Lupus nephritis (LN) treatment remains challenging because of the limited efficacy and substantial side effects of conventional immunosuppressive therapies. Traditional Chinese medicine (TCM), with its holistic and multitarget approach, offers unique therapeutic potential. The emerging gut–kidney axis theory provides a new framework for understanding LN pathogenesis by linking gut dysbiosis and intestinal barrier injury to renal inflammation. This review systematically examines the role of gut–kidney axis dysregulation in LN progression and establishes connections between the TCM spleen–kidney correlation theory and this modern concept. Accumulating evidence suggests that TCM compounds and active ingredients alleviate renal injury and improve LN through multiple mechanisms. TCM compounds modulate the gut microbiota composition, enhance intestinal barrier integrity, reduce endotoxin translocation, and suppress systemic inflammation. These findings position the gut–kidney axis as a critical target for TCM intervention. Through multicomponent synergy, TCM restores gut homeostasis and inhibits aberrant immune responses. Future studies should integrate multiomics approaches, including metagenomics and metabolomics, and prospective clinical trials should dynamically track the gut microbiota and metabolite profiles in LN patients. Such investigations will clarify the precise mechanisms by which TCM modulates the gut–kidney axis and facilitate the development of personalized TCM-based therapeutic strategies.

Engineered extracellular vesicles (EVs) have garnered significant attention due to their potential serving as both therapeutic agents and drug delivery vehicles. Real-time monitoring of engineered EVs-target interactions constitutes a critical need for advancing EVs-based therapeutics. Here, we present a novel biolayer interferometry (BLI)-based analytical platform for detecting dynamic interactions between collagen-binding domain (CBD)-engineered EVs and type I collagen (Col I). A stable CD63-CBD fusion protein-expressing mouse tendon cell line (designated TT-D6sCBD cells) was initially established using a lentiviral transduction system. Engineered EVs (TT-D6sCBDEVs) were subsequently isolated through optimized differential ultracentrifugation. Col I was covalently immobilized on AR2G biosensors for detecting EVs binding using BLI technology. Quantitative analysis revealed that TT-D6sCBDEVs-treated biosensors demonstrated significantly enhanced BLI signals versus control group (TT-D6sVecEVs), along with time-dependent signal accumulation. Correlative microscopy validation-including scanning electron microscopy (SEM) and confocal microscopy imaging-confirmed the enhanced EVs binding capacity in the test group compared to controls. This work establishes a paradigmatic methodology for characterizing binding kinetics between engineered EVs and their molecular targets, offering critical technical support for advancing precision EVs-based therapeutics.

Tendon injuries, particularly massive tendon defects, pose significant clinical challenges due to the limited regenerative capacity of tendons and suboptimal outcomes of current therapies. This study presents a bioinspired scaffold that integrates genetically engineered extracellular vesicles (EVs) with collagen-targeting capabilities into a decellularized bovine tendon sheet (DBTS) for tendon regenerative repair. Rat tendon-derived stem cells (TDSCs) were genetically modified to overexpress biglycan (Bgn) and fibromodulin (Fmod), producing bioactive EVs that drive tenogenic differentiation via the miR-145-5p/TGFβ2 signaling pathway. The incorporation of a collagen-targeting peptide (CTP) on EVs surfaces ensured efficient attachment and sustained release at the injury site. The resulting bioinspired scaffold provided a supportive microenvironment for tendon regeneration, demonstrated in vitro by improved stem cell proliferation, migration and tenogenic differentiation, and in vivo by enhanced collagen alignment, extracellular matrix remodeling, and biomechanical performance of regenerated Achilles tendons in rats. This scaffold represents an innovative approach in cell-free regenerative strategy, offering targeted modulation of the tendon niche with translational potential for treating massive tendon injuries.

Functional reconstruction and ligament-bone integration are a current challenge in anterior cruciate ligament (ACL) reconstruction. In previous studies, decellularized tendon matrix material was considered as a promising material for tendon and ligament repair due to its easy availability, good biocompatibility and low immunogenicity. In addition, extracellular vesicles derived from bone marrow mesenchymal stem cells (BMSCS-EVs) have been repeatedly reported in recent years to play a crucial role in promoting bone regeneration and graftbone integration, though their retention in vivo is low. This study designed a type I collagen (Col-I) targeting fusion peptide (TKKTLRTGGGGSCRHSQMTVTSRL) to engineer BMSCs-EVs. Further, the engineered BMSCs-EVs was coupled with decellularized porcine tendon sheets (DPTS) scaffold to construct a new bioactive scaffold DPTS@PEVs-DPTS-DPTS@PEVs for ACL reconstruction and its osseous integration. Our results confirmed that the bioactive scaffold improved the therapeutic concentration and duration of BMSCs-EVs in the graft-bone repair area. Moreover, the bioactive scaffold significantly promoted the adhesion, proliferation, migration and osteogenic differentiation of BMSCs, significantly inhibit M1 but promote M2 type polarization of macrophages. In addition, the novel DPTS@PEVs-DPTS-DPTS@PEVs bioactive scaffold showed good graft-bone integration and biomechanical properties after ACL reconstruction in New Zealand white rabbits, the above advantages may provide a promising new idea for surgical reconstruction of ACL in clinic.

The interrelationship between bone and fat can be described as a seesaw in bone homeostasis, in which both osteogenesis and adipogenesis occur in a delicate balance. Osteoblasts and adipocytes share a common origin and play key roles in osteogenesis and adipogenesis. Bone–fat balance indicates osteogenesis and adipogenesis keeps a balance for concordant distribution of trabecular bone and bone marrow adipose tissue in bone, thereby leading to the balance between bone metabolism and lipid metabolism. Bone–fat balance is crucial for metabolic health. When disrupted by various factors, this balance can lead to several bone-related metabolic diseases and systemic disorders, such as obesity, osteoporosis, and osteoarthritis. Recent research highlights the role of autophagy dysfunction in these metabolic conditions. Restoring autophagic function can help restore metabolic homeostasis and re-establish the bone–fat balance. The current review explores the factors that regulate bone–fat balance, the consequences of imbalance under pathological conditions, and the potential of autophagy modulation as a therapeutic approach. Overall, it can be concluded that targeting autophagy presents a promising strategy for treating metabolic disorders and restoring bone–fat balance.

BackgroundVascular calcification (VC) commonly occurs in diabetes and is associated with cardiovascular disease incidence and mortality. Currently, there is no drug treatment for VC. The Danlian-Tongmai formula (DLTM) is a traditional Chinese medicine (TCM) prescription used for diabetic VC (DVC), but its mechanisms of action remain unclear. This study aims to elucidate the effects of DLTM on DVC and explore the underlying mechanisms of action.MethodsUltra-high-performance liquid chromatography-mass spectrometry (UHPLC-MS) was used to identify the metabolites of DLTM. A DVC rat model was established using streptozotocin (STZ) combined with vitamin D3 (VitD3). The effects of DLTM on DVC were evaluated through alizarin red staining, calcium deposition, and changes in osteogenic and contractile markers. The specific molecular mechanism of DLTM in treating diabetic VC was comprehensively analyzed by transcriptomics, molecular docking and in vivo experimental verification.ResultsWe identified 108 major metabolites of DLTM. In vivo, high-dose DLTM significantly alleviated VC in diabetic rats. Transcriptomic analysis showed that DLTM treatment markedly altered the transcriptomic profile of rat aortas, which was associated with regulating the CCN3/NOTCH signaling pathway, promoting vascular smooth muscle contraction, and inhibiting the inflammatory responses. Molecular docking and molecular dynamics simulation demonstrated strong binding interactions between DLTM metabolites and key molecules within the CCN3/NOTCH pathway, including NOTCH1, DLL1, DLL4, hes1, and hey1. In vivo experiments confirmed that DLTM could upregulate CCN3, inhibit the activation of NOTCH signaling ligands DLL1 and downstream transcription factors hes1 and hey1, and reduce the release of inflammatory cytokines IL6, IL1β, and TNFα.ConclusionDLTM alleviates DVC by regulating the CCN3/NOTCH signaling axis to inhibit inflammatory responses. Our research provides experimental basis for clinical treatment and drug transformation of diabetic VC.

The selection of appropriate cell sources is vital for the regeneration and repair of tendons using stem cell-based approaches. Human adipose-derived stem cells (hADSCs) have emerged as a promising therapeutic strategy for tendon injuries. However, the heterogeneity of hADSCs can lead to inconsistent or suboptimal therapeutic outcomes. In this study, we isolated and identified a tenomodulin (TNMD)-positive subpopulation from hADSCs (TNMD+hADSCs) using flow cytometry and then assessed the cellular response of this subpopulation to decellularized tendon slices (DTSs), including cell proliferation, migration, and tenogenic differentiation, using the CCK-8 assay, transwell migration assay, and quantitative real-time polymerase chain reaction. Our findings revealed that TNMD+hADSCs maintained the general characteristics of stem cells and exhibited significantly higher expressions of tendon-related markers compared to hADSCs. Importantly, DTSs significantly enhanced the proliferation, migration, and tenogenic differentiation of TNMD+hADSCs. This study provides preliminary experimental evidence for the translational application of ADSCs for tendon regeneration and repair.

Arsenic exposure leads to vascular endothelial dysfunction (VED), which plays a driving role in the development of cardiovascular disease. Macroautophagy and chaperone-mediated autophagy (CMA), two major forms of autophagy in mammals, jointly maintain intracellular homeostasis. Our group has revealed that excessive macroautophagy induces VED. However, the function of CMA in arsenic-induced endothelial dysfunction as well as the regulatory relationship between macroautophagy and CMA have not been unveiled. Here, we demonstrate that the co-activation of macroautophagy and CMA promotes VED in vivo and in vitro. We also identify a damaging role of CMA in arsenic-induced vascular endothelial dysfunction, which contrasts with its previously reported protective effects. In addition, our results showed that macroautophagy and CMA were activated successively, and macroautophagy played a dominant regulatory role in VED induced by arsenic. Mechanistically, phosphorylation proteomics suggested that KEAP1 may play a pivotal role in arsenic-induced macroautophagy and CMA in mouse aortic endothelial cells. Moreover, a novel Keap1 phosphorylation site, Thr43, was significantly activated by the JNK pathway. Furthermore, when Keap1 levels decrease to a considerable lower level, macroautophagy and CMA decrease remarkably, endothelial dysfunction was accordingly alleviated. Collectively, our study demonstrates that the p-JNKThr183/Tyr185/p-Keap1Thr43/Keap1 axis mediates arsenic-induced VED by coordinately activating both CMA and macroautophagy, which revealing a new regulation mechanism of Keap1 in autophagy. Additionally, the genetic polymorphism of Keap1 was found have a significant correlation with the susceptibility to hypertension in arsenicosis areas. Collectively, these findings provide promising new ideas for the prevention and treatment of arsenic-induced CVD through regulating autophagy.

Psoriasis burdens children and adults, but the impact of air pollution and aging is unclear. This study examines the association between air pollution exposure and psoriasis risk, considering the mediating role of biological aging. A prospective cohort study of 284 544 adults (51.3% female, mean age 56.26 ± 8.10 years) from the UK Biobank examined long-term exposure to air pollutants (PM2.5, PM10, PM2.5-10, NO2, and NOX). Biological aging was assessed using phenotypic age algorithms. Cox proportional hazards models were constructed to analyze the relationships with the risk of psoriasis, adjusting for demographic, socioeconomic, and health-related factors. Mediation analysis explored the role of biological aging. During a median follow-up of 15.58 years, 3,446 (1.21%) participants developed psoriasis. After adjusting for all confounders, each ten-unit increase (10 μg/m³) in PM2.5, PM10, NO2, and NOx, corresponded to the significantly increased risk of psoriasis by 95.7% (HR = 1.957, 95% CI 1.435-2.671), 19.7% (HR = 1.197, 95% CI 1.006-1.426), 9.0% (HR = 1.090, 95% CI 1.043-1.138) and 4.4% (HR = 1.044, 95% CI 1.024-1.066), respectively. Moreover, all air pollutants are significantly associated with biologically aging, while each one-year increase in PhenoAge was associated with a 5.0% higher risk of psoriasis (HR = 1.050, 95% CI 1.045-1.056). Finally, accelerated biological aging partially mediated 5.96%-13.86% of these air pollutants. Long-term exposure to air pollution significantly affects psoriasis risk, with biological aging as a partial mediator. Reducing pollution may lower the risk of psoriasis by slowing biological aging.

Recent studies have indicated that demineralized cortical bone (DCB) may be used to repair tendons and ligaments, such as the patellar tendon and anterior cruciate ligament (ACL). Hydrogen peroxide (H2O2) has been shown to reduce the osteoinductivity of DCB, and heat treatment may also decrease the osteoinductivity of DCB. The purpose of this study was (i) to determine whether heat treatment reduces the osteoinductivity of DCB and (ii) to compare the effectiveness of heat treatment and H2O2 treatment on BMP-2 inactivation. DCB was prepared by immersion in 0.6 N hydrochloric acid, and DCB-H and DCB-HO were prepared by heat treatment (70°C for 8 h) and H2O2 treatment (3% H2O2 for 8 h), respectively. The surface topographies, elemental distributions and histological structures of the scaffolds were observed by scanning electron microscopy (SEM), Fourier transform infrared spectroscopy (FT-IR) and histological staining. The viability and osteogenic differentiation of TDSCs cultured on the scaffolds were evaluated via live/dead cell staining and Cell Counting Kit-8 (CCK-8) testing, real-time polymerase chain reaction (RT-PCR) and western bolt (WB) analysis, alkaline phosphatase activity (ALP) and alizarin red S (ARS) staining. The intramuscular implantation of the scaffolds in rats was also used to evaluate the effect of heat treatment and H2O2 treatment on the osteoinductivity of DCB. Our results demonstrated that both treatments removed BMP-2 and osteocalcin (OCN) within the DCB and that DCB-H and DCB-HO had good cytocompatibility and reduced the osteogenic differentiation of TDSCs. Moreover, the in vivo results indicated that the DCB-H and DCB-HO groups had smaller areas of osteoid formation than did the DCB group, and the DCB-HO group had the smallest area among the three groups. Our study demonstrated that heat treatment could reduce the osteoinductivity of DCB, and that H2O2 treatment was more effective than heat treatment.

Age-related macular degeneration (AMD) is a common retinal neurodegenerative disease among the elderly. Neovascular AMD (nAMD), a leading cause of AMD-related blindness, involves choroidal neovascularization (CNV), which can be suppressed by anti-angiogenic treatments. However, current CNV treatments do not work in all nAMD patients. Here we investigate a novel target for AMD. Granzyme B (GzmB) is a serine protease that promotes aging, chronic inflammation and vascular permeability through the degradation of the extracellular matrix (ECM) and tight junctions. Extracellular GzmB is increased in retina pigment epithelium (RPE) and mast cells in the choroid of the healthy aging outer retina. It is further increased in donor eyes exhibiting features of nAMD and CNV. Here, we show in RPE-choroidal explant cultures that exogenous GzmB degrades the RPE-choroid ECM, promotes retinal/choroidal inflammation and angiogenesis while diminishing anti-angiogenic factor, thrombospondin-1 (TSP-1). The pharmacological inhibition of either GzmB or mast-cell degranulation significantly reduces choroidal angiogenesis. In line with our in vitro data, GzmB-deficiency reduces the extent of laser-induced CNV lesions and the age-related deterioration of electroretinogram (ERG) responses in mice. These findings suggest that targeting GzmB, a serine protease with no known endogenous inhibitors, may be a potential novel therapeutic approach to suppress CNV in nAMD.

Purpose: To examine the 5-year incidence of age-related macular degeneration (AMD) and its associated factors in an adult Chinese population. Methods: The Tongren Health Care Study included individuals attending regular health care check-up examinations in the Beijing Tongren Hospital. Baseline examinations were performed from 2014 to 2015, with 5-year follow-up examinations conducted between 2019 and 2020. Fundus photographs were graded according to the Beckman Initiative guidelines. Results: A total of 5658 participants with gradable photographs at both examinations were included in the study, comprising 58.0% women, with a mean age of 54.9 +/- 11.0 years. The 5-year incidence of any, early, intermediate, and late AMD were 6.1% (95% confidence interval [CI], 5.5%-6.8%), 5.0% (95% CI, 4.4%-5.6%), 3.4% (95% CI, 2.9%-3.9%), and 0.3% (95% CI, 0.2%-0.4%), respectively. In multivariate analysis, incident early AMD was associated with older age (P < 0.001; odds ratio [OR], 1.04; 95% CI, 1.02-1.06), female sex (P = 0.011; OR, 1.42; 95% CI, 1.08-1.86), and a higher estimated glomerular filtration rate (P = 0.020; OR, 1.15; 95% CI, 1.02-1.30), whereas having diabetes was a protective factor (P= 0.019; OR, 0.61; 95% CI, 0.41-0.92). Incident intermediate AMD was associated with older age (P < 0.001; OR, 1.05; 95% CI, 1.04-1.07), a higher high-density lipoprotein cholesterol level (P < 0.001; OR, 1.97; 95% CI, 1.38-2.83) and a lower triglyceride level (P = 0.008; OR, 0.77; 95% CI, 0.64-0.93). Conclusions: A higher estimated glomerular filtration rate level was a risk factor for incident early AMD. A higher high-density lipoprotein cholesterol level and lower triglyceride level were risk factors for incident intermediate AMD. This finding may point to the role of renal circulation and lipid metabolism in incident AMD.

Tendon regeneration is greatly influenced by the oxidant and the inflammatory microenvironment. Persistent inflammation during the tendon repair can cause matrix degradation, tendon adhesion, and excessive accumulation of reactive oxygen species (ROS), while excessive ROS affect extracellular matrix remodeling and tendon integration. Herein, we used tannic acid (TA) to modify a decellularized tendon slice (DTS) to fabricate a functional scaffold (DTS-TA) with antioxidant and anti-inflammatory properties for tendon repair. The characterizations and cytocompatibility of the scaffolds were examined in vitro. The antioxidant and anti-inflammatory activities of the scaffold were evaluated in vitro and further studied in vivo using a subcutaneous implantation model. It was found that the modified DTS combined with TA via hydrogen bonds and covalent bonds, and the hydrophilicity, thermal stability, biodegradability, and mechanical characteristics of the scaffold were significantly improved. Afterward, the results demonstrated that DTS-TA could effectively reduce inflammation by increasing the M2/M1 macrophage ratio and interleukin-4 (IL-4) expression, decreasing the secretion of interleukin-6 (IL-6) and interleukin-1β (IL-1β), as well as scavenging excessive ROS in vitro and in vivo. In summary, DTS modified with TA provides a potential versatile scaffold for tendon regeneration.

Objectives: Epidemiological evidence has shown that genetics and environment are associated with the risk of hypertension. However, the specific SNP effects of a cluster of crucial genes in the RAAS system on the risk of hypertension are unclear. Methods: A case-control study was performed on the baseline participants of Environment and Chronic Disease in Rural Areas of Heilongjiang China (ECDRAHC) study. According to the inclusion and exclusion criteria, 757 subjects (428 hypertensive patients) were enrolled. A total of 32 SNP sites and related haplotypes, involved in AGT (angiotensinogen), ACE (angiotensin-converting enzyme), AGTR1, CYP11B2 (aldosterone-synthase), LDLR (low-density lipoprotein receptor), LRP5 (low-density lipoprotein receptor associated protein 5), LRP6 (low-density lipoprotein receptor associated protein 6), PPARG (peroxisome proliferator-activated receptor gamma) and ACE2 (angiotensin-converting enzyme 2) genes which exert important roles in renin-angiotensin-aldosterone system (RAAS) system were analyzed. Furthermore, a polygenic scoring model was established to assess individual risk of developing hypertension based on the comprehensive SNPs effects in genes related the RAAS system. Results: After controlling the impact of confounding factors, multivariate logistic regression analysis revealed that the distribution of AGT/rs5046, LRP6/rs12823243 and ACE2/rs2285666 was associated with susceptibility to essential hypertension. In genetic score model, the score >- 0.225 had a higher risk, the OR ( 95%CI) was 1.229 (1.110, 1.362). Conclusions: To the best of our knowledge, this is the first time a hypertension risk scoring model on RAAS associated gene cluster has been constructed, which will provide a novel approach for prevention and control of essential hypertension.

RATIONALEPatients with chronic obstructive pulmonary disease (COPD) and type 2 diabetes (T2D) have worse clinical outcomes compared to patients without metabolic dysregulation. Glucagon-like peptide 1 receptor agonists (GLP-1RA) reduce asthma exacerbation risk and improve forced vital capacity in COPD.OBJECTIVESTo determine whether GLP-1RA use is associated with reduced COPD exacerbation rates, and severe and moderate exacerbation risk, compared with other T2D therapies.METHODSRetrospective, observational, electronic health records-based study using an active comparator, new-user design of 1,642 patients with COPD at a U.S. health system (2012-2022). The COPD cohort was identified using a previously validated machine learning algorithm that includes a natural language processing tool. Exposures were defined as a prescription for GLP-1RAs (reference group), dipeptidyl-peptidase 4 inhibitors (DPP-4i), sodium-glucose cotransporter 2 inhibitors (SGLT2i) or sulfonylureas.MEASUREMENTS AND MAIN RESULTSUnadjusted COPD exacerbation counts were lower in GLP-1RA users. Adjusted exacerbation rates were higher in DPP-4i [IRR,1.48; 95% CI, (1.08 to 2.04); P=.02] and sulfonylurea [IRR, 2.09; 95% CI, (1.62 to 2.69); P <.0001] users compared to GLP-1RA users. GLP-1RA use was associated with significantly reduced risk of severe exacerbations compared to DPP-4i and sulfonylurea users, and of moderate exacerbations compared to sulfonylurea users. After adjustment for clinical covariates, moderate exacerbation risk was also lower in GLP-1RA compared to DPP-4i users. No significant difference in exacerbation outcomes was seen between GLP-1RA and SGLT2i users.CONCLUSIONSProspective studies of COPD exacerbations in patients with comorbid T2D are warranted. Additional study may elucidate mechanisms underlying observed associations with T2D medications.

Recent in vivo and ex vivo studies have demonstrated retinal vasculopathy may be associated with Alzheimer’s disease (AD). We investigated amyloid beta (Ab) localization relative to vessels in wholemount retinas from AD and control donors. We specifically tested whether extravascular retinal Ab aggregated toward vessels and whether the Ab localization pattern differed between the AD and control retinas. From 15 AD donors and 10 age-matched controls, free-floating punches were taken in the foveal, peri-foveal, and mid-peripheral temporal, superior, and inferior neuro-retina. Immunohistochemistry was performed for Ab (6F/3D, 12F4) with secondary antibodies tagged with Cy3. The punches were imaged at 543-nm using Zeiss LSM 510 confocal microscope focused at the ganglion cell layer in four non-overlapping 450mm x 450mm images. Blind raters segmented the images into intravascular and extravascular regions excluding cell bodies and artefacts. Quantitative analysis was performed as follows: Ab reactivity was detected pixel-wise by intensity thresholding, and the total vessel area, raw and normalized intra- and extravascular Ab load, and vessel proximity of extravascular Ab were computed. Out of 452 images 272 contained visible vessels. Total vessel area was lower in the AD retinas in the superior region (p = 0.004). There was no group difference in Ab load except in the temporal intravascular region (p = 0.007); however, intravascular Ab signal may be due to blood artefacts and requires caution in interpretation. Aggregation of Ab near vessels was tested by comparing the vessel proximity of extravascular Ab-positive pixels against that of all other pixels in the extravascular region. Extravascular Ab were located significantly closer to the vessels than the background in the control retinas in the peri-fovea (p = 0.0023) and temporal (p = 0.001) regions, but this was not observed in AD retinas. With our previous study on intracellular retinal Ab, the current study suggests that Ab deposition pattern in the retina is specific in spatial regions (eg. temporal, superior) and anatomical regions (eg. intracellular, intravascular). The non-specificity of Ab localization relative to the vessels in AD may indicate compromised Ab clearance via retinal vasculature.

Introduction: The aim of the study was to investigate associations between diabetic retinopathy (DR) and chronic kidney disease (CKD) in patients with type 2 diabetes (TD2). Methods: The participants of the cross-sectional, community-based Tongren Health Care Study underwent a detailed medical and ophthalmological examination. We defined TD2 by a fasting plasma glucose concentration of ≥7.0 mmol/L or a medical history. CKD was classified as either reduced estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 mm2 or presence of albuminuria. DR was assessed using color fundus photographs. Results: Out of 62,217 participants of the Tongren Health Care Study, 5,103 (8.2%) patients had TD2. The prevalence of DR was 12.8% (95% CI, 11.8%, 13.7%), CKD was 13.3% (95% CI, 12.4%, 14.3%), and the subtypes of CKD including reduced eGFR and albuminuria was 4.6% (95% CI, 4.2%, 5.1%) and 10.1% (95% CI, 9.3%, 10.9%), respectively. DR was detectable in 21.0% of the patients with CKD, while CKD was present in 20.9% of the DR patients. Higher DR prevalence was associated with higher prevalence of albuminuria and reduced eGFR (both p < 0.05). Factors independently associated with the presence of CKD instead of DR were older age (p < 0.001, OR = 1.05), a higher body mass index (p < 0.001, OR = 1.14), a higher serum concentration of triglycerides (p < 0.001, OR = 1.26), and a lower blood glucose (p < 0.001, OR = 0.93). Having hypertension was additionally associated with the presence of reduced eGFR as compared with DR (p = 0.005, OR = 4.47). Conclusions: TD2 patients of older age and with higher body mass index, hypertension, and dyslipidemia had a higher probability of being affected by CKD rather than DR, while those with a higher blood glucose level were more prone to DR than CKD.