Chronic urticaria and mesangial proliferative glomerulonephritis: a case report

Abstract

Background In glomerulonephritis (GN), glomerular deposition of immune complexes produces complement activation which usually results in hypocomplementemia. Decreased complement levels are most commonly found in patients with membranoproliferative GN and membranous nephropathy due to lupus or to hepatitis B virus infection, while IgA nephropathy and other forms of membranous nephropathy lead to less complement activation [1]. Furthermore, both hereditary complement deficiency and the presence of circulating factors that promote complement activation can cause or contribute to hypocomplementemia in GN. All forms of hereditary hyocomplemetemia are associated with a predisposition to immune complex diseases because of an impaired clearance of immune complexes. The most common deficiency is of C1q, and >90% of C1q deficient individuals develop systemic lupus erythematosus (SLE) [2]. Moreover, systemic diseases with renal involvement, such as acute atheroembolic disease, haemolytic-uraemic syndrome or thrombotic thrombocytopenic purpura and sepsis are necessarily excluded when hypocomplementemia is found in the setting of renal insufficiency. We hereby report on a patient with chronic urticaria who presented with an acute nephrotic syndrome caused by a mesangial proliferative GN and that had the particular feature of persistently depressed serum complement C4 levels.