Aims: Diabetic nephropathy (DN) is one of the main causes of chronic kidney disease (CKD), which increases the risk of cardiovascular diseases and progresses to end-stage renal failure. Thus, early diagnostic markers for diabetic patients are urgently needed to improve the prognosis of DN and predict DN progression.Materials and methods: PubMed, MEDLINE, EMBASE, and Scopus were searched for publications until February 24, 2021. Review Manager 5.4 software was used for meta-analysis. We performed the heterogeneity test using the I² statistic: P < 0.1 and I²> 50% meant statistical significance.Results: We included 13 studies. The urinary liver-type fatty acid-binding protein (uL-FABP) concentrations in the normal albuminuria group were significantly higher than those in the normal control group without diabetes mellitus (DM) [P = 0.009, SMD 1.72, 95% CI (0.44, 2.99)]. Urinary F-LABP levels were elevated in the macroalbuminuria group compared with those in the microalbuminuria group with DM [P = 0.002, SMD 2.82, 95% CI (1.03, 4.61)]. Urinary L-FABP levels were also significantly increased in the progression and CKD groups compared with non-progression and CKD subjects with DM [P = 0.02, P < 0.00001, respectively]. Furthermore, uL-FABP concentrations were positively correlated with the albumin-to-creatinine ratio and systolic blood pressure in patients with DM [Summary Fisher’s Z = 0.58 P < 0.00001; Summary Fisher’s Z = 0.24 P < 0.0001, respectively] and negatively correlated with estimated glomerular filtration rate in patients with DM [Summary Fisher’s Z = −0.36, P < 0.0001].Conclusion: Urinary L-FABP may be a potential marker for the detection of all stages of DN and for the prediction of the progression and severity of DN in patients with type 1 and 2 DM.

Background: It has been demonstrated that 12/15-lipoxygenase (LO) contributes to insulin resistance by promoting beta cells’ exposure to inflammation. We investigate the mechanism by which 12/15-LO regulates the expression of inflammatory factors in obesity-related glomerular disease (ORG). Methods: Glomerular mesangial cells were treated with metabolite of 12/15-LO, and the expression of inflammatory factors was measured. Cell histones methylation in 12/15-LO related metabolic memory process were evaluated by chromatin immunoprecipitation (ChIP) assays. Wild-type (WT) and 12/15-LO knockout mice were fed a high-fat diet (HFD) to induce ORG. Results: 12(S)-HETE increased TNF-α, MCP-1, and IL-6 mRNA expression. Inhibition of 12/15-LO reduced the expression of inflammatory factors stimulated by PA or TNF-α. ChIP assays showed that 12(S)-HETE increased H3K4me modification in the TNF-α, IL-6, and MCP-1 gene promoters, and decreased H3K9me3 modification in the MCP-1 and IL-6 gene promoter. Urinary albumin excretion was greater in HFD-fed than in standard fat diet-fed mice, but both urinary protein and microalbumin amounts were lower in HFD-fed 12/15-LO knockout than in WT mice. The levels of TNF-α, IL-6, and MCP-1 in serum and renal cortex were higher in WT than in 12/15-LO knockout mice. Conclusions: 12/15-LO may regulate the expression of inflammatory factors in ORG by methylation of histones in the promoter regions of genes encoding inflammatory factors, sustaining the inflammatory phenotype of ORG.

Background: Telitacicept is a biologic that specifically targets B-lymphocyte stimulator and a proliferation-inducing ligand, demonstrating significant potential for therapeutic applications in B-cell-mediated autoimmune diseases. Currently, telitacicept is primarily utilized in the treatment of systemic lupus erythematosus. However, its therapeutic effect on immunoglobulin A nephropathy (IgAN) after hematopoietic stem cell transplantation (HSCT) has not been reported. This case report presents the clinical outcome of telitacicept administration in the treatment of IgAN following HSCT.Case report: A 36-year-old Asian man developed IgAN following allogeneic HSCT for acute myeloid leukemia (AML). The patient presented with features of high-risk nephrotic syndrome, including a urinary protein quantification of 8.28 g/24 h and serum albumin level of 29 g/L. The patient showed significant clinical improvement following treatment with moderate-dose glucocorticoids combined with telitacicept. After the treatment process, the urine albumin quantification decreased to 0.23 g/24 h, and serum albumin increased to 45.8 g/L. During the treatment, estimated glomerular filtration rate (eGFR) increased from 67.3 to 79.83 mL/min/1.73m², and immune indicators immunoglobulin A (IgA), immunoglobulin G (IgG) and immunoglobulin M (IgM) also demonstrated steady levels (IgA: 6.78–10.1 g/L, IgG: 0.5–1.41 g/L, IgM: 0.17–0.6 g/L). Notably, the patient’s condition remained stable without any significant adverse effects throughout the rapid tapering of the glucocorticoid dose.Conclusion: This case suggests that telitacicept may be an effective treatment option for IgAN following HSCT, providing valuable insights into future therapeutic strategies for managing post-HSCT IgAN.