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Echocardiographic Imaging of Myocardial Inflammation
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Lipid microbubbles have been synthesized to augment their complement-mediated avidity to activated leukocytes by the incorporation of phosphatidyl serine into the microbubble shell (39). In a model of murine kidney ischemia-reperfusion, these micro-bubbles yielded greater persistent videointensity signal compared to standard lipid microbubbles (39). More recently, in a canine model of reperfused myocardial infarction, phosphatidyl serine microbubbles were used to ultrasonically demonstrate the postischemic region of inflamed myocardium (Fig. 4) (40). Similarly, because albumin microbubbles also adhere to activated leukocytes, MCE can be used to identify acute heart transplant rejection, as has been shown in a rat model of heterotopic heart transplantation (Fig. 5).
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
Kidney ischemia stimulates glycolysis, thus increasing the generation of protons and leading to a decrease in cellular pH (Chan, et al., 1982). Severe acidosis may be detrimental to cell survival in other organs, such as the heart (Williamson, et al., 1976; Neely and Grotyohann, 1984). The reduced pH inhibits glycolysis by inhibiting phosphofructokinase, the rate-limiting enzyme in glycolysis. Although severe acidosis has been proposed to be detrimental to the kidney (Bore, et al., 1981) we have demonstrated in renal tubular cells and isolated hepatocytes that mild acidosis (pH 6.9) protects cells against anoxia and substrate deprivation in vitro (Bonventre, 1984; Bonventre and Cheung, 1985). Weinberg also found protection of renal tubular cells with acidosis (Weinberg, 1985). This protection is associated with the prevention of any increase in total cell Ca2+ (Bonventre and Cheung, 1985). When tubules were incubated at high density and generated an extracellular pH of approximately 7.0 due to accumulation of products of metabolism, similar protection was observed (Weinberg, 1985). Acidosis was also found to be protective in the isolated perfused kidney (Shanley, et al., 1988). The mechanism of protection by mild degrees of acidosis is not known. The protection is not dependent upon preservation of cellular ATP levels (Bonventre and Cheung, 1985). Reduction in pH protects tubules exposed to ionomycin or mitochondrial inhibitors despite the fact that the tubules have increases in [Ca2+]i, equivalent to those changes observed in nonprotected tubules (Weinberg, et al., 1991). Acidosis has been reported to stabilize cell membranes (Bell, et al., 1971) and may decrease transmembrane calcium flux (Vogel and Sperelakis, 1977). It is possible that the protection is due to inhibition of an enzymatic process which would otherwise be detrimental to the cells. For example, we have found that at least two kidney PLA2 enzymes have alkaline pH optima (Bonventre, 1992; Nakamura, et al., 1991). When blood flow and oxygen delivery are reestablished the extracellular pH rapidly returns to normal. With the increase in intracellular pH upon reperfusion, activation of PLA2 would be enhanced. This might lead to further alteration in membrane structure and secondarily to enhanced Ca2+ permeability, which in turn will further enhance PLA2 activation. The increase in pH which occurs as a consequence of reperfusion may contribute in an important way to “reperfusion injury”.
Associations of urinary orosomucoid, N-acetyl-β-D-glucosaminidase, and albumin with blood pressure and hypertension after 7 years. The Tromsø Study
Published in Blood Pressure, 2022
Karl M. Brobak, Runa M. Andreassen, Toralf Melsom, Aud Høieggen, Jon V. Norvik, Marit D. Solbu
The proximal tubules are responsible for reabsorbing approximately 65% of filtered load and most low molecular weight proteins [63]. It is hypothesized that subclinical kidney injury, with the development of afferent arteriolopathy and tubulointerstitial disease, especially in the outer medulla, leads to kidney ischemia, inflammation and oxidative stress, which is associated with a decrease in sodium filtration and an increase in blood pressure [4]. Urinary NAG is a marker of proximal tubular cell function and is considered a sensitive marker related to inflammation and oxidative stress [25]. Earlier studies of urinary NAG in blood pressure and hypertension are limited in sample size or in the urine collection method [12,64–67]. A small study of patients with newly diagnosed hypertension without microalbuminuria found a significantly higher NAG activity in hypertensives compared to healthy controls [28]. Further, NAG, but not ACR, was significantly associated with incident hypertension among the HIV-uninfected women in the Women′s Interagency HIV Study [64]. In this general population cohort, consisting of participants with overall normal kidney function, urinary NAG yielded only weak or non-significant associations with blood pressure and hypertension in our multivariable models with CVD risk factors.
Transcriptional profile changes after treatment of ischemia reperfusion injury-induced kidney fibrosis with 18β-glycyrrhetinic acid
Published in Renal Failure, 2022
Yamei Jiang, Chengzhe Cai, Pingbao Zhang, Yongsheng Luo, Jingjing Guo, Jiawei Li, Ruiming Rong, Yi Zhang, Tongyu Zhu
According to a 2017 global epidemiological survey, the worldwide prevalence of chronic kidney disease (CKD) is about 9.1%. Death caused by CKD or impaired renal function accounted for 4.6% of all deaths in 2017, and CKD was the twelfth leading cause of death [1]. The immense public health burden of CKD has aroused great interest in research into the mechanism and potential therapy of this disease worldwide. In clinical settings, kidney ischemia and reperfusion (I/R) injury leaded acute kidney injury is a common complication of major surgery such as cardiac surgery (accounting for 20%) and abdominal surgery [2,3]. Furthermore, it is also a common reason for delayed graft function after kidney transplantation [4]. I/R injury eventually results in serious adverse outcome of progressing to CKD [5]. Renal fibrosis with deposition of collagens and other extracellular matrix proteins is the basic feature of CKD. Targeting cytokines, transcription factors, developmental, and signaling pathways has been shown to ameliorate kidney fibrosis in preclinical studies [6]. In addition, experts in various fields have collaborated to provide insights into novel strategies to prevent and treat CKD through animals and biomimetic studies [7]. In the current post-genomic era, the application of systems biology enables in-depth analysis of CKD at the molecular and subcellular level [8]. It is imperative to explore promising effective therapeutic strategies for CKD.
Evidence-based medicine, the number ‘three’ and its multiples in urological clinical rules
Published in Scandinavian Journal of Urology, 2021
Georges Mjaess, Fouad Aoun, Simone Albisinni, Michel Vanhaeverbeek, Thierry Roumeguère
Warm kidney ischemia is known to be ‘30 min’ among urologists during partial nephrectomy and is based on a canine study in 1975. However, while Funahashi et al. [3] have shown that warm ischemia time in order to preserve kidney function is ideally <20 min, Parekh et al. [4] have concluded that a human kidney can tolerate 30–60 min of controlled clamp ischemia, and the ancient concept that ‘every minute counts’ is revoked. Moreover, the typical window of opportunity for surgical intervention in testicular torsion is thought to be ‘6 h’ from onset of pain with a proved 90% salvage rate. However, a recent systematic review has demonstrated that survival of testis (1) can be much longer than 6 h ‘that is commonly taught’, and (2) is believed to be significant even after 24 h of testicular torsion [5].