Complement system inhibitors are emerging as promising therapies in nephrology, particularly for diseases where complement dysregulation is central to pathogenesis. This review summarizes the role of complement activation in kidney diseases and current evidence supporting complement-targeted treatments. As the complement system can be involved in the pathogenesis of different diseases to varying degrees, several research works have been conducted. These research efforts aim, firstly, to understand the mechanisms and role of complement cascade components in the most prevalent nephrological diseases and, secondly, to explore the potential of complement system inhibitors in these conditions and their possible clinical applications. Clinical trials demonstrate that complement inhibitors are most effective in conditions with significant complement involvement, such as C3 glomerulopathy (C3G), atypical hemolytic uremic syndrome (aHUS), and immune complex membranoproliferative glomerulonephritis (IC-MPGN). These agents show variable benefits in diseases with partial complement activation, including lupus nephritis and ANCA-associated vasculitis, while their role in disorders like diabetic nephropathy and focal–segmental glomerulosclerosis remains limited. Complement inhibition offers a targeted strategy to prevent disease progression and improve outcomes in selected nephrological disorders.

Calcific uremic arteriolopathy, also known as calciphylaxis, is a rare and often fatal condition most commonly occurring in patients with end-stage renal disease (ESRD). It is marked by extensive vascular calcification, resulting in tissue ischemia and the development of distinctive skin lesions. We report the case of a 38-year-old male with ESRD due to polycystic kidney disease, who developed calciphylaxis lesions following total parathyroidectomy (PTx). We also performed an electronic search of PubMed and Google Scholar from inception until December 2024, using the following keywords: ‘chronic kidney disease’, ‘dialysis’, ‘calciphylaxis’, ‘calcific uremic arteriolopathy’, ‘secondary hyperparathyroidism’, and ‘parathyroidectomy’. A literature review of calciphylaxis cases following PTx in chronic kidney disease (CKD) patients identified 14 cases reported up to the manuscript’s writing. Although PTx can be a treatment option for calciphylaxis related to severe secondary hyperparathyroidism (SHPT), leading to clinical improvement in some patients, there are atypical calciphylaxis cases occurring after PTx. While the mechanism is not fully understood, the sudden reduction in parathormone (PTH) levels leading to hypocalcemia and decreased bone turnover, together with an increased calcium loading in a patient at risk for abnormal mineralization, may promote vascular and soft tissue calcification. However, the long-term impact of severe SHPT with a delayed post-PTx manifestation cannot be ruled out. Clinicians should consider calciphylaxis in CKD patients with new painful skin lesions. Skin biopsy remains controversial, but a thorough clinical examination, and, in some cases, imaging are essential for a correct diagnosis. A multidisciplinary, personalized approach is crucial, with careful management of post-PTx hypocalcemia and calcium supplementation. Further research is needed to enhance understanding and treatment strategies.

Background and hypothesis. Mortality in hemodialysis (HD) remains high and cannot be entirely clarified by tradi-tional risk factors. The interplay between arterial stiffness, cardiac remodeling, and biomarker activation, such as galectin-3 and NT-proBNP, may be a potential driver of adverse outcomes in this setting. Combining biomarker profiling with NT-proBNP and galectin-3 may improve risk stratification. Methods. This was an observational study of 173 stable, asymptomatic HD patients, followed for more than 10 years. Patients were classified into four groups based on baseline NT-proBNP and galectin-3 medians (4,234 pg/mL and 28.1 ng/mL, respectively). Pri-mary outcomes were all-cause mortality, major cardiovascular events (MACE), and an exploratory outcome: all-cause mortality stratified by pulse wave velocity (PWV). Results. The overall mortality rate was 76.9% in our cohort: 21.1% died from cardiovascular causes, 21.1% from sepsis, and 22.6% of patients died from other causes. 31.6% of pa-tients were coded as sudden death. High NT-proBNP (Groups 3–4) was associated with the poorest survival (adjusted HR 2.58 and 1.93 vs. Group 1, p< 0.05). Age and PVW were independently associated with higher mortality risk. Each one-year increase in age was associated with a 4% higher risk of death, and each 1m/s increase in PVW corresponded to a 6% increase in mortality risk. MACE occurred in 26.8% and did not differ among biomarker groups. Conclusion. In this long-term HD cohort, biomarker profiles that included high NT-proBNP, pre-dicted all-cause mortality. Raised PWV further augmented risk, underlying the inter-play between cardiac stretch and vascular stiffness.

This article explores the multifaceted role of micro-ribonucleic acids (RNAs) (miRNAs) as critical posttranscriptional regulators in renal physiology and disease, with a focus on their emerging significance in glomerulopathies. miRNAs, small endogenous noncoding RNAs, modulate gene expression by promoting messenger RNA degradation or inhibiting translation, thereby orchestrating essential cellular processes such as proliferation, differentiation, apoptosis, and stress responses. Recent advances have revealed that aberrant miRNA expression profiles are intricately linked to the pathogenesis and progression of various renal diseases, including acute kidney injury, chronic kidney disease, alloimmune injury in solid organ transplantation and glomerulonephritis. This review summarizes the pathogenic and protective roles of miRNAs in major glomerulopathies, discusses their potential as diagnostic and prognostic biomarkers, and outlines future directions for their integration into personalized therapeutic strategies. At the moment, it is not fully established whether some of these mechanisms are the primary pathogenic driver or a secondary response. Combining miRNAs with other molecular markers may further enhance diagnostic and predictive accuracy, facilitating clinical translation, while selective targeting of specific miRNAs at different stages of disease progression could offer promising therapeutic opportunities.