Most cases are marked by asymmetric polyneuropathy, but progressive disease can lead to symmetric nerve involvement. Central nervous system involvement may cause strokes or seizures.Renal system: Kidney involvement is common and often leads to death of parts of the kidney. Involvement of the renal artery, which supplies the kidneys with highly oxygenated blood, often leads to high blood pressure in about one-third of cases. deposition of protein or blood in the urine may also be seen. Almost all patients with PAN have renal insufficiency caused by renal artery narrowing, thrombosis, and infarctions. Cardiovascular system: Involvement of the arteries of the heart may cause a heart attack, heart failure, and inflammation of the sac around the heart (pericarditis).Gastrointestinal system: Damage to mesenteric arteries can cause abdominal pain, mesenteric ischemia, and bowel perforation. Abdominal pain may also be seen. Musculoskeletal system: Muscle and joint aches are common. Complications
Stroke
Heart failure resulting from cardiomyopathy and pericarditis
Intestinal necrosis and perforation

Causes
PAN has no association with anti-neutrophil cytoplasmic antibodies, but about 30% of people with PAN have chronic hepatitis B and deposits containing HBsAg-HBsAb complexes in affected blood vessels, indicating an immune complex-mediated cause in that subset. Infection with the hepatitis C virus and HIV are occasionally discovered in people affected by PAN. PAN has also been associated with underlying hairy cell leukemia. The cause remains unknown in the remaining cases; there may be causal and clinical distinctions between classic idiopathic PAN, the cutaneous forms of PAN, and PAN associated with chronic hepatitis.
When the condition is active, the basement membrane is dissolved by the antibodies produced, and areas of skin lift away at the base, causing hard blisters which scar if they burst. In other words, this is a desquamating/blistering disease in which the epithelium "unzips" from the underlying connective tissue, allowing fluid to gather that subsequently manifest as bullae, or blisters. Diagnosis
Diagnostic techniques:

antibodies (IgG) precipitate complement (C3) in the lamina lucida of the basement membrane. Circulating auto-antibodies to BP-1 antigen (located in hemidesmosome). 50% have BP-2. Positive Nikolsky sign. IgG, C3 deposition at BM creating smooth line in immunofluorescent analysis. Management
The management depends upon the severity of the condition. For example, where there are lesions in the mouth alone, systemic drugs are less likely to be used. Where the condition is not limited to the mouth, or where there is poor response to Topical treatments, systemic drugs are more likely to be used. Conservative
Simple measures that can be taken include avoidance of hard, sharp or rough foods, and taking care when eating. Good oral hygiene is also usually advised, and professional oral hygiene measures such as dental scaling. Medications
Topical and intralesional (injected into the affected areas) corticosteroid drugs may be used, such as fluocinonide, clobetasol propionate or triamcinolone acetonide. Oral candidiasis may develop with long term topical steroid use, and sometimes antimycotics such as miconazole gel or chlorhexidine mouthwash are used to prevent this. Topical ciclosporin is sometimes used. Dapsone is sometimes used as a steroid sparing agent.