Hepatitis C virus infection complicating lupus nephritis.

Key words: hepatiti Cs virus; lupus nephritisIntroductionA certain prevalenc of hepatitie Cs virus (HCV) anti-bodies has been foun idn patients with chronic 'prim-ary' glomerulonephriti (GN) Howeve. sr ther are escarce and conflicting data describin the prevalenc g eof anti-HCV antibodie isn patients with GN. AlthoughHCV-associated GN seems to be infrequent in France[ 1 ], Spain [2] an, d Hong Kong [3], others investigatorshave foun ad high prevalenc of anti-HCe V antibodiesin patients with biopsy-prove GN inn Italy [4] and inJapan [5]. HCV infectio i associatesn d with membranopro-liferative type I GN [6-8] and membranous GN [9,10]. The pathogenesi of HCV-associates GdN i comples xand unclear. HCV-associated membranoproliferativetype I GN seem tso b relatee tdo th depositioe onfcirculating immune complexes containin HCV anti,g-HCV IgG an monoclonad l rheumatoi in d factors;contrast, it is possible that HCV-associated membran-ous GN could be relate tdo antibodies cross-reactingwith glomerular antigens [6,11-16]. However severalimportant questions need further investigations: natureof inciting antigens, compositio o circulatinf anndgdeposited immune complexes, host predispositio and nHCV genotypes [17]. Althoug a varieth y o f extrahep-atic immunologically mediated syndromes were recog-nized to complicat HCe infectioV n [14,15,17 the ]development of systemic lupus erythematosu has nos tbeen described previousl in detaily bu, t it i possibls ethat th deterioratioe on immunf e respons in lupue spatients can increas the e likelihood o f HCV infection[18]. We repor twt caseo s with severe lupus nephritis(LN) and HCV infection with liver damage. Althoughthis associatio ins probably not cause-effect related it ,offers th opportunite to discusy ths evolutioe anndmanagement of these conditions.Case reportsCase 1. A 50-year-old ha womad diagnosi an ofssystemic lupus erythematosu in 197s whe6n she pre-sented polyarthritis, malar erythema, photosensitivity,Raynaud's phenomenon, alopecia and positiv, e anti-nuclear an double-stranded DN antibodiesAd Th.epatient received antimalaria and aspiril drugn wits hgood response. Twelv she develope yeare s lated rnephrotic syndrome without rena or arterial failurlehypertension. Renal biopsy showed focal proliferativeglomerulonephitis (typ IIe I WHO) with active lesions.She was treated with prednisone plus azathioprin aned6 months later nephrotic range proteinuria decreasedto 0.5 g/24 Wit h. h these medication sh remainee s dwell for 5 years. Afterwards she presented a relapse o fnephrotic syndrome with decreased renal function(serum creatinine 176.8 umol/1), microscopic haemat-uria and elevated blood 'pressure In a secon. d renalbiopsy diffuse proliferative glomerulonephitis (typeIV WHO) wa diagnoses d (Figur 1). Simultaneousle yshe had elevatio onf live r enzymes value (GOTs 72U/L, GPT 94 U/l) an cryoglobulind s wer noet pres-ent. HCV serum antibodies were detecte the d usingsecond-generation HCV enzyme-linked immunoassay(Monolisa, Sanofi Diagnostic and s PasteurTM)recombinant immunoblot assay (RIBA2, ImmunoblotOrtho DiagnosticTM). Vira HCl V RNA was detected