Chronic kidney disease (CKD) affects many adults worldwide. Persistent low-grade inflammation is a substantial factor in its development and progression and has correlated with increased mortality and cardiovascular problems. This low-grade inflammation is a product of dysregulation of the normal balance between pro- and anti-inflammatory markers. Various factors such as increased innate immune system activation, reactive oxygen species production, periodontal disease, dysregulation of anti-inflammatory systems and intestinal dysbiosis result in the dysregulation of this balance. Furthermore, this low-grade inflammation has down-effects such as hypertension, renal fibrosis and acceleration of renal function decline. Moreover, low-grade inflammation over time has been linked to malignancy in CKD. As CKD progresses, many patients require dialysis, which has a negative bidirectional relationship with persistent inflammation. Treatment options for inflammation in CKD are vast, including cytokine inhibitors, statins and diets. However, more research is needed to create a standardized management plan. In this review, we will examine the normal physiology of the kidney and its relationship with the immune system. We will then delve into the pathology behind persistent inflammation, the various causes of inflammation, the downstream effects of inflammation, dialysis and potential treatments for inflammation in CKD.

Diabetic kidney disease (DKD) is a leading cause of chronic kidney disease and affects approximately 40% of individuals with diabetes . Cases of DKD continue to rise globally as the prevalence of diabetes mellitus increases, with an estimated 415 million people living with diabetes in 2015 and a projected 642 million by 2040. DKD is associated with significant morbidity and mortality, representing 34% and 36% of all chronic kidney disease deaths in men and women, respectively. Common comorbidities including hypertension and ageing-related nephron loss further complicate disease diagnosis and progression. The progression of DKD involves several mechanisms including glomerular endothelial cell dysfunction, inflammation, and fibrosis. Targeting these mechanisms has formed the basis of several therapeutic agents. Renin-angiotensin-aldosterone system (RAAS) blockers, specifically angiotensin receptor blockers (ARBs), demonstrate significant reductions in macroalbuminuria. Sodium-glucose transporter type 2 (SGLT-2) inhibitors demonstrate kidney protection independent of diabetes control while also decreasing the incidence of cardiovascular events. Emerging agents including glucagon-like peptide 1 (GLP-1) agonists, anti-inflammatory agents like bardoxolone, and mineralocorticoid receptor antagonists show promise in mitigating DKD progression. Many novel therapies including monoclonal antibodies CSL346, lixudebart, and tozorakimab; mesenchymal stem/stromal cell infusion; and cannabinoid-1 receptor inverse agonism via INV-202 are currently in clinical trials and present opportunities for further drug development.

Acute kidney injury (AKI), a common and severe complication following burn injuries, presents a significant challenge due to its broad clinical manifestations and diverse etiologies. AKI, previously known as acute renal failure, can present abruptly following burns or thermal injuries, causing detrimental health outcomes such as progressive kidney dysfunction, increased hospital length of stay, and requirement of renal replacement therapy (RRT). AKI affects the maintenance of homeostasis of fluid and electrolytes, elimination of metabolic wastes and byproducts, and acid–base balance. Aggressive nutritional support is particularly necessitated in burn patients to prevent protein-energy wasting and a negative nitrogen balance. Understanding the pathogenesis of AKI in burns and improving its prevention and early diagnosis are active areas of research in this field. Despite the potential benefits, the optimal timing and threshold for RRT initiation in burn patients with AKI remain unclear, warranting further studies. Ongoing investigations focus on refining RRT techniques, evaluating biomarkers for early detection of AKI, and exploring adjunctive therapies to enhance renal recovery. The aim of this study is to review the etiology, diagnostic tools, and interventions that improve outcomes associated with AKI in burn-related settings.

Congenital anomalies of the kidney and urinary tract (CAKUT) represent a broad range of diseases with differing mechanisms, clinical presentations, and prognoses. With an estimated prevalence of between 4 and 60 per 10,000 births, CAKUT represents a sizable number of patients for pediatric and adult nephrologists as therapies have progressed, allowing longer life spans. Many CAKUT disorders are associated with genetic mutations, and with advances in genomic sequencing, these genes are being identified at an increasing rate. Understanding these mutations provides insight into these conditions’ molecular mechanisms and pathophysiology. In this article, we discuss the epidemiology, presentation, and outcomes of CAKUT in addition to our current understanding of genetic and molecular mechanisms in these diseases.

Renal cystic diseases (RCDs) can arise from utero to early adulthood and present with a variety of symptoms including renal, hepatic, and cardiovascular manifestations. It is well known that common RCDs such as autosomal polycystic kidney disease and autosomal recessive kidney disease are linked to genes such as PKD1 and PKHD1, respectively. However, it is important to investigate the genetic pathophysiology of how these gene mutations lead to clinical symptoms and include some of the less-studied RCDs, such as autosomal dominant tubulointerstitial kidney disease, multicystic dysplastic kidney, Zellweger syndrome, calyceal diverticula, and more. We plan to take a thorough look into the genetic involvement and clinical sequalae of a number of RCDs with the goal of helping to guide diagnosis, counseling, and treatment.