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
risk factors for acute renal failure/injury
- age (renal reserve decreases with age)
- preexisting renal dysfunction
- certain surgical procedures (cardiac bypass >2 hours, aortic aneurysms with supra-renal clamping, ventricular dysfunctions)
- sepsis (hypovolemia, hemolysis, DIC, infection, acidosis)
- use of nephrotoxic agents
- DM
- HTN
contrast induced nephropathy (CIN)
- 3rd most common cause of hospital acquired acute renal injury and represents
- 12% of cases
- results from administration of iodinated contrast media
- transient and reversible
- treatment is mainly supportive –> fluid and electrolyte management, although dialysis may be required in some cases
risk factors that put a patient at increased risk for developing CIN.
- preexisting disease –> DM, HTN
- hypovolemic
- hypoperfusion
- obesity
- hepatorenal syndrome
- hypoxic
CIN Prevalence
- 6% after CT
- 9% after angiography
- 4% after IV pyelography
- LOW incidence in those with normal renal function 0-5%
- 12-27% in patients with preexisting renal impairment
- 50% in those with diabetic neuropathy
CIN pathophysiology
- not well understood
- worsened by hypoxia and hypoperfusion
- direct toxicity of contrast media which could be related to harmful effects of free radicals and oxidative stress
- in renal tubules, the excreted CM generates osmotic force causing marked increase in sodium and water excretion
- diuresis will increase intratubular pressure, which will reduce the GFR, contributing to the pathogenesis of acute renal failure
CIN treatment
- supportive
- prevention = important
- benefit vs risk
oliguria in the OR
- sign of inadequate systemic perfusion
- rapid recognition and treatment can help prevent renal insult
monitors used to assess fluid status in OR
- urinary catheter
- TEE
- CVP
- blood pressure
- SVV (stroke volume variation)
oliguria treatment
- assume pre-renal 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 (fenoldopam or “low dose” dopamine)
CKD in disadvantaged populations
- African, American Indian, Hispanic, Asian, and Aboriginal populations have higher incidences of DM and HTN, leading causes of chronic kidney disease
- higher risk of developing severe kidney disease and kidney failure
- Hispanic Americans 1.5 times greater risk
- ESRD rates 4 fold higher in African Americans compared to US whites
- Native Americans 1.8 times more likely to be diagnosed with renal failure
eGFR
- estimated glomerular filtration rate
- calculated using a formula that included a person’s body habitus, age, sex, serum Cr, and race
- RACIST - now they are finally getting rid of it
SES and cultural factors that increase risk of developing kidney disease.
- language barriers
- education and literacy levels
- low income
- unemployment
- lack of adequate health insurance
- certain culture-specific health beliefs and practices
chronic renal failure
- slow, progressive, irreversible
- decreased functioning nephrons
- decreased renal blood flow
- decreased GFR, tubular function, and reabsorptive capacity
common causes of chronic renal failure
- glomerulonephritis (inflammation of glomeruli, autoimmune)
- pyelonephritis (kidney inflammation)
- DM
- vascular or hypertensive insults
- congenital defects
decreased renal reserve stage
asymptomatic until <40% of normal nephrons remain
renal insufficiency stage
- 10-40% of functioning nephrons remain
- compensated, little renal reserve
end-stage renal failure or uremic stage
- > 95% of nephrons are functional
- GFR is <5-10% of normal
- severely compromised electrolyte, hematologic, and acid-base balances
- uremia (urine in blood) is eventually lethal
- dialysis dependent
chronic renal failure clinical manifestations
- hypervolemia
- acidemia
- hyperkalemia
- cardiorespiratory dysfunction
- anemia
- bleeding disturbances
treatment for chronic renal failure
- hemodialysis
- peritoneal dialysis
- kidney transplant
glucose
- freely filtered by glomerulus
- reabsorbed in proximal tubule
glycosuria
signifies the ability of renal tubules to reabsorb glucose has been exceeded by an abnormally heavy glucose load and is usually indicative of DM
BUN
- blood urea nitrogen
- not a direct renal function
- influenced by exercise, bleeding, steroids, and tissue breakdown
- elevated in kidney disease once GFR is reduced to ~75%
serum creatinine
- muscle tissue turnover and dietary intake of protein
- creatinine is freely filtered at the glomerulus and is neither reabsorbed or secreted
- best tool to assess kidney function
creatinine clearance
-good measure of GFR
GFR
- best measure of glomerular function
- normal 125 mL/min
- asymptomatic until GFR decreases to <30-50% of normal
electrocardiogram in renal disease
- reflects toxic effects of potassium excess more closely than determination of serum potassium concentration
- peaked T waves
- small or indiscernible P waves
hyperkalemia treatment
- CaCl (or gluconate)
- insulin and D50 (5-10 units and 1 amp)
- albuterol
- hyperventilate
clinical situations that contribute to increased K+ in renal failure
- protein catabolism
- hemolysis
- hemorrhage
- transfusion of stored RBCs
- meatbolic acidosis
- exposure to meds that inhibit K+ entry into cells or K+ secretions in distal nephron
stored blood and potassium
- blood storage slow and constant leak of potassium from the cells into plasma due to failure of sodium potassium ATPase pump failure
- plamsa potassium may increase by 0.5-1 mmol/L per day of refrigerator storage
prevention of hyperkalemia following a transfusion
- select blood collected less than 5 days prior to transfusion
- wash unit of blood immediately before infusion to remove excess potassium
- use of potassium absorption filters during transfusion
- rate and volume of transfusion affect potassium level
ultrasound + renal disease
- noninvasive
- minimal patient prep
- assess kidney size, hydronephrosis, vasculature, obstructions, and masses
CT + renal disease
detects stones of all kinds, masses may be evaluated using contrast
MRI + renal disease
- detailed tissue characterization
- nice alternative to contrast CT
- reduced radiation exposure
general anesthesia effect on renal function
-PPV and decreased CO –> depression of renal blood flow, GFR, urinary flow, and electrolyte secretion
regional anesthesia effect on renal function
-parallels with degree of SNS blockade, decreased venous return, and decrease in blood pressure
indirect effects on renal function
-circulatory, endocrine, SNS, patient positioning
direct effects on renal function
medications that target renal cellular function
surgery effect on renal function
stress and catecholamine release, fluid shifts, secretion of vasopressin and angiotensin
morphine in renal failure
- active metabolites that depend on renal clearance mechanisms for elimination
- morphine-3-glucuronide and morphine-6-glucuronide are excreted via kidney
meperidine (demerol) in renal failure
- active metabolite normeperidine depends on renal excretion
- accumulation can lead to CNS toxicity and seizures
fentanyl in renal failure
- not grossly altered by renal failure, but decrease in plasma protein binding may result in higher free fractions of drug
- probably drug of choice in those with renal failure
CKD and ketamine
- 8% of administered ketamine metabolized by the liver forming norketamine
- norketamine hydroxylated into water soluble metabolite and excreted by kidneys
- most clinicians believe dose modification for ketamine not necessary
gapapentenoids in renal failure
- gabapentin, pregabalin
- liberal administration of gabapentinoids may increase risk of over sedation and even coma
- these agents do not undergo hepatic metabolism and are excreted SOLEY by the kidney
- a reduction of 50% of the dose for each 50% decline in GFR or CCr and increasing time interval between doses is advised
inhalational agents in renal failure
- all can cause a decrease in blood pressure
- kidneys respond with compensatory increase in renal vascular resistance which decreases renal blood flow
isoflurane
decreases BP dose dependent
desflurane
with increased heart rate, may maintain a greater degree of CO and therefore renal perfusion
sevoflurane
- free fluoride ion metabolite
- was more pronounced and only proven with methoxyflurane (and greater than 5 MAC hours)
- clear evidence not established with sevo
compound A
- CO2 absorbents containing soda lime (KOH, NaOH, water, and Ca(OH)2) degrade sevo resulting in production of vinyl ether called compound A
- routinely used outside US
Risk of compound A development dependent on
- duration of gas exposure
- fresh gas flow rate
- concentration of sevo
amsorb
- replaces soda lime
- non-caustic and disposed of in domestic waste
- no compound A production even with low flows of sevo
propofol in renal failure
- does not adversely affect renal tubular function
- may be an extrahepatic site of propofol deposition
- prolonged infusion may result in green urine due to presence of phenolic metabolites
- PRIS can result in renal failure secondary to rhabdo, myoglobinuria, hypotension, metabolic acidosis
succinylcholine in renal failure
- can be used carefull
- metabolism catalyzed by pseudocholinesterase to yield the non-toxic end products of succinic acid and choline
- admin of succ causes rapid, transient increase of 0.5 mEq/L in serum potassium concentration
- can be exaggerated in those with renal failure
- ok to use of patient has received dialysis within 24 hours and normal serum K
non-depolarizing muscle relaxants in renal failure
the duration of action of muscle relaxants may be PROLONGED in patients with renal failure
sugammadex in renal failure
- cyclodextrin is the molecule that inactivates aminosteroidal NMBs
- resultant sugammadex NMB complex is excreted by the kidney
- in patients with severe renal disease, these complexes can accumulate
- insufficient data on what long term exposure to the complexes means
sodium nitroprusside in renal failure
- thiocyanate is final metabolic product
- half life normally more than 4 days, but can be prolonged in renal failure
- thiocyanate levels greater than 10 mg/dL = toxic
- hypoxia, nausea, tinnitus, muscle spasm, disorientation, psychosis
albumin in renal failure
FRIEND
-may be protective by maintaining renal perfusion, binding of endogenous toxins and nephrotoxic drugs, and preventing oxidative damage
hetastarch/dextran in renal failure
NOT FRIEND
-have been associated with acute kidney injury secondary to breakdown of synthetic carbs to degradation products that cause direct tubular injury and plugging of tubules
dopaminergics
- dopamine and fenoldopam
- dilate afferent and efferent arterioles and increase renal perfusion
anti-dopaminergics
- metoclopramide, phenothiazines, doperiodol
- may impair renal response to dopamine
renal cell carcinoma
- most common renal malignancy (80% of all solid renal masses)
- originates in lining of proximal tubules
- refractory to chemo or radiation
- surgical treatment is curative (often only option)
- 5-10% of patients, tumor extends into renal vein and IVC + RA –> may require CPB
classic triad presentation of renal cell carcinoma
- hematuria
- flank pain
- renal mass
renal dysplasia
- malformation in tubules during fetal development
- 1 in 4000 live births
- kidney has irregular cysts of varying sizes
- diagnosis by ultrasound in utero
- may also have ureteropelvic junction obstruction and vesicoureteral reflux
- linked to genetic mutation and illicit drug use by mother (cocain)
- bilateral = incompatible with life
- 90% of patients will have contralateral hypertrophy by adulthood
- leads to CKD, dialysis, and transplant
polycystic kidney disease (PKD)
- inherited (dominant or recessive), massive enlargement of the kidneys with compromised renal function
- cysts can also occur on other organs
- painful due to distention of cysts and stretching of fascia
- hemorrhage, rupture or infection exacerbate the pain
complications of PKD
- hypertension due to activation of RAAS
- cyst infections
- bleeding
- decline in renal function
treatment PKD
- symptom management
- dialysis
- transplant
wilms tumor (nephroblastoma)
- often presents unilaterally and a painless palable abdominal mass (<5% bilateral)
- can be associated with congenital or genetic defects
- most common malignant renal tumor in kids
- requires resection of possible chemo
- capacity for rapid growth
- metastasis usually to lungs
stage 1 wilms tumor
43% of cases
limited to kidney and is completely excised
stage 2 wilms tumor
23% of cases
tumor extends beyond kidney but completely excised
stage 3 wilms tumor
20% of cases
inoperable primary tumor or lymph node metastasis
stage 4 wilms tumor
lymph node metastases outside abdomino-pelvic region
stage 5 wilms tumor
bilateral renal involvement
total nephrectomy
- renal artery and vein ligated and then it involves removal of kidney, ipsilateral adrenal gland, perinephric fat, and surrounding fascia
- other kidney must be functional
partial nephrectomy
- nephron sparing
- considered for patients with a solitary functional kidney , small lesions (<4 cm), or bilateral tumors, OR patients with increased risk because of disease (DM, HTN)
- maybe open, laparoscopic, or robotic
pre-surgery
- flank mass
- HTN - started on antihypertensives
- ultrasound and CT
- biopsy -diagnosis
anesthesia for renal
- premed
- BP control –> wide fluctuations requiring volume and vasopressors
- PIVsx2, aline, CVC palced by surgeon if chemo or by anesthesia for IV immunosuppression med
anesthetic considerations for nephrectomy
- standard risk assessment
- ID smoking and age risk factors
- note any preexisting renal dysfunction
- many are anemic - CBC and T+C
- K+ = BMP
- regional anesthesia include blockage of nerve roots T8-L3
- ERAS
- opioid sparing
