Search Results (2,597)

Background/Objectives: Leukocyte telomere length (TL) is a marker of biological aging associated with cardiovascular disease, chronic kidney disease, and malignancy in the general population. Its long-term prognostic significance in systemic lupus erythematosus (SLE) remains unclear. We aimed to evaluate the association between baseline TL and long-term clinical outcomes in patients with SLE. Methods: Prospective cohort study including 97 Caucasian women with SLE. Relative TL was measured in whole blood using quantitative polymerase chain reaction (qPCR) at baseline. A control group of 50 healthy Caucasian women from the same geographical region was included for comparison. Patients were followed for a mean of 9.7 ± 2.8 years. Outcomes included thrombotic cardiovascular events, damage accrual, incident malignancy, and chronic kidney disease. Associations were assessed using multivariable regression models adjusted for potential confounders. Results: Mean age was 51.6 ± 13.8 years and mean relative TL was 4.3 ± 1.0. Relative TL was inversely associated with age (β = −0.20, p = 0.048) and was shorter in patients with hematological manifestations (p = 0.038). No differences in relative TL were observed between SLE patients and controls. Relative TL was not associated with disease activity, cumulative damage, cardiovascular risk factors, vitamin D levels, or subclinical atherosclerosis. During follow-up, 13.4% of patients experienced cardiovascular events, 10.3% developed malignancy, and 11.3% developed chronic kidney disease. Relative TL was initially associated with long-term damage accrual, glomerular filtration rate and cardiovascular events; however, after adjustment for age, only the association with glomerular filtration rate remained at the limit of statistical significance (p = 0.05). Conclusions: In this prospective cohort, relative TL was primarily associated with aging, hematological manifestations, and glomerular filtration rate, but not with disease activity or most long-term clinical outcomes. These findings suggest that TL reflects biological aging rather than disease-specific processes and has limited utility as a prognostic biomarker in SLE. Full article

Associated with high morbidity and mortality, cisplatin-induced acute kidney injury (AKI) is a common clinical complication characterized by oxidative stress, inflammation, and mitochondria-associated signaling. Although multiple signaling pathways have been implicated in AKI progression, effective interventions targeting these complex mechanisms are still lacking. As a medicinal fungus with antioxidant and anti-inflammatory properties, Schizophyllum commune (SC) has shown potential biological activities; however, its renoprotective effects in cisplatin-induced AKI remain unclear. Therefore, this study aimed to investigate SC’s protective effects and underlying mechanisms in a cisplatin-induced AKI mouse model. SC treatment improved renal function and attenuated histopathological damage. It reduced oxidative stress and inflammatory responses, as evidenced by the modulation of malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), and pro-inflammatory cytokines. Mechanistically, SC regulated multiple signaling pathways, including mitogen-activated protein kinase (MAPK), toll-like receptor 4/nuclear factor kappa B (TLR4/ NF-κB), PI3K/AKT, nuclear factor erythroid 2–related factor 2/heme oxygenase-1 (Nrf2/HO-1), and the calcium/calmodulin-dependent protein kinase kinase–AMP-activated protein kinase–sirtuin 1 (CaMKK–AMPK–Sirt1) axis. In addition, SC modulated apoptosis, autophagy, and PTEN-induced kinase 1 (PINK1)/Parkin-mediated mitophagy, suggesting improved mitochondrial homeostasis. These findings indicate that SC exerts renoprotective effects and may contribute to cisplatin-induced nephrotoxicity mitigation strategies. Full article

Background and Clinical Significance: IgG4-related disease (IgG4-RD) is a chronic fibroinflammatory, immune-mediated multisystem disorder that can mimic neoplastic, infectious, or autoimmune conditions. Among its head-and-neck manifestations, IgG4-related dacryoadenitis and sialadenitis, historically referred to as Mikulicz disease, should be distinguished from the classical Mikulicz syndrome, which describes secondary lacrimal and salivary gland enlargement due to other systemic disorders. Renal involvement, most commonly in the form of IgG4-related tubulointerstitial nephritis (IgG4-TIN), is less frequent but carries major prognostic implications because delayed diagnosis may lead to irreversible kidney damage. Case Presentation: A 49-year-old man with no relevant past medical history presented with a 2-year history of intermittent polyuria and foamy urine. Laboratory testing revealed advanced kidney dysfunction, with serum creatinine of 4.2 mg/dL, estimated glomerular filtration rate of 16 mL/min/1.73 m², and proteinuria of 2874 mg/day. Physical examination showed bilateral parotid enlargement, upper eyelid edema, lacrimal gland enlargement, and sicca symptoms, raising suspicion for IgG4-related dacryoadenitis and sialadenitis (Mikulicz disease). Further work-up demonstrated marked eosinophilia, polyclonal hypergammaglobulinemia, and significantly elevated serum IgG4 levels (3180 mg/dL), while infectious serologies and autoimmune studies were negative. Kidney biopsy revealed plasma cell-rich tubulointerstitial nephritis with lymphoplasmacytic and eosinophilic infiltrates, interstitial fibrosis, tubular atrophy, and more than 40 IgG4-positive plasma cells per high-power field, supporting the diagnosis of IgG4-related tubulointerstitial nephritis in the setting of systemic IgG4-RD. Treatment with prednisone followed by mycophenolate mofetil led to improvement in glandular manifestations and a partial reduction in proteinuria, but renal recovery remained incomplete. The patient subsequently developed a severe pulmonary infection complicated by sepsis and oligoanuric acute kidney injury superimposed on chronic kidney disease, and ultimately progressed to end-stage kidney disease requiring chronic maintenance hemodialysis. Conclusions: This case highlights that a Mikulicz disease phenotype may represent the initial manifestation of systemic IgG4-RD and should prompt evaluation for extraglandular involvement, particularly renal disease. In patients with glandular enlargement, eosinophilia, hypergammaglobulinemia, and unexplained renal dysfunction, IgG4-RD should be actively considered. Kidney biopsy remains essential for diagnostic confirmation and prognostic assessment, as delayed recognition may result in irreversible renal damage and progression to end-stage kidney disease. Full article

Acute kidney injury (AKI) caused by ischemia–reperfusion injury (IRI) involves rapid activation of innate immune responses, in which myeloid-derived immune cells critically shape injury severity. Y-box binding protein 1 (YB-1) regulates pro-inflammatory gene expression intracellularly and can be secreted to function extracellularly, yet how these two compartments jointly influence early IRI pathology remains poorly understood. To dissect the roles of intracellular myeloid versus extracellular YB-1, we subjected myeloid-specific Ybx1 knockout, Ybx1^fl/fl × LysM^cre, mice and wild-type (WT) littermates to unilateral renal IRI following administration of either a neutralizing anti-YB-1 antibody or control IgG. Kidney injury, inflammation, immune cell recruitment, neutrophil extracellular trap (NET) formation, antibody localization, and Fcγ receptor expression were assessed by qRT-PCR, histology, immunostaining, Western blotting, and flow cytometry. Myeloid-specific knockout of Ybx1 markedly reduced renal inflammation, neutrophil infiltration, NET formation, and tubular injury. This protective phenotype was lost when extracellular YB-1 was simultaneously reduced: anti-YB-1 treatment in knockout mice restored pro-inflammatory cytokine expression, increased tubular damage markers such as NGAL and KIM-1, exacerbated neutrophil recruitment and NET formation, and led to luminar accumulation of YB-1/anti-YB-1 immune complexes in tubular cells. Mechanistically, Ybx1-deficient myeloid cells exhibited significantly reduced CD16 expression, pointing to impaired Fcγ receptor-mediated phagocytosis as the cause of defective immune complex clearance. In contrast, wild-type mice efficiently cleared extracellular YB-1 complexes and showed no injury aggravation upon antibody treatment. Our findings identify myeloid YB-1 as a central regulator of early inflammatory injury in renal IRI and reveal that its protective depletion becomes pathogenic when extracellular YB-1 is simultaneously neutralized, likely due to unmasked defects in immune complex clearance. Full article

Mycotoxins are toxic secondary metabolites produced by filamentous fungi, which extensively contaminate agricultural products such as grains and nuts. Common mycotoxins, including aflatoxin B1, ochratoxin A, and deoxynivalenol, can induce liver cancer, kidney damage, neural tube defects, and immune suppression, necessitating highly sensitive detection methods to ensure food safety. Conventional techniques are limited by complex procedures and insufficient sensitivity. Electrochemiluminescence (ECL), owing to its high sensitivity, low background signal, and rapid response, has emerged as a promising strategy for mycotoxin analysis. In this context, metal–organic frameworks (MOFs), with their high surface area and tunable structures, have been widely employed in ECL sensors to improve sensing performance. This review summarizes the construction strategies of MOF-based ECL sensors, the diverse functional roles of MOFs in ECL sensing, the associated sensing mechanisms, and the applications of these sensors for the detection of mycotoxins in food. Current challenges, including material stability, sensor reproducibility, and practical applicability, are discussed, and future directions are outlined. Particular emphasis is placed on the development of stable MOF materials, their integration into portable and intelligent ECL sensing platforms, and the establishment of standardized and scalable production methods to enable practical food safety monitoring. Full article

Mori Cortex Radicis (MCR), which is abundant in resources and low in cost, is a Chinese herbal medicine with antitussive, anti-inflammatory, analgesic, and hypoglycemic effects; however, its application in the prevention and control of aquatic pathogens remains understudied. In this study, a MCR water extract (MCR-WE) was prepared, and its contents of polysaccharides, polyphenols, and proteins were found to be 0.63%, 1.17%, and 2.79%, respectively. LC-MS metabolomics revealed that L(+)-Arginine, 9,12,13-Todea, Citric acid, 1-Deoxynojirimycin, and 4-Guanidinobutanoic acid were the most abundant compounds. Subsequently, by feeding the MCR-WE to crucian carp (Carassius auratus) and challenging them with Aeromonas veronii, it was found that the MCR-WE enhanced the activities of immune factors (AKP, ACP, LZM) and the phagocytic activity of leukocytes (p < 0.05). Furthermore, the MCR-WE improved the survival rate of crucian carp (p < 0.05), reduced the bacterial load in the kidneys (p < 0.05), decreased the mRNA expression of inflammatory factors (IL-6, IL-1β, TNF-α), and lowered the expression levels of antioxidant-related factors (CAT, GSH-Px, SOD, MDA) and the mRNAs of oxidative stress pathway factors (Nrf2, HO-1, Keap1) (p < 0.05). Histopathological sections and immunofluorescence assays showed that the MCR-WE maintained the structural integrity of internal organs and reduced renal cell apoptosis and DNA damage. Therefore, MCR-WE is rich in immunologically active substances, can activate the immune response of crucian carp, reduce fish mortality, exert anti-inflammatory and antioxidant activities, and maintain the structural and functional integrity of internal organs. Thus, the MCR-WE holds promise as a therapeutic agent against A. veronii infection in fish. Full article

Objective: This study aimed to develop an oral celastrol-loaded self-microemulsifying drug delivery system (Cel-SMEDDS) to enhance the therapeutic efficacy against rheumatoid arthritis and reduce toxicity. Methods: The optimal Cel-SMEDDS formulation, identified through solubility screening, excipient compatibility assays, and pseudo-ternary phase diagram analysis, was characterized by particle size, PDI, zeta potential, in vitro release, and stability. In vitro anti-inflammatory activity was evaluated in LPS-induced RAW264.7 macrophages, while in vivo anti-RA efficacy was assessed in CIA mice via paw swelling, clinical scoring, serum TNF-α, and joint histopathology. Preliminary safety was examined by hematological, serum biochemical, and histopathological analyses in mice. Results: The optimal Cel-SMEDDS formulation consisted of LABRAFIL M 1944 CS-Kolliphor RH40-CAPRYOL 90 (0.2:0.48:0.32, w/w/w) with a drug loading of 1.5% (w/w). It spontaneously formed uniform microemulsions with a mean particle size of 26.70 nm, PDI of 0.067, and zeta potential of −2.87 mV. In vitro, Cel-SMEDDS showed enhanced cytotoxicity against M1-type macrophages (IC₅₀ = 0.1753 μg/mL vs. 0.2684 μg/mL for free Cel), significantly suppressed pro-inflammatory TNF-α and IL-1β expression, and upregulated anti-inflammatory IL-10. In CIA mice, oral Cel-SMEDDS reduced paw swelling by 37.42% (vs. 22.79% for free Cel), markedly decreased serum and intra-articular TNF-α levels, and alleviated articular cartilage damage. Preliminary safety evaluation demonstrated no significant abnormalities in hematological parameters, liver/kidney function, or major organ histology. Conclusions: The optimized oral Cel-SMEDDS effectively inhibits the expression of pro-inflammatory cytokine TNF-α both in vitro and in vivo, exhibits superior anti-RA activity compared to free Cel, and possesses favorable safety. This formulation addresses the key limitations of celastrol and shows promising potential for clinical translation in RA treatment. Full article

Objective: The development of nanobubble technology has expanded to various gas molecules, such as nitric oxide (NO). NO donors have been frequently used for both therapeutic and diagnostic purposes. However, the use of NO in nanoformulations has received little attention thus far. This research aimed to assess the subchronic toxicity of NO nanobubbles in a preclinical study design. Methods: Ninety days of subchronic toxicity testing based on modified OECD guidelines in Sprague Dawley rats was used in this study to assess potential adverse effects of intravenous administration of NO nanobubbles (NONBs). Hematological factors, serum biochemistry, and histology of the liver, kidney, heart, lung, and spleen were investigated. Results: The intravenous NONB injection trial using graded doses of 0.01 mL, 0.04 mL, and 0.06 mL resulted in no deaths during the 90-day treatment period. However, liver disturbance and electrolyte imbalance emerged. This condition was supported by histological findings in the liver and kidney, which showed potential reversible damage, and persistent hemorrhage of the spleen. Conclusions: Intravenous administration of NONBs at a dose of up to 0.06 mL in this subchronic toxicity test remains safe. Further studies with adjustments to the test formulation are highly encouraged before the clinical trial stage in humans. Full article

Dengue remains a major public health problem in tropical and subtropical regions, particularly in Latin America. Acute kidney injury (AKI) is one of the severe complications associated with dengue and has been linked to worse clinical outcomes, including prolonged hospitalization, need for renal replacement therapy, and increased mortality. This review aimed to summarize the available evidence on the epidemiology, pathophysiology, clinical manifestations, diagnosis, management, and prognosis of dengue-associated AKI, while also providing an overview of the literature from Latin America. This manuscript was developed as a narrative review. For the Latin America-specific overview, a focused structured search was conducted in PubMed, ScienceDirect, Cochrane Library, LILACS, and Web of Science, including studies published up to December 2025. The available data suggest that AKI in dengue is multifactorial, involving plasma leakage, renal hypoperfusion, endothelial dysfunction, tubular injury, rhabdomyolysis, thrombotic microangiopathy, and inflammatory renal damage. Clinically, AKI has been associated with oliguria, proteinuria, elevated serum creatinine, renal replacement therapy, and higher mortality. Only four eligible indexed studies from Latin America were identified in our search, all from Brazil, with small sample sizes and incomplete reporting of renal outcomes; however, additional unpublished or non-indexed local data may exist. In summary, dengue-associated AKI is a relevant complication of severe dengue, but the evidence available from Latin America remains limited. These findings highlight the need for improved renal surveillance and standardized reporting in dengue-endemic settings across Latin America. Full article

Acute kidney injury (AKI) is a life-threatening event prevalent in hospitalized patients but also not rare among endurance sports athletes. Hypoxia, oxidative stress, and sterile inflammation are the key pathophysiological factors driving kidney damage in AKI. Zinc is an essential trace element required for the intact function of approximately 3000 proteins (~10% of the human proteome), including over 300 enzymes for which zinc serves as a cofactor. Cell biological tasks of zinc signaling include adaptive responses to hypoxia and oxidative stress, as well as anti-inflammatory effects. The underlying molecular pathways involve modulation of hypoxia-inducible factor signaling, suppression of reactive oxygen species (ROS) generation, and inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), the latter being the major pro-inflammatory transcription factor. As a catalytic cofactor for the “classical” histone deacetylases, zinc is essential for epigenetic control of gene expression, thereby exerting further adaptive effects. Apart from the intracellular zinc signaling, extracellular zinc elicits cytoprotective and anti-inflammatory effects via the G Protein-Coupled Receptor 39 (GPR39). GPR39 activation by zinc binding may exert antioxidant and anti-inflammatory effects mediated by the zinc-finger protein A20 (TNFAIP3) and NF-κB suppression, followed by reduced production of pro-inflammatory cytokines such as tumor necrosis factor (TNF), interleukin-1β (IL-1β), and IL-6. At the same time, GPR39 signaling may stimulates the release of the anti-inflammatory cytokine IL-10, thus shifting the kidney tissue towards an anti-inflammatory milieu, promoting renal recovery. The present review focuses on the role of zinc in AKI to identify potential therapeutic strategies targeting zinc signaling for renoprotection and biomarker-based risk stratification. Full article

Background/Objectives: Arsenic (ARS) exposure is a major cause of kidney injury, driven by oxidative stress, inflammation, fibrosis, and apoptosis. This study evaluated the renoprotective effects of morin (MOR) and morin-loaded PLGA nanoparticles (MOR–PGNPs) against ARS-induced nephrotoxicity in rats. Methods: Sixty male Sprague Dawley rats were randomly allocated into six groups (n = 10 per group). The control group received corn oil. The MOR group received MOR (100 mg/kg), and the MOR–PGNPs group received the same dose of MOR encapsulated in PLGA nanoparticles. ARS was administered at 10 mg/kg for 14 days. Co-treated groups received ARS together with either MOR or MOR–PGNPs, with a 28 min interval between administrations. Renal function markers (serum urea, creatinine, uric acid, renal KIM-1), oxidative stress and antioxidant parameters (Nrf2/HO-1, CAT, SOD, GPx, ROS, MDA), inflammatory mediators (TLR4/NF-κB, TNF-α, IL-6, IL-1β), fibrotic markers (TGF-β1, fibronectin), and apoptotic proteins (caspase-3, caspase-8, Bax, Bcl-2) were assessed, alongside histopathological and ultrastructural evaluations. Results: ARS exposure significantly impaired renal function, increased KIM-1, suppressed Nrf2/HO-1 signaling, reduced antioxidant enzyme activities, and elevated ROS and MDA levels. It also activated TLR4/NF-κB signaling, upregulated pro-inflammatory cytokines and fibrotic markers, and increased pro-apoptotic proteins while downregulating Bcl-2. MOR co-treatment partially ameliorated these alterations. MOR–PGNPs produced potentially enhanced protection, restoring kidney function markers, enhancing antioxidant defenses, and markedly attenuating inflammation, fibrosis, and apoptosis. Histopathological and ultrastructural analyses confirmed preservation of glomerular and tubular architecture, mitochondrial integrity, and minimal cytoplasmic vacuolization in the MOR–PGNPs group. Conclusions: MOR–PGNPs at 100 mg/kg effectively mitigated ARS-induced renal damage through antioxidant, anti-inflammatory, antifibrotic, and anti-apoptotic mechanisms, supporting PLGA-based morin nanoparticles as a promising and safe renoprotective strategy. Full article

Nuclear factor-κB (NF-κB) is a critical regulator of inflammation and stress response signaling in acute kidney injury (AKI). Increasing evidence demonstrates that NF-κB signaling is directly related to oxidative stress, autophagy, mitochondrial malfunction, and apoptosis in the process of AKI. Injury-related stimuli, including ischemia–reperfusion, sepsis, nephrotoxins, reactive oxygen species (ROS) and damage-associated molecular patterns (DAMPs), activate canonical and non-canonical NF-κB pathways, resulting in renal inflammation and tubular injury. Recent investigations have shown that TLR4/NF-κB signaling, NLRP3 inflammasome activation, defective autophagy, and mitochondrial dysfunction mediate inflammatory and pro-apoptotic responses in AKI. On the other hand, autophagy-associated proteins such as microtubule-associated protein 1 light chain 3 beta (LC3B) and Beclin-1 may play renoprotective roles through the regulation of NF-κB signaling. This review tries to cover the knowledge regarding NF-κB signaling in AKI and to emphasize the possible function of NF-κB signaling in the control of inflammation, autophagy, and apoptosis. It also seeks to provide some insight into future research directions that may guide the development of more effective therapies for AKI. Full article

Preeclampsia (PE) is a severe pregnancy-specific hypertensive disorder characterized by immune microenvironment dysregulation at the maternal–fetal interface, with decidual macrophage phenotypic imbalance being a key pathological feature. The Ghrelin/growth hormone secretagogue receptor-1a (GHSR-1a) axis exerts immunomodulatory and anti-inflammatory effects, but its role in regulating decidual macrophage infiltration and phenotypic marker expression in PE remains unclear. In this study, we first detected the expression of the Ghrelin/GHSR-1a axis in decidual tissues from 10 healthy pregnant women and 12 PE patients via immunohistochemistry (IHC). We then established a lipopolysaccharide (LPS)-induced PE-like rat model to investigate the axis’s functional role and underlying mechanisms. Intriguingly, clinical analysis revealed a severity-dependent compensatory escalation of the Ghrelin/GHSR-1a axis in PE decidual tissues, potentially representing an endogenous antagonistic response to pregnancy-associated pathological stress. In the animal model, exogenous Ghrelin supplementation reversed LPS-induced PE-like phenotypes, including hypertension, proteinuria, fetal growth restriction (FGR), and placental dysfunction, and alleviated pathological damage to the maternal liver, kidney, and placenta. Mechanistically, Ghrelin modulated decidual macrophage phenotypic marker expression by downregulating the M1 marker CD86 and upregulating the M2 marker CD163 and promoted trophoblast invasion and spiral artery remodeling by restoring laminin, α-cytokeratin 7 (α-CK7), and α-smooth muscle actin (α-SMA) expression in placental tissue. All protective effects of Ghrelin were abrogated by co-administration of D-lys-3-GHRP-6, a specific GHSR-1a antagonist, confirming the dependence on the Ghrelin/GHSR-1a axis. Collectively, our findings suggest that the Ghrelin/GHSR-1a axis is compensatorily upregulated in PE and may exert a protective role by regulating decidual macrophage phenotypic marker expression and improving placental function, providing preliminary evidence that this axis merits further investigation as a potential research target for PE. Full article

Despite their reduced viability, kidneys from donors-after-circulatory-death (DCD) increase the pool of transplantable kidneys. Molecular hydrogen (H₂) is emerging as a gas with therapeutic potential against graft injury. We investigated the effect of H₂ in an ex vivo porcine model of DCD kidney transplantation. Renal arteries of male Yorkshire pigs (n = 6) were clamped in situ for 60 min to induce ischemia, and ureters and arteries were cannulated to mimic DCD kidney injury. Upon nephrectomy, kidneys were flushed with UW solution or H₂-saturated UW solution and then preserved by machine perfusion at 4 °C for 4 h followed by a 4-h reperfusion period with warm autologous blood. Urine and arterial blood samples were collected hourly. H₂ preserved renal architecture, evidenced by significantly reduced tubular necrosis and renal expression of damage markers, which corresponded with the downregulated renal expression of pro-inflammatory genes compared to the UW-only group (p < 0.05). H₂ also markedly reduced levels of serum creatinine, BUN and intrarenal resistance, while flow rate, creatinine clearance and urine output were significantly higher, which positively correlated with Trx-1 and HO-1 expression in comparison with UW only group (p < 0.05). Improvement in renal graft quality and function is associated with Trx-1/HO-1 activation, suggesting preliminary clinical trials in kidney transplantation. Full article

Background/Objective: Albuminuria is an early marker of kidney damage and cardiovascular risk. However, data on its prevalence and association with urine dipstick parameters in heterogeneous, hospital-based populations remain limited. The objective of this study was to determine the prevalence of elevated albuminuria measured by the urine albumin-to-creatinine ratio (UACR) in a diverse patient population and evaluate associations with semi-quantitative urine dipstick parameters. Methods: This cross-sectional study included 393 adults recruited from a tertiary-care hospital setting, comprising individuals undergoing clinical evaluation and routine health assessments. Given the hospital-based recruitment and enrichment with chronic conditions, the study population represents a high-risk cohort rather than the general population. Spot urine samples were analyzed for the UACR and dipstick parameters. Elevated albuminuria was defined as a UACR ≥ 30 mg/g. Associations were assessed using chi-square tests and multivariate logistic regression, with adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Results: Elevated albuminuria was observed in 64% of participants. This high prevalence likely reflects the underlying clinical characteristics of the study population, including a substantial burden of chronic kidney disease and other comorbidities, and should not be interpreted as representative of population-level prevalence. Chronic kidney disease was independently associated with elevated albuminuria (aOR 3.14, 95% CI 1.12–8.86, p = 0.030), as was male sex (aOR 1.54, 95% CI 1.01–2.34, p = 0.045). Dipstick-positive blood was significantly associated with elevated albuminuria (85% vs. 60% in those without dipstick blood positivity, p = 0.005). Dipstick albumin strongly correlated with the UACR (p < 0.001), although 22% of individuals with negative dipstick albumin still had an elevated UACR. Other urine dipstick parameters were not significantly associated with elevated albuminuria. Conclusions: In this high-risk, hospital-based cohort, elevated albuminuria was common and associated with kidney disease and male sex. Dipstick blood positivity is significantly associated with albuminuria and may warrant further investigation. However, reliance on dipstick testing alone may underestimate disease burden, supporting the need for broader implementation of UACR-based screening strategies. Full article