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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 juxtaglomerular apparatus (Figure 40.2) is formed where the ascending thick limb of the loop of Henle passes between the afferent and the efferent arterioles, close to the glomerulus. The three components of the juxtaglomerular apparatus are granular cells, the macula densa and mesangial cells. Granular cells produce and store renin and are found in the walls of the afferent arteriole. The macula densa is a morphologically distinct region of the thick ascending limb of the loop of Henle, which passes through the angle formed by the afferent and efferent arterioles of the same nephron. The cells of the macula densa contact the extraglomerular mesangial cells and the granular cells of the afferent arteriole and are involved in the control of renin production and renal blood flow.
The renal system, hypertension and pre-eclampsia
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
When glomeruli are damaged, plasma proteins pass through into the filtrate (they are normally too big to do so). Albumin is the most common plasma protein and it is a relatively small molecule. When there is significant loss in the urine, plasma oncotic pressure changes result in a shift of fluid out of the vascular space, resulting in oedema and a reduction in plasma volume. The juxtaglomerular apparatus detects the fall in blood flow to the kidneys, which stimulates the renin-angiotensin-aldosterone system to conserve water and sodium, setting up a vicious cycle of fluid retention and worsening oedema (Huether, 2006). Nephrotic syndrome occurs with glomerulonephritis, diabetic nephropathy or lupus nephritis, with the most common cause in pregnancy being preeclampsia. A low dietary intake of protein with anorexia or malnutrition may contribute to low levels of plasma albumin (Davison and Baylis, 2002).
Renal
Published in Sarah Armstrong, Barry Clifton, Lionel Davis, Primary FRCA in a Box, 2019
Sarah Armstrong, Barry Clifton, Lionel Davis
Hormonal system that helps regulate long-term blood pressure control and blood volumeReduced perfusion (e.g. hypovolaemia) of the renal juxtaglomerular apparatus causes the cells to release the enzymatic hormone renin. Secretion also increases in cardiac failure, cirrhosis and renal artery stenosisRenin cleaves angiotensinogen (inactive peptide) to angiotensin I in the kidneysAngiotensin I is cleaved to angiotensin II in the lung capillaries by angiotensin-converting enzyme (ACE)
Type 2 diabetes mellitus and cardiovascular risk; what the pharmacotherapy can change through the epigenetics
Published in Postgraduate Medicine, 2020
Pavlina A. Andreeva–Gateva, Ivelina D. Mihaleva, Ivanka I. Dimova
The renin-angiotensin system (RAS) is a cascade of successive activation of proteases starting from the renin with one of the important final effects on the aldosterone secretion, i.e. renin-angiotensin-aldosterone system (RAAS). Renin is produced from the juxtaglomerular apparatus as an inactive prorenin and sympathetic system by beta1-receptors, prostaglandins, and kinins can stimulate renin secretion. According to the classical, endocrine view of the systemic RAS, renin catalyzes the cleavage of angiotensin I, from the circulating angiotensinogen, a protein produced by the liver. Angiotensin I is subsequently hydrolyzed by angiotensin I-converting enzyme (ACE), located on endothelial cells, yielding the angiotensin II, the active end product of the RAS cascade [98]. Epigenetic mechanisms are involved in the regulation of the renin secretion by histone H4 acetylation [99]. Epigenetic regulation of the ACE expression via hypermethylation of the promoter region by the inflammatory cytokine TNFα in the endothelial cells was recently reported [100].
Development of transplant immunosuppressive agents – considerations in the use of animal models
Published in Expert Opinion on Drug Discovery, 2018
Russell Costello, Adrien Kissenpfennig, Paulo N Martins, James McDaid
Animal models have been used to determine the toxicity of immunosuppressive agents. The most important side effect of the calcineurin inhibitor cyclosporine is deterioration in kidney function (nephrotoxicity), accompanied by electrolyte disturbances (often high potassium, hyperkalemia). The histological changes and damage associated with cyclosporine administration in rats have been studied [100]. The changes seen in human vasculature, such as necrosis leading to ischemia, because of cyclosporine toxicity, are not seen in rats. Clinical use of cyclosporine is associated with hypertension [73]. The exact mechanism is not clear, the renin angiotensin system (RAS) is activated by constriction of renal afferent arterioles leading to peripheral hypertension. Cyclosporine also sensitizes endothelial and smooth muscle cells to vasopressin and angiotensin II leading to systemic hypertension. The effect of RAS differs between species, whilst the juxtaglomerular apparatus experiences hypertrophy in both species leading to an increase in renin secretion. The activation of the RAS appears to be more transient in humans, whilst rats do not appear to experience peripheral hypertension.
A comparative safety review between GLP-1 receptor agonists and SGLT2 inhibitors for diabetes treatment
Published in Expert Opinion on Drug Safety, 2018
Agostino Consoli, Gloria Formoso, Maria Pompea Antonia Baldassarre, Fabrizio Febo
SGLT2i reduce BP, mostly via a direct osmotic diuretic effect but probably also by a reduction in arterial stiffness. Local inhibition of the renin-angiotensin-aldosterone system secondary to increased delivery of sodium to the juxtaglomerular apparatus might also play a role [31,32]. BP reduction was observed in both efficacy and safety trials and was confirmed in meta-analyses of clinical trials conducted with different molecules of the class. Baker et al. [33] pooled together data from 27 randomized clinical trials (n = 12,960 subjects). SGLT-2i use resulted associated with a significant reduction from baseline in both systolic BP (weighted mean difference, −4.0 mm Hg; 95% confidence interval (CI) −4.4 to −3.5) and diastolic BP (weighted mean difference, −1.6 mm Hg; 95% CI, −1.9 to −1.3). Although postural hypotension has been reported in susceptible subjects, no significant increase in the incidence of orthostatic hypotension was observed in this pooled analysis [33].