Role of the renal sympathetic nervous system in mediating renal ischaemic injury-induced reductions in renal haemodynamic and excretory functions

Salman, Ibrahim M.; Ameer, Omar Z.; Sattar, M. A.; Abdullah, Nor Azizan; Yam, Mun Fei; Najim, Hafsa S.; Khan, Abdul Hye; Johns, Edward J.

doi:10.3109/00313021003631304

Cited by 24 publications

(26 citation statements)

References 29 publications

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“…Since AKI may increase volume retention, these episodes could exacerbate heart failure and myocardial ischemia [18]. AKI may also activate the sympathetic nervous system via ischemia in the kidney as a potential mechanism to increase risks of cardiovascular events and death [5,11,19].…”

Section: Discussionmentioning

confidence: 99%

Association of Acute Kidney Injury with Cardiovascular Events and Death in Systolic Blood Pressure Intervention Trial

et al. 2019

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Rationale and Objective: In the Systolic Blood Pressure Intervention Trial, the possible relationships between acute kidney injury (AKI) and risk of major cardiovascular events and death are not known. Study Design: Post hoc analysis of a multicenter, randomized, controlled, open-label clinical trial. Setting and Participants: Hypertensive adults without diabetes who were ≥50 years of age with prior cardiovascular disease, chronic kidney disease (CKD), 10-year Framingham risk score > 15%, or age > 75 years were assigned to a systolic blood pressure target of < 120 mm Hg (intensive) or < 140 mm Hg (standard). Predictor: AKI episodes. Outcomes: The primary outcome was a composite of myocardial infarction, acute coronary syndrome, stroke, decompensated heart failure, or cardiovascular death. The secondary outcome was death from any cause. Analytical Approach: AKI was defined using the Kidney Disease: Improving Global Outcomes modified criteria based solely upon serum creatinine. AKI episodes were identified by serious adverse events or emergency room visits. Cox proportional hazards models assessed the risk for the primary and secondary outcomes by AKI status. Results: Participants were 68 ± 9 years of age, 36% women (3,332/9,361), and 30% Black race (2,802/9,361), and 17% (1,562/9,361) with cardiovascular disease. Systolic blood pressure was 140 ± 16 mm Hg at study entry. AKI occurred in 4.4% (204/4,678) and 2.6% (120/4,683) in the intensive and standard treatment groups respectively (p < 0.001). Those who experienced AKI had higher risk of cardiovascular events (hazard ratio [HR] 1.52, 95% CI 1.05–2.20, p = 0.026) and death from any cause (HR 2.33, 95% CI 1.56–3.48, p < 0.001) controlling for age, sex, race, baseline systolic blood pressure, body mass index, number of antihypertensive medications, cardiovascular disease and CKD status, hypotensive episodes, and treatment assignment. Limitations: The study was not prospectively designed to determine relationships between AKI, cardiovascular events, and death. Conclusions: Among older adults with hypertension at high cardiovascular risk, intensive treatment of blood pressure independently increased risk of AKI, which substantially raised risks of major cardiovascular events and death.

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Section: Discussionmentioning

confidence: 99%

Association of Acute Kidney Injury with Cardiovascular Events and Death in Systolic Blood Pressure Intervention Trial

et al. 2019

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“…25,48,52 These haemodynamic changes can be prevented by local renal denervation at the beginning of the reperfusion phase. 25,48,52 These haemodynamic changes can be prevented by local renal denervation at the beginning of the reperfusion phase.…”

Section: Mitigates Experimental Ir-induced Renal Injurymentioning

confidence: 99%

“…25,48,52 These haemodynamic changes can be prevented by local renal denervation at the beginning of the reperfusion phase. 23,30,31,48 Diuresis and fractional sodium excretion (FE Na ) are elevated in the acute reperfusion phase, 23,52 likely reflecting early tubular damage and compromised concentrating ability of the kidneys. 23,30,31,48 Diuresis and fractional sodium excretion (FE Na ) are elevated in the acute reperfusion phase, 23,52 likely reflecting early tubular damage and compromised concentrating ability of the kidneys.…”

Section: Mitigates Experimental Ir-induced Renal Injurymentioning

confidence: 99%

“…23,30,31,48 Diuresis and fractional sodium excretion (FE Na ) are elevated in the acute reperfusion phase, 23,52 likely reflecting early tubular damage and compromised concentrating ability of the kidneys. 48 These differences may be related to the sequence of experimental procedures. 23 Renal denervation performed immediately after IR in animals with both kidneys and unilateral IR resulted in FE Na that was higher than in non-denervated kidneys exposed to IR.…”

Section: Mitigates Experimental Ir-induced Renal Injurymentioning

confidence: 99%

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The sympathetic nervous system in acute kidney injury

Grisk

2019

Acta Physiologica

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Acute kidney injury (AKI) is frequently accompanied by activation of the sympathetic nervous system (SNS). This may result from pre-exisiting chronic diseases associated with sympathetic activation prior to AKI or it may be induced by stressors that ultimately lead to AKI such as endotoxins and arterial hypotension in circulatory shock. Conversely, sympathetic activation may also result from acute renal injury. Focusing on studies in experimental renal ischaemia and reperfusion (IR), this review summarizes the current knowledge on how the SNS is activated in IR-induced AKI and on the consequences of sympathetic activation for the development of acute renal damage. Experimental studies show beneficial effects of sympathoinhibitory interventions on renal structure and function in response to IR. However, few clinical trials obtained in scenarios that correspond to experimental IR, namely major elective surgery, showed that peri-operative treatment with centrally acting sympatholytics reduced the incidence of AKI. Apparently, discrepant findings on how sympathetic activation influences renal responses to acute IR-induced injury are discussed and future areas of research in this field are identified.

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“…While some have postulated an opiate receptor, which is known to aid in proximal reabsorption in rats, 55 it is unclear whether such a receptor exists in humans. Usually, in water deprivation states, sodium is avidly reabsorbed from the glomerular filtrate as a result of suppression of natriuretic peptide, 56 activation of renal nervous system 57 and renin-angiotensin-aldosterone system axis, and local changes in peritubular hemodynamics 58 ( Figure 1). …”

Section: Renal Physiology In Water Deprived States Sodium Chloridementioning

confidence: 99%

Toward the optimal clinical use of the fraction excretion of solutes in oliguric azotemia

et al. 2010

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While the fractional excretion of solutes have long been considered excellent research tools to investigate tubular physiology, their clinical use has become common over the last 40 years in the diagnoses of many disorders; however, none have reached the clinical utility of the fractional excretion of sodium in the ability to distinguish pre-renal azotemia from acute tubular necrosis. Nevertheless, there are many drugs and medical conditions that interfere with that utility and recently other solutes, including urea, uric acid and lithium, have been recently investigated to improve the diagnostic ability in clinical situations where the fractional excretion of sodium is known to be unreliable. We review the tubular physiology of these solutes and show how the differences in tubular physiology might be exploited to develop a strategy for their optimal clinical use.

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Role of the renal sympathetic nervous system in mediating renal ischaemic injury-induced reductions in renal haemodynamic and excretory functions

Cited by 24 publications

References 29 publications

Association of Acute Kidney Injury with Cardiovascular Events and Death in Systolic Blood Pressure Intervention Trial

Association of Acute Kidney Injury with Cardiovascular Events and Death in Systolic Blood Pressure Intervention Trial

The sympathetic nervous system in acute kidney injury

Toward the optimal clinical use of the fraction excretion of solutes in oliguric azotemia

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