Renal, hepatic, cardiac, and GI involvement is most frequent.
Renal lesions are of two types: large-vessel (the lesion is a tubular infarction, and renal failure is uncommon) and microvascular, including the glomerular afferent arterioles (the lesion is diffuse, and renal failure is common and occurs early).
Of patients with massive hepatic infarction, 50% have polyarteritis nodosa, although this complication is rare.
Milder degrees of hepatic tenderness and increased concentrations of liver enzymes usually reflect focal areas of hepatic capsular vasculitis.
Several polyarteritis nodosa-associated syndromes are separated from typical polyarteritis nodosa by pathogenic or clinical differences:
hypersensitivity angiitis;
Churg-Strauss syndrome (the vasculitis includes lung involvement,
eosinophilia,
necrotizing granulomas,
and severe asthma);
Cogan's syndrome (the disease begins as interstitial keratitis and inner ear infarction);
pure mesenteric polyarteritis nodosa (recognized in IV methamphetamine addicts);
Kawasaki's disease (mucocutaneous lymph node syndrome in infants and children complicated by coronary arteritis with early aneurysm formation);
and necrotizing arteritis associated with hepatitis B infection (either acute hepatitis or chronic active liver disease).
Many patients with essential cryoglobulinemia causing small- and medium-sized vasculitis (ie, palpable purpura, digital vessel occlusion, glomerulonephritis) are chronically infected with hepatitis C.
The interrelationships of idiopathic polyarteritis nodosa and these forms of arteritis are unclear.
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