Renal injury, a prevalent clinical outcome with multifactorial etiology, imposes a substantial burden on society. Currently, there remains a lack of effective management and treatments. Extensive research has emphasized the diverse biological effects of natural polysaccharides, which exhibit promising potential for mitigating renal damage. This review commences with the pathogenesis of four common renal diseases and the shared mechanisms underlying renal injury. The renoprotective roles of polysaccharides in vivo and in vitro are summarized in the following five aspects: anti-oxidative stress effects, anti-apoptotic effects, anti-inflammatory effects, anti-fibrotic effects, and gut modulatory effects. Furthermore, we explore the structure-activity relationship and bioavailability of polysaccharides in relation to renal injury, as well as investigate their utility as biomaterials for alleviating renal injury. The clinical experiments of polysaccharides applied to patients with chronic kidney disease are also reviewed. Broadly, this review provides a comprehensive perspective on the research direction of natural polysaccharides in the context of renal injury, with the primary aim to serve as a reference for the clinical development of polysaccharides as pharmaceuticals and prebiotics for the treatment of kidney diseases.

Rationale: Multiorgan/system injury was observed in severely infected coronavirus disease 2019 (COVID-19) patients, in addition to viral pneumonia. Recognizing and correcting the key and immediate dysfunctions may reduce mortality. Patient concerns: A 66-year-old previously healthy male patient was referred to the isolation ward in Guanggu Branch of Hubei Province Maternity and Childcare Hospital with a high fever and nonproductive cough for twenty days. Diagnoses: Diagnosis of severe COVID-19 infectious pneumonia was established by travel history, clinical features, chest imaging, and a positive oropharyngeal swab specimen result for the severe acute respiratory syndrome coronavirus 2 RT-PCR assay. Interventions: In addition to standard supportive care, combined inflammatory cytokine depletion therapy (double filtration plasma pheresis and tocilizumab) and convalescent plasma were administered. Outcomes: The patient's homeostatic parameters (blood pressure, heart rate, spontaneous respiration, SPO2, and blood gas) recovered, along with the recovery on chest imaging. All the intravenous catheters were removed. Supportive care continued for several days, and the patient was transferred to a non-ICU isolation ward. Lessons: It is not safe to draw causal conclusions between cytokine depletion and clinical manifestation improvement with only 1 case, but this is a potential research direction in facing the COVID-19 crisis.

Fibroblast Growth Factor 23 (FGF23) is a bone-derived hormone regulating phosphate and vitamin D metabolism, now recognized as a dynamic biomarker across acute and chronic kidney disorders. Elevated FGF23 is a hallmark of chronic kidney disease (CKD), but also rises acutely in acute kidney injury (AKI) and appears disproportionately high in autosomal dominant polycystic kidney disease (ADPKD), underscoring condition-specific regulation. This review explores the correlation and heterogeneity of FGF23 expression in AKI, CKD, and ADPKD, highlighting shared and divergent mechanisms and the diagnostic and therapeutic implications. We summarize FGF23 expression kinetics in each condition, elucidate known and proposed molecular drivers of its elevation, and discuss how FGF23 serves as a unifying yet disease-divergent marker in renal pathology. In AKI, inflammation, ischemia, and acute metabolic stress drive a rapid FGF23 surge, whereas in CKD, phosphate retention and Klotho deficiency promote a sustained, maladaptive FGF23 elevation. ADPKD shows early FGF23 increases independent of glomerular filtration rate (GFR), potentially due to ectopic production (liver and cysts) and unique tubular defects. Clinically, FGF23 has emerged as an indicator of disease severity and outcomes in these contexts: it can signal early AKI and predict progression, is a strong prognostic factor for mortality and cardiovascular complications in CKD, and correlates with cystic disease burden and kidney growth in ADPKD. We also examine FGF23’s systemic effects (notably on cardiovascular remodeling) and potential therapeutic targets, from modulating phosphate balance and iron metabolism to novel interventions in development. Understanding the nuanced regulation of FGF23 across acute injury, chronic degeneration, and genetic kidney disease provides insight into acute-chronic disease intersections and guides precision diagnostics and therapies for improved patient outcomes.

Background: Tislelizumab, a humanized IgG4 anti-PD-1 monoclonal antibody has been approved in China and Europe. According to the published clinical research, tislelizumab shows satisfactory safety profile. No severe hepatotoxicity or acute kidney injury were reported.Case presentation: We presented a case study of a 74-year-old man who developed acute kidney injury (grade 3) and acute liver injury (grade 4) after being administered tislelizumab for the treatment of esophageal squamous cell carcinoma. We reviewed the patient’s history, physical examination, and laboratory findings and provided comprehensive differentials of the possible causes of the toxicities. Immune Checkpoint Inhibitors (ICI) hepatotoxicity and nephrotoxicity were confirmed clinically. We also discussed the management of toxicities associated with ICIs and the need for a multidisciplinary approach to care.Conclusions: The case highlights the importance of close monitoring and prompt management of toxicities associated with ICIs and the need for further research to better understand the risk factors for these toxicities and to identify effective treatments for them.