Department of Rheumatology, Saint-Antoine Hospital, Paris and Department of Nephrology, Tenon Hospital, Paris, France
SIR, Shunt nephritis is an immune complex-mediated glomerulonephritis [1]. It commonly occurs in patients with infected ventriculo-atrial shunts implanted for congenital or acquired hydrocephaly. Arthritis-related shunt nephritis has only been reported in two children [2, 3] and adolescents [1, 4]. This report describes a case of arthritis-related shunt nephritis in an adult suffering from arthritis.
A ventriculo-atrial shunt was implanted in a 41-yr-old woman in July 1995 to treat hydrocephalus due to an empty sella syndrome. She gradually developed inflammatory polyarthralgia in her hands. Arthritis of the wrists and arthralgia of the elbows occurred 3 yr later, along with febrile purpura of her legs and asthenia. Because of the occurrence of clinically palpable symmetrical synovitis in her wrists, she was diagnosed as suffering from rheumatoid arthritis by a rheumatologist 3 months later. She was given prednisone (1 mg/kg daily) for 3 weeks and gradually reduced to 5 mg/day for 2 months, but her arthralgia persisted. She was admitted to our department, at which time she had symmetrical arthralgia in her hands (first, second and third metacarpophalangeal and proximal interphalangeal joints), wrists with palpable synovitis and swelling, low back pain and a petechial purpura of the lower legs. Laboratory tests revealed a white blood count of 12 500/mm3 with neutrophils 10 500/mm3, haemoglobin 10.2 g/dl, platelets 156 000/mm3, erythrocyte sedimentation rate (ESR) 60 mm/h and C-reactive protein (CRP) 26 mg/l. Her urine sediment showed proteinuria at 0.94 g/24 h, haematuria 200/mm3 and leucocyturia 70/mm3. The urine culture was sterile. Renal function was normal. Total haemolytic complement CH100 was 22 IU/l (normal: 4881150 IU/ml), C3 complement was 0.65 g/l (normal: 0.751.40 g/l) and C4 complement was 0.11 g/l (normal: 0.100.34 g/l). Rheumatoid factors, antinuclear antibodies and double-stranded DNA antibodies were negative. A type III mixed cryoglobulinaemia was present (0.22 g/l). Blood cultures were positive for a coagulase-negative staphylococcus and her cerebrospinal fluid was positive for a coagulase-negative staphylococcus and Propionibacterium acnes. An echocardiogram did not reveal endocarditis. The diagnosis of shunt nephritis was proposed and the ventriculo-atrial shunt removed. Cultures of the ventriculo-atrial shunt were positive for a coagulase-negative staphylococcus. Parenteral oxacillin and pefloxacin were prescribed. Her arthralgia/arthritis and purpura were gradually resolved over 1 month. Her urinalyses returned to normal in 6 months.
There have been many reports of shunt nephritis [5]. Its incidence after insertion of a ventriculo-atrial shunt is 0.72.3%. The most common manifestations are haematuria, proteinuria, hypertension and renal insufficiency due to an immune complex-related glomerulonephritis. The initial event is infection of the shunt, most commonly with a coagulase-negative staphylococcus, leading to the release of bacterial antigens and the formation of immune complexes in the systemic circulation. Arthritis may occur via the same immunological mechanism. Our case indicates that arthritis can reveal shunt nephritis not only in children [2, 3] or adolescents [1, 4], but also in adults (Table 1). The prognosis for renal function is good, provided that the ventriculo-atrial shunt is removed soon after onset of the disease. However, renal function can rapidly deteriorate when diagnosis and treatment are delayed [6]. In our case, even though there was a long delay in diagnosis, the renal outcome was excellent. We hypothesize that the prescription of corticosteroids, because of their immunosuppressive properties, slowed down the immunological process and decreased the formation of immune complexes.
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We therefore suggest that shunt nephritis should be considered in patients with a ventriculo-atrial shunt who present with arthritis, even adults, and that the arthritis may be an early indicator of an infected shunt.
Notes
Correspondence to: F. Berenbaum, Saint-Antoine Hospital, Department of Rheumatology, 184 rue du faubourg Saint-Antoine, 75012 Paris, France. E-mail: francis.berenbaum{at}sat.ap-hop-paris.fr
References