Renal pathophysiology Flashcards
The kidneys receive __________ percent of total cardiac output
15 to 25%
95% of this blood is directed to the renal cortex
5% is directed to the medulla
The amount of blood through the renal arteries is
1-1.25 L/min
Renal medullary papillae are more vulnerable to
ischemic insults
Kidneys successfully autoregulate their blood flow between
60-160 mmHg mean arterial pressures
Since it is intrinsic,
autoregulation is intact even in the denervated kidneys
Autoregulation is
an INTRINSIC MECHANISM that causes vasodilation & vasoconstriction of renal afferent arterioles to regulate renal blood flow
The capillaries are lined with
endothelial cells known as PODOCYTES
The glomerular filtration rate is
the rate at which blood is filtered through all of the glomeruli measure overall kidney function
The resistance in the efferent arterioles creates
HYDROSTATIC PRESSURE within the glomerulus to provide force for ultrafiltration
The glomerulus separates the
afferent (brings blood) arterioles from the efferent (takes it away) arterioles
SNS activation will
reduce renal blood flow ****
Shunts blood to more important places in times of stress
SNS activation reduces renal blood flow by
shunting 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
Anesthetics that decrease renal blood flow include
Propofol
PPV
retractors
among many other things
Perioperative causes of ADH release include**:
hemorrhage positive pressure ventilation upright position nausea medications
The half-life of antidiuretic hormone is
16-24 minutes
2 primary functions of ADH include
increases reabsorption of sodium & water in the kidneys
causes vasoconstriction and PVR to increase blood pressure
Antidiuretic hormone is synthesized in the
hypothalamus & is released from the posterior pituitary
Antidiuretic hormone is released in response to
DECREASED stretch receptors in the atrial & arterial wall (low fluid in system means decreased volume and decreased stretch)
INCREASED osmolality of the plasma (monitored by hypothalamus)
Renin is an enzyme secreted by the kidneys that
hydrolyzes angiotensin to angiotensin I
Renin is released from the
juxtaglomerular cells located near the afferent arterioles in response to
a decreased arterial blood pressure
a decrease in NA load delivered to the distal tubules
& SNS (beta 1 receptors)
Angiotensin I is converted in the lungs by
angiotensin-converting enzyme into angiotensin II
Angiotensin II is a
potent vasoconstrictor & stimulates the hypothalamus to secrete ADH
Aldosterone is a
mineralocorticoid hormone released from the adrenal gland
The plasma half-life of aldosterone is
20 minutes
Aldosterone stimulates epithelial cells in the distal tubule & collecting ducts to
REABSORB SODIUM & WATER
-exchanges potassium to maintain electroneutrality
Aldosterone is the complete opposite of
atrial natriuretic hormone function
Spironolactone is a
potassium sparing diuretic that blocks the aldosterone receptors
Acute kidney injury is the
sudden inability of the kidneys to vary urine volume & content appropriately
develops rapidly but may resolve
AKI has a ______ mortality rate
50%
Causes of AKI include
pre-renal
intrinsic-renal
post-renal
Pre-renal AKI is a result of
hemodynamic or endocrine factors that impair perfusion
hypoperfusion or hypovolemia
Factors that can cause hypoperfusion or hypovolemia in pre-renal AKI include
skin loss (e.g. burns) fluid loss hemorrhage sequestration vascular occlusion (e.g. thrombosis, aortic, or renal artery clamping)
Pre-renal AKI will activate
mechanism to conserve salt & water
-RAAS, ADH, low urine sodium with high osmolality)
Pre-renal AKI can progress to
permanent parenchymal damage
Renal or acute tubular necrosis is the result of
tissue damage from
- prolonged ischemia
- nephrotoxic injury (e.g. antibiotics, chemotherapeutics, & contrast dye)
- glomerulonephritis
Patients with parenchymal disease will have trouble
concentrating urine
-high urine Na & low osmolality
Nephrotoxic drugs include
aminoglycosides, amphotericin B, chemotherapeutic drugs, cyclosporine modified, NSAIDs, penicillin antibiotics (when used in combo with other nephrotoxic drugs), & radiocontrast dye
Post-renal AKI is a result of
obstruction (e.g. calculi, blood clots, & neoplasm)
surgical ligation
edema
Oliguric is described as
<0.5 mL/kg/hr
Non-oliguric
also known as anuric is an ominous sign
Polyuric is defined as
> 2.5 L/day of non-concentrated urine
Risk factors for acute renal failure/injury include:
increasing age preexisting renal dysfunction certain surgical procedures- mainly cardiac sepsis use of nephrotoxic agents diabetes, HTN
For each year after age 50, creatinine clearance
decreases by 1.5 mLs and renal plasma flow by 8 mL
Surgical procedures that increase risk for AKI include
cardiac bypass >2 hours aortic aneurysms (supra-renal aortic clamping) ventricular dysfunctions
Sepsis can contribute to AKI because of
hypovolemia, hemolysis, DIC, infections, & acidosis
_________ of renal insult is far more successful than management
Prevention
The 3rd most common cause of hospital acquired AKI include
contrast induced nephropathy
1st- renal hypoperfusion
2nd- postoperative renal injury
Contrast induced nephropathy results from
administration of iodinated contrast media
it is a transient & reversible form of acute renal failure
Treatment of contrast induced nephropathy is
mainly supportive, consisting of careful fluid & electrolyte management, although dialysis may be required in some cases (dialysis does not remove contrast)
In regards to CIN treatment,
treatment is only supportive
prevention is important!
the benefit for CM-based diagnostic studies or interventional procedures should always be weighed against the risk of CIN
Contrast induced nephropathy is worsened by
hypoxia & hypoperfusion
Direct toxicity of contrast media could be related to
harmful effects of free radicals & oxidative stress
- thought that activation of cytokine-induced inflammatory mediators by reactive free radicals is responsible
In the renal tubules, the excreted contrast media
generates osmotic force causing marked increase in sodium & water excretion
The diuresis as a result of contrast media will
increase intratubular pressure, which will reduce the GFR & contribute to the pathogenesis of acute renal failure
The incidence of CIN is low in patients with
normal renal function
CIN is as high as
50% in patients with diabetic nephropathy
Oliguria is often a sign of
inadequate systemic perfusion
Rapid recognition and treatment of oliguria in the OR can help
prevent renal insult intraoperatively
Monitors used to assess fluid status intraoperatively include
urinary catheter TEE CVP Blood pressure SVV
Treatment of oliguria includes
assume prerenal oliguria is related to FLUID until proven otherwise
blood?
diuretics- do not give in the setting of intravascular hypovolemia- furosemide & mannitol
selective dopamine DA1 receptor agonists-causes renal arteriolar vasodilation- low dose dopamine
______ are more likely to suffer from CKD
disadvantaged populations; such as African Americans, American Indian, Hispanics, Asian, & aboriginal populations are more likely to suffer from higher rates of DM & HTN which are leading causes of CKD
____ have a 1.5 times greater risk for developing kidney failure
Hispanic Americans
ESRD rates are nearly 4-fold higher among_______
African Americans as compared to US whites despite similar prevalence rate of early CKD
_______ are about 1.8 times more likely to be diagnosed with kidney failure
Native Americans-
diabetes is the leading cause of kidney failure among this population
What increases the risk of developing kidney disease & limit access to preventive measures & treatment in communities with socioeconomic & cultural differences?
language barriers education & literacy levels low income unemployment lack of adequate health insurance certain culture-specific health beliefs & practices
For most Low Middle income countries, transplantation is rare due to
lack of infrastructure, & survival can be complicated by the affordability of immunosuppressive drugs, malnutrition and infectious disease, in particular tuberculosis
Chronic renal failure is a
slow, progressive, irreversible disease
decreased functioning nephrons, decreased renal blood flow
decreased GFR, tubular function & reabsorptive capacity
Common causes of chronic renal failure include
glomerulonephritis- inflammation of glomerulus (e.g. autoimmune)
pyelonephritis- kidney inflammation (e.g. UTI 70-80% are due to E. Coli)
diabetes
vascular or hypertensive insults
congenital defects
States of chronic renal failure include ****
decreased renal reserve
renal insufficiency
End-stage renal failure or uremia
Describe the chronic renal failure phase of decreased renal reserve
asymptomatic until <40% of normal nephron remain
Describe the chronic renal failure phase of renal insufficiency
10-40% of functioning nephrons remain
compensated, little renal reserve
Describe the chronic renal failure phase of end-stage renal failure or uremia.
> 95% of nephrons are nonfunctioning
GFR is <5-10% of normal
severely compromised electrolyte, hematologic, & acid-base balances
uremia (urine in the blood) is eventually lethal
dialysis dependent
Chronic renal failure manifests as
hypervolemia acidemia hyperkalemia cardiorespiratory dysfunction anemia & bleeding disturbances
Treatment of chronic renal failure includes
hemodialysis
peritoneal dialysis
kidney transplant
