French Guiana ranks among the French overseas territories with the highest prevalence of systemic lupus erythematosus (SLE). However, local data on lupus flares and renal involvement remain limited. This study aimed to determine the frequency of lupus flares and identify associated factors among patients with lupus nephritis (LN) compared with those without renal involvement. We conducted an observational historical cohort study using data from the West Guyanese lupus cohort between January 2018 and December 2022. Patients with confirmed SLE were consecutively included and classified according to the presence or absence of LN. Clinical, biological, and immunological data were extracted from medical records. Lupus flare was defined as documented disease worsening requiring therapeutic intensification. Factors associated with flares were assessed using multivariable logistic regression. Sixty-two patients were included, of whom 45 (72.6%) had LN. Overall, 53% experienced at least one flare. Flares occurred more frequently in patients with LN than in those without LN (62.2% vs. 29.4%). Higher anti-dsDNA and anti-Smith antibody levels, higher SLEDAI scores, fever, pleural effusion, and cutaneous manifestations were significantly associated with flares. In multivariable analysis, LN (OR 3.64; 95% CI 1.00–13.23; p=0.049) and higher anti-dsDNA antibody levels (p=0.033) were independently associated with flares. Lupus flares were frequent and occurred more often in patients with LN. LN and higher anti-dsDNA antibody levels were independently associated with flares, supporting close monitoring of patients with renal involvement to identify disease activity and optimize management.
Irwing R. Benites-Flores, Javier Rodríguez Revilla, Alvaro Taype-Rondan, Liliana C. Fernández-Anticona, Pedro Augusto Prado Ramírez, Nelly Seminario Alegre, Celia Rodríguez Tudero, Esperanza Moral Berrio, Elena Jimenez Mayor, Avinash Chandu Nanwani, José C. De la Flor
Accurate volume assessment in maintenance hemodialysis remains challenging because no single bedside method fully characterizes extracellular fluid overload. We evaluated discordance among clinical examination, bioimpedance spectroscopy, and abbreviated six-zone lung ultrasound, the prevalence of subclinical pulmonary congestion, and factors associated with pulmonary congestion. In this single-center cross-sectional study, 116 adults receiving maintenance hemodialysis without clinically recognized heart failure underwent standardized clinical examination, whole-body bioimpedance spectroscopy, and predialysis six-zone lung ultrasound. Subclinical pulmonary congestion was defined as a prespecified total B-line count of ≥3 in clinically euvolemic patients. Agreement was assessed using Cohen’s kappa, and independent associations were evaluated using multivariable Poisson regression. Among 49 clinically euvolemic patients, 27 (55.1%) had subclinical pulmonary congestion, representing 23.3% of the cohort. Clinical examination showed fair agreement with lung ultrasound for ≥3 B-lines (κ = 0.28; 95% CI, 0.11–0.45), whereas agreement between lung ultrasound and bioimpedance-defined overhydration was slight (κ = 0.16; 95% CI, −0.03 to 0.35). Bioimpedance-derived overhydration, but not interdialytic weight gain, was independently associated with subclinical pulmonary congestion. Discordance among clinical examination, bioimpedance spectroscopy, and lung ultrasound was common and is consistent with the hypothesis that these modalities capture partially distinct aspects of volume status and pulmonary congestion. Abbreviated lung ultrasound frequently identified clinically occult pulmonary congestion despite apparent clinical euvolemia, supporting a multidimensional approach to bedside volume assessment in maintenance hemodialysis.
Leonardo A. Sechi, Luca Bulfone, Antonio Vacca, Jacopo Comand, Stefano Marcante, Gabriele Brosolo, Claudio Pagano, Cristiana Catena
Epidemiological evidence demonstrates that atherosclerotic cardiovascular disease (ASCVD) is a major cause of death and disability in patients with chronic kidney disease (CKD). From the early stages of CKD, and in addition to specifically related conditions, the coexistence of traditional risk factors contributes to a process of accelerated atherosclerosis. In patients with CKD, increased cardiovascular risk persists even after correction of hypertension, dyslipidemia, and diabetes, indicating a residual risk likely related to additional subtle factors. Lipoprotein(a) [Lp(a)] is an LDL-like particle containing apoB100 covalently linked to apo(a) and is now recognized as a genetically determined risk factor for ASCVD. Following its initial description, Lp(a) aroused extraordinary interest, which then waned in the late-1990s due to the controversial results of some prospective studies and the lack of effective interventions to reduce its circulating levels. Over the past two decades, clinical studies have provided robust evidence supporting the causal and independent contribution of Lp(a) to ASCVD, also suggesting a significant contribution to residual cardiovascular risk. This contribution may be particularly significant in patients with CKD, who exhibit elevated Lp(a) levels from the earliest stages of disease. The recent development of potent Lp(a)-lowering drugs offers an exciting opportunity to effectively address residual risk in the general population and in patients with CKD. No data are yet available on their use in patients with CKD but pending future definition of their efficacy on cardiovascular outcomes, approval, dosing, and long-term safety, these drugs might possibly represent a useful tool for cardiovascular prevention in these patients.
Kidney disease is a major global public health challenge. The pathological mechanisms linking chronic kidney disease (CKD) and age-related kidney function decline are complex. Cellular senescence and its senescence-associated secretory phenotype (SASP) act as key links between kidney aging and disease progression. Although publications in this field have surged, a systematic bibliometric analysis is needed to outline its knowledge framework, research hotspots, and future trends. This study aims to quantitatively analyze global publication trends, core contributors (countries, institutions, journals, and authors), and cooperation networks to map the dynamic evolution of this field. We conducted a comprehensive literature search across both the Web of Science Core Collection (WoSCC) and Scopus databases to retrieve original articles and reviews concerning cellular senescence and kidney aging published between 2000 and 2025. After merging the datasets and removing duplicates, a meticulous bibliometric analysis was executed using Excel 365, CiteSpace, VOSviewer, and Bibliometrix (an R package) to map the knowledge framework and cooperation networks. This analysis included 2,191 relevant papers involving 16,545 researchers. The overall publication volume showed significant growth, reaching a peak in 2025. The United States leads the field with the most publications and the highest citation frequency. China ranks second in publications but fourth in citations, reflecting a gap in research quality. The collaboration network indicates that the United States is the core node, maintaining close ties with countries like China and Germany. The American Journal of Physiology-Renal Physiology ranked first in publication volume, while the Journal of the American Society of Nephrology achieved the highest citation frequency. Xiang-Mei Chen and Anette Melk were identified as core contributing scholars. Keyword analysis established “aging” (825 times) and “cellular senescence” (330 times) as the central concepts. Emerging topics such as “machine learning,” “ferroptosis,” and “Mendelian randomization” are rapidly rising as research hotspots. This study maps the evolutionary trends of research on cellular senescence and related kidney diseases, identifying current frontiers and providing data to support future research. The rise of concepts like machine learning, ferroptosis, and Mendelian randomization marks a deep shift in the research paradigm, offering new perspectives for future scientific exploration.
Light chain (AL) amyloidosis is typically associated with plasma cell dyscrasias but can rarely arise from low-grade B-cell non-Hodgkin lymphoma. Renal involvement may present with nephrotic-range proteinuria, acute kidney injury, edema, anasarca, and hypoalbuminemia. Recognizing lymphoma-associated AL amyloidosis is essential because diagnosis requires tissue confirmation, and treatment must target the underlying clonal B-cell disorder. We report a rare case of severe renal AL amyloidosis in a patient with known low-grade B-cell non-Hodgkin lymphoma previously treated with rituximab. The patient presented with witnessed syncope, progressive peripheral edema, anasarca, and hypotension. Initial evaluation showed acute kidney injury with nephrotic-range proteinuria, including a urine protein-to-creatinine ratio greater than 10 g/g. Workup for autoimmune, infectious, and malignant causes of proteinuric kidney disease revealed positive hepatitis C antibody, mildly elevated serum lambda free light chains, a mildly decreased kappa-to-lambda ratio, and serum immunofixation positive for an IgM monoclonal lambda gammopathy. Renal biopsy demonstrated severe AL amyloidosis with predominant renal involvement. Bone marrow biopsy showed low-grade B-cell non-Hodgkin lymphoma involving 85% of the marrow, with CD20-positive immunophenotyping. This case highlights a rare presentation of renal AL amyloidosis secondary to low-grade B-cell non-Hodgkin lymphoma. Persistent nephrotic-range proteinuria in patients with B-cell lymphoma, particularly with IgM lambda monoclonal gammopathy, should prompt evaluation for amyloidosis with renal biopsy and hematologic assessment.
