Membranous nephropathy associated with psoriasis.

This is a 62-year-old Caucasian hypertensive woman with known history of severe erythrodermic psoriasis and psoriatic arthritis marginally controlled on cyclosporin therapy, who was seen in June 2001 for evaluation of proteinuria. She had 1 gram of protein on 24-hour urine collection and a creatinine of 0.8 mg/dl. Additional laboratory testing, including serum and urine protein electrophoresis, ANA, ANCA, rheumatoid factor, serum complements, hepatitis B, hepatitis C and HIV screen, were all normal. She was started on lisinopril and hydrochlorothiazide. She returned in June 2002 with worsening hypertension and proteinuria, with urine protein/creatinine ratio of 7.5 and serum creatinine of 1.8. Examination showed diffuse psoriatic lesions and no edema. Renal biopsy showed stage 1 membranous glomerulopathy with complete effacement of foot processes. Biopsy also showed mild interstitial fibrosis and tubular atrophy consistent with cyclosporine toxicity. Her protein/creatinine ratio declined following initiation of benazepril and irbesartan to 2.1 in December 2002 and further to 0.49 by January 2003. However, her serum creatinine rose over that period from 1.5 to 1.9. In March 2003, her rheumatologist started etanercept for treatment of refractory psoriasis and discontinued cyclosporin, following which the psoriatic lesions improved. The follow-up creatinine in April 2003 was 1.7 and in June 2003 was 1.5. Urine protein/creatinine ratio also improved to 0.16 in August 2003. Only four cases of membranous glomerulopathy associated with psoriasis have been described worldwide. The exact relationship remains unclear, but an autoimmune mechanism most likely links the two. Psoriatic patients are also at an increased risk of developing microalbuminuria. The postulated mechanism involves vascular lesions in the glomeruli formed by systemic exposure of glomerular antigens, which result in hyperfiltration of protein. The timing of the improvement in proteinuria makes it difficult to judge whether this was due to adequate psoriatic control, direct effect of etanercept, natural history of the disease or discontinuation of cyclosporin. The latter seems less likely as nephrotic proteinuria is not a typical feature of cyclosporin toxicity. We postulate that psoriatic control with etanercept has contributed to continued remission of membranous glomerulopathy in this case.

Tinoy Kizhakekuttu, MD, David Ringold, MD, Benjamin R. Pflederer, MD, and Lisa M. Antes, MD. UICOM-P, Peoria, IL. UIHC, Iowa City, IA.