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Cellular and Molecular Mechanisms of Ischemic Acute Renal Failure and Repair
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Joseph V. Bonventre, Ralph Witzgall
This chapter will focus on the cellular and molecular consequences of ischemia in the kidney. The result of generalized and/or localized ischemia to renal tissue is damage to the tubular cells themselves. Damaged tubular cells swell in size due to abnormalities in volume regulation. Membrane blebs are formed which break off and are released into the tubular lumen. These blebs, together with other released “cellular debris”, then result in cast formation (Bayati, et al., 1989), tubular lumen obstruction, and elevated tubular pressures (Arendshorst, et al., 1975; Mason, et al., 1977). The damaged cells sluff leaving a denuded basement membrane. The resultant enhanced tubular fluid backleak into the peritubular capillaries results in an effective reduction in GFR which is likely much more important than glomerular endothelial and epithelial cell changes and resultant effects on the glomerular capillary ultrafiltration coefficient (Daugharty, et al., 1974; Hostetter and Brenner, 1988).
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.
Renal Effects
Published in Lars Friberg, Tord Kjellström, Carl-Gustaf Elinder, Gunnar F. Nordberg, Cadmium and Health: A Toxicological and Epidemiological Appraisal, 2019
Fowler and co-workers66 also reported renal vascular changes in rats exposed to cadmium chloride in drinking water (0 to 200 mg Cd per liter) for up to 12 weeks. There were constrictions of smaller renal arteries, mild dilatation of larger arteries, and a diffuse dose-related scarring of peritubular capillaries.
Andrographis paniculata mitigates first-line anti-tubercular drugs-induced nephrotoxicity in Wistar rats
Published in Biomarkers, 2022
Varsha Sharma, Radhika Sharma, Vijay Lakshmi Sharma
Not only liver as a detoxifying organ can be adversely affected by the drugs and their toxic metabolites but also, these have to show an adverse impact on kidneys because of their involvement in waste elimination (Pazhayattil and Shirali 2014, Sharma et al. 2019a). The kidney performs various functions in the body, such as maintenance of electrolytes through acid-base balance, the continuance of homeostasis, detoxification, and excretion of drugs and their metabolites. Human kidneys have to accept 20% of the cardiac output but also play an important role in filtering and concentrating a range of chemical substances from the excretory fluid. Whenever the amounts of these substances reach the highest level only then become toxic to renal tissue. RMs with the aid of indispensable charge and size can filtrate out and consequently through pinocytosis/endocytosis run into cells of renal tubular epithelial (Lee and Kim 2004). Many drugs through peritubular capillaries make a path towards the basolateral surface of renal tubular epithelial cells where they are taken up by anionic and cationic transporters and ultimately discharged into tubular lumen (Khrunin et al. 2010). Thus, kidneys also endure these eliminated metabolites which result in performed impaired functions (Loh and Cohen 2009). In the loop of Henle elevated drug concentration leads to water reabsorption which is one of the reasons for tubular cells destruction. High metabolic activity in tubular cells of the collecting duct and loop of Henle is a causative factor of renal toxicity and also escorts the cells towards hypoxic conditions. Therefore, RMs that are the byproducts of drug metabolism are also liable for drug-mediated renal toxicity.
Pro- and anti-fibrotic effects of vascular endothelial growth factor in chronic kidney diseases
Published in Renal Failure, 2022
Changxiu Miao, Xiaoyu Zhu, Xuejiao Wei, Mengtuan Long, Lili Jiang, Chenhao Li, Die Jin, Yujun Du
Renal microvascular rarefaction can be defined as loss of renal capillaries. Peritubular capillaries are an integral part of the renal microvasculature. Branches of glomerular efferent arterioles consist of a capillary network which supplies oxygen and nutrients to tissues along the proximal and distal tubules [4]. Rarefaction of peritubular capillaries is a characteristic feature of renal fibrosis. A close link between capillary rarefaction and fibrosis has been demonstrated in animal models of diabetic nephropathy, chronic allograft nephropathy, obstructive nephropathy, and anti-glomerular basement membrane glomerulonephritis [5–8]. These findings strongly suggest the involvement of peritubular capillaries rarefaction in fibrosis progression. Exposure of kidney tissue to pathogenic factors disturbs the blood flow in peritubular capillaries, resulting in decreased perfusion in the adjacent renal interstitial region, which may lead to a loss of capillaries and renal fibrosis. The consequent hypoxia promotes the infiltration of inflammatory cells and the deposition of extracellular matrix, inducing renal fibrosis. The most dominant mechanism of renal microvascular rarefaction is believed to involve an imbalance between proangiogenic and anti-angiogenic factors [9]; for example, upregulation of antiangiogenic factors thrombospondin-1 and endothelin, and downregulation of angiogenic factors such as vascular endothelial growth factor (VEGF) and angiogenin. Among these, VEGF is the most important regulator of angiogenesis. The role of VEGF in kidney diseases has attracted increasing attention over the years, because in addition to regulation of angiogenesis, it also plays a role in the progression of renal fibrosis (Figures 1 and 2).
The paradigm shift from polycythemia to anemia in COPD: the critical role of the renin–angiotensin system inhibitors
Published in Expert Review of Respiratory Medicine, 2022
Vassilios Vlahakos, Katerina Marathias, Sofia Lionaki, Stelios Loukides, Spyros Zakynthinos, Demetrios Vlahakos
In addition to hypoxia, RAS activation may enhance erythropoiesis in patients with COPD and contribute to the development of polycythemia. We have previously shown that both plasma renin and aldosterone levels were threefold greater in patients with polycythemia compared to equally hypoxemic COPD patients with normal hematocrit values. No difference in erythropoietin levels was observed between patients with or without polycythemia and only renin levels and PaO2 were independently and significantly associated with hematocrit values [45]. The mechanism(s) by which RAS increases red blood cell mass has not yet been fully elucidated, but currently available evidence indicates that angiotensin II, the active octapeptide of RAS, participates in the regulation of erythropoiesis. First, angiotensin II, a selective vasoconstrictor of the efferent arteriole, decreases blood supply in the peritubular capillaries, causes ischemia in renal tubulointerstitium and affects the hypoxia inducible-factor 1, which augments EPO production and secretion [46]. The stimulatory effect of the RAS on EPO secretion appears to be mediated by the angiotensin II type 1 (AT1) receptor, since losartan can completely block EPO oversecretion induced by angiotensin II infusion in healthy volunteers [47]. On the other hand, angiotensin II may act, as a direct growth factor of erythroid progenitors by activating specific AT1 receptors on their surface, as revealed in in-vitro experiments [48]. In order to facilitate erythropoiesis, angiotensin II is capable to stimulate iron absorption and utilization. For example, angiotensin II infusion in experimental animals decreased hepcidin levels, increased the expression of duodenal iron transporters and increased ferritin levels. All these effects were blocked by selective angiotensin receptor blockers [49,50].