarction in systemic lupus: association with
anticardiolipin antibodies. Clin Exp Rheumatol 2:47-51, 1984
7. Asherson RA, Mackworth-Young CG, Harris E N , Gharavi AE,
Boey M L , Hughes GRV: Multiple venous and arterial thromboseij associated with the lupus anticoagulant and antibodies to
cardiolipin in the absence of S L E . Rheumatol Int 5:91-93, 1985
8 . Hughes GRV. Asherson RA: Atypical lupus with special reference to ANA negative lupus and lupus subsets, Advances in
Nephrology. Edited by J P Grunfeld, MH Maxwell. Chicago,
Year Book Medical Publishers, 1985, pp 333-346
9. Jinidal MK, Martin MFR, Gayner A: Gangrene developing after
minor surgery in a patient with undiagnosed systemic lupus
erythematosus and lupus anticoagulant. Ann Rheum Dis
42.347-349. 1983
10. Asherson RA, Harris E N , Gharavi AE, Hughes GRV: Clinical
manifestations associated with the lupus anticoagulant and
elevations of antibodies to cardiolipins in S L E and other conditions, Progress in Rheumatology. Vol. 11. Edited by I Machtey,
Israel, Hasharon Hospital, 1984, pp 323-329
595
gm/day. After 3 months of treatment, the patient was clinically improved, but in February 1984. she developed a
generalized edema and was hospitalized.
At that time, laboratory investigations revealed the
following: serum creatinine of 2 mgl100 ml, creatinine clearance of 46 mliminute, proteinuria at 4.5 gmi24 hours (moderately selective according t o Cameron’s index), hypoalbuminemia at 1.9 gmilOO ml, hypercholesterolemia at 3 0 mgilO0
ml. Immunologic studies revealed normal levels of C3, C4,
and CH50, and tests for fluorescent antinuclear antibodies,
anti-double-stranded DNA, cryoglobulins, and circulating
immune complexes ( C l q and conglutinin binding tests)
showed negative results. H L A identification showed that
she had A29,B I ~ , B ~ ~ , C W ~ , D R ~ , D R,MT2.
S,MTI
A renal biopsy was performed, and under light
microscopy, the sample showed normal glomeruli. Immunofluorescence analysis of the specimen gave negative results
using antisera against IgG, IgM, IgA. C l q . C3, C4, and
fibrinogen. Using electron microscopy, the only abnormality
noted was a complete loss of the foot processes of the
epithelial cells (foot process disease) (Figure I ) . Withdrawal
of the tiopronin (total cumulative dose 70 gm) and institution
of prednisone treatment ( I mglkgiday) completely resolved
the nephrotic syndrome within 1 month.
There are many similarities in the nephrotic syndrome induced by tiopronin and that induced by D-penicillamine, both drugs having a chemical structural affinity (6-1 I ) .
First, the highest incidence of disease occurs during the first
year of treatment, showing no correlation between mean
daily dose and toxicity. Second, the glomerular injury is
mediated by an immunologic mechanism, and it appears to
be self-limiting upon withdrawal of the offending drug.
Nephirotic syndrome induced by tiopronin: association
with the HLA-DR3 antigen
To the Editor:
The role of tiopronin as a useful disease-remittive
drug in rheumatoid arthritis (RA) has been established in
clinical trials (1-3). Pasero et al (4), in a multicenter trial
comparing tiopronin treatment with D-penicillamine treatment, have demonstrated comparable efficacy. In Pasero’s
study, proteinuria ranging from 2-3 gmlday (but not associated with nephrotic syndrome) occurred in 4 patients in the
tiopronin-treated group. We describe a patient who developed nephrotic syndrome during treatment with tiopronin,
and was also found to have the HLA-DR3 antigen.
In October 1983, a 60-year-old woman was diagnosed
as haking definite RA. according to American Rheumatism
Association criteria (5). Treatment with tiopronin was started, with gradually increasing doses, until she was taking 1
Figure 1. Electron micrograph of renal biopsy specimen from a 60year-old woman with tiopronin-induced nephrotic syndrome, showing complete loss of the foot processes of epithelial cells (original
magnification x 5,000).
LETTERS
596
Third, the morphologic basis of glomerulopathy consists of
both membranous and minimal change glomerular lesions.
The pathogenesis of tiopronin-induced nephropathy
is still unclear. The renal injury may be an immune complexmediated membranous nephropathy similar to the D-penicillamine-induced lesions. The antigenic role of tiopronin has
been demonstrated by Stratta e t al (9), who have shown a
positive result on immune complex elution testing after
incubation of kidney sections with tiopronin. According to
Lupo et al(8), in tiopronin-induced minimal change nephropathy, a sensitization mechanism similar to that described in
minimal change nephropathy associated with exposure to
allergens may occur. In patients with HLA-DR3, Speerstra
et a1 (12) showed that there is an increased risk of nephrotic
syndrome during treatment with D-penicillamine. Our observation suggests a similar immunogenetic susceptibility for
the renal damage induced by tiopronin; however, further
studies will be necessary to prove whether this association is
statistically significant.
Carlo Salvarani, M D
PierLuigi Macchioni, M D
Fulvia Rossi, MD
Ido Iori, MD
Giordano Filippi, M D
Hospital of Reggio Emilia
Reggio Emilia, Italy
I . Pasero G , Ciompi ML: Thiopronine therapy in rheumatoid
arthritis (letter). Arthritis Rheum 222303404, 1979
2. Pasero G, Pellegrini P, Ciompi ML, Colamussi V, Barbieri P,
Mazzoni MR: La tiopronine, nouveau traitement de fond de la
polyarthrite rhumatoi’de: Ctude ouverte de 158 cas. Rev Rhum
Ma1 Osteoartic 47: 163-168, 1980
3. Amor B, Mery C, de Gery A: La tiopronine: nouvel antirhumatismal i action lente dans la polyarthrite rhumatoide. Rev Rhum
Ma1 Osteoartic 47: 157-162, 1980
4. Pasero G, Pellegrini P, Ambanelli U , Ciompi ML, Colamussi V ,
Ferraccioli G , Barbieri P, Mazzoni MR, Menegale G , Trippi D:
Controlled multicenter trial of tiopronin and D-penicillamine for
rheumatoid arthritis. Arthritis Rheum 25:923-929, 1982
5. Ropes MW, Bennett GA, Cobb S , Jacox R, Jessar RA: 1958
revision of diagnostic criteria for rheumatoid arthritis. Bull
Rheum Dis 9:175-176, 1958
6. Bacon PA, Tribe CR, Mackenzie JC, Verrier-Jones J, Cumming
RH, Amer B: Penicillamine nephropathy in rheumatoid arthritis. Q J Med 45:661-684, 1976
7. Falck HM, Tornroth T, Koch B, Wegelius 0: Fatal renal
vasculitis and minimal change glomerulonephritis complicating
treatment with penicillamine. Acta Med Scand 205: 133-138,
I979
8. Lupo A, Faraggiana T, Loschiavo C, Parolini C, Maschio G:
Nephrotic syndrome during 2-mercapto-propionyl-glycine
(thiola) therapy. Nephron 28:96-99, 1981
9. Stratta P, Coratelli P, Camussi G , Passavanti G , Segoloni GP,
Coppo R, Amerio A, Vercellone A: Sindrome nefrosica durante
trattamento con 2-mercaptopropionilglicina. Minerva Nefrol
25:87-92, 1978
10. Fruttero B, Dall’Aglio PP, Bruno M, Rossi E, Pozzo L, Ferrari
C, Linari F, Migone L: Sindrome nefrosica indotta dalla 2mercapto-propionil-glicina. Symposium on Metabolic, Physiochemical and Therapeutical Aspects of Urolithiasis. Edited by F
Linari, M Brund, B Fruttero, M Marancella. Milan, Italy,
Wichtig, 1983, pp 131-135
11. kzzoni G , Pavanello L, Dussini N , Chiandetti L, Zacchello G:
Nephrotic syndrome during treatment with alpha-mercaptopropionylglycine. J Urol 122:381-382, 1979
12. Speerstra F, Reekers P, Van de Putte LBA, Vandenbroucke JP,
Rasker JJ, de Rooij DJRAM: HLA-DR antigens and proteinuria
induced by aurothioglucose and D-penicillaminein patients with
rheumatoid arthritis. J Rheumatol 10:948-953, 1983
Idiopathic thrombocytopenic purpura with high-titer,
speckled pattern antinuclear antibodies: possible
marker for systemic lupus erythematosus
To the Editor:
Idiopathic thrombocytopenic purpura (ITP) has been
associated, in a small number of patients, with the subsequent development of systemic lupus erythematosus (SLE)
( I , 2 ) . Several histologic features resembling those described
in S L E have been found in the spleens of some ITP patients
(3), supporting the concept that an ITP-like syndrome can be
the initial manifestation of S L E . Since S L E is a chronic and
potentially fatal disease, it is of prognostic importance to
identify ITP patients who are at risk of developing SLE. In
this report we provide evidence suggesting that ITP patients
presenting with high-titer, speckled pattern, antinuclear antibodies (ANA) appear to be at risk of developing SLE.
Between 1976 and 1983, we studied 18 patients in
whom the diagnosis of ITP was made. All patients presented
with easy bruising, petechiae and/or bleeding, and platelet
counts ranging from 5,000-15,000/mm3. None of the patients
had ingested drugs known to induce thrombocytopenia, nor
did they have evidence of any other underlying disease. All
patients were female, with a mean age of 29 years (range 1038). Patients were followed for a mean of 3.4 years (range 10
months-7 years). At the time of diagnosis of ITP, all patients
had serum drawn for rheumatoid factor (latex fixation),
complement levels (C3 and C4), antibodies to double-stranded DNA, and ANA determinations. In those sera exhibiting
speckled pattern ANA, the presence or absence of antibodies directed against the nuclear antigens R N P and/or Sm was
determined (4). The diagnosis of S L E was established using
the American Rheumatism Association preliminary criteria
(5). Presence of 4 or more criteria was required before the
diagnosis of S L E was made.
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tioproninassociation, induced, hla, syndrome, antigen, dr3, nephrotic
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