Search Results (56)

(1) Background: Whether spatial predictive patterns in non-communicable disease mortality persist after accounting for socio-demographic development and biomarkers remains understudied in East Africa. (2) Methods: This study used heterogeneous graph transformer (HGT) models and other techniques to model spatial patterns in cause- and sex/age-specific mortality (hypertensive heart disease [HHD], ischaemic heart disease [IHD], stroke, and diabetes), incorporating risk factors and socio-demographic development (SDI), using data from the Global Burden of Disease (GBD) study, 1990–2023, across Burundi, Kenya, Rwanda, Tanzania, and Uganda. (3) Results: HGT achieved higher performance than OLS spatial lag benchmarks (R² 0.948–0.970 vs. 0.194–0.376). Spatial predictive patterns were disease-specific. Stroke was the only disease with consistent positive spatial structure (SDI-only: 0.645%, 95% CI [0.380, 0.907]), with spatial structure strengthening after 2015. HHD exhibited severe and stable degradation (Risk-only: −137.892%, 95% CI [−181.908, −96.380]), driven by the interaction between metabolic risk covariates and geographic adjacency. Diabetes showed consistently severe degradation (SDI + Risk: −201.941%, 95% CI [−257.349, −150.082]). IHD patterns were weak and unstable. Sex disaggregation revealed stronger stroke spatial signals, indicating latent sex-specific patterns masked by aggregation. GBD measurement uncertainty contributed less than 0.025% of result variance, with model randomness dominating. (4) Conclusions: Spatial predictive patterns in NCD mortality in East Africa are disease-specific. Stroke shows emerging cross-border spatial structure after 2015, while HHD and diabetes reflect country-specific determinants. Sex-disaggregated graph construction reveals latent spatial heterogeneity invisible to aggregate models, supporting disease-specific, sex-stratified regional health strategies. Full article

Arterial hypertension in adolescents is increasingly a lifestyle-driven disorder, and a growing share of cardiovascular risk in this age group is hidden from conventional office measurement. Intensive nighttime screen use, together with the chronic sleep loss that accompanies it, may disrupt circadian control of the cardiovascular system, an effect we designate, as a proposed integrative concept, digital chronotoxicity. Through melatonin suppression, sustained sympathetic and neuroendocrine activation, oxidative stress, and metabolic dysregulation, this exposure is hypothesized to attenuate the physiological nocturnal fall in blood pressure and to contribute to the non-dipper phenotype, a predictor of early vascular aging that remains invisible to office readings. This narrative review traces the mechanistic pathway from screen exposure to the loss of nocturnal dipping and reframes the problem as a diagnostic one. Twenty-four-hour ambulatory blood pressure monitoring is positioned as the reference standard for detecting the at-risk phenotype and masked hypertension; the cardiac, vascular, renal, autonomic, and neurocognitive biomarkers of early hypertension-mediated organ damage are reviewed; and emerging wearable and artificial-intelligence tools for continuous, preventive screening are examined. An integrated screening pathway is proposed, on the premise that the evaluation of a hypertensive adolescent is incomplete without a digital and sleep history alongside ambulatory monitoring. Reframed in this way, pediatric hypertension becomes a detectable chronobiological disease. Full article

Arterial stiffness is a determinant of cardiovascular risk and has been increasingly associated with obstructive sleep apnea (OSA), although its independent contribution remains unclear due to the presence of comorbidities, the most important of which is hypertension. This narrative review synthesizes current evidence on the relationship between OSA, hypertension, and arterial stiffness, with a particular focus on the mediating role of hypertension and its clinical phenotypes. Evidence from observational and longitudinal studies indicates that OSA is generally associated with increased arterial stiffness, particularly in younger and normotensive individuals. A stepwise increase in pulse wave velocity (PWV) is consistently observed across control, OSA, hypertension, and combined OSA–hypertension groups, supporting an additive vascular burden. Hypertension emerges as a central correlate and amplifier of vascular remodeling, with its presence attenuating the independent association between OSA and arterial stiffness. Findings regarding masked hypertension are heterogeneous, with some studies showing increased PWV in OSA while others demonstrate minimal differences after adjustment. In contrast, resistant hypertension is consistently associated with high-risk hemodynamic and metabolic profiles, although the independent contribution of OSA to arterial stiffness in this group is often limited after multivariable adjustment. Large cohort evidence further suggests that associations between OSA and arterial stiffness surrogates are largely explained by age, blood pressure status, and cardiometabolic comorbidities. Because the evidence base is predominantly cross-sectional, these findings should be interpreted as showing that OSA’s association with arterial stiffening is closely intertwined with the presence and development of hypertension, rather than establishing a causal or temporal sequence. Future longitudinal and interventional studies are needed to clarify causal pathways and therapeutic implications. Full article

Continuous and noninvasive blood pressure (BP) monitoring is important for hypertension screening and long-term cardiovascular management. Continuous BP estimation using photoplethysmography (PPG) and electrocardiography (ECG) has become a promising alternative to conventional cuff-based measurements. However, handcrafted feature-based methods are sensitive to fiducial point detection, while end-to-end deep models often require large labeled datasets and may ignore subject-specific BP baselines. This study proposes a personalized calibration and hybrid feature fusion framework for continuous BP estimation from ECG and PPG signals. The framework integrates physiologically interpretable handcrafted features, self-supervised waveform representations, and subject-specific prior BP information to predict systolic and diastolic BP. The handcrafted branch extracts pulse transit time, heart rate variability, and PPG morphological descriptors, whereas a masked reconstruction-based self-supervised encoder learns latent waveform embeddings without BP labels. Personalized calibration incorporates base BP from the earliest calibration file through an alpha-weighted strategy, and the fused representation is fed into XGBoost regressors. The framework was evaluated on a private dataset and the BP-UCI dataset, achieving SBP/DBP MAEs of 7.25/3.98 mmHg and 7.85/4.02 mmHg, respectively. Comparative and ablation results indicate improved baseline performance in the current experimental setting, suggesting the methodological feasibility of the proposed framework for small-sample continuous BP estimation. Further validation with larger and more diverse cohorts is still required. Full article

Cardiac tamponade in pregnancy is an exceptional maternal–fetal emergency in which physiological tachycardia, hypervolaemia and dependent oedema mask the classical signs of tamponade. Corynebacterium amycolatum is a non-diphtherial, Gram-positive coryneform commensal of human skin and mucosa that is increasingly recognised as a true invasive pathogen, although pericardial infection has rarely, if ever, been reported. We aimed to describe the diagnostic and decompression strategy in such a case. We report a 29-year-old woman at 30 + 4 weeks of gestation with class III obesity (pre-pregnancy body mass index 36 kg/m²), pregnancy-induced hypertension and diet-controlled type 2 diabetes referred after a routine echocardiogram suggested tamponade despite preserved haemodynamic compensation. Transthoracic echocardiography demonstrated a large circumferential pericardial effusion with diastolic right-atrial and right-ventricular collapse, a plethoric inferior vena cava and respiratory mitral-inflow variation. Severe maternal obesity superimposed on advanced gestation degraded the acoustic windows, elevated the diaphragm, displaced the heart anteriorly and brought the gravid uterus into the subxiphoid corridor, rendering percutaneous pericardiocentesis prohibitively hazardous. After multidisciplinary heart-team review, a left anterior mini-thoracotomy with pleuro-pericardial window evacuated approximately 1000 mL of fluid. Aerobic culture yielded C. amycolatum (MALDI-TOF), with histological pericarditis and a consistent antibiogram; autoimmune, viral and neoplastic causes were excluded, although blood cultures and extended viral testing were not performed. Targeted intravenous cefazolin was given, and the patient delivered a healthy term neonate at 39 weeks, with a normal 7-month echocardiogram. To the best of our knowledge, this is among the first reported cases of C. amycolatum pericardial tamponade in pregnancy. Because blood cultures and molecular confirmation of pericardial involvement were not obtained, a contaminant or incidental role for the organism cannot be entirely excluded, and the causal attribution should be regarded as probable rather than definitive. The case highlights heart-team-based individualised decompression and the cautious microbiological interpretation of organisms traditionally regarded as commensals. Full article

Background: Routine fundus photography is widely accessible; however, its utility in stratifying systemic vascular risk in asymptomatic, general populations remains understudied. We utilized a large-scale health screening cohort in South Korea to evaluate the clinical validity of the retinal arteriosclerosis index (RAI) in a generally healthy population. Methods: We conducted a cross-sectional study of 74,608 adults who underwent routine health screening (2003–2010) at a tertiary center. Retinal arteriosclerosis was graded (0–4) by masked readers with a modified Scheie classification; a higher eye grade was defined as a person-level grade. High-grade RAI was prespecified as ≥2. Associations with systemic conditions (hypertension, type 2 diabetes, hyperlipidemia, metabolic syndrome, cardiovascular disease, and stroke) were examined by using multivariable logistic regression adjusted for demographic, lifestyle, and laboratory covariates; moreover, analyses were stratified by age and sex. Results: High-grade RAI was present in 4.5% of the participants and increased with age. After adjustment, high-grade RAI was associated with hypertension (OR, 2.97; 95% CI, 2.73–3.23), diabetes mellitus (OR, 1.35; 95% CI, 1.22–1.50), cardiovascular disease (OR, 1.46; 95% CI, 1.25–1.71), metabolic syndrome (OR, 1.63; 95% CI, 1.49–1.78), and stroke (OR, 1.98; 95% CI, 1.41–2.79) but not with hyperlipidemia. Sex-stratified analyses revealed broadly similar patterns, although high-grade RAI was associated with stroke in women and cardiovascular disease in men. Age-stratified analyses demonstrated consistent associations with hypertension, metabolic syndrome, and stroke across all age groups, with stronger effect sizes being observed in younger individuals. With respect to lifestyle factors, frequent alcohol consumption was associated with higher odds of high-grade RAI. Laboratory correlates included higher uric acid levels and lower red blood cell, albumin, and bilirubin levels (all p < 0.001). Conclusions: Fundus-defined arteriosclerotic changes were independently associated with multiple systemic vascular and metabolic conditions. An association with stroke in adults younger than 40 years of age was also observed, although this finding should be interpreted with caution given the cross-sectional design and limited number of events. These findings support the potential role of retinal vascular changes as cross-sectional correlates of systemic vascular health. Longitudinal studies are needed to clarify temporal relationships and causality. Full article

Background: Kounis syndrome is an allergic acute coronary syndrome precipitated by coronary vasospasm, plaque destabilization, stent thrombosis, or bypass occlusion. Cardiac surgery represents a uniquely high-risk setting due to cardiopulmonary bypass–associated inflammation and exposure to multiple pharmaceutical agents. Importantly, Kounis syndrome remains underrecognized in this context, as classical signs of anaphylaxis may be masked under general anesthesia and cardiopulmonary bypass, while ischemic manifestations may be misattributed to other perioperative conditions. Methods: A narrative review of PubMed-indexed literature was conducted to synthesize current evidence on the pathophysiology, perioperative triggers, clinical presentation, diagnostic strategies, and management of Kounis syndrome in cardiac surgery, with emphasis on intraoperative recognition and surgical decision-making. Published cases were retrieved involving perioperative cardiac surgery patients with a definite diagnosis of Kounis syndrome. Additionally, cases presenting with severe perioperative anaphylaxis and life-threatening cardiovascular involvement (grade III with cardiovascular collapse and grade IV with cardiac arrest) were included as possible Kounis syndrome, reflecting real-world diagnostic uncertainty in the intraoperative setting. Results: The literature review identified five cases of definite Kounis syndrome and ten cases of possible Kounis syndrome, including three cases with cardiovascular collapse and seven cases with cardiac arrest. Recurrent episodes were reported in several patients, particularly due to re-exposure to the triggering agent. In the context of cardiac surgery, Kounis syndrome is most frequently triggered by chlorhexidine, protamine, antibiotic prophylaxis, and anesthetic agents. The clinical presentation is often subtle during cardiopulmonary bypass. Vasoplegia, pulmonary hypertension, ventricular dysfunction, new regional wall-motion abnormalities, and hyperdynamic ventricles on transesophageal echocardiography commonly precede overt electrocardiographic changes. Diagnosis is primarily clinical and relies on intraoperative ultrasound, hemodynamic monitoring, serum tryptase, serum troponin, and, when indicated, coronary angiography. A dual-pathway approach addressing both anaphylaxis and myocardial ischemia is essential; however, one component may predominate, particularly in perioperative patients with limited clinical information, potentially leading to misdiagnosis. A multidisciplinary approach is therefore required for rapid diagnosis and individualized management. In refractory cases, cardiopulmonary bypass or ventricular assist devices may provide lifesaving support. Conclusions: Kounis syndrome remains underrecognized in cardiac surgery but carries significant morbidity. Increased clinical awareness, multidisciplinary collaboration, structured diagnostic approaches, and preventive strategies are essential to improve outcomes and reduce the risk of recurrence during future procedures. Full article

Emergent tracheal intubation in critically ill patients is a common, yet high-risk, intervention. It is frequently complicated by peri-intubation hypoxemia, hemodynamic instability, and metabolic derangements that increase the risk of arrhythmias, hypotension, cardiac arrest, and death. Because the highest-risk interval often occurs in the minutes surrounding induction, when apnea, derecruitment, and abrupt cardiopulmonary shifts converge, oxygenation failure frequently reflects a mismatch between preoxygenation strategy and the underlying physiology rather than inadequate oxygen delivery alone. This review proposes a phenotype-based approach to peri-intubation oxygenation and focuses on four high-risk phenotypes in whom standard preoxygenation strategies commonly fail: obesity, neuromuscular disease, right ventricular dysfunction or pulmonary hypertension, and post-operative respiratory failure with altered respiratory mechanics or airway anatomy. We summarize the key mechanisms that shorten safe apnea time, including reduced functional residual capacity, intrapulmonary shunt, elevated oxygen consumption, rapid derecruitment after induction, and impaired oxygenation–hemodynamics coupling. We then compare preoxygenation modalities as physiologic tools, including facemask oxygen, high-flow nasal cannula (HFNC), noninvasive ventilation (NIV), and controlled bag-mask ventilation (BMV), and integrate contemporary randomized trial evidence that informs bedside selection and combination of these approaches. Finally, we synthesize these concepts into a practical, physiology-informed framework to guide clinicians in choosing and troubleshooting preoxygenation strategies in high-risk patients undergoing emergent intubation. Full article

Background and Clinical Significance: Pulmonary hypertension (PH) is a recognized complication of chronic liver disease, most commonly manifesting as portopulmonary hypertension (POHP) prior to liver transplantation. While the natural history and management of pre-transplant PH are well described, the development of de novo pulmonary arterial hypertension (PAH) following liver transplantation remains exceedingly rare and poorly understood. In such cases, establishing true causality is challenging, and alternative explanations—including previously unrecognized or masked disease—must be carefully considered. This entity poses significant diagnostic and therapeutic challenges and may adversely affect post-transplant outcomes if not promptly recognized and treated. Case Presentation: We report the case of a 46-year-old man with end-stage liver disease secondary to alcohol use who underwent deceased donor liver transplantation without preoperative evidence of PH. His pre-transplant evaluation revealed preserved biventricular function and no measurable PH. Eight days postoperatively, he was readmitted with acute dyspnea, hypoxemia, and signs of right ventricular failure. Transthoracic echocardiography demonstrated severe right ventricular dilation and dysfunction with markedly elevated pulmonary artery systolic pressure. Right heart catheterization confirmed severe PAH. Secondary causes of PH were excluded. The patient was initiated on sildenafil and continuous intravenous epoprostenol, resulting in clinical, echocardiographic, and hemodynamic improvement. Subsequent follow-up demonstrated sustained response to therapy despite concurrent progression of coronary artery disease requiring complex percutaneous intervention. Conclusions: This case highlights a rare presentation of severe PAH occurring shortly after liver transplantation, in the absence of documented pre-transplant PH. While a causal relationship cannot be definitively established, the temporal association raises important clinical considerations. It underscores the need for heightened clinical vigilance for pulmonary vascular disease in post-transplant patients presenting with cardiopulmonary symptoms. Further research is warranted to elucidate the underlying mechanisms, risk factors, and optimal management strategies for PAH diagnosed after liver transplantation. Full article

Background/Objectives: Laparoscopic sleeve gastrectomy (LSG) treats severe obesity, but data on its effects on 24 h blood pressure (BP) patterns, blood pressure variability (BPV), and cardiac autonomic nervous system (CANS) in obese patients without hypertension or diabetes are limited. We evaluated these parameters before and after LSG. Methods: 78 patients with severe obesity (BMI ≥ 40 kg/m²) without hypertension or diabetes who underwent LSG between January 2016 and December 2019 were included in the study. Patients underwent ambulatory blood pressure monitoring (ABPM), ambulatory electrocardiographic monitoring, and laboratory tests before and six months after surgery. Results: Preoperative ABPM was characterized by a significant proportion of masked hypertension (43.5%), high 24 h BP (mean SBP 138.9 ± 5.5 mmHg, DBP 81.1 ± 4.9 mmHg), high BP load (39% SBP, 38% DBP), and a non-dipper pattern (67.9%). After LSG, significant improvements were observed in mean 24 h SBP, DBP (p < 0.001), BPV, BP load, and non-dipper patterns. HRV parameters (SDANN, RMSSD) increased significantly (p < 0.001) and HRT parameters improved: TO became more negative from −0.54 ± 1.73 to −2.53 ± 1.97, TS increased from 5.98 ± 3.49 to 9.87 ± 4.28 ms/RR (p < 0.001). We found a strong association between decreased body mass index and BP changes. Changes in glucose, HbA1c, and HOMA-IR predicted CANS improvement (β = 0.24–0.38; R² = 20.8–29.7%). Conclusions: Six months after LSG, significant improvements in BP, BPV, and CANS were observed. BP reduction was primarily associated with weight loss, while glucose control was associated with autonomic improvements. LSG was associated with early improvements in surrogate cardiovascular risk markers through combined weight-dependent and metabolic-hormonal mechanisms. Full article

Hypertension has traditionally been viewed as a hemodynamic disorder leading to cardiac and renal injury; however, growing evidence suggests that, in many individuals, elevated blood pressure is instead the earliest clinical expression of subtle cardiorenal dysfunction. Early abnormalities—such as low-grade albuminuria, increased renal resistive index, arterial stiffness, and masked or nocturnal hypertension—can appear before estimated glomerular filtration rate decline or elevated office blood pressure, indicating early impairment of pressure–natriuresis, heightened tissue renin–angiotensin–aldosterone system (RAAS) activity, and increased renal microvascular impedance. The aim of this review is to summarize mechanistic, clinical, and phenotypic evidence supporting the concept that hypertension functions as an early biomarker along the cardiorenal continuum. Incorporating vascular and renal biomarkers, ambulatory blood pressure phenotyping, and targeted laboratory indices into routine assessment may identify individuals transitioning from functional disturbances to structural organ damage. These abnormalities reflect a mechanistic triad of arterial stiffening, salt-sensitive RAAS activation, and circadian blood pressure disruption, collectively defining the early cardiorenal–hypertensive phenotype. Viewing hypertension through a cardiorenal lens underscores a critical opportunity for earlier detection and mechanism-oriented intervention, which may modify disease trajectory and prevent progression to overt chronic kidney disease and heart failure. Full article

Hypertension in adolescence causes early vascular injury manifesting as endothelial dysfunction (ED), which signifies elevated cardiovascular risk. This review synthesizes recent insights (2020–2025) into ED’s mechanisms and detection in hypertensive youth. We highlight how reduced nitric oxide bioavailability, oxidative stress, inflammation, and hormonal changes in puberty contribute to ED and consequent vascular remodeling. Non-invasive diagnostic tools (e.g., flow-mediated dilation, peripheral arterial tonometry) reveal that even asymptomatic hypertensive adolescents have measurable ED linked to arterial stiffness and cardiac changes. Encouragingly, ED in youth appears reversible: exercise and dietary interventions improve endothelial function, and pharmacotherapy (ACE inhibitors, ARBs) can restore endothelial health beyond blood pressure control. Early identification of ED in hypertensive adolescents is therefore critical—it not only refines risk stratification (e.g., unmasking high-risk “white-coat” hypertension) but also presents an opportunity to initiate lifestyle modifications and therapy to preserve vascular function. Full article

Background: For patients on hemodialysis, routine blood pressure (BP) measurements taken shortly before or after dialysis provide inaccurate estimates of the BP load during the interdialytic period. In this study, we used peridialytic recordings in combination with interdialytic ambulatory BP monitoring (ABPM) aiming to provide a more precise assessment of hypertension in a sample of 70 stable hemodialysis patients. Methods: The evaluation of hypertension in the study cohort was performed using the following approaches: (i) routine predialysis and postdialysis BP measurements taken by the dialysis-unit staff were prospectively recorded over six consecutive dialysis sessions; (ii) ABPM was performed using the Microlife WatchBPO3 device (20 min intervals during an entire 44 h interdialytic period). The diagnostic thresholds of hypertension were ≥140/90 mmHg for predialysis, ≥130/80 mmHg for postdialysis and ≥130/80 mmHg for 44 h ambulatory BP, respectively. Patients receiving ≥1 antihypertensive medication also were classified as hypertensives. Results: The prevalence of hypertension was 88.6% by predialysis, 92.9% by postdialysis and 90.0% by ambulatory BP measurements. In all, 87.1% of patients were being treated for hypertension. When the combination of predialysis and 44 h ambulatory BP was evaluated, the prevalence of sustained normotension, white-coat, masked and sustained hypertension was 52.9%, 21.4%, 5.7% and 20.0%, respectively. A similar distribution of patients into these phenotypes was observed when postdialysis BP was used for the classification of the severity of hypertension (50.0%, 24.3%, 5.7% and 20.0% for sustained normotension, white-coat, masked and sustained hypertension, respectively). Interdialytic ABPM revealed that just one patient had abnormal BP solely during the daytime period. Conversely, isolated nocturnal hypertension was diagnosed in 27.1% of patients. Conclusions: This study shows that among patients on hemodialysis, peridialytic BP is an inaccurate proxy of interdialytic ambulatory BP. In approximately 30% of patients, there is discordance between routine peridialytic recordings and interdialytic ABPM for the diagnosis of hypertension. ABPM also facilitates the diagnosis of isolated nocturnal hypertension, which is another frequent BP phenotype in this high-risk patient population. Full article

Background/Objectives: This exploratory study aimed to assess the prevalence of retinal ischemic perivascular lesions (RIPLs) in individuals with cardiovascular disease (CVD) or associated risk factors and to investigate their potential role as non-invasive biomarkers of systemic ischemia using optical coherence tomography (OCT). Methods: A prospective observational study was conducted between July and October 2022. A total of 665 participants aged 40–90 years underwent macular OCT imaging using the Topcon Maestro 2 system. Participants were classified into two groups: those with ischemic CVD or risk factors (n = 297) and healthy individuals without cardiovascular conditions (n = 368). RIPLs were defined by inner nuclear layer thinning and outer nuclear layer expansion in perivascular regions and were identified by masked consensus of three independent evaluators. Results: The overall prevalence of RIPLs was 0.75% (five cases), exclusively observed in the diseased group (1.68%), with no cases identified among healthy individuals (p = 0.044). Stratified analysis showed an increase in RIPL prevalence with age, reaching 2.24% in the 70–79 years cohort. Statistically significant associations were found between RIPLs and hypertension, dyslipidemia, ischemic heart disease, and thrombosis (all p < 0.001). No significant association was observed with sex, myocardial infarction, or RIPL presence as an independent predictor (p = 0.08). Conclusions: Their identification through OCT during routine ophthalmologic examinations highlights a possible new avenue for early cardiovascular risk stratification. Nevertheless, the extremely low number of RIPL cases detected (only five out of six hundred and sixty-five participants; 0.75%) significantly limits the statistical power of the analysis and precludes strong conclusions. These findings should be regarded as preliminary and hypothesis-generating, requiring confirmation in larger, more diverse populations. Full article

Background/Objectives: Masked uncontrolled hypertension (MUCH) is a blood pressure phenotype prevalent among chronic kidney disease (CKD) patients. It has been associated with an elevated risk of cardiovascular morbidity and mortality. Identifying MUCH predictor factors in this population is crucial in facilitating anticipation of adverse outcomes and complications. Methods: For a period of 7 years (2017–2023), hypertensive patients presenting CKD and in-office normotension (<140/90 mmHg) were consecutively selected. After ambulatory blood pressure monitoring (ABPM), we classified the patients into controlled hypertension (CH) or MUCH. We used epidemiological, clinical, anthropometric, and laboratory data to develop a predictor model of the MUCH phenotype. Results: From 220 participants, 109 (49.5%) had MUCH (mean age: 60 ± 16 years; 45% men; 35% with obesity). Higher diastolic BP (DBP) values were observed in the MUCH group (72 vs. 75; p = 0.01). In contrast, a higher body mass index was observed in the CH group (26 vs. 28; p < 0.01), while elevated albuminuria was observed in the MUCH group (69 vs. 275; p < 0.01). After multivariate analysis, DBP ≥75 mmHg (Odds Ratio: 1.93, 95%CI 1.03–3.64; p = 0.04), BMI ≤25 Kg/m² (Odds Ratio: 2.21, 95%CI 1.08–4.52; p = 0.03), and albuminuria ≥ 300 mg/g (Odds Ratio: 3.26, 95%CI 1.71–6.19; p < 0.01) were identified as predictors of MUCH phenotype Conclusions: MUCH is common in patients with arterial hypertension (AH) and CKD. DBP ≥ 75 mmHg, BMI ≤ 25 Kg/m², and albuminuria ≥ 300 mg/g were predictors of MUCH in these patients. Full article