The nephrotic syndrome holds significant clinical importance and is characterized by a substantial protein loss in the urine. Damage to the glomerular basement membrane or podocytes frequently underlies renal protein loss. There is an increasing belief in the involvement of the complement system, a part of the innate immune system, in these conditions. Understanding the interactions between the complement system and glomerular structures continually evolves, challenging the traditional view of the blood–urine barrier as a passive filter. Clinical studies suggest that a precise inhibition of the complement system at various points may soon become feasible. However, a thorough understanding of current knowledge is imperative for planning future therapies in nephrotic glomerular diseases such as membranous glomerulopathy, membranoproliferative glomerulonephritis, lupus nephritis, focal segmental glomerulosclerosis, and minimal change disease. This review provides an overview of the complement system, its interactions with glomerular structures, and insights into specific glomerular diseases exhibiting a nephrotic course. Additionally, we explore new diagnostic tools and future therapeutic approaches.

INTRODUCTION: The exocrine pancreas is an important determinant of the intestinal microbiome composition and stability. Although chronic pancreatitis (CP) is known to severely affect the bacterial community, its impact on the intestinal mycobiome is currently unknown. METHODS: A total of 93 patients with clinical and imaging evidence of CP were prospectively recruited and compared with 2 equally sized matched control cohorts. One control group was matched for age, sex, body mass index, and smoking (Con-1), and the other additionally for exocrine pancreatic function (stool elastase) and diabetes (Con-2). Fecal samples were collected from all 279 individuals to determine the fecal mycobiome by internal transcribed spacer 2 sequencing. RESULTS: In CP patients, fungal reads were increased (3.7-fold and 2.0-fold) as compared with Con-1 and Con-2. In comparison with Con-1, CP patients demonstrated higher total abundance of Candida (4.5-fold, q = 0.009) and higher mean relative abundance (11.4% vs 1.0%, q = 0.014) and presence (25.8% vs 9.7%, q = 0.025) of Nakaseomyces. In contrast to Con-2, CP patients showed higher Candida total abundance (1.9-fold, P = 0.016) which was, however, not significant after correction for multiple testing (q = 0.056). DISCUSSION: Not only the microbiome but also the mycobiome in CP patients is characterized by distinct changes, with higher abundances of Candida or Nakaseomyces. Exocrine pancreatic dysfunction in CP patients likely contributes to this observation. This may result in increased rates of fungal infections, chronic inflammation, and could be contributing to the development of pancreatic cancer.