China
Africa
Explore chapters and articles related to this topic
Cardiovascular Risk Factors
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Dietary fructose intake in conjunction with high salt intake can contribute to hypertension. Fructose can impair insulin signaling in insulin-responsive tissues and can contribute to insulin resistance (Baena et al., 2016). In the setting of insulin resistance, more circulating insulin is present which can lead to increased sympathetic response that further elevates blood pressure (Figure 5.2). Fructose can also influence intestinal sodium absorption leading to increase expression of sodium and hydrogen transport proteins, and rat models demonstrate that fructose can increase reabsorption within the kidney proximal tubule, the site of sodium reabsorption. In fact, rat models have shown that at a fructose consumption of 40% of daily caloric intake led to an increased tail cuff blood pressure reading. A renal proximal tubule mechanism was suggested by increased proximal tubule expression of sodium transporters compared to control rats in the study (Gonzalez-Vicente, et al. 2018).
Urolithiasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Phosphate is a urinary buffer.Filtered by the glomerulus and reabsorbed in the proximal tubule.
Systemic complications following vascular reconstruction
Published in Sachinder Singh Hans, Mark F. Conrad, Vascular and Endovascular Complications, 2021
Srihari K. Lella, Mark F. Conrad
With acute renal ischemia, large accumulations of cytosolic and mitochondrial calcium develop that result in renal vasoconstriction, especially in the afferent arterioles of the glomerulus. Secondarily, the outer medulla of the kidney develops significant congestion with worsening of the hypoxia and a proposed resultant worsening of endothelial damage from increased oxidant injury. Following reperfusion, the proximal tubules lose their polarity and brush border. Reactive oxygen species develop with resulting cell death, and these dead cells are then shed into the tubular lumen. This creates the formation of casts that causes tubular obstruction and reduces the glomerular filtration rate (GFR).72
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).
The effects of apelin-13 against cisplatin-induced nephrotoxicity in rats
Published in Drug and Chemical Toxicology, 2023
Atilla Topcu, Sinan Saral, Tolga Mercantepe, Kerimali Akyildiz, Levent Tumkaya, Adnan Yilmaz
Examination of the control group kidney tissue sections under light microscopy revealed a normal structure in the epithelial cells of the renal corpuscles and tubules (Table 2; Figures 1(A,B), 2(A,B); median RHDS: 0 (0–1)). Similarly, typical glomerular (g) and tubular epithelial cells were observed in the kidney tissue sections from the AP-13 only group (Table 2; Figures 1(C,D), 2(C,D); median RHDS: 1 (0–1)). In contrast, necrotic tubules associated with diffuse vacuolization in the cytoplasm of tubular epithelial cells were detected in the kidney tissue sections from the CP group. Loss of brush border in the proximal tubule was particularly conspicuous. Widespread leukocyte infiltrations and fibrosis formations were also observed in interstitial areas (Table 2; Figures 1(E,F), 2(E,F); median RHDS: 9 (8–9.5)). Light microscopy examination of the CP + Apelin-13 group kidney sections displayed normal tubular epithelial cells, along with a small number of necrotic tubular epithelial cells. The brush border structure of the proximal tubule cells was clearly visible. Nonetheless, the inflammation in the interstitial area was reduced (Table 2; Figures 1(G,H), 2(G,H); median RHDS: 2 (0.5–2)).
The anti-hypertensive effects of sodium-glucose cotransporter-2 inhibitors
Published in Expert Review of Cardiovascular Therapy, 2023
Luxcia Kugathasan, Lisa Dubrofsky, Andrew Advani, David Z.I. Cherney
Under normal physiological conditions, blocking sodium transport in the proximal tubule increases distal tubular load and promotes a compensatory enhancement of sodium, chloride, and potassium reabsorption at the loop of Henle primarily by Na-K-2Cl (NKCC2) cotransporters. However, owing to the natriuretic-diuretic coupling effect of SGLT2 inhibition at the proximal tubule, it has been postulated that a diluted load with a low chloride concentration is delivered to the distal nephron and renders tubular reabsorption at the loop of Henle ineffective (Figure 3) [96]. Specifically, since the proximal tubule is highly permeable to water and SGLT2 inhibition renders glucose non-resorbable, isotonicity between the tubular fluid and blood is maintained by osmoregulation. The resulting diuresis is thought to decrease the chloride ion concentration in the proximal tubular filtrate [92]. Therefore, it is speculated that the requirement of two chloride ions for each cotransport at the thick ascending limb subsequently reduces NKCC2 cotransporter activity in a diluted chloride environment [92,96]. The off-target impact of SGLT2 inhibitors at the thick ascending limb may indicate similar activity to that of a loop diuretic to promote plasma volume contraction, although this effect has yet to be proven [96].