scholarly journals Arterial Hypertension and Unusual Ascending Aortic Dilatation in a Neonate With Acute Kidney Injury: Mechanistic Computer Modeling

2019 ◽  
Vol 10 ◽  
Author(s):  
Luis Altamirano-Diaz ◽  
Andrea D. Kassay ◽  
Baran Serajelahi ◽  
Christopher W. McIntyre ◽  
Guido Filler ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Arterial Hypertension ◽  
Computer Modeling ◽  
Kidney Injury ◽  
Aortic Dilatation

scholarly journals Arterial hypertension and unusual ascending aortic dilatation in a neonate with acute kidney injury: mechanistic computer modelling

2018 ◽  
Author(s):  
Sanjay R Kharche
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Ascending Aorta ◽  
Small Vessel ◽  
Aortic Dilatation ◽  
Small Vessels ◽  
Left Ventricle Hypertrophy ◽  
Vessel Resistance ◽  
Underlying Mechanisms ◽  
Ventricle Hypertrophy

Background: Neonatal asphyxia caused acute kidney injury and severe hypertension in a newborn patient. An unusually dilatated ascending aorta developed within a few weeks. Dialysis and hypertensive treatment led to partial recovery of the aortic diameters. It was hypothesized that the aortic dilatation may be associated with cardiovascular changes induced by the acute kidney injury. Mathematical modelling was used to better understand the underlying mechanisms of hypertension and aortic dilatation.Methods: Patient observation included systolic blood pressure recording and echocardiographic exams. To explore underlying mechanisms of aortic dilatation and hypertension, a previous whole-body lumped parameter hemodynamics model was adapted to this study. Computer simulations were designed to permit dissection of individual mechanisms. The hypertension inducing effects of altering systemic vascular resistances, stiffnesses, and heart rate on blood flows and pressures were simulated.Results: In agreement with our clinical diagnosis, the mathematical model showed that an increase of systemic small vessel resistance is the prime cause of hypertension. Further, aortic stiffening may also cause hypertension, it was found to be secondary to the potency of systemic small vessel resistance. The cardiac output, as quantified using pressure-volume loop area, reduced significantly due to hypertension. Simultaneous left ventricle hypertrophy and small vessel blocking increased ascending aorta blood flow as well as pressure indicating an enlarged ascending aorta. In contrast, increased arterial stiffness appeared to lower the aortic blood flow and pressures.Conclusions and discussion: Systemic small vessel resistance is an important factor in arterial hypertension, and may also be a key clinical therapeutic target. Left ventricle hypertrophy may also be simultaneously ameliorated when treating systemic small vessels. Treatment of arterial stiffness appears to provide significant benefit but may be secondary to treatment of the systemic small vessels. The quantitative grading of pathophysiological mechanisms provided by the modelling may contribute to treatment recommendations. Further development and individualization of the model will augment its applicability in clinical practice.

scholarly journals Contrast-associated acute kidney injury in patients with arterial hypertension and stable coronary artery disease

2020 ◽  
Vol 17 (3) ◽  
pp. 48-52
Author(s):  
Olga Iu. Mironova ◽  
Viktor V. Fomin
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Acute Kidney Injury ◽  
Coronary Artery ◽  
Arterial Hypertension ◽  
Contrast Media ◽  
Stable Coronary Artery Disease ◽  
Kidney Injury ◽  
Baseline Creatinine ◽  
Artery Disease

Relevance.The combination of stable coronary artery disease (CAD) and arterial hypertension (AH) is one of the most common seen by cardiologists. The administration of contrast media might increase the risk of development of acute kidney injury, especially in patients with comorbidities. The influence of iodine contrast media administration on the risk of development of contrast-associated acute kidney injury (CA-AKI) in patients with stable CAD and AH was studied in our work. Materials and methods.863 patients with stable CAD and AH and indications for interventions requiring intraarterial administration of contrast media were included in the prospective open observational cohort study (ClinicalTrials.gov ID NCT04014153). CA-AKI was defined according to KDIGO criteria as the elevation of serum creatinine 25% and more above baseline or 0.5 mg/dl (44 mkmol/l) and more in 48 hours after intraarterial administration of contrast media. The primary endpoint was the development of CA-AKI. Results.Diabetes mellitus, obesity and hyperuricemia were not statistically significant risk factors of CA-AKI development according to the contingency tables analyses, unlike proteinuria. A logistic regression model was built (area under the curve 0.7638,p0.0001, 95% confidence interval 0.7130.815) and included the following risk factors: age, weight, body mass index, female gender, heart failure, proteinuria, AH, anemia, baseline creatinine. Proteinuria, baseline creatinine and contrast volume were statistically significant ones. Conclusion.The rate of CA-AKI was 12.6%. Proteinuria, baseline creatinine and contrast volume were statistically significant risk factors of CA-AKI in logistic regression model. Key words:contrast-induced acute kidney injury, contrast-induced nephropathy, contrast-associated acute kidney injury, coronary artery disease, percutaneous coronary intervention, arterial hypertension, stable coronary artery disease, prognosis.

scholarly journals Hyperuricemia in patients with stable coronary artery disease and arterial hypertension and percutaneous coronary interventions

2020 ◽  
Vol 22 (12) ◽  
pp. 20-22
Author(s):  
Olga Iu. Mironova ◽  
◽  
Viktor V. Fomin ◽  
Keyword(s):  
Coronary Artery Disease ◽  
Acute Kidney Injury ◽  
Coronary Artery ◽  
Linear Regression ◽  
Arterial Hypertension ◽  
Stable Coronary Artery Disease ◽  
Kidney Injury ◽  
Multiple Linear Regression Model ◽  
Artery Disease ◽  
Stable Cad

Aim. To assess the influence of hyperuricemia on the risk of contrast-induced acute kidney injury (CI-AKI) in patients with stable coronary artery disease (CAD) and arterial hypertension. Materials and methods. Patients receiving optimal medical therapy and with indications for coronary angiography and possible coronary angioplasty, with stable CAD and arterial hypertension were included in the study. We conducted an observational open prospective cohort study, that was registered in clinicaltrials.gov with ID NCT04014153. Results. We included 1023 patients with chronic CAD. 863 had arterial hypertension. Hyperuricemia was diagnosed in 31 patients, 832 had normal levels of uric acid on admission. Contrast-induced acute kidney injury developed in 2 (6.5%) patients suffering from hyperuricemia. In patients with stable CAD, AH and no hyperuricemia the rate of CI-AKI was 107 (12.9%) patients. The difference between groups was not statistically significant (95% CI -0.056–0.183, р=0.292). We built a multiple linear regression model that included age, weight, female gender, heart failure, diabetes mellitus, kidney diseases in past medical history, protei-nuria, anemia, baseline glomerular filtration rate, contrast volume and difference between baseline creatinine and creatinine after contrast administration. No risk factor showed any statistical significance in the model. Conclusion. Contrast-induced acute kidney injury developed in 2 (6.5%) patients suffering from hyperuricemia. The rate of CI-AKI in patients without hyperuricemia was twice higher but the results were not statistically significant. Among the risk factors included in the multiple linear regression model none was statistically significant.

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