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Hypertension
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Plasma volume usually decreases as BP increases. In rare cases, the plasma volume stays at normal levels or increases. It is usually high in a hypertensive person because of primary aldosteronism or renal parenchymal disease. Plasma volume can be very low as well, because of pheochromocytoma. As the diastolic BP increases and arteriolar sclerosis develops, blood flow through the kidneys gradually decreases. Until much later, the glomerular filtration rate (GFR) remains normal. The filtration fraction increases because of this. Blood flow in the cerebral, coronary, and muscle blood vessels is normal unless severe atherosclerosis is present.
An Overview of Drug-Induced Nephropathies *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Jean Paul Fillastre, Michel Godin
Some studies have now been made of the primary alterations of renal function after cisplatin. Offerman et al. (1984) measured GFR and renal plasma flow in ten patients receiving cisplatin infusion at a dose of 20 mg/m2 over 4 h. These measurements were made before, during, and after the administration of cisplatin on the first day of treatment. The patients were hydrated with intravenous saline during the whole study period. In all of them there was a decrease in renal plasma flow during, or within 3 h of, cisplatin infusion, with no important changes in GFR. Thus, an increase in the corresponding filtration fraction was found in all patients. Subsequently, a decreased GFR was also detected. The fall in renal plasma flow that occurred before any change in GFR was suggestive of an increase in renal vascular resistance.
Glomerular Filtration
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 plasma flow is 600 mL/min, and the GFR is 125 mL/min. The filtration fraction, the fraction of renal plasma flow filtered off into the tubule, is 125/600, or about 20%. The increase in oncotic pressure of glomerular capillary plasma is directly proportional to the filtration fraction. This means that the greater the percentage of volume filtered from plasma, the greater the increase in oncotic pressure of glomerular capillary plasma.
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].
Impact of obesity with or without hypertension on systemic haemodynamic and renal responses to lower body negative pressure
Published in Blood Pressure, 2021
Nima Vakilzadeh, Dusan Petrovic, Marc Maillard, Lucie Favre, Eric Grouzmann, Gregoire Wuerzner
The clearance of inulin, PAH or lithium (ml/min) was calculated using the standard formula Cx = Ux * V/Px, where Ux and Px are the urine and plasma concentrations of x and V is the urine flow rate in ml/min. Urinary electrolyte excretion rate was calculated as Ux * V. The fractional excretions were calculated as the clearance of x divided by the measured GFR. Renal blood flow (RBF) was calculated as RBF = RPF/(1 – Hematocrit) and renal vascular resistance (RVR) as RVR = mean blood pressure/RBF. Finally, the filtration fraction (FF) was calculated as inulin clearance/PAH clearance and free water clearance was calculated as ClH2O = (1 − urine osmolality/plasma osmolality) *urinary flow rate. Cumulated urinary normetanephrine and metanephrine were calculated as Cumulated x = (volume T1*UxT1) + (volume T2*UxT2) + (volume T3*UxT3), where T1, T2 and T3 are hourly timing before, during and after LBNP.
Obesity, acute kidney injury and mortality in patients with sepsis: a cohort analysis
Published in Renal Failure, 2018
Joana Gameiro, Miguel Gonçalves, Marta Pereira, Natacha Rodrigues, Iolanda Godinho, Marta Neves, João Gouveia, Zélia Costa e Silva, Sofia Jorge, José António Lopes
Obesity dramatically alters renal hemodynamics, which could explain an increased susceptibility to AKI in obese patients [27]. Although the pathophysiology is not completely understood, the increased renal plasma flow and GFR resulting from altered hemodynamics could lead to a higher filtration fraction or hyperfiltration syndrome, potentially contributing to an increased renal susceptibility to damage [28]. A recent study by Billings et al. found that markers of oxidative stress appear to affect renal function by reducing renal perfusion, reducing creatinine clearance, and instigating cellular and functional renal damage in experimental models, and demonstrated that these biomarkers were a strong predictor of AKI in cardiac surgery patients [23]. Adipose production of inflammatory mediators, as well as adipokines such as leptin, and decreased production of adiponectin, in response to acute illness have been associated with a heightened AKI risk [29]. Another factor that could contribute to obesity’s influence on AKI is the challenge to correctly assess the intravascular volume status and to prescribe adequate fluid therapy and/or vasopressors. Dosing of potentially nephrotoxic agents may also be demanding, since obesity impacts many pharmacokinetic factors, and the dose itself may be variable depending on whether it was based on actual body weight or on formulae-based weight adjustment, not obesity [30]. Notably, obese ICU patients are at an increased risk for elevated intra-abdominal pressure, which may, in itself, cause renal dysfunction from both venous congestion and poor arterial organ perfusion [31,32].