الفهرس 
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Abstract
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that preferentially affects women from early adulthood through mid-adulthood (Somers et al., 2014).
SLE is characterised by autoantibody formation against nuclear antigens with resultant inflammation in organs such as the kidney, skin and joints. SLE is notorious for its markedly heterogeneous clinical phenotype, with a multifactorial aetiology that depends on genetic, epigenetic and environmental influences (Tsokos, 2011).
Lupus nephritis (LN) is a form of glomerulonephritis and constitutes one of the most severe organ manifestations of SLE. LN is histologically classified into six distinct classes that represent differ¬ent manifestations and severities of renal involvement in SLE (Yan et al., 2021).
Most patients with SLE who develop LN do so within 5 years of an SLE diagnosis, although it is not uncommon for LN to develop at later times. In many cases, LN is the presenting manifestation that results in the diagnosis of SLE. Understanding of the genetic and pathogenetic basis of LN has improved substan¬tially over the past few decades. (Cervera et al., 2003).
One of the challenges in the management of patients with SLE relies on the optimal control of cardiovascular (CV) risk. In fact, patients with SLE are known to have an increased risk of cardiovascular events (CVE), due to both traditional and disease-specific risk factors, including inflammation, endothelial dysfunction, accelerated atherosclerosis and lupus nephritis (LN) (Kostopoulou et al., 2019).
To date, CVE represent the most common cause of death in SLE, with CV and cerebrovascular diseases having tremendous burden of morbidity. Lupus nephritis itself leads to increased risk for CVE. This condition, indeed, comprises a variety of disease-specific detrimental factors that further increase CV risk. These include well-recognised factors, such as proteinuria, nephrotic syndrome, prolonged use of glucocorticoids, higher prevalence of arterial hypertension, dyslipidaemia, chronic kidney disease (CKD), end stage renal disease (ESRD), but also other less-defined players, endothelial dysfunction, injury and inflammation. It has been shown that LN patients are much more prone to accelerated atherosclerosis than non-LN SLE patients (Gustafsson et al., 2017).
Lupus nephritis has an additional (up to 8.5-fold) CV risk when compared with nonrenal lupus, consequently leading to an overall increased mortality (Reppe Moe et al., 2019).
On this basis, patients with SLE would generally benefit from additional CV screening and more intensive prevention strategies (Hallajzadeh et al.,2018)
To estimate subclinical atherosclerosis, different non-invasive approaches have been used, including carotid intima-media thickness (cIMT), pulse wave velocity and myocardial perfusion strategies. Among those approaches, ultrasound evaluation of cIMT is one of the most used for risk stratification in SLE patients, being characterized by a high sensitivity9 and with a high predictive value for adverse CV events (Kao et al., 2013).
The aim of this study was done to investigate the association between lupus nephritis, impaired renal function and atherosclerosis measured by carotid and femoral arteries intima-media thickness (IMT) in patients with SLE.
This study was conducted on 50 clinically diagnosed SLE patients and 50 healthy controls.
The patents were diagnosed according to The new 2019 EULAR/ACR classification criteria for SLE which requires a positive ANA as obligatory entry criterion. Other criteria were chosen from 7 clinical (constitutional, hematologic, neuropsychiatric, mucocutaneous, serosal, musculoskeletal, renal) and 3 immunologic (antiphospholipid antibodies, complement proteins, SLE-specific antibodies) categories, and weighted from 2 to 10 (Aringer M et al., 2019).
All were subjected to full clinical history and examination, complete blood count, ESR, C-reactive protein, ANA, Ds DNA, C3, C4, liver enzymes serum creatinine, uric acid, Complete urine analysis ,24 hours urinary protein, Doppler ultrasound on both commo carotid and common femoral arteries.
Renal biopsy was done and classified according to the to the classification of lupus nephritis by the International Society of Nephrology/Renal Pathology Society (ISN/RPS) (Weening et al.,2004).
This study demonstrated the following:
• The Carotid and Femoral intima media thickness (IMT) was statistically significant higher among studied SLE patients with LN compared with SLE patients without LN .
• The Carotid and Femoral intima media thickness (IMT) was significantly correlated with the SLEDAI scores, CRP, ESR, TAG, LDL URIC acid, & lupus nephritis .
Conclusion:
This study findings indicate that LN (Lupus Nephritis) in combination with impaired renal function is strongly associated with presence of atherosclerosis detected by CIMT (Carotid Intima Media Thicness) and FIMT (Femoral Intima Media Thickness) in SLE (Systemic Lupus Erythematosus) patients.