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Medicines in neonates
Published in Evelyne Jacqz-Aigrain, Imti Choonara, Paediatric Clinical Pharmacology, 2021
Evelyne Jacqz-Aigrain, Imti Choonara
The action of prostanoids on the kidney is mediated through prostaglandin receptors belonging to the G-protein family [2]. The role of COXs in renal development appears increasingly evident while, by far, not fully understood [3]. In the fetus, COX-2 is crucial for nephrogenesis in mid-pregnancy [4–6]. Arachidonic acid metabolites modulate some enzyme activities along the nephron with an age-dependent developmental effect [7]. Experimental studies show that cortical as well as medullar COX-2 are over-expressed in fetal life and in the first days of life. This accounts for the high amount of vasodilator prostaglandins being secreted [3]. Both the fetus and the neonate, in the first postnatal days of life, face a high vascular resistance environment. In the renal glomerular vasculature, the efferent arteriole is under the influence of vasoconstrictive agents, such as angiotensin II (ANG II). Maintaining a high vascular resistance at this level during this period is the way by which the immature kidney is able to filtrate. PGE2 and PGI2 are the main vasodilator prostanoids which act on the glomerular afferent arterioles. These prostanoids counteract this high renal vascular resistance in utero in the first days of life and maximise the glomerular filtration through the EP2 and EP4 receptors (EP for E-prostanoid), and the IP2 receptor (IP for I-prostanoid). EP2 prostaglandins appear to play a role in regulating renin release through their receptors on renal juxtamedullar cells, providing a useful feedback mechanism [8].
Functions of the Kidneys and Functional Anatomy
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 afferent arterioles to the high-pressure glomerular capillaries arise from small branches of the renal artery. The glomerular capillaries form distinct loops before joining together and are drained by the efferent arteriole. Blood from the efferent arterioles is distributed to supply (i) the low-pressure peritubular capillaries that receive the large amount of fluid and electrolytes reabsorbed by the tubules and (ii) the vasa recta.
The Urinary System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
After the efferent arteriole leaves the glomerular capsule, it branches into secondary capillary plexuses around both the proximal and distal convolutions before finally reaching the renal vein. Through these capillaries, the circulatory system selectively reabsorbs some of the filtrate from the Bowman's capsule. Ions and glucose are reabsorbed early in the proximal convolution, and other nutrients and much of the water are reabsorbed in the distal convolution, converting glomerular filtrate into urine by the time it reaches the collecting tubules for transport to the renal pelvis.
Treatment with human umbilical cord blood serum in a gentamicin-induced nephrotoxicity model in rats
Published in Drug and Chemical Toxicology, 2022
Naser Mirazi, Fatemeh Baharvand, Reza Moghadasali, Alireza Nourian, Abdolkarim Hosseini
Prior to the implementation of eosin and hematoxylin staining, from the kidney tissues, 5 µ-size sections were deparaffinized and rehydrated. The reagents and stains were bought from Sigma (St. Louis, MO, USA). An Olympus BX-50 microscope, with the integration of a color digital camera (Olympus, Japan, DP-72), was utilized for observing the histological sections. Protective effects of hUCBS on kidney were quantitatively assessed by measuring the glomerular surface area (GA), glomerular volume (GV) and number of proximal tubular cell nuclei (PTN). For each group, 20 superficial cortical glomeruli were selected according to the following criteria: 1) presence of afferent or efferent arterioles at the glomerular vascular pole; 2) presence of the beginning of proximal convoluted tubule at the glomerular urinary pole. GA was measured by outlining a perimeter along the glomerular periphery (Gilbert et al.1991) using image analysis software (Image J v1.53). Assuming glomeruli as spheres, we calculated GV using the following formula: GV = 1.2545 × GA (Rangan and Tesch 2007). PTN was counted in 10 proximal convoluted tubular sections close to the renal corpuscles on which the glomerular measurements were performed. The numbers of epithelial cells were calculated as number of nuclei per 100 µm of perimeter of proximal convoluted tubules using Olympus DP2-BSW application software (v2.2). The images were all taken with a magnification of ×400 from H&E-stained renal tissue sections.
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.
Neprilysin, the kidney brush border neutral proteinase: a possible potential target for ischemic renal injury
Published in Toxicology Mechanisms and Methods, 2020
Runali Sankhe, Manas Kinra, Jayesh Mudgal, Devinder Arora, Madhavan Nampoothiri
Exogenous infusion of ANP in a rat model of ischemic kidney injury preserved the glomerular filtration rate and attenuated renal tissue damage (Lieberthal et al. 1990). ANP has been shown to be a potent inhibitor of aldosterone secretion by its direct action on the adrenal gland (Maack et al. 1984; Lieberthal et al. 1990), as well as indirectly by inhibiting renin release from the kidney (Maack et al. 1984; Vesely 2003). In the kidney, ANP increases the glomerular capillary hydrostatic pressure leading to rise in glomerular filtration rate and dilation of afferent arterioles with slight constriction of efferent arterioles (Saito 2010). ANP and BNP have similar diuretic and natriuretic effects; however the half-life of BNP is 100-fold shorter than ANP. CNP is present in human kidney, but CNP did not affect renal function.