Aims: Mutation of the KRAS gene predicts the clinical response to the monoclonal antibody cetuximab in patients with advanced colorectal cancer (CRC). This study aimed to perform KRAS mutation detection on formalin-fixed paraffin-embedded (FFPE) tumour tissue by two different methods for comparison. Methods: The FFPE sample was microdissected to enrich for tumour cells. KRAS exon 2 mutations were performed on 100 Chinese patients with CRC by direct nucleotide sequencing and high-resolution melting (HRM) analysis. Results: KRAS exon 2 mutations were detected in a total of 62 patients with the two methods combined, comprising 11 different mutant alleles. Three common mutations p.Gly12Asp, p.Gly12Val and p.Gly13Asp accounted for approximately 70% of all cases. The concordant rate between the two methods was 95%. Four mutations not initially detected by direct sequencing were identified by HRM and confirmed by sequencing of the HRM amplicons. One mutation detected by direct sequencing was inadvertently grouped as a wild-type allele by HRM software, but this was readily rectified through manual review. Conclusion: HRM analysis is a sensitive method of detecting KRAS mutation on FFPE tumour tissue to guide cetuximab treatment and is applicable to routine molecular diagnostic service. Utilisation of HRM to screen for mutations upfront economises the resource used in the sequencing reaction.

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide. Recently, there have been multiple advances in the understanding of IgAN pathophysiology and therapeutic options. Despite the advent of new treatment options, individual risk stratification of the disease course and choosing the best treatment strategy for the patient remains challenging. A multitude of clinical trials is ongoing, opening multiple opportunities for enrollment. In this brief review we discuss the current approach to the management of IgAN and highlight the ongoing clinical trials.

IgA nephropathy (IgAN) is characterized by the deposition of poorly-O-galactosylated IgA1 (also referred to as galactose-deficient IgA1 or gd-IgA1) containing immune complexes in the glomerular mesangium. This triggers a variable degree of glomerular inflammation that leads to progressive kidney damage and often kidney failure. The acceptance of proteinuria reduction as a reasonably likely surrogate end point for treatment effects on progression to kidney failure has led to many clinical trials evaluating novel and repurposed therapies for IgAN. New treatments leverage different aspects of IgAN pathophysiology, including the modulation of mucosal immunity, mechanisms of B-cell activation, and complement activity. The approval of the first treatments evaluated specifically for IgAN (including delayed-release budesonide, sparsentan, atrasentan, and iptacopan) represent meaningful advancements in the management landscape, and promisingly, many more treatments seem poised to arrive. This review compiles a list of current active trials for IgAN and highlights the necessity for ongoing research to optimize therapeutic strategies to further improve outcomes for those living with IgAN.

Lupus nephritis (LN), a severe complication of systemic lupus erythematosus (SLE), leads to significant kidney inflammation and damage and drastically increases mortality risk. Predominantly impacting women in their reproductive years, LN poses specific risks during pregnancy, including pre-eclampsia, growth restrictions, stillbirth, and preterm delivery, exacerbated by lupus activity, specific antibodies, and pre-existing conditions like hypertension. Effective management of LN during pregnancy is crucial and involves carefully balancing disease control with the safety of the fetus. This includes pre-conception counseling and a multidisciplinary approach among specialists to navigate the complexities LN patients face during pregnancy, such as distinguishing LN flare-ups from pregnancy-induced conditions. This review focuses on exploring the complex dynamics between pregnancy and LN, emphasizing the management difficulties and the heightened risks pregnant women with LN encounter.

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder marked by the development of cysts in the kidneys and other organs, leading to diverse clinical manifestations, including kidney failure. The psychological burden of ADPKD is substantial, with significant contributors including pain, daily life disruptions, depression, anxiety, and the guilt associated with transmitting ADPKD to offspring. This review details the psychological impacts of ADPKD on patients, addressing how they navigate physical and emotional challenges, including pain management, genetic guilt, mood disorders, and disease acceptance. This review also underscores the need for comprehensive research into the psychological aspects of ADPKD, focusing on the prevalence and contributing factors of emotional distress and identifying effective strategies for managing anxiety and depression. Furthermore, it highlights the importance of understanding the diverse factors that influence patients' quality of life and advocates for holistic interventions to address these psychological challenges.

Background: Acute Kidney Injury (AKI) is a common and critical condition associated with significant morbidity and mortality across various patient populations. The recovery process following AKI is complex and involves a multitude of biological, clinical, and environmental factors. Despite considerable research, there remains substantial debate regarding the exact role and significance of these factors, as well as how they interact with one another. Summary: This systematic review aims to examine the currently available evidence on the key factors influencing AKI recovery. We hope to offer a clearer understanding of the complex dynamics in AKI recovery, including where current evidence remains inconclusive or contradictory. Key Messages: This review will provide valuable insights for clinicians and researchers aiming to improve treatment strategies and patient outcomes in AKI recovery.