Renal Cortical Necrosis: Experimental Induction by Hormones (Contributions to Nephrology, Vol. 28) - kelloggchurch.org

Renal Cortical Necrosis in Postpartum HemorrhageA Case.

Jul 01, 2016 · Pregnancy-related acute kidney injury AKI is a rare complication in high-income countries, with an estimated incidence from 1.5 to 4.5 per 10,000 deliveries.1, 2 Except for women with preexisting hypertension or chronic kidney disease, the long-term outcome of pregnancy-related AKI is usually favorable unless renal cortical necrosis RCN occurs.3, 4, 5 RCN is defined as ischemic. Dec 01, 2016 · Acute kidney injury AKI occurs when there is a rapid decline in glomerular filtration rate GFR; see Glossary, Box 1, usually accompanied by impaired microcirculation, inflammation and/or tubular injury or necrosis and reduced renal blood flow Basile et al., 2012.AKI is initiated by various clinical insults, including hypotensive shock, sepsis, surgery or the administration of nephrotoxic. INTRODUCTION. Idiopathic calcium oxalate CaOx stone disease is a common urological disorder affecting 6-10% of the US population and costing over 2 billion dollars/year 1.The incidence of kidney stones is on the rise and in the United States of America rose by 37% between 1976–1980 and 1988–1994 in both genders 2.A number of animal models, specifically rat models have been utilized to. Introduction. Few diseases give rise to such diverse renal manifestations as does sickle cell disease SCD. Such involvement adversely affects virtually all major physiological processes in the kidney, and leads to complications that are common and chronic on the one hand such as impaired urinary concentrating ability, and those that are rare and uniformly fatal on the other such as renal.

Oxidative stress has a critical role in the pathophysiology of several kidney diseases, and many complications of these diseases are mediated by oxidative stress, oxidative stress-related mediators, and inflammation. Several systemic diseases such as hypertension, diabetes mellitus, and hypercholesterolemia; infection; antibiotics, chemotherapeutics, and radiocontrast agents; and. BMJ 3:559-561, 1970 sen RA: The induction of renal papillary necrosis in Gunn rats by analgesics and analgesic mixtures. Br J Exp Pathol 56:92-97, 1975 and EA: Experimental renal papillary necrosis. Kidney Int 13:5-14, 1978 er I: Experimental analgesic nephropathy: A reassessment of the role of phenacetin and other analgesics.

Mar 01, 2011 · Ischemia is the most common cause of acute kidney injury AKI in hospitalized patients. The authors of this Review describe the morphological and functional responses of kidney. Mar 01, 2011 · Apoptosis and necrosis are major mechanisms of cell death that have. when cortical blood flow might have returned to n ear acute renal failure. Kidney Int. 66, 496–499 2004. Nov 20, 2007 · The kidney is sensitive to changes in oxygen delivery. This sensitivity has the merit of facilitating the kidneys in their adjustment of erythropoietin EPO production to changes in oxygen supply. The main determinant of EPO synthesis is the transcriptional activity of its gene in kidneys, which is related to local oxygen tensions. Regulation of EPO production is mediated by hypoxia-inducible. Experimental AKI also increased renal cortical mRNA levels for α-fetoprotein albumin's embryonic equivalent. A correlate in patients was increased urinary α-fetoprotein excretion. We conclude that AKI can unmask, in the kidney, the normally silent renal albumin and α-fetoprotein genes. Gentamicin accumulates in the renal cortex see next section and induces renal morphological changes and an overall syndrome very similar in humans and experimental animals Luft et al., 1977.

Dec 23, 2010 · Castration renders male rats less susceptible compared with sham‐operated rats, indicating that sex hormones may contribute to the pathogenesis of Adriamycin‐induced renal injury. 22 Because of the difference in severity of renal injury, choice of sex is a major factor in designing an experiment using AN as a model of renal injury. J B Hook's 260 research works with 4,816 citations and 793 reads, including: Hepatic and Renal Conjugation Phase II Enzyme Activities in Young Adult, Middle-Aged, and Senescent Male Sprague. Sep 05, 2007 · 8 Padanilam, B. J. 2003 Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis. Am. J. Physiol. Renal. Physiol. 284,F608-F627 Crossref Medline, Google Scholar.

Of Mice and MenExperimental Induction of Calcium Oxalate.

Johnson JP, Grillo FG 1994 Thyroid hormone induction of ornithine decarboxylase in ischemic acute renal failure. Ren Fail 164:433–442 Google Scholar Kashgarian M, Siegel NJ, Ries AI et al. 1976 Hemodynamic aspects in development and recovery phases of experimental post-ischemic acute renal. Chronic kidney disease CKD is common in geriatric cats, affecting up to 49% of cats older than 15 years, 23 but most cases have nonspecific renal lesions. In a postmortem study of 64 cats with CKD, 8 specific renal diseases, including neoplasia, chronic pyelonephritis, polycystic kidney disease, and amyloidosis, were identified in approximately half the cats. The present study was performed to assess the effects of the platelet-derived growth factor PDGF receptor kinase inhibitor imatinib mesylate on the renal morphological changes occurring during the development of malignant hypertension in transgenic rats with inducible expression of the Ren2 gene [TGRCyp1a1Ren2]. Arterial blood pressure was measured by radiotelemetry in male Cyp1a1-Ren2. Background: Cancer immunotherapy, such as anti-cytotoxic T-lymphocyte-associated protein 4 CTLA-4 and anti-programmed death 1 PD-1, has revolutionized the treatment of malignancies by engaging the patient's own immune system against the tumor rather than targeting the cancer directly. These therapies have demonstrated a significant benefit in t.

Oct 03, 2016 · Results. In the stenotic kidney, the median magnetization transfer ratio showed progressive increases from baseline to 6 weeks after surgery increases of 13.7% [P =.0006] and 21.3% [P =.0005] in cortex and medulla, respectively, which were accompanied by a progressive loss in renal volume, perfusion, blood flow, and oxygenation.The 6-week magnetization transfer ratio map showed. mandatory for renal CaOx deposits. Intraperitoneal administration: In Sprague-Dawley rats i.p. administration of high dose of HyP 2, 5 g/kg, is followed by a massive deposition of calcium oxalate in renal parenchyma within 24 h with presumably an acute renal failure: Increased kidney volume and weight kidney, inflammation and oedema[17]. Introduction. Acute kidney injury AKI is characterized by a rapid decrease in renal function over the course of hours to days and is associated with significant morbidity and mortality ∼40% Uchino et al., 2005.Despite recent efforts to better understand AKI, mortality associated with this clinical disorder has remained unchanged over the last five decades Thadhani et al., 1996; Waikar. Semiautomated image registration and segmentation of the 3D MR renography data sets were performed to produce iliac artery, renal cortical, and renal medullary signal intensity versus time curves 27 Fig 2 and measures of the whole kidney, cortical, and medullary renal volumes.

A portion of the renal cortex from each kidney was homogenized in liquid nitrogen and resuspended in 4 vol of ice-cold 50 mM Tris·HCl pH 7.4. The samples were sheared by passing them through a 19-gauge needle and agitated on ice for 30 min. Four volumes of 0.1% Triton X-100 were added to each sample and the samples were agitated on ice for. Contrast-induced nephropathy CIN remains a leading cause of iatrogenic acute kidney injury, as the usage of contrast media for imaging and intravascular intervention keeps expanding. Diabetes is an important predisposing factor for CIN, particularly in patients with renal functional impairment. Renal hypoxia, combined with the generation of reactive oxygen species, plays a central role in.

The contribution of oxidative stress to impaired renal hemodynamic and tubular function has been reviewed. 35,36 Renal oxidative stress is common in experimental models of hypertension, and studies continue to point to reactive oxygen species as an important mediator of AngII hypertension. Interleukin IL-18 is a member of the IL-1 family of cytokines and was described originally as an interferon γ-inducing factor. Aldosterone plays a central role in the regulation of sodium and potassium homoeostasis by binding to the mineralocorticoid receptor and contributes to kidney and cardiovascular damage. Aldosterone has been reported to induce IL-18, resulting in cardiac fibrosis.

Jul 13, 2018 · Kidney tissue samples were homogenized in a buffer containing 2 mM MgCl 2, 1 mM EGTA, 1 mM DTT, and 0.5% vol/vol Triton X-100. Homogenates were centrifuged at 13,000 rpm for 10 min 4 °C and protein in the collected supernatant quantified BCA protein assay Kit Heat shock protein 70 Hsp70 is a potent antiapoptotic agent. Here, we tested whether it directly regulates renal cell survival and organ function in a model of transient renal ischemia using Hsp70 knockout, heterozygous, and wild-type mice. The kidney cortical Hsp70 content inversely correlated with tubular injury, apoptosis, and organ dysfunction after injury. Kidney cortex from C57BL/6 and TNFR1-KO mice showed extensive histological damage, such as tubular dilation, cast formation and necrosis, and sloughing of renal epithelial cells arrowheads. Kidneys from TNFR2-KO mice had better preserved morphology. Magnification: ×10 A–C; ×40 D–F. 1,25-Dihydroxyvitamin D3 levels begin to drop early in the course of kidney disease, leading to elevated parathyroid hormone levels and disrupted mineral metabolism. Impaired mineral metabolism seems to be associated not only with bone disease but also with vascular calcification. Animal models have identified molecular mechanisms by which high mineral levels and other uremic substances induce. In contrast, COX2 is expressed predominantly in the renal medullary interstitial cells and in cortical thick ascending limb and cells associated with the macula densa 15, 28, 32. The expression of COX2 in these cells can be induced after a variety of physiological stresses see following sections.

All experimental procedures were approved by the Institutional Ethical Research Board of the University of Sao Paulo, Brazil. CKD in mice model and study design. For the induction of CKD in mice, C57/BL-6 animals were fed with a 0.2% adenine-containing diet Sigma,. In contrast to the renal cortex, renal medullary ET-1 reduces blood pressure by directly inhibiting sodium reabsorption on the collecting duct and increasing medullary blood flow through activation of the ET B receptor. Inner medullary collecting ducts produce the most ET-1 within the kidney ≈10 times more than any other nephron segment.

A portion of the renal cortex from each kidney was homogenized in liquid nitrogen and resuspended in 4 vol of ice-cold 50 mM Tris-HCl pH 7.4. The samples were sheared by passing them through a 19-gauge needle and agitated on ice for 30 min. Four volumes of 0.1% Triton X-100 were added to each sample, and the samples were agitated on ice for. Kidney; cat, ischemia/reperfusion injury, cortical biopsies, kidney injury molecule-1 KIM-1 immunohistochemistry. a Biopsy obtained immediately after clamping of renal artery. There is cell swelling and loss of whole cells into the lumen of S1 and S2 proximal tubules arrows in the cortex, and light granular KIM-1 staining of individual.

Forefronts in Nephrology 487 Fig. 1. Stains of human cadaveric kidney with ischemic acute tubular necrosis ATN 1 week post-transplant. A Hematoxylin and eosinstain. The patient exhibited delayed graft function in the absence of. In histopathological examination, our mouse model of ZP-induced kidney injury displayed vacuoles, denatured cytoplasm, and aggregated eosinophilic materials, probably reflecting cellular necrosis. In ZP-induced kidney injury in the clinic, renal cortical necrosis was observed Darwish et al., 1984. Thus, the results observed in the present. Discoveries have emerged highlighting the complex nature of the interorgan cross-talk between the kidney and the lung. Vascular rigidity, neurohormonal activation, tissue hypoxia, and abnormal immune cell signaling have been identified as common pathways leading to the development and progression of chronic kidney disease. Mar 16, 2010 · Aldosterone is a steroid hormone that is mainly recognized for its action on sodium reabsorption in the distal nephron of the kidney. In addition,.

The kidney is a major clearance organ of the body and is responsible for the elimination of many xenobiotics and prescription drugs. With its multitude of uptake and efflux transporters and metabolizing enzymes, the proximal tubule cell PTC in the nephron plays a key role in the disposition of xenobiotics and is also a primary site for toxicity. In this minireview, we first provide an. Oct 04, 2013 · Kidney injuries provoke considerable adjustment of renal physiology, metabolism, and architecture to nephron loss. Despite remarkable regenerative capacity of the renal tissue, these adaptations often lead to tubular atrophy, interstial and glomerular scaring, and development of chronic kidney disease. The therapeutic strategies for prevention of the transition from acute kidney damage.

Chronic kidney disease CKD is characterized by changes in mineral metabolism associated with alterations of its hormonal regulation and various forms of bone disease. In the past, these associations focused attention on the kidney–bone axis. The last decade has seen renewed interest on interactions among mineral metabolism disorders and extraosseous and cardiovascular calcifications. Oct 20, 2016 · MCP-1 is predominantly expressed in renal monocytes, endothelial cells, and mesangial cells and is highly regulated by tumor necrosis factor-alpha TNF-α and interleukin IL-1 174, 191. In addition, MCP-1 was found to be upregulated in the glomerulus and tubulointerstitium in experimental. Post-Translational Loss of Renal TRPV5 Calcium Channel Expression, Ca2D Wasting, and Bone Loss in Experimental Colitis VIJAYABABU M. RADHAKRISHNAN, 1RAJALAKSHMY RAMALINGAM, CLAIRE B. LARMONIER, ROBERT D. THURSTON,1 DANIEL LAUBITZ,1 MONICA T. MIDURA–KIELA,1 RITA–MARIE T. MCFADDEN,1,3 MAKOTO KURO–O,4 PAWEL R. KIELA,1,2,§ and FAYEZ K.. 20 September 2007 American Journal of Nephrology, Vol. 28, No. 1 Renal mitochondrial impairment is attenuated by AT 1 blockade in experimental Type I diabetes American Journal of Physiology-Heart and Circulatory Physiology, Vol. 294, No. 1.

Nov 05, 2015 · Cholesterol is essential for diverse cellular functions and cellular and whole-body cholesterol homeostasis is highly controlled. Cholesterol can also influence cellular susceptibility to injury. The connection between cholesterol metabolism and inflammation is exemplified by the Tm7sf2 gene, the absence of which reveals an essential role in cholesterol biosynthesis under stress conditions but.

  1. Get this from a library! Renal cortical necrosis: experimental induction by hormones. [Ferenc A László].
  2. Vol. 198, 2019 available Active subscription CKD-Associated Complications: Progress in the Last Half Century Editors: Nakanishi, Takeshi Nishinomiya/Kobe.
Renal Cortical Necrosis: Experimental Induction by Hormones (Contributions to Nephrology, Vol. 28)

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