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European Heart Journal Jun 2017Increased neurohumoral stimulation resulting in excessive sodium avidity and extracellular volume overload are hallmark features of decompensated heart failure.... (Review)
Review
Increased neurohumoral stimulation resulting in excessive sodium avidity and extracellular volume overload are hallmark features of decompensated heart failure. Especially in case of concomitant renal dysfunction, the kidneys often fail to elicit effective natriuresis. While assessment of renal function is generally performed by measuring serum creatinine-a surrogate for glomerular filtration-, this only represents part of the nephron's function. Alterations in tubular sodium handling are at least equally important in the development of volume overload and congestion. Venous congestion and neurohumoral activation in advanced HF further promote renal sodium and water retention. Interestingly, early on, before clinical signs of heart failure are evident, intrinsic renal derangements already impair natriuresis. This clinical review discusses the importance of heart failure (HF) induced changes in different nephron segments. A better understanding of cardiorenal interactions which ultimately result in sodium avidity in HF might help to treat and prevent congestion in chronic and acute HF.
Topics: Acute Disease; Cardio-Renal Syndrome; Diuretics; Glomerular Filtration Rate; Homeostasis; Humans; Kidney Glomerulus; Kidney Tubules; Phenotype; Renal Circulation; Renal Insufficiency, Chronic; Sodium; Sodium Potassium Chloride Symporter Inhibitors
PubMed: 28329085
DOI: 10.1093/eurheartj/ehx035 -
Methods in Molecular Biology (Clifton,... 2021Dynamic contrast-enhanced (DCE) MRI monitors the transit of contrast agents, typically gadolinium chelates, through the intrarenal regions, the renal cortex, the...
Dynamic contrast-enhanced (DCE) MRI monitors the transit of contrast agents, typically gadolinium chelates, through the intrarenal regions, the renal cortex, the medulla, and the collecting system. In this way, DCE-MRI reveals the renal uptake and excretion of the contrast agent. An optimal DCE-MRI acquisition protocol involves finding a good compromise between whole-kidney coverage (i.e., 3D imaging), spatial and temporal resolution, and contrast resolution. By analyzing the enhancement of the renal tissues as a function of time, one can determine indirect measures of clinically important single-kidney parameters as the renal blood flow, glomerular filtration rate, and intrarenal blood volumes. Gadolinium-containing contrast agents may be nephrotoxic in patients suffering from severe renal dysfunction, but otherwise DCE-MRI is clearly useful for diagnosis of renal functions and for assessing treatment response and posttransplant rejection.Here we introduce the concept of renal DCE-MRI, describe the existing methods, and provide an overview of preclinical DCE-MRI applications to illustrate the utility of this technique to measure renal perfusion and glomerular filtration rate in animal models.This publication is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction is complemented by two separate publications describing the experimental procedure and data analysis.
Topics: Animals; Biomarkers; Contrast Media; Diffusion Magnetic Resonance Imaging; Glomerular Filtration Rate; Humans; Image Enhancement; Image Processing, Computer-Assisted; Kidney; Monitoring, Physiologic; Perfusion; Renal Circulation; Software
PubMed: 33476002
DOI: 10.1007/978-1-0716-0978-1_12 -
Hypertension (Dallas, Tex. : 1979) Apr 2022The collateral circulation can adapt to bypass major arteries with limited flow and serves a crucial protective role in coronary, cerebral, and peripheral arterial... (Review)
Review
The collateral circulation can adapt to bypass major arteries with limited flow and serves a crucial protective role in coronary, cerebral, and peripheral arterial disease. Emerging evidence indicates that the renal collateral circulation can similarly adapt and thereby limit kidney ischemia in atherosclerotic renovascular disease. These adaptations predominantly include recruitment of preexisting microvessels for arteriogenesis, with de novo vessel formation playing a limited role. Yet, adaptations of the renal collateral circulation in renovascular disease are often insufficient to fully compensate for the limited flow within an obstructed renal artery and may be hampered by the severity of obstruction or patient comorbidities. Experimental strategies have attempted to circumvent limitations of collateral formation and improve the prognosis of patients with various ischemic vascular territories. These have included pharmacological approaches such as endothelial growth factors, renin-angiotensin-aldosterone system blockade, and I channel-blockers, as well as interventions like preconditioning, exercise, enhanced external counter-pulsation, and low-energy shock-wave therapy. However, few of these strategies have been implemented in atherosclerotic renovascular disease. This review summarizes current understanding regarding the development of renal collateral circulation in atherosclerotic renovascular disease. Studies are needed to apply lessons learned in other vascular beds in the setting of atherosclerotic renovascular disease to develop new treatment regimens for this patient group.
Topics: Atherosclerosis; Collateral Circulation; Female; Humans; Hypertension, Renovascular; Ischemia; Kidney; Kidney Diseases; Male; Renal Artery; Renal Artery Obstruction; Renal Circulation
PubMed: 35135307
DOI: 10.1161/HYPERTENSIONAHA.121.17960 -
American Journal of Physiology. Renal... Mar 2021Renal autoregulation is critical in maintaining stable renal blood flow (RBF) and glomerular filtration rate (GFR). Renal ischemia-reperfusion (IR)-induced kidney injury...
Renal autoregulation is critical in maintaining stable renal blood flow (RBF) and glomerular filtration rate (GFR). Renal ischemia-reperfusion (IR)-induced kidney injury is characterized by reduced RBF and GFR. The mechanisms contributing to renal microvascular dysfunction in IR have not been fully determined. We hypothesized that increased reactive oxygen species (ROS) contributed to impaired renal autoregulatory capability in IR rats. Afferent arteriolar autoregulatory behavior was assessed using the blood-perfused juxtamedullary nephron preparation. IR was induced by 60 min of bilateral renal artery occlusion followed by 24 h of reperfusion. Afferent arterioles from sham rats exhibited normal autoregulatory behavior. Stepwise increases in perfusion pressure caused pressure-dependent vasoconstriction to 65 ± 3% of baseline diameter (13.2 ± 0.4 μm) at 170 mmHg. In contrast, pressure-mediated vasoconstriction was markedly attenuated in IR rats. Baseline diameter averaged 11.7 ± 0.5 µm and remained between 90% and 101% of baseline over 65-170 mmHg, indicating impaired autoregulatory function. Acute antioxidant administration (tempol or apocynin) to IR kidneys for 20 min increased baseline diameter and improved autoregulatory capability, such that the pressure-diameter profiles were indistinguishable from those of sham kidneys. Furthermore, the addition of polyethylene glycol superoxide dismutase or polyethylene glycol-catalase to the perfusate blood also restored afferent arteriolar autoregulatory responsiveness in IR rats, indicating the involvement of superoxide and/or hydrogen peroxide. IR elevated mRNA expression of NADPH oxidase subunits and monocyte chemoattractant protein-1 in renal tissue homogenates, and this was prevented by tempol pretreatment. These results suggest that ROS accumulation, likely involving superoxide and/or hydrogen peroxide, impairs renal autoregulation in IR rats in a reversible fashion. Renal ischemia-reperfusion (IR) leads to renal microvascular dysfunction manifested by impaired afferent arteriolar autoregulatory efficiency. Acute administration of scavengers of reactive oxygen species, polyethylene glycol-superoxide dismutase, or polyethylene glycol-catalase following renal IR restored afferent arteriolar autoregulatory capability in IR rats, indicating that renal IR led to reversible impairment of afferent arteriolar autoregulatory capability. Intervention with antioxidant treatment following IR may improve outcomes in patients by preserving renovascular autoregulatory function and potentially preventing the progression to chronic kidney disease after acute kidney injury.
Topics: Animals; Arterioles; Blood Pressure; Glomerular Filtration Rate; Homeostasis; NADPH Oxidases; Rats; Reactive Oxygen Species; Renal Circulation; Renal Insufficiency, Chronic; Reperfusion Injury
PubMed: 33491564
DOI: 10.1152/ajprenal.00500.2020 -
Comprehensive Physiology Jan 2015Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially... (Review)
Review
Heat stress increases human morbidity and mortality compared to normothermic conditions. Many occupations, disease states, as well as stages of life are especially vulnerable to the stress imposed on the cardiovascular system during exposure to hot ambient conditions. This review focuses on the cardiovascular responses to heat stress that are necessary for heat dissipation. To accomplish this regulatory feat requires complex autonomic nervous system control of the heart and various vascular beds. For example, during heat stress cardiac output increases up to twofold, by increases in heart rate and an active maintenance of stroke volume via increases in inotropy in the presence of decreases in cardiac preload. Baroreflexes retain the ability to regulate blood pressure in many, but not all, heat stress conditions. Central hypovolemia is another cardiovascular challenge brought about by heat stress, which if added to a subsequent central volumetric stress, such as hemorrhage, can be problematic and potentially dangerous, as syncope and cardiovascular collapse may ensue. These combined stresses can compromise blood flow and oxygenation to important tissues such as the brain. It is notable that this compromised condition can occur at cardiac outputs that are adequate during normothermic conditions but are inadequate in heat because of the increased systemic vascular conductance associated with cutaneous vasodilation. Understanding the mechanisms within this complex regulatory system will allow for the development of treatment recommendations and countermeasures to reduce risks during the ever-increasing frequency of severe heat events that are predicted to occur.
Topics: Baroreflex; Cardiovascular System; Cerebrovascular Circulation; Heat Stress Disorders; Hemodynamics; Humans; Muscle, Skeletal; Renal Circulation; Splanchnic Circulation
PubMed: 25589263
DOI: 10.1002/cphy.c140015 -
Current Opinion in Nephrology and... Jan 2021Many forms of acute and chronic disease are linked to changes in renal blood flow, perfusion, vascular density and hypoxia, but there are no readily available methods to... (Review)
Review
PURPOSE OF REVIEW
Many forms of acute and chronic disease are linked to changes in renal blood flow, perfusion, vascular density and hypoxia, but there are no readily available methods to assess these parameters in clinical practice. Dynamic contrast enhanced ultrasound (DCE-US) is a method that provides quantitative assessments of organ perfusion without ionising radiation or risk of nephrotoxicity. It can be performed at the bedside and is suitable for repeated measurements. The purpose of this review is to provide updates from recent publications on the utility of DCE-US in the diagnosis or assessment of renal disease, excluding the evaluation of benign or malignant renal masses.
RECENT FINDINGS
DCE-US has been applied in clinical studies of acute kidney injury (AKI), renal transplantation, chronic kidney disease (CKD), diabetic kidney disease and to determine acute effects of pharmacological agents on renal haemodynamics. DCE-US can detect changes in renal perfusion across these clinical scenarios and can differentiate healthy controls from those with CKD. In sepsis, reduced DCE-US measures of perfusion may indicate those at increased risk of developing AKI, but this requires confirmation in larger studies as there can be wide individual variation in perfusion measures in acutely unwell patients. Recent studies in transplantation have not provided robust evidence to show that DCE-US can differentiate between different causes of graft dysfunction, although it may show more promise as a prognostic indicator of graft function 1 year after transplant. DCE-US can detect acute haemodynamic changes in response to medication that correlate with changes in renal plasma flow as measured by para-aminohippurate clearance.
SUMMARY
DCE-US shows promise and has a number of advantages that make it suitable for the assessment of patients with various forms of kidney disease. However, further research is required to evidence its reproducibility and utility before clinical use can be advocated.
Topics: Acute Kidney Injury; Contrast Media; Diabetic Nephropathies; Hemodynamics; Humans; Kidney; Kidney Diseases; Kidney Transplantation; Renal Circulation; Renal Insufficiency, Chronic; Reproducibility of Results; Ultrasonography
PubMed: 33186215
DOI: 10.1097/MNH.0000000000000664 -
Medicina Intensiva Mar 2017Acute kidney injury (AKI) is a growing concern in Intensive Care Units. The advanced age of our patients, with the increase in associated morbidity and the complexity of... (Review)
Review
Acute kidney injury (AKI) is a growing concern in Intensive Care Units. The advanced age of our patients, with the increase in associated morbidity and the complexity of the treatments provided favor the development of AKI. Since no effective treatment for AKI is available, all efforts are aimed at prevention and early detection of the disorder in order to establish secondary preventive measures to impede AKI progression. In critical patients, the most frequent causes are sepsis and situations that result in renal hypoperfusion; preventive measures are therefore directed at securing hydration and correct hemodynamics through fluid perfusion and the use of inotropic or vasoactive drugs, according to the underlying disease condition. Apart from these circumstances, a number of situations could lead to AKI, related to the administration of nephrotoxic drugs, intra-tubular deposits, the administration of iodinated contrast media, liver failure and major surgery (mainly heart surgery). In these cases, in addition to hydration, there are other specific preventive measures adapted to each condition.
Topics: Acute Kidney Injury; Contrast Media; Critical Care; Diuretics; Fenoldopam; Fluid Therapy; Hemodynamics; Humans; Intensive Care Units; Liver Failure; Postoperative Complications; Renal Circulation; Rhabdomyolysis; Risk Factors; Secondary Prevention; Sepsis; Vasoconstrictor Agents
PubMed: 28190602
DOI: 10.1016/j.medin.2016.12.004 -
Contributions To Nephrology 2017It has become apparent that inflammation and inflammatory reactions can evoke renal injury and promote chronic kidney disease (CKD) progression. Under physiological... (Review)
Review
It has become apparent that inflammation and inflammatory reactions can evoke renal injury and promote chronic kidney disease (CKD) progression. Under physiological condition, intrarenal vascular distribution is heterogeneous, and medulla is hypoxic. To avoid energy deprivation in the low pO2 regions of the kidney, an array of hormones, autocoids, and vasoactive substances, including medullipin, prostaglandins, endothelins, nitric oxide, angiotensin II, kinins, and adenosine, tonically regulates the microvasculature to ensure a perfect match of the microcirculation (O2 supply) and renal tubules (O2 demand). Inflammation, systemic or intrarenal, not only can abolish the microvascular response to its regulators, but also induces an array of tubular toxins, including reactive oxygen species, leading to tubular injury, nephron dropout, and onset of CKD. Positive acid balance, electrolyte alterations, and intestinal dysbiosis can perpetuate CKD progression. Understanding the role of inflammation in the genesis and progression of CKD will foster the development of strategies to prevent and treat the underlying inflammation and improve CKD outcomes.
Topics: Disease Progression; Humans; Inflammation; Kidney Tubules; Microcirculation; Renal Circulation; Renal Insufficiency, Chronic
PubMed: 28910792
DOI: 10.1159/000479257 -
Nature Reviews. Nephrology Jul 2022
Topics: Humans; Kidney; Microcirculation; Renal Circulation
PubMed: 35668234
DOI: 10.1038/s41581-022-00595-8 -
Nephron 2023Alterations of renal hemodynamics play an essential role in renal homeostasis and kidney diseases. Recent data indicated that semaphorin 3C (SEMA3C), a secreted...
BACKGROUND
Alterations of renal hemodynamics play an essential role in renal homeostasis and kidney diseases. Recent data indicated that semaphorin 3C (SEMA3C), a secreted glycoprotein involved in vessel development, can modulate renal vascular permeability in acute kidney injury, but whether and how it might impact systemic and renal hemodynamics is unknown.
OBJECTIVES
The objective of the study was to explore the effect of SEMA3C on systemic and renal hemodynamics.
METHODS
SEMA3C recombinant protein was administered intravenously in two-month-old wild-type mice, and the variations of mean arterial pressure, heart rate, renal blood flow, and renal vascular resistance were measured and analyzed.
RESULTS
Acute administration of SEMA3C induced (i) systemic hemodynamic changes, including mean arterial pressure decrease and heart rate augmentation; (ii) renal hemodynamic changes, including reduced vascular resistance and elevated renal blood flow. Continuous perfusion of SEMA3C had no significant effect on systemic or renal hemodynamics.
CONCLUSION
SEMA3C is a potent vasodilator affecting both systemic and renal hemodynamics in mice.
Topics: Mice; Animals; Hemodynamics; Kidney; Vascular Resistance; Heart Rate; Renal Circulation; Semaphorins
PubMed: 36580904
DOI: 10.1159/000528259