China
Africa
Explore chapters and articles related to this topic
Pathophysiologic Mechanisms of Acute Renal Failure
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
At the nephron level, several mechanisms have been proposed as being responsible for renal dysfunction in acute renal failure (Table 1). There are basically two categories of explanations for impaired renal function after ischemic or toxic insult. The vascular theories suggest that intense renal vasoconstriction leading to a reduction in renal blood flow is responsible for the decrease in glomerular filtration rate (GFR). An additional vascular factor involving the specialized capillaries of the glomeruli suggests that a decrease in glomerular permeability (K1) contributes to impaired filtration in acute renal failure. The tubular injury theories suggest that cellular necrosis results in a denuded tubular basement membrane allowing backleak of glomerular filtrate. Furthermore, necrotic cells and cellular debris displaced into the urinary space form casts leading to obstruction of the nephrons (Figure 1). Either or both of these phenomena then contribute to diminished glomerular filtration. An additional theory implicates activation of tubuloglomerular feedback mechanisms as responsible for diminished GFR. All of these potential mechanisms will be elaborated upon below.
The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
The physiological role of the tubulo-glomerular feedback system may be to set glomerular filtration rate at levels appropriate to the tubular reabsorptive capacity of the nephron and to the needs of the whole organism for increases or decreases in salt excretion. The sensitivity of the tubuloglomerular feedback system is appropriately modified by the sodium status of the animal.430,431 In sodium deprived animals, tubuloglomerular feedback was active and was progressively diminished by higher sodium intakes. These observations support a role for the system in overall sodium homeostatis.
The renal system
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Tubuloglomerular feedback involves the activity of the juxtaglomerular apparatus (see Figure 10.1). This structure is located where the distal tubule comes into contact with the afferent and efferent arterioles, adjacent to the glomerulus. The juxtaglomerular apparatus is composed of the following: Macula densaGranular cells
Increased mean perfusion pressure variability is associated with subsequent deterioration of renal function in critically ill patients with central venous pressure monitoring: a retrospective observational study
Published in Renal Failure, 2022
Yudie Peng, Buyun Wu, Changying Xing, Huijuan Mao
The microvascular system of the kidney is most vulnerable to the adverse effects of larger BPV which is associated with higher albuminuria [10]. In healthy people, the kidney can maintain its perfusion through tubuloglomerular feedback when mean arterial pressure (MAP) fluctuates in the range of 80 ∼ 180mmHg [11]. However, the physiological regulation function is impaired in critically ill patients. Affected by factors like sepsis, nephrotoxin, and insufficient blood perfusion [12–14], abnormal BPV may be a hit to the kidney and finally deteriorate renal function. Previous studies have rarely focused on the population of critically ill patients. One study conducted by Xie and his colleagues has shown that in critically ill patients, higher systolic BPV was related to the incidence of acute kidney injury (AKI) [15], which is a clinical syndrome characterized by a significant acute reduction in glomerular filtration rate and occurs in more than 50% of patients admitted to intensive care units [16]. However, the sample size of this study was relatively small and had no external verification. In addition, they also did not distinguish between the time of BPV monitoring and the time of AKI occurrence. Moreover, traditional index like systolic blood pressure (SBP) and diastolic blood pressure (DBP) has some physiological deficiencies, especially the failure to consider venous outflow pressure. Obtained by the difference between MAP and central venous pressure (CVP), mean perfusion pressure (MPP) was recently proposed to personalized management tissue perfusion pressure instead of MAP [17,18].
Proteinuria in early referral to spectral domain optical coherence tomography for macular edema detection in type 2 diabetes individuals: results from the Brazilian diabetes study
Published in Current Medical Research and Opinion, 2022
Joaquim Barreto, Fernando Chaves, Vicente H. R. Fernandes, Daniel Campos de Jesus, Mauricio Abujamra Nascimento, Rodrigo P. C. Lira, Wilson Nadruz, Carlos Arieta, Andrei C. Sposito
The influence of proteinuria on DME was not affected by the baseline GFR. In a matter of fact, our study showed using a mediation analysis that proteinuria directly affected the risk of maculopathy, which was only marginally influenced by GFR. This observation is in accordance with prior studies. For example, Hsieh et al.12 showed in a national, prospective cohort that micro- and macroalbuminuria were related to 1.6- and 2.7-fold increased incidence of DME, respectively, while low GFR was not significantly related to the risk of DME even among individuals with GFR < 30 mL/min/1.73m.2 At least partially, this event is attributed to the influence of T2D on the tubuloglomerular feedback, which promotes glomerular hyperfiltration leading to increased GFR levels despite disease progression compromising the relationship between this marker and T2D-related complications36,37. Furthermore, the cornerstone of both DME and proteinuria is endothelial dysfunction and plasma leakage, whereas GFR estimation is susceptible not only to changes in transglomerular pressure gradient, but it also has an expected decline with age which may influence the way it relates to retinal disorders35,38–40.
Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging
Published in Temperature, 2021
Christopher L. Chapman, Blair D. Johnson, Mark D. Parker, David Hostler, Riana R. Pryor, Zachary Schlader
There is great interest in accurately quantifying changes in renal blood flow because it is a highly controlled variable that has implications for the regulation of blood pressure and water and electrolytes. Thus, it is also important to note that the kidneys have an intrinsic ability to maintain blood flow at varying arterial pressures (i.e., autoregulate). Renal blood flow autoregulation is mediated by actions of the afferent arterioles and interlobular arteries and their myogenic response to constrict or relax in response to changes in perfusion pressure [173-175]. Approximately, 50% of the total autoregulatory response [176,177] rapidly occurs within 3-10 seconds [178,179], which is contributed to by unloading of the renal baroreceptors and tubuloglomerular feedback provided by the juxtaglomerular apparatus [180,181]. Tubuloglomerular feedback also results in renin release by the afferent arterioles in response to sensation of decreased NaCl delivery to the macula densa in the distal tubule [182], which ultimately ensures a relatively stable renal blood flow and glomerular filtration rate (see Glomerular filtration rate). These neural (discussed previously in Autonomic control of kidney function), hormonal (discussed previously in PHYSIOLOGY AND ASSESSMENT OF BODY WATER REGULATION), and autoregulatory mechanisms offer a complex and highly redundant control of renal blood flow to maintain homeostasis utilizing many systems.