Renal autoregulation

Cisplatin induces DNA damage and subsequently DNA damage response proteins such as ataxia telangiectasia-mutated ATM proteins are activated leading to p53 phosphorylation. The threshold is dependent to some extent on the rate of filling and is higher when filling is slow; and training affects the amount the bladder can retain.

For all patients, these should include the following: Concentration in circuit at different fresh gas flow rates The above graph shows anaesthetic concentrations in a typical paediatric circle system as a fraction of the out-of-circuit vaporiser concentration, using different fresh gas flow rates 0.

Cisplatin significantly decreased cytochrome P content and increased bleomycin-detectable iron in the kidney. In another study by Kim et al.


Such variation is normal, and a fixed low specific gravity is an indication of chronic renal disease. Direct caspase-3 or apoptosis inhibition has not been reported to protect against cisplatin-induced AKI supporting the lack of a direct role of caspasemediated apoptosis in causing the functional derangements in AKI.

ADH regulates water excretion by increasing the permeability of the collecting ducts to water and salt and by accelerating water and ion transfer in a direction determined by the osmotic gradient.

The pathophysiology of cisplatin-induced AKI involves proximal tubular injury, oxidative stress, inflammation, and vascular injury in the kidney. This induction was shown to be dependent on p53 because PUMA was also inhibited by both pharmacological pifithrin and genetic ablation of p They are useful in detecting tumours of the kidney or adjacent structures and in distinguishing tumours from cysts.

Caspase-1 and Apoptosis In the study by Faubel et al. The usual bolus dose of 5 mg to 10 mg may be repeated every 20 to 30 minutes as needed.

The X-rays Renal autoregulation indicate the position, size, and presence of scarring or tumours in the organs and provide an approximate comparison of function in the two kidneys. Autophagy was found to promote cellular survival and delay the onset of apoptosis in RTECs exposed to cisplatin [ 52 ].

Until recently, the FasL- associated apoptotic stimulus was thought to be mediated only through the T lymphocytes [ 81 ]. In the study by Yuan et al. Angiotensin IV has a wide range of activities in the central nervous system. Thus voluntary initiation and control of micturition is effected partly by an active process of stimulating parasympathetic sacral nerve outflow, partly by removing the normal inhibition exerted by the higher centres on the reflex centres in the spinal cord.

If by contrast, the GFR were too low, the kidneys could not eliminate enough wastes, excess electrolytes, and other materials that should be excreted. Surgery decision should not be based solely on MIBG scan alone. This will not only slow induction and recovery, but will also tend to increase consumption of the inhalation anaesthetic.

In vivo, U prevented the loss of cilia from proximal tubules during cisplatin treatment and protected against AKI. The clearance of inulin and some other compounds is not altered by raising its plasma concentration, because the amount of urine completely cleared of the agent remains the same.

The desire to micturate begins at around a content of millilitres, but it can be voluntarily overridden until the content reaches — millilitres, with a resulting pressure within the bladder of up to millimetres of water.

Magnesium should be replaced adequately according to serum magnesium levels [ 22 ]. In clinical practice, various types of cisplatin-induced vascular toxicities can be caused by cisplatin such as thrombotic microangiopathy and myocardial infarction. In this paper, we aim to review the pathophysiological mechanisms of cisplatin-induced AKI and discuss the most recent experimental strategies and molecules to prevent cisplatin-induced AKI.

autoregulation (redirected from Renal autoregulation) Also found in: Dictionary, Thesaurus. Understanding renal blood flow and autoregulation Clinical relevance of understanding renal blood flow and autoregulation When faced with a patient suspected of having, or proven to have AKI, intrinsic renal disease and obstruction should always be excluded.


Attenuated renal autoregulation contributes to renal damage in many, but not all, models of renal, diabetic, and hypertensive diseases. This review provides a summary of our current knowledge regarding underlying mechanisms enabling renal autoregulation in health and disease and methods used for its study.

diseases of hypothalamus (see also physiology of hypothalamus); diseases of hypophysis / pituitary gland; diseases of anterior hypophysis / adenohypophysis (see also physiology of adenohypophysis) (anterior) panhypopituitarisms / Simmonds' syndrome: generalized or particularly severe hypopituitarism, which in its complete form leads to absence of gonadal function and insufficiency of thyroid.

Renal autoregulation involves feedback mechanisms intrinsic to the kidney that cause either dilation or constriction in the afferent arteriole so as to counteract blood pressure changes and keep a steady GFR. For instance, if the mean arterial pressure increases, renal autoregulation causes the afferent arteriole to constrict, preventing the pressure.

Hypertensive renal diseases are the most common medical disorders seen in pregnancy. Whereas preeclampsia (acute pregnancy-induced hypertension) is the etiology of hypertension in most (approximately 70%), chronic hypertension or renal disease .

Renal autoregulation
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The Worldwide Physiologist - Vascular Autoregulation