الفهرس 
Introduction and Aim of WorkOnly 14 pages are availabe for public view
 |  | from | 194 |  |  |
| | | from | 194 | | |
Abstract
Systemic sclerosis (SSc, scleroderma) is a multisystem autoimmune rheumatic disease that causes inflammation, vascular damage and fibrosis. It is uncommon, affecting approximately one in 10, 000 but has a very high morbidity and the highest case-specific mortality of any rheumatic disorder, with 50% of patients dying or developing major internal organ complications within 3 years of diagnosis (Denton & Black, 2005). There are two major clinical subsets: limited cutaneous SSc (lcSSc) and diffuse cutaneous SSc (dcSSc). Depending on the extent of skin involvement, dcSSc typically is most active in the first 3 years from onset, and this is the time during which major complications develop in the lungs, kidney and heart. The skin disease usually plateaus or improves over 1–2 years (Shand et al., 2007). Raynaud’s phenomenon is observed in 90-98 % of SSc patients. It may precede SSc for years and its presence may have predictive value for the subsequent development of SSc, in particular in association with abnormal nailfold capillaries and the occurrence of antinuclear antibodies (ANA) (Haustein, 2002). Pulmonary manifestations of systemic sclerosis include interstitial lung disease, pulmonary hypertension, pleuritis, pleural effusion, and aspiration pneumonia. Scleroderma renal crisis is characterized by an abrupt rise in blood pressure and rapid progressive renal failure (Eisenberg et al., 2008). Sudden renal episodes are not the only problem of rheumatologists and nephrologists. Patients with systemic sclerosis are exposed to chronic and progressive renal damage, which can lead to renal failure. So far, the pathogenesis of renal changes in systemic sclerosis, both acute and chronic, has not been known (Lewandowski et al., 2005).