Background Lupus Nephritis (LN) is one of the most severe forms of systemic lupus erythematosus (SLE) (1). Angiotensinogen (AGT) gene encodes the only glycoprotein known to be a precursor of the vasopresor angiotensin II (Ang II). Ang II is also a growth factor and a profibrogenic cytokine (2). In kidney transplantation AGT has been founded down expressed in biopsies with chronic allograft dysfunction (3). In LN, AGT deserves evaluation.
Objectives To investigate AGT expression in biopsies and urines from LN patients.
Methods 32 biopsies/urines paired from 32 LN patients was included. Kidney biopsies were evaluated according to the ISN/RPS classification system. Levels of AGT were evaluated using Quantitative Real Time PCR. Threshold cycle (Ct) scores were averaged for calculations of relative expression values. The Ct scores were normalized against Ct scores by subtracting β2Microglobuline control, or ΔCt=Ct,gene- Ct,B2M. Data expressed as ΔCt are inversely proportional to gene expression level. Nonparametric Mann Whitney test analysis and Anova with Bonferroni test were performed.
Results 26 (81.3%) patients were female with a mean age at biopsy time of 31.9±29 years. The SLEDAI at the time of biopsy was 10.5 (IQR 0–15.7) and SLICC ≥1 in 13 (32.5%), hypocomplementemia 13/31 (41.9%) and positive DNA in 11/29 (37.9%) patients. Biopsies from patients with proteinuria ≥0.5 and renal failure (n=23), proteinuria isolated (n=14), LN remission (n=9), renal failure (n=7) and nephrotic syndrome (n=2) were performed. The mean value of ΔCt AGT gene expression in renal biopsy was 4.50 (IQR 3.51 – 5.67) and AGT in urine samples was 13.94 (IQR 11.66 – 17.89).
Conclusions In the present study we found a potential utility of AGT mRNA levels in samples of active vs remission LN patients. Prospective studies are needed for confirming these results.
Yajuan Li et al. Biomarkers Profiling for Lupus Nephritis. Genomics Proteomics Bioinformatics 11; 158–165, 2013.
Eriguchi M et al. Assessment of urinary angiotensinogen as a marker of podocyte injury in proteinuric nephropathies. Am J Physiol Renal Physiol 310: F322–F333, 2016.
Mas V et al. Establishing the molecular pathways involved in chronic allograft nephropathy for testing new non-invasive diagnostic markers. Transplantation. 83:448–57, 2007.
Disclosure of Interest None declared