Patients affected by chronic kidney disease (CKD) are generally considered to be frailer than those with preserved renal function. We cross-sectionally evaluated the associations between frailty, malnutrition–inflammation syndrome and circulating inflammatory cytokines in 115 older individuals with advanced CKD. As for frailty definition, we adopted Fried’s frailty phenotype (FP), while malnutrition–inflammation syndrome was assessed using the Malnutrition–Inflammation Score (MIS) and circulating inflammatory cytokines (IL-6; TNFα; MCP-1). A total of 48 patients were frail, and mean eGFR was comparable in both frail and non-frail patients (24 ± 10 vs. 25 ± 11 mL/min/1.73 m²; p = 0.63). Frail patients had higher MIS (6 [4–11] vs. 4 [3–5]; p < 0.0001) but cytokine concentrations were comparable in both groups. At multivariate regression, FP was independently associated with MIS, age, gender and pre-albumin but not with cytokines. However, we found some associations between inflammatory cytokines and some specific frailty criteria: weight loss and slowness were associated with MCP-1 (respectively p = 0.049 and p < 0.0001) and weakness with IL-6 (p = 0.005); in conclusion, in older patients with advanced CKD, frailty is strictly associated with malnutrition–inflammation syndrome but not with circulating inflammatory cytokines.

Dietary studies conducted in chronic kidney disease (CKD) patients were focused on the quantities of single nutrients, however it is possible that the excessive attention put on the restriction of proteins, sodium, potassium and phosphorus may compromise the overall quality of the diet in terms of micronutrients and palatability. Instead, concentrating on the nutritional quality healthy dietary patterns, may provide a better approach to improve nutritional prescriptions in CKD patients. All these dietary regimens share common features as reduced content of red meat, salt and saturated fatty acids, and higher fiber content, but may differ in terms of single nutrients consumption. In particular, Mediterranean Diet (Med Diet) has been associated with reduced incidence of diabetes, cardiovascular diseases and obesity, all conditions that are also strictly related to CKD. Given its low content of animal proteins and high contents of fiber it is possible that Med Diet may exert also positive effects on CKD as well as on its metabolic complications. In this review we summarize the role of Med Diet in primary prevention of CKD and on its progression.

Background: In patients with chronic kidney disease (CKD), Fibroblast Growth Factor 23 (FGF23) is markedly increased and has been proposed to interact with systemic inflammation. Methods: In this cross-sectional study, we evaluated the correlations of intact FGF23, c-terminal FGF23, and the FGF23 ratio (c-terminal to intact) with some inflammatory cytokines in 111 elderly patients with advanced CKD not yet in dialysis. Results: Estimated glomerular filtration rate (eGFR) was inversely correlated with intact FGF23 and c-terminal FGF23, as well as with interleukin 6 (IL-6), tumor necrosis factor alpha (TNFα), and monocyte chemoattractant protein-1 (MCP-1). Intact FGF23 levels were directly correlated with IL-6 (r = 0.403; p < 0.001) and TNFα (r = 0.401; p < 0.001) while c-terminal FGF23 was directly correlated with MCP-1 (r = 0.264; p = 0.005). The FGF23 ratio was, instead, inversely correlated with IL-6 (r = −0.326; p < 0.001). Multivariate analysis revealed that intact FGF23 was directly associated with TNFα [B = 0.012 (95% CI 0.006, 0.019); p = 0.003] and c-terminal FGF23 was directly associated with MCP-1 [B = 0.001 (95% CI 0.000, 0.002); p = 0.038], while the FGF23 ratio was inversely correlated with IL-6 [B = −0.028 (95% CI −0.047, −0.010); p = 0.002]. Conclusions: Our data demonstrate that, in CKD patients, intact FGF23 and the metabolites deriving from its proteolytic cleavage are differently associated with some inflammatory pathways. In particular, intact FGF23 is mainly associated with IL-6 and TNFα, c-terminal FGF23 with MCP-1, and the FGF23 ratio with IL6.

IgA Nephropathy (IgAN) and Membranous Nephropathy (MN) are primary immune-mediated glomerular diseases with highly variable prognosis. Current guidelines recommend that greater immunologic activity and worse prognosis should guide towards the best treatment in an individualized approach. Nevertheless, proteinuria and glomerular filtration rate, the current gold standards for prognosis assessment and treatment guidance in primary glomerular diseases, may be altered with chronic damage and nephron scarring, conditions that are not related to immune activity. In recent years, thanks to the development of new molecular technologies, among them genome-wide genotyping, RNA sequencing techniques, and mass spectrometry, we have witnessed an outstanding improvement in understanding the pathogenesis of IgAN and MN. In addition, recent genome-wide association studies have suggested potential targets for immunomodulating agents, stressing the need for the identification of specific biomarkers of immune activity. In this work, we aim to review current evidence and recent progress, including the more recent use of omics techniques, in the identification of potential biomarkers for immune monitoring in IgAN and MN.

In recent years, advancements in immunosuppressive medications and post-transplant management have led to a significant decrease in acute rejection rates in renal allografts and consequent improvement in short-term graft survival. In contrast, recent data have shown an increased incidence of post-transplant glomerular diseases, which currently represent a leading cause of allograft loss. Although pathogenesis is not fully understood, growing evidence supports the role of inherited and immunological factors and has identified potential pre- and post-transplant predictors. In this review, we illustrate recent advancements in the pathogenesis of post-transplant glomerular disease and the role of risk factors and immunological triggers. In addition, we discuss potential prevention and management strategies.

Lupus nephritis (LN) is seeing more and more enriching immunotherapies, but important unmet needs remain. Here, we discuss how to focus on histologic signs of immunologic activity triggering immunotherapy versus signs of irreversible kidney injury requiring care for CKD. In addition, the correct interpretation of residual proteinuria requires dissecting immunologic activity from glomerular hyperfiltration, e.g ., by repeat biopsy. Despite modern triple immunotherapy, per-protocol biopsies still document irreversible injury to occur in the first year. Immediate inhibition of the complement system may address this unmet need and may even help to ultimately replace early glucocorticoid therapy. We advocate the concept of a clone-directed therapy to sufficiently suppress the autoreactive clones of memory B and T cells inside the lymphoid tissues as well as the long-lived plasma cells in the bone marrow that maintain activity of SLE and drive disease flares. Numerous B-cell and plasma cell–targeting therapies are gradually becoming available, and their parenteral route of application may also avoid oral drug nonadherence. Replacing oral and toxic medications such as steroids, mycophenolate, and calcineurin inhibitors is now a goal for the next decade. Obtaining orphan disease designation for LN would accelerate progress and is supported by latest data on LN prevalence. With these conceptual and management improvements, LN, once “complex” and frequently fatal, may become easy-to-manage as other autoimmune diseases.