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Major obstetric haemorrhage
Published in Jennifer Duguid, Lawrence Tim Goodnough, Michael J. Desmond, Transfusion Medicine in Practice, 2020
The hypothalamo-pituitary adrenal response is also important, although it is slower. Reduced renal blood flow stimulates intrarenal baroreceptors, which mediate renin release from the juxta-glomerular apparatus. This in turn leads to the conversion of circulating angiotensinogen to angiotensin I and then angiotensin II (in the lung). Angiotensin II is a powerful arteriolar vasoconstrictor that also stimulates aldosterone release from the adrenal cortex, and arginine vasopressin (AVP – also known as antidiuretic hormone, ADH) release from the posterior pituitary. AVP release is also stimulated by atrial receptors, which respond to the decrease in extracellular volume. These changes enhance sodium-ion and water reabsorption at the distal renal tubule as the body attempts to conserve fluid.
Hepatorenal tyrosinemia/fumarylacetoacetate hydrolase deficiency
Published in William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop, Atlas of Inherited Metabolic Diseases, 2020
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop
Renal disease is another characteristic feature of this disease. Among 32 patients [40], 47 percent had enlargement of the kidneys, often palpable [31]; 47 percent had increased echogenicity of the kidneys and 16 percent had nephrocalcinosis. In another eight patients [41], 50 percent had nephromegaly. The renal tubular disease is that of a typical renal Fanconi syndrome in which there is phosphaturia, aminoaciduria, and often glycosuria. There may be proteinuria. Systemic metabolic acidosis may result from renal tubular dysfunction. The phosphate losses lead to hypophosphatemia and clinical rickets (Figures 22.5–22.7). There may also be a variable reduction in glomerular function. In the series of 32 patients [40], 48 percent had decreased glomerular filtration; 82 percent had aminoaciduria, 67 percent hypercalcinuria, and 59 percent renal tubular acidosis. Affected infants have been observed to have vitamin D-resistant rickets at less than four months [25], which is unusual.
The kidneys
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Two main groups of diseases affect the renal tubules: Ischaemic or toxic injury leading to acute tubular necrosis.Inflammatory reactions involving the tubules and interstitium, known as tubulointerstitial nephritis.
Targeted drug delivery strategy: a bridge to the therapy of diabetic kidney disease
Published in Drug Delivery, 2023
Xian Chen, Wenni Dai, Hao Li, Zhe Yan, Zhiwen Liu, Liyu He
Glomerular basement membrane (GBM) thickening is considered as the earliest observed pathological feature in patients with DKD, which is appeared within 1–2 years after the onset of DM (Tervaert et al., 2010; Ponchiardi et al., 2013). Endothelial cells play an important role in the progression of DKD. With the development of DKD, the fenestrated ECs are decreased in diabetic patients, which correlates with albuminuria and the loss of GFR (Dou and Jourde-Chiche, 2019). Mesangial expansion, caused by Mesangial cells (MCs) enlargement and accumulation of glomerular matrix protein, is the most common renal pathological change in DKD (Reidy et al., 2014; Zhang et al., 2019). On the glomerular capillary side of MCs, without the surrounding of GBM and podocytes, drugs can be delivered to MCs for treating kidney diseases (Scindia et al., 2008). Podocytes are glomerular epithelial cells which contain 3 separate elements: cell body, extending processes and foot processes (Garg, 2018). Podocytes injury in DKD is induced by many compound factors, such as inflammatory reaction, mechanical stress, oxidative stress, renin angiotensin aldosterone system activation, TGF-β1 induction, and AGEs accumulation, and any part of the pathway is expected to be the target of DKD therapy (Kawanami et al., 2016). The renal tubules consist of the proximal tubules, collecting tubules and distal tubules. The morphological and functional changes of the renal tubules are involved in the pathogenesis and progression of DKD (Duan et al., 2021). Most renal tubular targeted systems are directed at the proximal tubules (Christensen et al., 2012).
Balancing renal Ang-II/Ang-(1–7) by xanthenone; an ACE2 activator; contributes to the attenuation of Ang-II/p38 MAPK/NF-κB p65 and Bax/caspase-3 pathways in amphotericin B-induced nephrotoxicity in rats
Published in Toxicology Mechanisms and Methods, 2023
Amany A. Azouz, Doaa M. Abdel-Rahman, Basim Anwar Shehata Messiha
As well, our results showed that amphotericin B produced serum electrolyte imbalance, where serum levels of Na+, K+, and Mg2+ were significantly reduced. The binding of amphotericin B to membrane cholesterol results in the formation of pores in renal tubular cell membrane with subsequent leakage of electrolytes and tubular dysfunction (Wu and Huang 2018). Besides, the amphipathic character of amphotericin B and the presence of lipophilic part in its structure contribute to the induced damage in renal cell membrane (Katopodis et al. 2020; Berto and Dalzochio 2021). Increased levels of unabsorbed electrolytes in renal tubules produces further deterioration in kidney function due to vasoconstriction and reduced glomerular filtration by TGF and Ang-II stimulation (Loo et al. 2013; Karimzadeh et al. 2015b). In addition, Yano et al. (2009) have demonstrated that increased intracellular Na+ concentration due to membrane pores formed by amphotericin B leads to injury of renal cells by activation of MAPKs and increased intracellular Ca2+ concentration.
Safety of current antiviral drugs for chronic hepatitis B
Published in Expert Opinion on Drug Safety, 2022
Chiara Masetti, Nicola Pugliese, Alessio Aghemo, Mauro Viganò
All oral antiviral agents are excreted in active form by the kidney through active uptake by proximal tubular cells and the subsequent elimination in the urinary space. Proximal renal tubule seems most commonly involved in nephrotoxicity induced by oral antiviral agents, as these cells are particularly rich in mitochondria and therefore more susceptible to damage. Renal tubular dysfunction may be difficult to detect, as early indicators, such as fractional excretion of phosphate and retinol-binding protein (RBP), are not commonly used in clinical practice, while commonly used indicators for renal function (glomerular filtration rate, eGFR, and creatinine clearance) may underestimate renal tubular injury [29]. Reductions in renal tubular function may lead to a Fanconi-like syndrome, characterized mainly by metabolic acidosis, hypophosphatemia, hyperphosphaturia, and glycosuria, which can become life-threatening. Conversely, acute tubular necrosis is more frequently observed in patients with preexistent kidney disease [12].