Renal Pathophysiology Flashcards
how much cardiac output do the kidneys receive?
15-25%
how much blood goes to the renal cortex?
95%
how much blood goes to the renal medulla?
5%
blood flow through renal arteries
1-1.25 L/min
kidney autoregulation of blood flow
- kidneys autoregulate their blood flow between 60-160 mmHg mean arterial pressures
- intrinsic mechanism that causes vasodilation and vasoconstriction of the renal afferent arterioles regulates the autoregulation of renal blood flow
- because it is intrinsic, autoregulation is intact even in denervated kidneys
glomerulus
- separate afferent arterioles from efferent arterioles
- the resistance in the efferent arterioles creates hydrostatic pressure within the glomerulus to provide force for ultrafiltration
- capillaries are lined with endothelial cells (podocytes)
- the rate at which blood is filtered through all the glomeruli (GFR) is a measure of overall kidney function
SNS activation + renal blood flow
- reduction of renal blood flow
- shunt to skeletal muscle during exercise
- surgical stimulation can increase vascular resistance
- stimulates the adrenal medulla –> catecholamine release
- if BP decreases, SNS will also stimulate RAAS
antidiuretic hormone
- released in response to decreased stretch receptors in atrial and arterial wall
- released in response to increased osmolality of the plasma (monitored by hypothalamus)
- synthesized in hypothalamus and released from posterior pituitary
- half life = 16-24 min
2 primary functions of ADH
- increases reabsorption of sodium and water in the kidneys
- causes vasoconstriction and PVR to increase blood pressure
perioperative causes of ADH release
- hemorrhage
- positive pressure ventilation (decreased VR)
- upright position
- nausea
- medications
renin
- enzyme secreted by the kidneys that hydrolyzes angiotensinogen to angiotensin I
- released from the JG cells located near afferent arterioles
what is renin released in response to?
- a decreased arterial blood pressure
- a decrease in sodium load delivered to the distal tubules
- SNS (beta 1 receptors)
Angiotensin I
converted in the lungs by angiotensin-converting enzyme into angiotensin II
Angiotensin II
potent vasoconstrictor and stimulates the hypothalamus to secrete ADH
aldosterone
- mineralocorticoid hormone released from adrenal gland
- plasma half life = 20 minutes
- stimulates epithelial cells in distal tubule and collecting ducts to reabsorb sodium and water (exchanges potassium to maintain electroneutrality)
- complete opposite of atrial natriuretic hormone function
spironolactone
potassium sparing diuretic that blocks aldosterone receptors
acute renal failure
- the sudden inability of the kidneys to vary urine volume and content appropriately
- develops rapidly but may resolve
- has a 50% mortality rate
pre-renal acute renal failure
- hemodynamic or endocrine factors that impair perfusion
- hypoperfusion or hypovolemia –> skin loss (burns), fluid loss, hemorrhage, sequestration, vascular occlusion (thrombosis or renal artery/aortic clamping)
- will activate mechanism to conserve salt and water (RAAS, ADH)
- can progress to parenchymal damage
pre renal failure labs
- low urine sodium
- high urine osmolality
renal or acute tubular necrosis (intrarenal)
- tissue damage - prolonged ischemia, nephrotic injury (abx, contrast, chemo), glomerulonephritis
- patients with parenchymal disease will have trouble concentrating urine
intrarenal failure labs
- high urine sodium
- low urine osmolality
post-renal acute renal failure
- obstruction (calculi, blood clot, neoplasm)
- surgical ligation
- edema
oliguric
<0.5 mL/kg/hr
polyuric
> 2.5 L/day of non-concentrated urine