Injury In Hypertensive Patients Research Articles

The potential Role of CYP2D6*10(c.100 C>T) Gene Polymorphism in Kidney Injury of Patients with Hypertension Complicated with Non-Elevated Cystatin C.

This study aims to investigate the potential role of CYP2D6*10 (c.100 C>T) gene polymorphism in renal function injury among hypertensive patients without elevated cystatin C. A cohort of hypertensive patients without elevated cystatin C was enrolled between 2021 and 2024 in the Fourth Affiliated Hospital of Soochow University, and their peripheral venous blood was used for total RNA extraction and CYP2D6*10 genotype analysis. Based on kidney injury status, patients were categorized into two groups, hypertensive patients with kidney injury (n = 94) and those without (n = 893). General characteristics such as age, gender and hyperlipemia were compared between the two groups. Multiple genotype models were investigated between the two groups, including allele models, dominant models, recessive models, co-dominant models, and super-dominant models. The results revealed that in the co-dominant gene model (CC vs. CT vs. TT), the risk of hypertension combined with renal injury was lower with the CT genotype compared to the CC genotype (Odds Ratio (OR) = 0.55, 95% Confidence Interval (CI) = 0.32-0.93, p = 0.02). In the overdominance model (CC + TT vs. CT), the risk of hypertension and renal injury in CC and CT genotypes was 0.42 times lower than that in the CT genotype (OR = 0.42, 95% CI = 0.27-0.64, p < 0.001). This study proposes CYP2D610 gene polymorphism as a potential predictor of renal function injury in hypertensive patients with normal cystatin C levels.

THE POTENTIAL ROLE OF CYP2D6∗10(C.100 C&gt;T) GENE POLYMORPHISM IN KIDNEY INJURY OF PATIENTS WITH HYPERTENSION COMPLICATED WITH NON-ELEVATED CYSTATIN C

Objective: This study aims to investigate the potential role of CYP2D6∗10 (c.100 c&gt;t) gene polymorphism in renal function injury among hypertensive patients without elevated cystatin C. Design and method: A cohort of hypertensive patients without elevated cystatin C was recruited, and the CYP2D6∗10 genotype was analyzed. The objective was to evaluate the association between CYP2D6∗10 gene polymorphism and renal function injury by comparing patients with different genotypes. Genetic equilibrium was assessed using the Hardy-Weinberg equilibrium test. Polymorphic genotype frequencies between case and control groups were examined using the Chi-square test, with statistical significance set at p&lt;0.05. Results: Among the hypertensive patients in the study, a significant correlation was observed between CYP2D6∗10 genotype and renal function injury (p&lt;0.05) in codominant model and super-dominant model. Patients with the CYP2D6∗10 genotype exhibited more severe renal function damage. Conclusions: This study proposes CYP2D610 gene polymorphism as a potential predictor of renal function injury in hypertensive patients with normal cystatin C levels. Further research is crucial to validate this association and delve into the specific mechanisms through which the CYP2D610 genotype influences renal function injury in hypertensive individuals.

Association between obstructive sleep apnea and vascular injury in hypertensive patients

Objective: To investigate the relationship between obstructive sleep apnea (OSA), apnea hypopnea index (AHI) and vascular injury in hypertensive patients. Methods: This cross-sectional study enrolled patients admitted to the Hypertension Department of TEDA International Cardiovascular Hospital from April 2020 to April 2023, who finished portable sleep monitoring. Sleep monitoring indicators, flow-mediated vasodilation (FMD), carotid artery ultrasound, carotid intima-media thickness, cervical and femoral pulse wave conduction velocity (cfPWV), brachial and ankle pulse wave conduction velocity (baPWV) were analyzed. OSA was classified into mild (5 times/h≤AHI<15 times/h), moderate (15≤AHI<30 times/h), and severe (AHI≥30 times/h) based on AHI levels. FMD<6.0% was defined as vascular endothelial injury, and cfPWV>10 m/s and/or baPWV>18 m/s was defined as arterial stiffness. Multivariate logistic regression analysis was used to explore the correlation between AHI, OSA severity and vascular injury, and subgroup analysis was performed in young (age≤45 years) and middle-to-old patients (age>45 years). Sensitivity analysis was performed by excluding patients with diabetes, cerebrovascular disease and coronary heart disease. The correlation between AHI and vascular injury index was analyzed by restricted cubic spline. Results: A total of 555 adult hypertensive patients were included, the mean age was (39.7±9.2) years, 422 were males (76.0%), and the prevalence of OSA was 66.7% (370/555). Multivariate logistic regression analysis showed that moderate OSA (OR=2.83, P=0.019) and severe OSA (OR=3.40, P=0.016) were positively correlated with vascular endothelial injury after adjusting for age, sex, body mass index and mean arterial pressure. Subgroup analysis showed that log AHI (OR=1.99, P=0.035), moderate OSA (OR=4.83, P=0.010) and severe OSA (OR=4.64, P=0.015) were associated with vascular endothelial injury in young hypertensive patients. The results of sensitivity analysis were similar to the above results. The results of restricted cubic spline analysis showed that AHI was correlated with FMD (P=0.022), and the slope of the curve was the largest when AHI was between 0 and 10 times/h. There was no correlation between log AHI and OSA severity and carotid intima-media thickening and arterial stiffness (all P<0.05). Conclusions: OSA is associated with vascular endothelial injury in hypertensive patients, especially in young patients.

New insights on the mechanisms of myocardial injury in hypertensive patients with COVID-19

Abstract Introduction Cardiac comorbidities, particularly hypertension, are highly prevalent in patients hospitalized with COVID-19 and are related directly to the risk of clinical disease progression. Cardiac injury is the most frequently reported cardiac abnormality in these patients. Diverse forms and mechanisms of myocardial injury, including acute myocardial ischemia due to plaque rupture, oxygen supply/demand imbalance, non-ischemic injuries such as myocarditis, direct virus-mediated injury, and immune system dysregulation, have been described in patients with COVID-19. Purpose The mechanism of the association among hypertension, COVID-19 and cardiac injury and the reasons for worse clinical progression in these patients have not been elucidated clearly. Considering that myocardial injury due to direct SARS-CoV-2 infection is rare and that the immune system is often dysregulated in patients with COVID-19, and also that cytokine storm and lymphopenia are important immune markers of progression to severe disease, the present study aimed to investigate the immune profile of hypertensive patients with COVID-19 and myocardial injury to obtain a better understanding of the immune dysregulation and to provide new insights on the mechanism of myocardial injury in hypertensive patients with this disease. Methods All patients were selected prospectively from a multicenter registry of adults hospitalized with confirmed COVID-19. Cases had hypertension and myocardial injury, defined by troponin levels above the 99th percentile upper reference limit, and controls were hypertensive patients with no myocardial injury. Biomarkers and immune cell subsets were quantified and compared between the two groups. A multiple logistic regression model was used to analyze the associations of clinical and immune variables with myocardial injury. Results The sample comprised 193 patients divided into two groups: 47 cases and 146 controls. Relative to controls, cases had lower total lymphocyte count, percentage of T lymphocytes, CD8+CD38+ mean fluorescence intensity (MFI), and percentage of CD8+ human leukocyte antigen DR isotope (HLA-DR)+ CD38–cells and higher percentage of natural killer lymphocytes, natural killer group 2A (NKG2A)+ MFI, percentage of CD8+CD38+cells, CD8+HLA-DR+MFI, CD8+NKG2A+MFI, and percentage of CD8+HLA-DR–CD38+cells. On multivariate regression, the CD8+HLA-DR+MFI, CD8+CD38+MFI, and total lymphocyte count were associated significantly with myocardial injury. Conclusion Our findings suggest that lymphopenia, CD8+CD38+MFI, and CD8+HLA-DR+MFI are immune biomarkers of myocardial injury in hypertensive patients with COVID-19. The immune signature described here may aid in understanding the mechanisms underlying myocardial injury in these patients. The study data might open a new window for improvement in the treatment of hypertensive patients with COVID-19 and myocardial injury.

New Insights on the Mechanisms of Myocardial Injury in Hypertensive Patients With COVID-19.

Myocardial injury is common in hypertensive patients with 2019 coronavirus disease (COVID-19). Immune dysregulation could be associated to cardiac injury in these patients, but the underlying mechanism has not been fully elucidated. All patients were selected prospectively from a multicenter registry of adults hospitalized with confirmed COVID-19. Cases had hypertension and myocardial injury, defined by troponin levels above the 99th percentile upper reference limit, and controls were hypertensive patients with no myocardial injury. Biomarkers and immune cell subsets were quantified and compared between the two groups. A multiple logistic regression model was used to analyze the associations of clinical and immune variables with myocardial injury. The sample comprised 193 patients divided into two groups: 47 cases and 146 controls. Relative to controls, cases had lower total lymphocyte count, percentage of T lymphocytes, CD8+CD38+ mean fluorescence intensity (MFI), and percentage of CD8+ human leukocyte antigen DR isotope (HLA-DR)+ CD38-cells and higher percentage of natural killer lymphocytes, natural killer group 2A (NKG2A)+ MFI, percentage of CD8+CD38+cells, CD8+HLA-DR+MFI, CD8+NKG2A+MFI, and percentage of CD8+HLA-DR-CD38+cells. On multivariate regression, the CD8+HLA-DR+MFI, CD8+CD38+MFI, and total lymphocyte count were associated significantly with myocardial injury. Our findings suggest that lymphopenia, CD8+CD38+MFI, and CD8+HLA-DR+MFI are immune biomarkers of myocardial injury in hypertensive patients with COVID-19. The immune signature described here may aid in understanding the mechanisms underlying myocardial injury in these patients. The study data might open a new window for improvement in the treatment of hypertensive patients with COVID-19 and myocardial injury.

Correlation between perioperative dexmedetomidine administration and postoperative acute kidney injury in hypertensive patients undergoing non-cardiac surgery.

Background: Previous studies have suggested that dexmedetomidine may have a protective effect on renal function. However, it is currently unclear whether perioperative dexmedetomidine administration is associated with postoperative acute kidney injury (AKI) incidence risk in hypertensive patients undergoing non-cardiac surgery. Methods: This investigation was a retrospective cohort study. Hypertensive patients undergoing non-cardiac surgery in Third Xiangya Hospital of Central South University from June 2018 to December 2019 were included. The relevant data were extracted through electronic cases. The univariable analysis identified demographic, preoperative laboratory, and intraoperative factors associated with acute kidney injury. Multivariable stepwise logistic regression was used to assess the association between perioperative dexmedetomidine administration and postoperative acute kidney injury after adjusting for interference factors. In addition, we further performed sensitivity analyses in four subgroups to further validate the robustness of the results. Results: A total of 5769 patients were included in this study, with a 7.66% incidence of postoperative acute kidney injury. The incidence of postoperative acute kidney injury was lower in the dexmedetomidine-administered group than in the control group (4.12% vs. 8.06%, p < 0.001). In the multivariable stepwise logistic regression analysis, perioperative dexmedetomidine administration significantly reduced the risk of postoperative acute kidney injury after adjusting for interference factors [odds ratio (OR) = 0.56, 95% confidence interval (CI): 0.36-0.87, p = 0.010]. In addition, sensitivity analysis in four subgroups indicated parallel findings: i) eGRF <90mL/min·1.73/m2 subgroup (OR = 0.40, 95% CI: 0.19-0.84, p = 0.016), ii) intraoperative blood loss <1000mL subgroup (OR = 0.58, 95% CI: 0.36-0.94, p = 0.025), iii) non-diabetes subgroup (OR = 0.51, 95% CI: 0.29-0.89, p = 0.018), and iv) older subgroup (OR = 0.55, 95% CI: 0.32-0.93, p = 0.027). Conclusion: In conclusion, our study suggests that perioperative dexmedetomidine administration is associated with lower risk and less severity of postoperative acute kidney injury in hypertensive individuals undergoing non-cardiac surgery. Therefore, future large-scale RCT studies are necessary to validate this benefit.

S-38-3: LONG NONCODING RNA P21 ALLEVIATES ENDOTHELIAL PROGENITOR CELLS DAMAGE AND PROMOTES ENDOTHELIAL REPAIR IN HYPERTENSION THROUGH ENHANCING AUTOPHAGY

Objective: Vascular damage of hypertension has been the focus of hypertension treatment, and endothelial progenitor cells (EPCs) play an important role in the repair of vascular endothelial damage. Functional damage and decreased number of EPCs are observed in the peripheral circulation of hypertensive patients, but its mechanism is not yet elucidated. Methods: Peripheral circulating endothelial progenitor cells of hypertensive patients were labeled and detected by flow cytometry. At the same time, the endothelial progenitor cells of hypertensive patients were cultured in vitro to detect their cell function and aging. The rat bone marrow-derived endothelial progenitor cells were isolated and cultured in vitro. After the intervention of AngII, the cell function, autophagy, and cell senescence were detected. PCR and WB were used to measure the expression and phosphorylation of SESN2, AMPK and TSC2. Results: Our results showed that the number of EPCs in hypertensive patients is significantly lower than that of normal population, and the cell function decreases with a higher proportion of EPCs at later stages. A decrease in autophagy is responsible for the senescence and damage of EPCs induced by AngII. Moreover, lncRNA-p21 plays a critical regulator role in the senescence and dysfunction of EPCs. Furthermore, lncRNA-p21 activates SESN2/AMPK/TSC2 pathway by promoting the transcriptional activity of p53 and lncRNA-p21 overexpression enhanced autophagy via AMPK/TSC2/mTOR pathway to protect against AngII-induced EPC damage. EPCs with lncRNA-p21 knockdown showed poor adhesion ability and vascular repair function. These results suggest that lncRNA-p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway. Conclusion: The data provide evidence that a reversal of decreased autophagy serves as the protective mechanism of EPC injury in hypertensive patients, and lncRNA-p21 is a new therapeutic target for vascular endothelial repair in hypertension.

高血压合并睡眠呼吸暂停低通气综合征患者发生肾损伤的研究进展

高血压合并睡眠呼吸暂停低通气综合征患者发生肾损伤的研究进展

Abstract 033: Anti-hypertensive Treatment With Acei Vs Arbs: The Differential Effect On Brain Microstructural Integrity Parameters Of Raas-targeting Treatments

Treating hypertension by drugs targeting the RAAS either blocking the Angiotensin receptor (ARBs) or inhibiting the Angiotensin Converting Enzyme (ACEi) have beneficial effects on cardiovascular health, preventing MI, stroke and global CV mortality. It is worth noting that no study investigated whether the two strategies targeting the RAAS have different effects on brain injury in hypertensive patients. To this aim, we investigated the correlation among microstructural integrity by DTI-MRI and the use of either class of drug. We recruited 51 hypertensives on ACEi or ARBs treatment and subjected them to advanced neuroimaging. DTI measures were normalized and analyzed by general linear model with age, sex, BMI, alcohol, smoke, SBP and DBP levels, heart rate as confounders to highlight alterations correlated to either treatment. The analysis shows that ARBs and ACEi exhibit an opposite and significant correlation with the microstructural integrity of the anterior commissure and the temporal subsection of the cingulum, reflecting a preserved microstructure in patients treated with ARBs compared with ACEi. This difference is also shown in pairwise comparison on anterior commissure (Table 1). In conclusion, our data suggest that ARBs may preserve specific white matter tracts integrity, suggesting that in hypertensive patients with cognitive dysfunction the use of ARBs should be preferred to protect brain microstructural integrity.

Aerobic Exercise Training Improves Renal Injury in Spontaneously Hypertensive Rats by Increasing Renalase Expression in Medulla.

We aimed to examine the effects of aerobic exercise training on renal function in spontaneously hypertensive rats (SHR) and elucidate their possible mechanisms. Adult male SHR and age-matched Wistar-Kyoto rats (WKY) were divided into four groups: WKY sedentary group, SHR sedentary group, low-intensity training group, and medium-intensity training group. Using molecular and biochemical approaches, we investigated the effects of 14-week training on renalase (RNLS) protein levels, renal function, and apoptosis and oxidative stress modulators in kidney tissues. In vitro, angiotensin II (Ang II)-induced human kidney proximal epithelial cells (HK-2) were treated with RNLS, and changes in apoptosis and oxidative stress levels were observed. Our results show that moderate training improved renal function decline in SHR. In addition, aerobic exercise therapy significantly increased levels of RNLS in the renal medulla of SHR. We observed in vitro that RNLS significantly inhibited the increase of Ang II-inducedapoptosis and oxidative stress levels in HK-2. In conclusion, aerobic exercise training effectively improved renal function in SHR by promoting RNLS expression in the renal medulla. These results explain the possible mechanism in which exercise improves renal injury in hypertensive patients and suggest RNLS as a novel therapy for kidney injury patients.

Long noncoding RNA p21 enhances autophagy to alleviate endothelial progenitor cells damage and promote endothelial repair in hypertension through SESN2/AMPK/TSC2 pathway

Vascular damage of hypertension has been the focus of hypertension treatment, and endothelial progenitor cells (EPCs) play an important role in the repair of vascular endothelial damage. Functional damage and decreased number of EPCs are observed in the peripheral circulation of hypertensive patients, but its mechanism is not yet elucidated. Here, we show that the number of EPCs in hypertensive patients is significantly lower than that of normal population, and the cell function decreases with a higher proportion of EPCs at later stages. A decrease in autophagy is responsible for the senescence and damage of EPCs induced by AngII. Moreover, lncRNA-p21 plays a critical regulator role in EPCs’ senescence and dysfunction. Furthermore, lncRNA-p21 activates SESN2/AMPK/TSC2 pathway by promoting the transcriptional activity of p53 and enhances autophagy to protect against AngII-induced EPC damage. The data provide evidence that a reversal of decreased autophagy serves as the protective mechanism of EPC injury in hypertensive patients, and lncRNA-p21 is a new therapeutic target for vascular endothelial repair in hypertension.

Serum Neutrophil Gelatinase-associated Lipocalin: A Biomarker of Renal Impairment in Hypertensive Patients

Background and Aim: Hypertension is one of the leading causes of chronic kidney disease (CKD). Neutrophil gelatinase-associated lipocalin (NGAL) is a novel and sensitive biomarker in acute and chronic renal injury. The present study investigated serum and urinary NGAL as markers of kidney damage in hypertensive and CKD patients. Materials and Methods: This case-control study was performed on 28 hypertensive patients, 28 patients with CKD, and 33 healthy volunteers. Serum and urinary NGAL levels were measured using the ELISA method. Creatinine and urea concentrations were measured by the routine methods. Receiver-operating characteristic (ROC) curve analysis was employed to find the best serum and urinary NGAL cut-off values for detecting renal function. Results: Both serum and urinary NGAL levels were higher in CKD patients than in hypertensive patients and healthy controls (serum NGAL: 193.48±50.62 vs 99.47±26.65 and 48.74±12.07, P&lt;0.001; urinary NGAL: 63.78±16.54 vs 23.24±6.87 and 11.36±3.4, P&lt;0.001 respectively). There was a significant positive correlation between serum and urinary NGAL with serum urea and creatinine. Serum and urinary NGAL levels showed a significant inverse correlation with the estimated glomerular filtration rate. In ROC analysis, serum NGAL had the best diagnostic profile with an AUC of 0.938 (95% CI: 0.865–0.978) and the best cut-off value of 64.61 ng/mL (sensitivity 97.73%; specificity 77.27%. Conclusion: These results revealed that serum NGAL is a reliable marker for early diagnosis of renal injury in hypertensive patients.

MIR-338-3P DOWN-REGULATION IN SMALL ARTERIES OF HYPERTENSIVE PATIENTS WITH CHRONIC KIDNEY DISEASE MAY ACT VIA UP-REGULATION OF ALKALINE CERAMIDASE 2 AND GLUTATHIONE PEROXIDASE 3

Objective: Hypertension (HTN) is associated with vascular damage characterized by vascular remodeling and stiffening and endothelial dysfunction, which is a cause of end-organ damage such as chronic kidney disease (CKD). microRNAs are small non-coding RNA that regulate gene expression by binding to their target messenger RNAs (mRNAs), leading to mRNA degradation or translational repression. Their participation in mechanisms leading to vascular injury remains unclear. We aimed to identify differentially expressed (DE) microRNAs in small arteries of human subjects with HTN associated or not with CKD to gain insight into pathophysiological molecular mechanisms in these conditions. Design and method: Normotensive subjects and patients with HTN associated or not with CKD grades 3-4 were studied (n = 15-16). Blood pressure was determined by automated office measurement (AOBP). Small arteries were isolated from subcutaneous gluteal biopsies and RNA extracted for small and total RNA sequencing using Illumina HiSeq-2500. Differentially expressed (DE) genes were identified with a P &lt; 0.05. The selected DE miRNAs were confirmed by reverse transcription-quantitative PCR (RT-qPCR). Putative microRNA targets were validated using gain- and loss-of-function in human aortic vascular cells by RT-qPCR and luciferase reporter assay. Results: Small RNA sequencing identified DE microRNAs uniquely associated with HTN (3 up and 6 down), CKD (42 up and 39 down) or both groups (2 up). One of 14 tested DE microRNAs was validated. RT-qPCR showed that miR-338-3p was decreased by 59% in CKD (P &lt; 0.05). miR-338-3p and three of its predicted targets were highly expressed in human aortic endothelial cells (HAECs). Two of them, alkaline ceramidase 2 (ACER2) and glutathione peroxidase 3 (GPX3), were up-regulated by 48% and 90% in human aortic endothelial cells (HAECs) transfected with anti-miR-338-3p, respectively (P &lt; 0.05). miR-338-3p mimic co-transfection in HAECs decreased respectively by 13% and 24% luciferase activity of reporter vectors containing the conserved wild-type but not mutated ACER2 or GPX3 3’ untranslated transcribed region miR-338-3p-5p binding sites (P &lt; 0.05). Conclusions: miR-338-3p down-regulation in small arteries may act via mRNA up-regulation of alkaline ceramidase 2 and glutathione peroxidase 3 to play a role in vascular injury in hypertensive patients with chronic kidney disease.

Implications of AB0 blood group in hypertensive patients with covid-19

BackgroundHypertension is the most frequent co-morbidity in patients with covid-19 infection, and we might speculate that a specific blood group could play a key role in the clinical outcome of hypertensive patients with covid-19.MethodsIn this prospective study, we compared 0 vs. non-0 blood group in hypertensive patients with covid-19 infection. In these patients, we evaluated inflammatory and thrombotic status, cardiac injury, and death events.ResultsPatients in non-0 (n = 92) vs. 0 blood group (n = 72) had significantly different values of activated pro-thrombin time, D-dimer, and thrombotic indexes as Von Willebrand factor and Factor VIII (p < 0.05). Furthermore, patients in non-0 vs. 0 blood group had higher rate of cardiac injury (10 (13.9%) vs. 27 (29.3%)) and death, (6 (8.3%) vs. 18 (19.6%)), (p < 0.05). At the multivariate analysis, Interleukin-6 (1.118, CI 95% 1.067–1.171) and non-0 blood group (2.574, CI 95% 1.207–5.490) were independent predictors of cardiac injury in hypertensive patients with covid-19. D-dimer (1.082, CI 95% 1.027–1.140), Interleukin-6 (1.216, CI 95% 1.082–1.367) and non-0 blood group (3.706, CI 95% 1.223–11.235) were independent predictors of deaths events in hypertensive patients with covid-19.ConclusionsTaken together, our data indicate that non-0 covid-19 hypertensive patients have significantly higher values of pro-thrombotic indexes, as well as higher rate of cardiac injury and deaths compared to 0 patients. Moreover, AB0 blood type influences worse prognosis in hypertensive patients with covid-19 infection.

The influence of mean arterial blood pressure during cardiopulmonary bypass on post-operation acute kidney injury in hypertensive patients

Introduction: Over a period of time, kidney blood vessels will be damaged in those patients suffering from hypertension. Objectives: This study aimed to investigate the effect of mean arterial pressure during cardiopulmonary bypass (CBP). Patients and Methods: The present observational prospective study was conducted on 90 high risk patients, having records of hypertension and being candidates for open heart surgery. Patients divided into three groups based on their mean arterial pressure (MAP), lower than 60 mmHg (first group), between 60 to 70 mm Hg (second group) and higher than 70 mm Hg (third group) respectively during cardiopulmonary bypass. Clinical outcomes being studied included cardiac surgery-associated acute kidney injury (CSA-AKI) (RIFLE class), serum creatinine levels, glomerular filtration rate (GFR) and urinary output up to 24 hours after the surgery. Results: Data related to 90 case-patients have been analyzed. There was no difference between the groups in terms of demographic information. Prevalence of AKI in preliminary course after cardiac surgery was different among the groups. AKI occurred in six patients (15%) of the first group, five patients (12.5%) of the second group and two patients (5%) of the third group (P = 0.03). There have been no differences in terms of serum creatinine levels, GFR and urinary output during 24 hours after cardiac surgery, among the groups. However, delta creatinine level and delta GFR were significant in those groups with MAP of lower than 60 mm Hg and also between 60-70 mm Hg. Conclusion: This study showed that MAP level during CBP directly affects occurrence of AKI in patients after open heart surgery. High risk patients such as those suffering from hypertension have to be constantly monitored during CBP regarding their MAP. We concluded that MAP drops to lower than 70 mm Hg has to be prevented in hypertensive patients.

Early identification of tubulointerstitial renal injury in hypertensive patients: a comparative evaluation of the urine biomarkers NGAL and KIM 1

Objective. The aim of the study was a comparative assessment of urine NGAL (neutrophil gelatinase associated lipocalin) and KIM‑1 (kidney injury molecule‑1) as biomarkers of early detection of tubulointerstitial renal damage in patients with arterial hypertension (HTN) without concomitant diabetes mellitus and kidney disease.Design and methods. The study involved 52 patients of both sexes (17 man and 35 women, mean age 60,2 ± 6,54 years) hospitalized for aggravation of HTN 1–3 degrees, which were divided into 3 groups with glomerular filtration rate (GFR) &gt; 90 ml/min/1,73 m 2 (n = 21), 60–90 ml/min/1,73 m 2 (n = 19) and &lt; 60 ml/min/1,73 m 2 (n = 12). In a separate group, patients with albuminuria in the range 10–29 mg/g urine creatinine were isolated. The comparison group consisted of 15 normotensive individuals (6 men and 9 women, mean age 49,8 ± 9,68 years) with no obvious signs of renal, cardiovascular or other diseases. All patients and controls underwent examination, and albumin, NGAL (Human NGAL ELISA kit) and KIM‑1 (Human KIM‑1 Immunoassay ELISA) levels were assessed in the first morning urine portion.Results. In the group of patients with GFR 67,7 ± 4,92 ml/min/1,73 m 2 (mildly reduced kidney function) and in the group of patients with GFR 55,8 ± 4,44 ml/min/1,73 m 2 (renal dysfunction) urine NGAL level increased by 3,43 (р &lt; 0,05) and 3,92 times (р &lt; 0,05), respectively, as compared with the control group. The urine concentration of KIM‑1 increased by 2,06 times (р &lt; 0,05) was observed only in patients with renal dysfunction. Based on the ROC analysis AUC for the urine NGAL level in patients with mildly reduced kidney function is 0,78 (95 % confidence interval, 95 %CI: 0,70–0,86; p &lt; 0,001), specificity — 89,6 %, sensitivity — 66,7 %. Similar indicators for KIM‑1 are 0,72 (95 % CI: 0,64–0,80; p &lt; 0,001), specificity — 85,3 %, sensitivity — 16,7 %. In the group of patients with mildly reduced kidney function the urine level of NGAL correlated with the HTN severity (r = 0,8944, р &lt; 0,001) and its duration (r = 0,8953, р &lt; 0,001).Conclusions. Urine NGAL as compared with KIM‑1 is a more sensitive biomarker, which indicates tubulointerstitial injury in HTN patients without diabetes mellitus and kidney diseases in the early stage of impairment renal function.

Nighttime blood pressure decline as a predictor of renal injury in patients with hypertension: a population-based cohort study.

We explored whether the nighttime blood pressure (BP) decline predicts renal function decline in a population-based cohort with primary hypertension. We measured the baseline ambulatory BP and glomerular filtration rate (GFR) in a cohort of 1,042 primary hypertensive patients. We repeated the GFR measurements and calculated the rate of GFR decline after a median follow-up of 5.8 years. The estimated GFR (eGFR) declined by −0.23 to −0.20 mL/min per year as the nighttime systolic BP (SBP), diastolic BP (DBP), and mean BP decline rates increased by 1% (P < 0.001). In the fully adjusted model, the nighttime SBP, DBP, and mean BP were all related to a steeper rate of eGFR decline by −0.25 to −0.22 mL/min per 1% increase. The adjusted multivariable results indicated that the odds of an eGFR decline were reduced by 46% when the nighttime SBP decline rate increased by 1% (OR= 0.54, 95% CI: 0.46–0.62). The restricted cubic spline model indicated a non-linear dose-response relationship with the nighttime SBP, DBP, and mean BP. Nighttime BP may be an important biomarker of renal function injury in hypertensive patients.

Comparison of Left Ventricular Mass Calculation Methods via Two-Dimensional Echocardiogram in Children, Adolescents, and Young Adults With Systemic Hypertension

Left ventricular (LV) mass is a major determining tool for myocardial injury in hypertensive patients. Issues with LV mass calculations exist given that there are multiple methods to assess mass, including from the parasternal long axis (PLA), parasternal short axis (PSA), and 2-dimensional (2D) volumetric methods. The aim of this study was to compare the agreement of LV mass calculations using the PLA, PSA, and 2D volumetric methods. This study retrospectively reviewed 200 consecutive, initial echocardiograms for the indication of hypertension. A single reader calculated the LV mass in each patient via the PLA, PSA, and 2D volumetric methods. Percent differences for each study were calculated. LV mass threshold cutoffs of 51 g/m2.7 (cardiac organ injury) and 38.6 g/m2.7 (elevated LV mass) were used to compare categorical differences between the different measurement methods. Paired comparisons demonstrated an absolute mean percent difference of 8.46% to 9.41% among the different methods. LV mass calculated by the 2D volumetric method was less compared with PLA and PSA methods (31.64 vs 33.90 vs 35.51 g/m2.7; p < 0.0001). Fewer patients were classified as having cardiac target organ injury or elevated LV mass via 2D volumetric calculation, compared with PLA and PSA methods (p = 0.02 and p = 0.03, respectively). In conclusion, there is a small but important difference in LV mass calculations for patients with hypertension. These results emphasize the need for consistency within echocardiography laboratories as surveillance studies are common in this patient population.

MicroRNA-34a promotes hypertension-induced vascular injury by targeting B-lymphocytoma-2

Objective To investigate the level of microRNA (miRNA, miR)-34a in serum of hypertensive patients and its effect on proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) by targeting B cell lymphoma/leukemia-2 (bcl-2), and clarify the underlying mechanism of hypertension-induced vascular injury. Methods Real-time quantitative polymerase chain reaction (qPCR) was used to detect the level of miR-34a in serum of 98 hypertensive patients and 65 healthy controls; the potential targets of miR-34a was predicted by TargetScan; the interaction between miR-34a and bcl-2 was measured by dual luciferase reporter assay, western blot and qPCR; the effect of miR-34a on proliferation and apoptosis of HUVECs was detected by methyl thiazol tetrazolium (MTT) and flow cytometry. Results The level of miR-34a in serum of 98 hypertensive patients (2.432±0.201) was significantly higher than that of 65 healthy controls (0.996±0.112, P 0.05). The protein and mRNA level of bcl-2 in HUVECs after overexpressing miR-34a (0.403±0.041, 0.206±0.018) decreased significantly than that in Blank group (1.000±0.098, 1.000±0.067) and miR-NC group (0.996±0.087, 1.012±0.049). The proliferation of HUVECs after overexpressing miR-34a (48 h: 0.269±0.021, 72 h: 0.324±0.028) decreased significantly than that of the Blank group (48 h: 0.324±0.025, 72 h: 0.458±0.044) and miR-NC group (48 h: 0.335±0.028, 72 h: 0.469±0.051, P<0.05), and apoptosis (23.54±2.65) was significantly higher than that of Blank (6.45±0.42) and miR-NC (7.32±0.54, P<0.05). Conclusion MiR-34a is overexpressed in serum of hypertensive patients. Overexpressing miR-34a can inhibit proliferation of HUVECs by targeting bcl-2 expression, which may be one of the potential mechanisms of vascular injury in hypertensive patients and provide experimental basis for using miR-34a as a new target to diagnose and treat hypertension in the future. Key words: MicroRNA-34a; B cell lymphoma/leukemia-2; Hypertension; Vascular injury

Loss of Renal Peritubular Capillaries in Hypertensive Patients Is Detectable by Urinary Endothelial Microparticle Levels.

Hypertension, an important cause of chronic kidney disease, is characterized by peritubular capillary (PTC) loss. Circulating levels of endothelial microparticles (EMPs) reflect systemic endothelial injury. We hypothesized that systemic and urinary PTC-EMPs levels would reflect renal microvascular injury in hypertensive patients. We prospectively measured by flow cytometry renal vein, inferior vena cava, and urinary levels of EMPs in essential (n=14) and renovascular (RVH; n=24) hypertensive patients and compared them with peripheral blood and urinary levels in healthy volunteers (n=14). PTC-EMPs were identified as urinary exosomes positive for the PTC marker plasmalemmal-vesicle-associated protein. In 7 RVH patients, PTC and fibrosis were also quantified in renal biopsy, and in 18 RVH patients, PTC-EMPs were measured again 3 months after continued medical therapy with or without stenting (n=9 each). Renal vein and systemic PTC-EMPs levels were not different among the groups, whereas their urinary levels were elevated in both RVH and essential hypertension versus healthy volunteers (56.8%±12.7% and 62.8%±10.7% versus 34.0%±17.8%; both P≤0.001). Urinary PTC-EMPs levels correlated directly with blood pressure and inversely with estimated glomerular filtration rate. Furthermore, in RVH, urinary PTC-EMPs levels correlated directly with stenotic kidney hypoxia, histological PTC count, and fibrosis and inversely with cortical perfusion. Three months after treatment, the change in urinary PTC-EMPs levels correlated inversely with a change in renal function ( r=-0.582; P=0.011). Therefore, urinary PTC-EMPs levels are increased in hypertensive patients and may reflect renal microcirculation injury, whereas systemic PTC-EMPs levels are unchanged. Urinary PTC-EMPs may be useful as novel biomarkers of intrarenal capillary loss.