Diabetic kidney disease (DKD), a major microvascular complication of diabetes mellitus, has become the second cause of end-stage renal disease enhancing the mortality rate of diabetes. However, there are still few treatment approaches to combat it. Traditional Chinese medicine (TCM) has been applied for a long time to treat DKD. However, there is a lack of research on how does TCM plays the role in treating DKD due to the complex of composition of TCM. In recent decade, gut microbiota is increasingly recognized for its contributions to host health, and the occurrence of gut–kidney axis also attracts many interests about microbiota in kidney injury. Some of the studies have already revealed that TCM can alleviate the symptoms of DKD through regulating gut microbiota and ameliorate a vicious circle caused by imbalance of gut–kidney axis. However, the problems of which specific species mediates the efficacy of TCM and how gut microbiota influences the process of DKD are urgent to solve. Therefore, this review systematically summarized the application of TCM and the importance of gut microbiota in DKD. More importantly, the review provided a new insight to find biomarkers for diagnosis and treatment of DKD. In future study, targeted manipulation of the gut microbiota will be progressively recognized as a way to enhance human health.

Evidence has been furnished that immune cells, and immune-podocytes interactions have increasingly become the focus of proteinuric kidney diseases, which affect millions of patients worldwide. Podocytes are highly specialized, terminally differentiated epithelial cells that wrap around the glomerulus to maintain the integrity of the glomerular filtration barrier. More recent studies demonstrate that podocytes express many elements of the innate and adaptive immune system including the complement components and receptors, through which podocytes can be involved in immune-mediated glomerular injuries and as a therapeutic target to alleviate the podocyte injury and progression to chronic kidney disease. The present review will shed light on recent findings, which have furthered our understanding of the immune mechanisms involved in podocyte injury, as well as the therapeutic implications in the treatment of immune-mediated glomerular injury.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has resulted in an ongoing worldwide pandemic since it was first recognized in December 2019. The kidney is one of the organs most easily affected by COVID-19. The injury of the kidney by COVID-19 manifested as hematuria, proteinuria, serum creatinine fluctuations, and even acute kidney injury (AKI). Critically ill patients with COVID-19 are much more prone to suffer from AKI. Moreover, AKI is related to poor outcomes in the patients infected with SARS-CoV-2. Therefore, early detection and active prevention of kidney injury are very important. In this article, we reviewed the epidemiology, clinical characteristics, pathogenesis, pathological manifestations, treatment, and prognosis of kidney injury in patients with COVID-19. It is expected to provide valuable insights for disease prevention and control from the perspective of nephrologists.

Membranoproliferative glomerulonephritis (MPGN) is usually characterized by refractory nephrotic syndrome and is associated with a poor prognosis. An older patient diagnosed with MPGN had a 20-year history of proteinuria and had clinical manifestations of nephrotic syndrome in the past 2 years. MPGN. Before the patients received an 11-month traditional Chinese medicine (TCM) treatment, the patient was treated with prednisone, tacrolimus, mycophenolate mofetil, and rituximab for 11 months. After 22 months, the urine protein level decreased to <1 g/d, with normal plasma albumin level, and remarkably increased glomerular filtration rate. Combination of TCM with Western medicine for 22 months was effective for the treatment of MPGN.

Background and Objective: The traditional Chinese Tangshen formula (TSF) has been reported to ameliorate diabetic kidney disease (DKD) in humans and animals. However, the effect of TSF on renal fibrosis remains unclear. Transforming growth factor-β1 (TGF-β1)/Smad3 signaling and lncRNA MEG3 are important in renal fibrosis. In this study, we examined the therapeutic effect of TSF on renal fibrosis and explored whether it was related to the modulation of TGFβ1/Smad3 signaling and lncRNA MEG3 expression. Materials and Methods: Experiments were performed in rats in vivo and in the HK2 cells in vitro. DKD was induced in rats by uninephrectomy combined with a single streptozotocin injection. The HK2 cells were stimulated by high glucose (HG) to explore the mechanism of TSF effects in vitro. Results: TSF significantly attenuated renal injury by lowering proteinuria and renal histological damage in DKD rats. TSF reduced collagen deposition by decreasing the expression of the fibrotic indicators collagen I, collagen IV, and fibronectin at the protein and mRNA levels, which suggested that TSF ameliorated DKD by decreasing renal fibrosis. Furthermore, TSF decreased TGF-β1 expression and suppressed the levels of phosphorylated Smad3 and Smad2/3 in vivo. Moreover, TSF downregulated the lncRNA MEG3 level in DKD rats. TSF reversed the upregulation of collagen I and fibronectin expression and downregulated Smad2/3 phosphorylation in the HK2 cells stimulated with HG. Conclusions: TSF ameliorates renal fibrosis in rats with DKD by suppressing TGF-β1/Smad3 signaling and lncRNA MEG3 expression.