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Role of Metabolism in Chemically Induced Nephrotoxicity
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Those conjugates that undergo glomerular filtration are either excreted in the urine (generally the mercapturates) or are reabsorbed into renal proximal tubular cells by active, sodium-dependent transport across the brush border membrane (Schaeffer and Stevens, 1987). Because only 30% of plasma is filtered through the glomerulus during a single pass through the renal circulation, a significant portion of chemicals cleared by the kidneys are taken up by processes localized to the basal-lateral membrane (Lash et al., 1988). Transport processes have been identified for several conjugates and their metabolites on the basal-lateral membrane in various in vitro systems, including renal cortical slices, membrane vesicles, isolated perfused kidney, isolated proximal tubules, and isolated proximal tubular cells (Boogaard et al., 1989; Inoue et al., 1981, 1984; Lash and Jones, 1983, 1984, 1985; Lash and Anders, 1989; Lock and Ishmael, 1985; Lock et al., 1986; Ulrich et al., 1989; Wolfgang et al., 1989; Zhang and Stevens, 1989).
Renal Blood Flow
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The renal blood flow amounts to 20% of the cardiac output, whereas the kidneys are only less than 1% of the body weight. Although the kidneys have a high metabolic rate, the renal blood flow is still 10 times more than is required. A very high renal blood flow is required for the production of large amounts of glomerular filtrate, which is necessary for the urinary excretion of waste products. Most of the blood perfuses the renal cortex (which contains the corpuscles), with the medullary flow being 10 times less (although the latter is still equivalent to brain blood flow). The main resistance vessels in the renal circulation are the afferent and efferent arterioles, and contraction of either reduces renal blood flow.
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.
The current and future status of inotropes in heart failure management
Published in Expert Review of Cardiovascular Therapy, 2023
Angelos Arfaras-Melainis, Ioannis Ventoulis, Effie Polyzogopoulou, Antonios Boultadakis, John Parissis
Dopamine is an endogenous molecule that can activate dopaminergic type 1 and 2, beta-1, and alpha-1 adrenergic receptors. When used at doses up to 2.5 µg/kg/min, it induces renal vasodilation by binding to the postsynaptic type 1 dopaminergic receptors, as well as splanchnic vasodilation by binding to the presynaptic type 2 dopaminergic receptors [8,39]. This effect leads to an increase in renal circulation, irrespective of cardiac output increases [40]. However, the clinical significance of the renal effects conferred by low-dose dopamine is disputed. For example, in the DAD-HF-II (Dopamine in Acute Decompensated Heart Failure II) study, the addition of low-dose dopamine to low-dose intravenous furosemide did not show any improvement in renal function, mortality or HF outcomes, when compared to the single low-dose furosemide treatment arm [21]. Additionally, the ROSE-AHF (Renal Optimization Strategies Evaluation in Acute Heart Failure) trial also failed to demonstrate any significant improvement in 72-hour urine volume or decongestion markers in patients who received dopamine [22]. When used at moderate doses (3–5 µg/kg/min), dopamine primarily enhances cardiac contractility and chronotropy by acting on the cardiac beta-1 receptors. When used at high doses (>5 µg/kg/min), it leads to a net vasoconstrictive effect by stimulating alpha-1 receptors. It is worth mentioning that tachyarrhythmias occur with the use of dopamine especially at higher doses closer to 10 µg/kg/min or above, as well as in the setting of underlying hypertension [8,41,42].
The effect of whole blood viscosity on contrast-induced nephropathy development in patients undergoing percutaneous coronary intervention
Published in Postgraduate Medicine, 2022
Mustafa Kinik, Sencer Çamci, Selma Ari, Hasan Ari, Mehmet Melek, Tahsin Bozat
The relationship between lowness of WBV and CIN can be explained by the tubuloglomerular feedback mechanism in the kidneys. The inability of the glomeruli, which have adapted to the low viscosity environment, to adapt to the sudden increase in viscosity caused by the deformation created by contrast material and contrast on the erythrocytes may cause CIN development [26]. Vasodilation in afferent arterioles and vasoconstriction in efferent arterioles occur to provide the necessary glomerular filtration in a low-viscosity environment. However, in case of a sudden increase in viscosity in the distal tubule, renin- and adenosine-mediated mechanisms cause vasoconstriction in afferent arterioles and the medullary vascular bed, causing a decrease in GFR [26]. This GFR decline is one of the main causes of CIN development. Because of decreased GFR, the removal of the contrast material from the body is delayed, and CIN develops because of this event, causing a vicious circle on the kidneys. Since the WBV values in non-STEMI and STEMI patients were higher than those in elective PCI patients, the tubuloglomerular feedback mechanism adapted to a more viscous environment. Therefore, since the viscosity increase in distal renal tubules in these patients is relatively less, the effectiveness of the feedback mechanism and the GFR decrease are less. The second explanation about the relationship between lowness of WBV and CIN; lower WBV conditions lead to a constricted renal circulation, associated with a condition of decreased NO bioavailability [27]. These may explain that WBV values are not CIN development predictors in these groups.
What should clinicians know about the renal effect and the mechanism of action of levosimendan?
Published in Expert Opinion on Drug Safety, 2021
Patrick M Honore, Sebastien Redant, Sofie Moorthamers, Thierry Preseau, Keitiane Kaefer, Leonel Barreto Gutierrez, Rachid Attou, Andrea Gallerani, Willem Boer, David De Bels
In view of the body of knowledge at our disposal, we can conclude that levosimendan increases overall KBF, but not at the price of medullary hypoxemia, and go along with an increase in GFR [11]. Levosimendan caused no significant changes in renal oxygen consumption, renal oxygen extraction or filtration fraction [11]. Filtration fraction (FF) is the fraction of renal plasma flow (RPF) filtered across the glomerulus [11] (calculated as GFR divided by RPF [11]). FF is about 20% indicating that the remaining 80% continues its pathway through the renal circulation. When the FF increases, the protein concentration of the peritubular capillaries increases [11]. This leads to additional absorption in the proximal tubule [11]. When the FF decreases, the amount of fluid being filtered across the glomerular filtration barrier per unit time consequently decreases [11]. The protein concentration downstream in the peritubular vessels decreases and the absorptive capacity of the proximal tubules lessens too [11].