Background Kidney transplantation is the treatment of choice for most patients with end-stage renal disease. To improve patient and transplant survival, non-invasive diagnostic methods for different pathologies are important. Leucine-rich alpha-2-glycoprotein (LRG-1) is an innovative biomarker that is elevated in cases of angiogenesis, inflammation, and kidney injury. However, there are limited data about the diagnostic role of LRG-1 in kidney transplant recipients. The aim of this study was to evaluate the association between serum LRG-1, urine LRG-1, and kidney transplant function and injury. Material/Methods We enrolled 35 kidney transplant recipients in the study. LRG-1 in the serum and urine was detected using ELISA. We evaluated the correlation of serum and urine LRG-1 with traditional serum and urine kidney injury markers. Results A higher level of serum LRG-1 correlates with a higher level of urine LRG-1. Serum LRG-1 has a positive correlation with transplant age, serum urea, serum creatinine, serum cystatin C, proteinuria, and fractional excretion of sodium (FENa) and a negative correlation with hemoglobin and estimated glomerular filtration rate (eGFR). Urine LRG-1 has a positive correlation with serum cystatin C, proteinuria, and urine neutrophil gelatinase-associated lipocalin (NGAL). Conclusions Higher levels of serum and urine LRG-1 are associated with kidney transplant injury and functional deterioration. Thus, LRG-1 might be also as a biomarker for tubular dysfunction in patients after kidney transplantation.

BACKGROUND AND AIMS Leucine-rich alpha-2-glycoprotein (LRG1) is a novel proangiogenic factor involved in the abnormal angiogenesis and renal fibrosis in diabetic nephropathy by potentiating endothelial transforming growth factor-beta/activin receptor-like kinase 1 (TGF-β/ALK1) signalling [1]. TGF-β mediates mesangial matrix accumulation culminating in the development of glomerulosclerosis [2], which also occurs in immunoglobulin A nephropathy (IgAN) patients. Our study aims to evaluate LRG1 as a marker of mesangial cell proliferation in IgAN patients. METHODS: Adults with a morphologically confirmed IgAN by the presence of IgA deposits by immunofluorescence microscopy were included in the study. Diabetes mellitus, oncology, acute inflammation processes were exclusion criteria. Serum LRG1 was detected using ELISA. RESULTS A total of 73 patients with IgAN were included [mean age 41 years, interquartile range (IQR) 35–47; range, 21–65; 65.8% men]. The median estimated glomerular filtration rate (eGFR) was 44 (IQR 24–83, range 4–133) mL/min/1.73m2. Kidney biopsies were analyzed according to the Oxford classification: M0 in 10 (13,7%), M1 in 56 (76.7%) patients. The median serum LRG1 was 49 µg/mL (IQR 40.7–57.7, range 29–133.3). Bivariate analyses showed that plasma LRG1 was negatively associated with eGFR (rho = −0.342, P = 0.003). A linear model showed that GFR decline for 1 mL/min was associated with an increase of LRG1 for 0.194 µg/mL. In IgAN patients with an M1-score LRG1 was higher (P = 0027, Mann–Whitney U test), the area under the ROC curve value for serum LRG1 was 0.739. CONCLUSION Serum LRG1 increases with GFR decline in patients with IgAN and at the same time correlates with mesangial hypercellularity according to Oxford classification. Therefore, LRG1 might be a potential marker of advanced disease in IgAN.

BACKGROUND AND AIMS The current strategy to fight against the COVID-19 pandemic involves active patient vaccination. Patients with renal and autoimmune diseases are in high risk for severe COVID-19 infection [1]. Therefore they should be prioritized for vaccination. Immunoglobulin A nephropathy (IgAN) is one of the most common primary glomerulonephritis triggered by mucous membrane alteration; however, there is a discussion about vaccination-caused IgA flare [2]. The immunological nature of IgAN and misleading information in public sources leaves patients skeptical about whether to get vaccinated [3]. The study aimed to investigate the impact of SARS-CoV-2 vaccination on the clinical course of IgA nephropathy. METHOD Adult patients treated in Pauls Stradins Clinical University Hospital with morphologically proven IgAN were included in the study. Patients with secondary IgAN were excluded. Evaluation of clinical and laboratory markers was performed on inclusion visit and on the second visit 6 months later. SARS-CoV-2 vaccination type and status were noted on both visits. Estimated GFR was calculated with CKD-EPI creatinine–cystatin equation. IBM SPSS Statistics version 27 and Microsoft Excel 10 were used for data analysis. RESULTS The study involved 54 patients, 36 were unvaccinated and 18 were fully vaccinated. A significant difference between the two groups was observed by baseline proteinuria. Other differences were not observed. Fourteen patients were vaccinated with mRNA vaccine, 13 with Comirnaty and 1 with Spikevax, and four patients were vaccinated with Vaxzevria vector vaccine. The differences between the two groups are shown in Table 1. During study period, two patients had COVID-19 infection; a patient in the vaccinated group had COVID-19 prior to vaccination. CONCLUSION SARS-CoV-2 vaccination did not affect the clinical course of IgA nephropathy. Our study results indicate that SARS-CoV-2 vaccination in IgA nephropathy patients was safe regarding renal function and disease activity markers.