Clinico-serological associations of urinary activated leukocyte cell adhesion molecule in systemic lupus erythematosus and lupus nephritis.

BACKGROUND: Lupus nephritis (LN) is one of the major complications associated with Systemic Lupus Erythematosus (SLE). Activated leukocyte cell adhesion molecule (ALCAM or CD166) is a promising urine biomarker that binds to CD6, a receptor found on lymphocytes. This binding results in T-cell activation, proliferation, and recruitment, which causes tissue inflammation and may explain the pathophysiology of LN. AIM OF WORK: Investigate the urinary ALCAM level in SLE, study its relationship to disease activity, and clarify the association with LN activity and histopathology. PATIENTS AND METHODS: A case-control study was performed on 60 patients with SLE and 20 matched controls. The SLE disease activity index (SLEDAI) and the activity of renal disease (rSLEDAI) were evaluated. Renal biopsy and uALCAM levels were also investigated. RESULTS: Urinary ALCAM levels were higher significantly in active LN patients than inactive LN patients, active and inactive non-LN SLE, and the control group (p < 0.001). The cut-off value for identifying active and inactive LN was above 270 ng/mg (p < 0.001). ALCAM levels were greater in proliferative (class III, IV, and IV/V) than in non-proliferative (class II and V) LN (p < 0.001). ALCAM exhibited high positive correlations with SLEDAI and rSLEDAI (p < 0.001 each) and negative significant correlations with C3 (p < 0.001) and C4 (p = 0.005). CONCLUSION: Urinary ALCAM is a sensitive biomarker evaluating LN in SLE patients. Levels above 270 ng/mg can help distinguish between active and inactive LN. ALCAM levels are correlated positively with SLEDAI and rSLEDAI but have a negative correlation with C3 and C4. Key Points • Urinary ALCAM shows promise as a biomarker for evaluating kidney dysfunction in SLE patients. • It is a non-invasive marker that can differentiate between proliferative and non-proliferative LN. • A urinary ALCAM level above 270 ng/mg can indicate active LN, while lower levels indicate inactive LN. • Urinary ALCAM levels are correlated positively with SLEDAI and rSLEDAI scores but correlated negatively with C3 and C4.

Association Between Renalase Gene Polymorphism (rs2296545) and Hypertension in Egyptian Chronic Kidney Disease Patients.

Background Renalase gene polymorphisms are associated with an increased risk of essential hypertension, chronic kidney disease (CKD), heart disease, diabetes, and stroke. One of these polymorphisms is a common missense (rs2296545) polymorphism, which was reported to be related to hypertension. The aim of this work was to investigate the possible relation between renalase gene polymorphism (rs2296545) and hypertension in patients with CKD patients. Subjects and methods Ninety patients were included in this case-control study: 30 normotensive CKD patients, 30 hypertensive CKD patients, and 30 apparently healthy controls. Genomic deoxyribonucleic acid (DNA) was extracted from peripheral whole blood, and renalase gene (rs2296545) polymorphism was genotyped in all patients and controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Odds ratios (OR) and their 95% CIs were calculated. Results We found that the CC genotype and the C allele renalase (rs2296545) were statistically associated with the risk of CKD (OR= 9.4; 95%CI 1.2-7.2; P= 0.036) and (OR= 3.78; 95%CI 1.57-9.08; P= 0.003), respectively. There was a statistically significant difference between the hypertensive CKD patients and the controls regarding the CC genotypes and the C allele, (26.7% versus 3.3%, P= 0.018) and (40% versus 11.7%, P< 0.001) for the CC genotype and the C allele, respectively. The mean values of systolic and diastolic blood pressure were higher in the normotensive CKD patients with the CC genotype compared to other genotypes (P= 0.014 and P= 0.022, respectively) and also were higher in hypertensive CKD patients with the CC genotype when compared to other genotypes (P= 0.001 for both). Conclusion This study demonstrated a statistically significant increase in the renalase gene (rs2296545) CC genotype and the C allele in CKD patients, especially hypertensive CKD.

Heme oxygenase and iron status in exosomes of psoriasis patients.

Psoriasis is an autoimmune skin disease characterized by hyperproliferation of keratinocytes due to interplay between keratinocytes and immune cells. Iron status plays an important role in modifying the function of the immune system. Heme oxygenase (HO), heme-degrading enzyme, plays important role in protective response to oxidative cellular stress. We aimed in this study to map the iron status and HO levels and declare the role HO enzyme in iron homeostasis and immune-modulation in psoriasis. Fifty-one patients with psoriasis and 50 age- and sex-matched healthy controls were enrolled in this study. 5 mL blood sample was withdrawn from each subject. Hepcidin, iron soluble transferring receptor (sTfR), and total iron binding capacity (TIBC) were estimated using ELISA technique and, HO-1 gene level was detected using RT-PCR (reverse transcription-polymerase chain reaction). Iron levels, TIBC, and hepcidin were significantly lower in cases compared to controls. On the contrary, sTfR and HO-1 were significantly over-expressed in cases compared to controls (p < 0.05 in all). HO-1 expression negatively correlated with PASI score and disease extent (%) (r = - 0.614-, p = 0.001; r = - 0.807-, p = 0.001 respectively). There were no significant associations between HO-1 expression and iron, TIBC, hepcidin, sTfR levels (p > 0.05 in all). Iron supplements for the patients with psoriasis are important to maintain haematopoiesis. The induction of HO-1 might have be a promising approach for the treatment of psoriasis through antioxidant ability, immunomodulatory role as well as its role in heme synthesis.