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Embryology, Anatomy, and Physiology of the Kidneys and Ureters
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Paul Sturch, Sanjeev Madaan, Seshadri Sriprasad
Factors that influence renal blood flow:Angiotensin II constricts afferent and efferent arterioles → reduces flow.ADH, adenosine triphosphate (ATP), platelet-activating factor (PAF), and endothelin → vasoconstriction → reduce flow and GFR.Nitric oxide (NO), prostaglandin → vasodilatation → increases blood flow.Atrial natriuretic peptide (ANP) → afferent arteriole dilatation → increases flow and GFR.
Disease
Published in Thomas F. Lüscher, Paul M. Vanhoutte, The Endothelium: Modulator of Cardiovascular Function, 2020
Thomas F. Lüscher, Paul M. Vanhoutte
Of all causes of acute renal failure, rhabdomyolysis and hemorrhage with increased blood and urine levels of myoglobin and hemoglobin are most relevant to endothelium-dependent responses.714 Indeed, myoglobin and hemoglobin are potent inhibitors of endothelium-dependent relaxations of isolated blood vessels757,805 (see Chapter 3). These large molecules bind nitric oxide at their ligand sites in the ferrous rings in vitro; they also interfere with the formation of cyclic GMP in vascular smooth muscle.731,805 Hemoglobin blocks the increase in cyclic GMP evoked by EDRF in cultured mesangial cells.1111 Thus, high plasma levels of hemoglobin and/ or myoglobin in vivo may, by inhibiting EDRF, increase vascular tone. In the renal circulation, this may help to decrease renal blood flow and reduce glomerular filtration.
Kidney Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
The glomerular filtration rate remains relatively constant despite variations in renal perfusion pressure. This is the result of autoregulation of renal blood flow. Over a wide range of renal perfusion pressures (estimated to be 80 to 160 mmHg in humans), renal blood flow remains nearly the same. Two mechanisms are primarily responsible for autoregulation: myogenic adjustments in preglomerular vascular resistance4 and tubuloglomerular feedback.5
Values of serum sFlt-1, PLGF levels, and sFlt-1/PLGF ratio in diagnosis and prognosis evaluation of preeclamptic patients
Published in Clinical and Experimental Hypertension, 2020
Xiaohe Zhu, Limin Chen, Ran Li
For a long time, preeclampsia is diagnosed based on proteinuria. Proteinuria occurs because of damage to capillary endothelial cells in the glomerulus, leading to diffuse swelling, and the lumen of the capillaries is compressed by the swollen endothelial cells. As a result, the renal blood flow is significantly reduced. When the kidney is in an ischemic and hypoxic environment, the permeability of blood vessel wall is increased, and plasma albumin and globulin are filtered from the glomerulus to induce proteinuria. Meanwhile, the renal tubular reabsorption is impaired. Therefore, the urinary protein level can reflect the degrees of glomerular ischemia, hypoxia, and functional damage, as an index for evaluating the progression of GH (3). However, the correlation between urinary protein level and severity of preeclampsia has become controversial recently.
Impact of increased venous pressure on kidney function and mortality in cardiovascular patients with preserved ejection fraction
Published in Current Medical Research and Opinion, 2020
Anastasios Milkas, Konstantinos Tsioufis, Leonidas Koliastasis, Eleftherios Tsiamis, Dimitris Tousoulis, Jozef Bartunek, Marc Vanderheyden
Respectively, perfusion, estimated by renal blood flow and unobstructed efferent flow is known to regulate renal function. Thus, kidneys constitute another anatomical area where left and right heart hemodynamics interact. While hypertension induces kidney dysfunction through decrease of renal blood flow and activation of detrimental neurohormonal mechanisms, the association of blood pressure levels within the normal range or after antihypertensive treatment and eGFR may be blunted. Elevated LV filling pressures can maintain cardiac output and renal perfusion, but the venous system might fail to accommodate an increased unstressed volume without a concomitant increase in CVP and RAP.25 Given that in our study almost two third of the patients were hypertensive patients under treatment, the different elastic properties and different response to volume re-distribution of the venous and arterial system may explain to some degree the paradoxical lack of association between LV hemodynamic parameters and eGFR.
The investigation of TIMI risk index for prediction of contrast-induced acute kidney injury in patients with ST elevation myocardial infarction
Published in Acta Cardiologica, 2020
Tufan Çınar, Yavuz Karabağ, Veysel Ozan Tanık, Metin Çağdaş, İbrahim Rencüzoğulları, Ahmet Öz
Previously, several studies have demonstrated that advanced age and hemodynamic status, which is reflected by heart rate and systolic blood pressure, are important risk factors for the development of CI-AKI after primary PCI [8,22]. It has been reported that aging is undoubtedly associated with structural changes in the kidney, including progressive loss of functional nephron, impaired endothelial function, and the decreased regenerative capacity of the renal parenchyma after acute injury [23]. Hemodynamic instability, namely increasing heart rate and decrease blood pressure, may cause decrease renal blood flow, which may activate the renin angiotensin aldosterone and sympathetic nervous systems in the body. Consequently, all of these changes can ultimately lead to constriction of the renal artery and renal medullary hypoxia, resulting in the development of CI-AKI [24].