Search Results (46)

Background/Objectives: DEFA3 and DEFA5 are alpha-defensins, which are small cationic antimicrobial peptides that are part of the innate immune system. DEFA3 encodes human neutrophil peptide-3 (HNP-3), primarily expressed in neutrophils, while DEFA5 encodes human defensin-5 (HD-5), predominantly expressed in Paneth cells of the small intestine. Both defensins show elevated levels in diabetes and are strongly associated with diabetic nephropathy, with the highest concentrations found in patients with this complication. We evaluated serum levels of DEFA3 and DEFA5 in 160 participants (93 patients with T2DM and 67 controls without carbohydrate disturbances) and their associations with diabetic nephropathy, as well as peripheral and cardiac autonomic neuropathy and anthropometric and metabolic parameters. Methods: This was a monocentric, cross-sectional, observational study conducted at the Endocrinology and Metabolic Disorders Clinic of Alexandrovska Hospital in Sofia. Main methods included detailed clinical and anthropometric assessments, diagnosis of peripheral neuropathy via the Neuropathy Disability Score (NDS), evaluation of cardiac autonomic neuropathy using heart rate variability analysis and Ewing cardiovascular reflex tests, comprehensive laboratory investigations with fasting blood samples, and measurement of serum DEFA3 and DEFA5 levels by ELISA kits. Results: Serum DEFA3 and DEFA5 levels did not differ significantly between patients with T2DM and controls without carbohydrate disturbances, nor by sex or menopausal status. Patients with diabetic nephropathy showed significantly higher levels of both DEFA3 (345.7 ± 77.9 pg/mL vs. 299.2 ± 100.3 pg/mL; p = 0.042) and DEFA5 (5.3 ± 10.1 pg/mL vs. 2.9 ± 2.9 pg/mL; p = 0.044). DEFA5 levels were also elevated in participants with increased albumin-to-creatinine ratio (4.9 ± 9.9 pg/mL vs. 2.2 ± 1.5 pg/mL; p = 0.043). No significant differences were observed in patients with peripheral neuropathy, cardiac autonomic neuropathy, retinopathy, or macroangiopathy, although a non-significant trend toward higher values was noted. DEFA3 demonstrated moderate discriminatory ability for diabetic nephropathy (AUC = 0.641; p = 0.037), superior to DEFA5 (AUC = 0.570; p = 0.303). DEFA3 showed multiple weak positive correlations with diabetes duration, body weight, BMI, total and LDL-cholesterol, serum creatinine, and uric acid, while DEFA5 correlated only with total cholesterol. Conclusions: Circulating DEFA3 and DEFA5 are associated with diabetic nephropathy and selected metabolic and renal parameters in patients with type 2 diabetes, with DEFA3 showing moderate discriminatory capacity. The associations were largely attenuated after covariate adjustment, suggesting that these alpha-defensins likely reflect downstream innate immune activation and renal stress rather than acting as independent drivers of complications. Full article

Background: Autonomic dysfunction is increasingly recognized as a key mechanism in disorders involving the brain–gut axis and gastrointestinal symptom generation. Transcutaneous vagus nerve stimulation (tVNS) is a noninvasive neuromodulatory technique investigated for its potential effects on autonomic regulation. Methods: A systematic review and meta-analysis were conducted following PRISMA guidelines, with protocol registration in PROSPERO. Randomized controlled trials (RCTs) investigating auricular or cervical tVNS in patients with visceral disorders were included. Continuous outcomes were pooled using mean differences (MDs) or standardized mean differences (SMDs) with 95% confidence intervals (CIs). When multiple publications originated from the same trial population, only independent datasets were considered for quantitative synthesis to avoid double-counting participants. Risk of bias was assessed using the PEDro scale and certainty of evidence with the GRADE approach. Results: Seven RCTs met the inclusion criteria. tVNS demonstrated a small but statistically significant improvement in gastrointestinal symptoms based on change-from-baseline GSRS scores (MD −0.19; 95% CI −0.29 to −0.09; p < 0.001; I² = 0%). Although statistically significant, the magnitude of this effect was modest, and its clinical relevance remains uncertain. No significant effects were observed on cardiac vagal tone (SMD 0.19; 95% CI −0.53 to 0.90; p = 0.61; I² = 73%) or systolic blood pressure (MD −1.24 mmHg; 95% CI −6.69 to 4.21; p = 0.66; I² = 0%). Evidence regarding cardiac autonomic neuropathy (CAN) was limited to a single independent randomized controlled trial, which found no significant differences between tVNS and sham stimulation. Conclusions: tVNS provides modest statistically significant improvements in gastrointestinal symptoms, supporting its role as a symptomatic neuromodulatory intervention. However, the available evidence for this outcome was based on only two studies, and the clinical relevance of the observed effect remains uncertain. No statistically significant pooled effects were observed for the cardiovascular autonomic markers assessed in this review. Evidence regarding CAN was limited to a single independent study. Therefore, the available evidence remains limited and heterogeneous, and further high-quality randomized controlled trials are warranted. Full article

Carbonyl stress, chronic inflammation, and progressive tissue injury accompany type 2 diabetes mellitus (T2DM) and obesity. Yet, the molecular systems that connect these processes with cardiac, vascular and neuronal complications are incompletely defined. This review examines the AGE–RAGE–DIAPH1 axis as a mechanistic link between metabolic dysfunction and diabetic myocardial and neuronal injury, with emphasis on vascular and myocardial remodeling and emerging implications for autonomic neuronal vulnerability. We summarize current evidence on the formation and accumulation of advanced glycation end-products and other RAGE ligands in metabolic disease, DIAPH1’s structural and signaling role as an intracellular effector of RAGE, and the cellular consequences of pathway activation in vascular, neural, and cardiac tissues. Across experimental models, this signaling axis promotes oxidative stress and inflammatory activation, leading to endothelial dysfunction and barrier failure. Subsequent fibrotic remodeling provides a biologically plausible route through which metabolic stress may be translated into persistent organ injury. In the heart, these mechanisms are linked to coronary microvascular dysfunction, altered cardiomyocyte phenotype, calcium handling abnormalities, and myocardial fibrosis. In the autonomic nervous system, limited but emerging data connect RAGE activation to oxidative injury and mitochondrial dysfunction, abnormal neuronal excitability, and structural vulnerability. Direct evidence linking DIAPH1 to autonomic neurons is lacking. We also review biomarker candidates related to this pathway, including circulating AGEs and soluble RAGE isoforms, skin AGE measurements, imaging markers of myocardial remodeling, and autonomic functional measures. Finally, we discuss pharmacological and natural compounds that target AGE formation, ligand accumulation, RAGE signaling, or intracellular protein interactions linked to this axis. Overall, the available evidence supports the AGE–RAGE–DIAPH1 axis as a credible mechanistic concept and a potentially informative translational hypothesis in T2DM. However, the AGE–RAGE component is supported more strongly than DIAPH1-specific involvement in human diabetic myocardial disorder or cardiovascular autonomic neuropathy. The value of DIAPH1 as a biomarker or therapeutic target in these neurocardiac complications remains to be established. Full article

Background and Objectives: We investigate whether a preoperative autonomic vulnerability phenotype and intraoperative regional cerebral oxygen saturation (rcSO₂) variables are associated with postoperative delirium (POD) in elderly patients undergoing non-cardiac, non-neurological surgery, and whether autonomic vulnerability modifies the association between cerebral desaturation and POD. Materials and Methods: This retrospective propensity score–matched cohort study included patients aged 65 years or older who underwent general anesthesia with intraoperative rcSO₂ monitoring. The preoperative autonomic vulnerability phenotype was defined using clinical features documented before surgery, including autonomic neuropathy, diabetic autonomic neuropathy, orthostatic hypotension, syncope or presyncope suggestive of autonomic dysfunction, and unexplained resting bradycardia or chronotropic incompetence not attributable to rate-limiting medication. The primary outcome was POD within 5 postoperative days. Patients were matched 1:1 using nearest-neighbor propensity score matching with a caliper of 0.2 standard deviations of the logit of the propensity score, and conditional logistic regression was used in the matched cohort. Results: A total of 412 patients were included; 112 had the phenotype and 300 did not. After matching, 98 pairs were analyzed. POD occurred in 27.6% of patients with the phenotype and 14.3% of patients without it. In the matched cohort, the phenotype (odds ratio [OR] 2.12, 95% confidence interval [CI] 1.18–3.82, p = 0.012), rcSO₂ decrease ≥20% (OR 2.45, 95% CI 1.31–4.58, p = 0.005), and longer duration of rcSO₂ < 80% of baseline (OR 1.02 per min, 95% CI 1.01–1.04, p = 0.008) were independently associated with POD. The phenotype-by-desaturation interaction was exploratory (OR 2.10, p = 0.032) and was not uniformly robust across sensitivity analyses. Conclusions: A preoperative autonomic vulnerability phenotype and intraoperative cerebral desaturation were independently associated with POD. The association between rcSO₂ decrease and POD appeared stronger in patients with autonomic vulnerability, but this interaction should be interpreted as hypothesis-generating rather than confirmatory. Full article

Background/Objectives: Angiopoietin-like proteins 4 and 8 (ANGPTL4 and ANGPTL8) are key regulators of lipid metabolism and inflammatory processes, with a potential role in the pathogenesis of type 2 diabetes mellitus (T2DM) and its complications. This monocentric observational study evaluated serum levels of ANGPTL4 and ANGPTL8 in 160 participants (93 patients with T2DM and 67 controls without carbohydrate disturbances) and their associations with peripheral and cardiac autonomic neuropathy. Methods: This is a monocentric, cross-sectional, observational study conducted at the Endocrinology and Metabolic Disorders Clinic of Alexandrovska Hospital in Sofia, involving 160 participants and approved by the Ethics Committee of Medical University–Sofia, with all subjects providing written informed consent in accordance with the Declaration of Helsinki. The main methods included detailed clinical and anthropometric assessments, diagnosis of peripheral neuropathy via the Neuropathy Disability Score (NDS), evaluation of cardiac autonomic neuropathy using heart rate variability analysis and Ewing cardiovascular reflex tests, comprehensive laboratory investigations with fasting blood samples, measurement of serum ANGPTL4 and ANGPTL8 levels by ELISA kits, and statistical analysis performed with IBM SPSS version 25, using parametric and non-parametric tests, correlations, logistic regression, and ROC curves. Results: ANGPTL4 levels were significantly lower in patients with T2DM (12.6 ± 23.1 ng/mL vs. 21.5 ± 29.3 ng/mL; p = 0.033). In a multivariate model, higher values remained associated with lower odds of T2DM (OR per 1 SD = 0.634; p = 0.0424). ANGPTL8 demonstrated moderate discriminatory ability for cardiac autonomic neuropathy (AUC = 0.678; p = 0.007) in unadjusted analysis, but the association did not persist after covariate adjustment. ANGPTL4 showed inverse correlations with body weight, basal metabolic rate, and GGT. Conclusions: The results support the role of ANGPTL4 as a potential biomarker in metabolic disturbances and complications in T2DM, while ANGPTL8 remains mainly insignificant after correction for potential confounding factors. Full article

Type 2 diabetes mellitus is associated with major cardiovascular complications, including cardiac autonomic neuropathy, which contributes to sympathetic–parasympathetic imbalance and increases susceptibility to arrhythmias and sudden cardiac death. Heart rate variability, assessed through R–R intervals on electrocardiography and 24 h Holter monitoring, represents a sensitive, non-invasive marker of autonomic dysfunction and arrhythmogenic risk. In patients with type 2 diabetes mellitus, chronic hyperglycaemia, oxidative stress, and metabolic inflammation lead to early impairment of the autonomic nervous system, manifested by consistent reductions in SDNN, RMSSD, pNN50, total power, and the high-frequency component, indicating diminished parasympathetic tone and sympathetic predominance. Nonlinear HRV indices demonstrate a loss of complexity and fractal organisation, providing additional prognostic value beyond conventional time- and frequency-domain analyses. Reduced HRV correlates with the severity of cardiac autonomic neuropathy, duration of diabetes, and poor glycaemic control, identifying patients with increased arrhythmogenic vulnerability. HRV analysis enables prediction of arrhythmic risk, facilitating the identification of high-risk individuals and guiding personalised interventions. The integration of HRV assessment into routine clinical practice may improve the early detection of subclinical autonomic neuropathy and optimise cardiovascular risk stratification and management in patients with type 2 diabetes mellitus. Full article

Diabetes mellitus is projected to affect more than 1.3 billion people worldwide by 2050, with millions remaining undiagnosed or in a prediabetic state. Cardiovascular complications account for nearly half of diabetes-related deaths, highlighting the need for scalable tools capable of identifying metabolic dysregulation before irreversible cardiac damage develops. This review synthesizes current mechanistic, clinical, and computational evidence linking diabetes to cardiac electrophysiological remodeling and examines electrocardiography (ECG) as a non-invasive modality for early detection of dysglycaemia. Chronic hyperglycaemia, insulin resistance, oxidative stress, microvascular dysfunction, and cardiac autonomic neuropathy collectively contribute to measurable ECG alterations, including QT/QTc prolongation, increased QT dispersion, changes in Tp–e indices, and reduced heart rate variability. These changes often precede overt cardiovascular disease and correlate with glycaemic burden and diabetes duration. Recent advances in signal processing and artificial intelligence have expanded the diagnostic potential of ECG. Both classical machine learning approaches and large-scale deep learning models demonstrate that ECG contains latent signatures associated with incident type 2 diabetes and glycaemic status. Despite promising results, heterogeneity in study design, limited representation of prediabetes, and lack of standardized validation frameworks remain major barriers to clinical translation. Prospective, multi-ethnic studies are needed to establish ECG-based screening as a reliable component of early diabetes detection strategies. Full article

Background/Objectives: Aortic stenosis is associated with autonomic nervous system (ANS) imbalance, while diabetes mellitus is a major contributor to cardiac autonomic neuropathy. Their coexistence may result in more pronounced autonomic dysfunction not fully captured by conventional assessment. This study aimed to compare ANS function in patients with severe aortic stenosis undergoing transcatheter aortic valve replacement (TAVR), according to diabetes status. Methods: This cross-sectional study included 74 patients with severe aortic stenosis referred for TAVR, including 21 patients with diabetes mellitus. Autonomic function was evaluated using non-invasive ECG-based analysis, incorporating short-term and 24 h Holter-derived heart rate variability (HRV), nonlinear Poincaré plot indices, and deceleration and acceleration capacity. Ambulatory blood pressure monitoring and standard clinical and echocardiographic assessment were performed. Results: Patients with diabetes mellitus demonstrated significantly lower long-term HRV parameters and reduced nonlinear Poincaré plot indices compared with non-diabetic patients, indicating altered autonomic modulation. Short-term HRV showed similar trends without statistical significance. Echocardiographic severity of aortic stenosis and left ventricular systolic function were comparable between groups. Conclusions: Autonomic dysfunction appears to be more pronounced in patients with severe aortic stenosis and diabetes mellitus, predominantly affecting parasympathetic modulation. ECG-derived autonomic parameters may offer complementary insight into ANS involvement in this population and warrant further investigation. Full article

The autonomic nervous system (ANS) plays a key role in cardiovascular regulation by maintaining hemodynamic and metabolic homeostasis through balanced sympathetic and parasympathetic activity. While autonomic dysfunction is classically associated with diabetes, neurodegenerative diseases, autoimmune neuropathies, and chronic cardiovascular conditions, growing evidence suggests that disturbances in iron metabolism represent an underrecognized contributor to cardiac autonomic dysregulation. This narrative review summarizes data from 107 studies on ANS disorders, including 49 investigating cardiovascular involvement. Reported abnormalities included reduced heart rate variability and baroreflex sensitivity, prolonged P-wave duration and QT dispersion, and deviations in non-invasive autonomic testing parameters. In iron overload states, these changes appear to be driven primarily by oxidative stress, whereas in iron deficiency they are likely mediated by tissue hypoxia. Importantly, several studies indicate that normalization of iron homeostasis may partially reverse autonomic dysfunction. This potentially reversible component underscores the clinical relevance of screening for and correcting iron imbalance not only to improve hematological status but also to reduce cardiovascular risk. Large-scale, multicenter studies using standardized autonomic assessment protocols are required to clarify prognostic implications and inform evidence-based clinical guidelines. Full article

Background and Objectives: Diabetes mellitus (DM) is a major risk factor for cardiovascular diseases (CVD), including acute myocardial infarction (MI), and is frequently associated with cardiac autonomic neuropathy (CAN). Post-MI autonomic dysfunction contributes to adverse outcomes, but data on prognostic markers in diabetic patients remain limited. This study aimed to (1) compare autonomic nervous system (ANS) function between patients with MI and DM (MI/DM), MI without DM, and DM without MI; (2) assess differences in MI/DM patients based on survival status; and (3) identify prognostic factors for all-cause mortality in diabetic patients following MI. Materials and Methods: This retrospective–prospective study included 375 patients: 93 MI/DM, 229 MI, and 53 DM. MI patients were treated with fibrinolytic or conservative therapy. All participants underwent cardiovascular reflex tests (CARTs) and 24 h Holter ECG with heart rate variability (HRV) analysis; DM patients without MI were tested in an outpatient setting. The primary endpoint was all-cause mortality during a median follow-up of 38 months. Univariable and multivariable Cox regression analyses were performed to determine mortality predictors. Results: Autonomic dysfunction was prevalent in all groups, with MI/DM patients showing the most pronounced impairment, particularly in parasympathetic function. MI/DM patients had significantly lower SDNN values and higher prevalence of definite parasympathetic dysfunction than other groups. In the MI/DM group, abnormal Valsalva maneuver (VM) was more frequent among non-survivors. Multivariable analysis identified abnormal VM and NSTEMI as predictors of overall mortality. Conclusions: Diabetic patients after MI exhibit the most severe autonomic impairment, predominantly parasympathetic, which may contribute to their increased cardiovascular risk. In this high-risk group, abnormal VM and NSTEMI presentations independently predict long-term mortality. Assessment of autonomic function, particularly VM, may provide valuable prognostic information and aid in risk stratification. Full article

Cardiac amyloidosis (CA) is an increasingly recognized cause of restrictive cardiomyopathy in which extracellular amyloid deposition leads to progressive structural and functional impairment. Beyond myocardial infiltration, growing evidence highlights the central role of autonomic nervous system dysfunction (ANS) —particularly the vagal nerve involvement—as a contributor to orthostatic intolerance, syncope, exercise limitation, arrhythmias, and reduced quality of life. Emerging data suggest that autonomic impairment may precede overt cardiac manifestations, offering a potential window for earlier recognition. This narrative review summarizes current knowledge on the mechanisms and clinical relevance of autonomic dysfunction in CA, emphasizing the novelty of the “vagal link” as a unifying framework connecting with a specific focus on the vagus nerve (VN) and its complex interplay with cardiac structure and function. We further discuss diagnostic approaches and the potential role of autonomic assessment in early detection, risk stratification, and personalized treatment strategies. A clearer understanding of vagal dysfunction may provide new insights into disease progression and identify opportunities for therapeutic innovation. Full article

Background and Objectives: Cardiac autonomic neuropathy (CAN) is a common but also underdiagnosed complication of diabetes mellitus (DM), associated with high cardiovascular risk and mortality. Sudomotor dysfunction can serve as an early indicator of autonomic dysfunction. This study evaluated the association between sudomotor dysfunction and the severity of CAN in patients with type 2 diabetes (T2D). Materials and Methods: In this cross-sectional study, 109 patients with T2D were evaluated for diabetic peripheral neuropathy, cardiovascular autonomic dysfunction, and sudomotor dysfunction. Additionally, clinical and biochemical data were collected from patients’ medical records. Results: Sudomotor dysfunction (SUDO+) was present in 59.6% of patients. The presence of SUDO+ was associated with a higher age, longer duration of diabetes, lower eGFR (estimated glomerular filtration rate) values, and more severe signs of peripheral neuropathy. SUDO+ patients showed significantly greater orthostatic systolic and diastolic BP (blood pressure) changes, lower RR interval ratios, and lower feet ESC (electrochemical skin conductance) values. ROC (receiver operating characteristic) analysis for feet ESC in identifying pathological RR ratio showed an AUC of 0.689 (95% CI: 0.593–0.774, p = 0.0022), with a sensitivity of 46.7% and a specificity of 94.7% at a cutoff of ≤68 µS. For orthostatic hypotension and QTc prolongation, the ESC values had limited discriminative power. Chi-squared analysis showed a significant association between feet sudomotor impairment and pathological RR ratio (χ² = 6.521, p = 0.0107). Conclusions: Sudomotor dysfunction is associated with indicators of CAN. SUDOSCAN can be used as a complementary tool for early CAN detection in clinical practice. Full article

Background/Objectives: Sarcoidosis is a systemic inflammatory disease that can cause cardiac autonomic dysfunction (SCAD), often underrecognized despite its clinical importance. While [¹⁸F]fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography ([¹⁸F]FDG PET/CT) and cardiac magnetic resonance imaging (CMR) assess cardiac involvement, [¹²³I]-meta-iodinebenzylguanidine ([¹²³I]MIBG) scintigraphy evaluates cardiac sympathetic innervation, offering complementary insights to potentially improve SCAD detection and management. This retrospective study explores the role of [¹²³I] MIBG scintigraphy in detecting SCAD among patients with unexplained cardiac symptoms. It focuses on its potential to provide complementary diagnostic information in patients where established imaging techniques, such as [¹⁸F]FDG PET/CT and CMR, fail to detect cardiac sarcoidosis. Methods: Sarcoidosis patients referred to the St. Antonius Hospital (2017–2024) who underwent [¹²³I]MIBG scintigraphy were included. Collected data encompassed demographics, SCAD symptoms, cardiac imaging findings, and carvedilol treatment outcomes. [¹²³I] MIBG abnormalities were defined as a heart-to-mediastinal ratio ≤1.6 or a washout rate ≥20%. Results: Among the final cohort of 40 sarcoidosis patients with unexplained cardiac symptoms and normal [¹⁸F]FDG PET/CT and CMR findings, 19 patients (48%) showed abnormal [¹²³I] MIBG scintigraphy results suggestive of SCAD. No significant differences were observed in clinical characteristics between patients with normal and abnormal [¹²³I]MIBG findings. Of the 16 patients treated with carvedilol, 88% reported symptom improvement, although 50% experienced side effects. Conclusions: [¹²³I]MIBG scintigraphy revealed abnormalities in a substantial number of sarcoidosis patients with unexplained cardiac symptoms despite normal [¹⁸F]FDG PET/CT and CMR. These findings indicate a potential role for [¹²³I]MIBG in detecting SCAD, but prospective studies are needed to confirm their clinical significance. Full article

Background/Objectives: Diabetic neuropathy (DN) is one of the most common and disabling complications of diabetes mellitus (DM), affecting motor, sensory, and autonomic nerves. Genetic factors, particularly polymorphisms in the Angiotensin-converting enzyme (ACE) gene, have been proposed as contributors to DN susceptibility. This study aimed to synthesize the scientific evidence on ACE gene polymorphisms and their association with DN through a scoping review combined with scientometric analysis. Methods: A comprehensive search of PubMed, Scopus, and Web of Science was performed in February 2025, following JBI and PRISMA-ScR guidelines. Observational studies involving individuals with DN and the genotyping of ACE polymorphisms were included. Scientometric mapping was conducted using the Bibliometrix package in RStudio to identify publication trends and key thematic terms. Results: From 100 screened articles, 11 met the inclusion criteria. Most studies (72.7%) addressed diabetic peripheral neuropathy, while 27.3% investigated cardiac autonomic neuropathy. All studies analyzed the I/D polymorphism in intron 16 of the ACE gene. The D allele and DD genotype were associated with increased susceptibility to DN in over half of the studies (6/11), while the II genotype was reported as protective in 3/11. Findings varied by ethnicity and study design. The scientometric analysis identified ‘peripheral diabetic neuropathy’, type 2 diabetes’, and ‘ACE gene polymorphism’ as the most frequently co-occurring terms, indicating that research on this topic has been concentrated around these themes, while showing limited diversity in geographic origin and scope. Conclusions: ACE I/D polymorphism appears to modulate susceptibility to DN, though interethnic variability and methodological heterogeneity challenge definitive conclusions. Broader, standardized studies are needed to validate its utility as a predictive biomarker. Full article

Aim: To compare diabetic polyneuropathy (DPN) and cardiac autonomic neuropathy (CAN) between T1DM and T2DM patients. Methods: This study enrolled 66 T1DM and 79 T2DM patients. DPN was evaluated using three different methods: clinical examination, using neuropathy symptom score (NSS) and neuropathy disability score (NDS), current perception threshold (CPT) using Neurometer, and nerve conduction studies (NCSs). CAN was assessed by cardiovascular autonomic reflex tests (CARTs). Results: The prevalence of DPN did not differ between T1DM and T2DM (p > 0.05 for all), however, the proportion of DPN depended on the method used and was highest with CPT (53.0% vs. 46.8%), followed by NCSs (44.1% vs. 41.2%) and clinical examination (25.8% vs. 31.6%). T2DM vs. T1DM patients were more often diagnosed with painful DPN (51.9% vs. 27.3%, p = 0.004), reduced perception of vibration (72.2% vs. 48.5%, p = 0.006), and autonomic neuropathy (59.5% vs. 32.3%, p = 0.001), while NCSs revealed more prevalent motor nerve dysfunction in T1DM compared to T2DM (41.2% vs. 19.6%). Multivariate regression analysis showed increased DPN risk with age and CAN risk with worsening of eGFR in T1DM. No significant associations remained after multivariate adjustment for T2DM. Conclusions: The prevalence of DPN is highly varied and depends on the diagnostic method used. T2DM patients more often had symptoms and signs of diabetic neuropathy. However, stronger associations with risk factors were observed in T1DM. Full article