Renal Pathophysiology Flashcards
kidneys receive how much total cardiac output
15-25%
how much of the blood directed towards the kidneys is directed towards the renal cortex
95%
how much of the blood directed towards the kidneys is directed towards the medulla
~5%
how many L/min of blood flows through the renal arteries
1-2.5L/min
what part of the kidney is most vulnerable to ischemic insults
renal medullary papillae
what is the mmHg range in which kidneys auto regulate their mean arterial pressures
60-160mmHg
is auto regulation intact in a denervated kidney
yes
what regulates autoregulation of the kidneys
intrinsic mechanisms of the kidney itself. they auto regulate via vasodilation and vasoconstriction of renal afferent arterioles
what separates the afferent arterioles from the efferent arterioles
glomerulus
how is hydrostatic pressure created in the kidney
resistance from efferent arterioles, which provides force for ultrafiltration
podocytes
endothelial cells that line the capillaries in the kidney
glomerular filtration rate
the rate at which blood is filtered through all of the glomeruli, measures overall kidney function
how does SNS activation affect renal blood flow
reduces renal blood flow
stimulated via adrenal medulla to release catecholamines of if BP decreases SNS will also stimulate RAAS
how does surgical stimulation affect vascular resistance
it increases vascular resistance
when is ADH released
in response to decreased stretch receptors in the atrial and arterial wall
released in response to increased osmolality of the plasma (monitored by hypothalamus) aka dehydration
where is ADH synthesized and released
hypothalamus, released from posterior ptuitary
half life of ADH
16-24h
2 primary functions of ADH
increases reabsorption of sodium and water in the kidneys
causes vasoconstriction and PVR to increase BP
perioperative causes of ADH (5)
hemorrhage PPV upright position of position changes nausea medications
role of renin
secreted by kidneys, hydrolyzes angiotensin to angiotensin 1
what is released from the juxtaglomerular cells
renin
what is renin released at the juxtaglomerular cells in response to (3)
decreased arterial BP
decrease in sodium load delivered to distal tubules
SNS (beta 1 receptors)
angiotensin I and II conversion
angiotensin I is converted in the lungs by angiotensin converting enzyme (ACE) into angiotensin II
role of angiotensin II
potent vasoconstrictor, stimulates hypothalamus to secrete ADH
aldosterone released from
minteralcorticoid hormone released from adrenal gland
plasma half life of aldosterone
20 minutes
role of aldosterone
stimulates epithelial cells in distal tubule and collecting ducts to reabsorb sodium and water. exchanges potassium to maintain electroneutrality
what is the complete opposite of aldosterone function
atrial natriuretic peptide (ANP)
spironolactone works by
potassium sparing diuretic that blocks aldosterone receptors
causes of AKI can be categorized as (3)
prerenal, infrarenal, postrenal
definition of pre renal AKI
hemodynamic or endocrine factors that impair perfusion. can progress to permanent parenchymal damage
causes of pre renal AKI (7)
hypo perfusion or hypovolemia
skin loss (burns)
absolute decrease in ECF volume (fluid loss, hemorrhage)
sequestration
vascular occlusion (thrombosis, aortic or renal artery clamping)
decreased renal blood flow (heart failure, renal artery stenosis)
altered hemodynamics (abdominal compartment syndrome, hepatorenal, hypercalcemia, sepsis, drugs)
pre-renal AKI usual pathology to correct itself
RAAS, ADH, low urine sodium with high osmolality
reasons for renal or acute tubular necrosis (ATN)
tissue damage from prolonged ischemia, nephrotic injury (antibiotics, chemotherapeutics, contrast dye), glomerulonephritis
what do you expect with a urinalysis from an ATN patient
patients with parenchymal disease will have trouble concentrating urine
you will see high urine sodium and low osmolality
nephrotoxic drugs include
aminoglycosides!!!!!! (gentamicin, tobramycin)
chemotherapeutic agents
NSAIDS
radiocontrast dye
post renal AKI causes
obstruction (calculi, blood clots, neoplasm)
surgical ligation
edema
oliguria
polyuria
> 2.5L/day of non concentrated urine
renal failure risk based on creatinine, UOP, GFR
creatinine increase x1.5 OR
GFR decrease >25%
UO
renal injury based on creatinine, UOP, GFR
increased creatinine x2 OR
GFR decrease >50%
UOP
renal failure based on creatinine, UOP, GFR
increased creatinine x3 OR
GFR decrease >75% OR
creating >4mg/100mL
UOP
risk factors for acute renal failure/injury
renal reserve decreasing with age preexisting renal dysfunction certain surgical procedures sepsis use of nephrotoxic agents diabetes, HTN
risk factors for acute renal failure/injury: how much does renal reserve decrease with age
for each year after age 50, creatinine clearance decreases by 1.5mL’s and renal plasma flow by 8mL
risk factors for acute renal failure/injury: certain surgical procedures include
cardiac bypass >2h aortic aneurysms (supra renal aortic clamping) ventricular dysfunctions
risk factors for acute renal failure/injury: sepsis includes
hypovolemia hemolysis DIC infections acidosis
2 ways to prevent renal insult
hydration
BP maintenance
contrast induced nephropathy (CIN) result from
results from administration iodinated contrast media. transient and reversible form of acute renal failure
(iodinated=worst for kidneys)
contrast induced nephropathy (CIN) treatment
mainly supportive, consisting of careful fluid and electrolyte management, although dialysis may be required in some cases
what are some risk factors that place a patient at increased risk for CIN
preexisting AKI
HTN
volume status
hepatorenal syndrome
CIN pathophysiology
worsened by hypoxia and hypoperfuson
direct toxicity of contrast media (CM) which could be related to harmful effects of free radicals and oxidative stress
in the renal tubules, excreted CM generates osmotic force causing marked increase in sodium and water excretion
this diuresis will increase intra tubular pressure, which will reduce GFR, contributing to pathogenesis of renal failure.
CIN and free radicals
it is thought that activation of cytokine induced inflammatory mediators by reactive free radicals is the responsible mechanism. conversely, the inhibition or reduction of free radicals formation might reduce CIN by alkalinizing tubular cells
CIN tx
only supportive, prevention is important
benefit for CM based diagnostic studies or interventional procedures should always be weighted against the risk of CIN
oliguria in the OR
often a sign of inadequate systemic perfusion. rapid recognition and tx can help prevent renal insult intra operatively
monitors to assess fluid status intra operatively
urinary catheter TEE CVP BP SVV
what is the differential diagnosis for oliguria in the OR
pump problem versus volume status problem versus vasodilation problem
SVV >10% =
volume bolus indication (7mL/kg)
SVV <10%, CI <2.5L/min
catecholamines (epi until CI >2.5L/min)
SVV >10%, CI >2.5L/min, MAP <60mmHg
vasopressor (norepinephrine until MAP >60)
oliguria treatment
assume prerenal oliguria is related to fluid until proven otherwise
- diuretics to consider are furosemide and mannitol, but do not consider these in the setting of hypovolemia
- selective dopa agonist cases renal arteriolar vasodilation (fenoldapam, low dose dopa)
examples of intra renal AKI reasons
tubular injury (ischemia or nephrotoxicity) interstitial nephritis (allergy or NSAID type) glomerular DO's (glomerulonephritis, thrombotic micorangiopathies, atheroembolic disease)
examples of post renal AKI reasons
anastomotic obstruction of bladder outlet, ureter) tubular obstruction (crystals, drug induced, proteins)
leading causes of CKD
diabetes and HTN
hispanic americans are at how much greater risk for developing kidney failure
1.5x
how much higher are ESRD rates in african americans
4x
native americans are how much more likely to be diagnosed with kidney failure?
1.8x
chronic renal failure overview
slow, progressive, irreversible
decreased functioning nephrons
decreased renal blood flow
decreased GFR, tubular function, reabsorptive capacity
common causes of chronic renal failure (5)
glomerulonephritis (inflammation of glomerulus)
pyelonephritis (kidney inflammation, usually UTI r/t E.coli)
DM
vascular or hypertensive insults
congenital defects
chronic renal failure stages (3)
decreased renal reserve ->
renal insufficiency ->
end stage renal failure or uremia
chronic renal failure stage 1: decreased renal reserve
asymptomatic until <40% of functioning nephrons remains
chronic renal failure stage 2: renal insufficiency
10-40% of functioning nephrons remains
compensated, little renal reserve
chronic renal failure stage 3: ESRF or uremia
> 95% of nephrons are non functioning
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 manifestations (6)
hypervolemia acidemia hyperkalemia cardiorespiratory dysfunction anemia (EPO) bleeding disturbances
chronic renal failure treatment (3)
HD, PD, transplant
SG reflects
tubular function. ability to concentrate urine
glucose filtration and reabsorption in kidneys
freely filtered at glomerulus, reabsorbed in proximal tubule
glycosuria
signifies ability of renal tubules to reabsorb glucose has been exceeded by abnormally heavy glucose lead and is usually indicative of DM
lab test for renal function: blood urea nitrogen (BUN)
not a direct renal function. influenced by exercise, bleeding, steroids, and tissue breakdown. elevates in kidney disease once GFR is reduced to ~75%
lab test for renal function: serum creatinine
muscle tissue turnover and dietary intake of protein. creatinine is freely filtered at glomerulus and is neither reabsorbed nor excreted
lab test for renal function: GFR
best measure of glomerular function. normal is 125mL/min. asymptomatic until GFR decreases to <30-50% of normal
conditions causing elevation of serum creatinine independent of GFR
ketoacidosis
cephalothin, cefoxitin
flu cytosine
other drugs including aspirin, cimetidine, probenecid, trimethoprim
conditions causing decrease of serum creatinine independent of GFR
physiologic decrease in muscle mass, pathologic decrease in muscle mass, decreased hepatic creatine synthesis and cachexia
when giving PRBC’s to ESRD, consider the following to reduce incidence of hyperkalemia
select <5d old blood
wash any unit of blood immediately before transfusion to remove extracellular K
using filters helps
rate and volume of transfusion also plays a role
imaging studies in renal disease: ultrasound
noninvasive, minimal patient prep, assess kidney size, hydronephrosis, vasculature, obstructions, masses
imaging studies in renal disease: CT
detects stones of all kinds, masses may be evaluated using contrast
imaging studies in renal disease: MRI
detailed tissue characterization, nice alternative to a contrast CT, reduced radiation exposure (ex preggo)
gadolinium
paramagnetic intravenous contrast agent commonly used in MRA images
peri operative effects on renal function: GA
PPV and decreased CO depresses renal blood flow, GFR, urinary blood flow, and electrolyte sevretion
peri operative effects on renal function: regional anesthesia
parallels with degree of SNS blockade, decreased VR, and decrease in blood pressure
peri operative effects on renal function: indirect effects
circulatory, endocrine, SNS, patient positioning
peri operative effects on renal function: direct effects
medications that target renal cellular function
peri operative effects on renal function: surgery
stress and catecholamine release, fluid shifts, secretion of vasopressin and angiotensin
morphine
active metabolites that depend on renal clearance mechanisms for elimination. principally metabolized by conjugation in the liver, and the water soluble glucoronides are excreted by kidney. morphine 6 glucoronide is active
dont give this drug in ARF
meperidine
active metabolite normeperidine depends on renal excretion. accumulation can lead to CNS toxicity and seizures
fentanyl
not grossly altered by renal failure, but a decrease in plasma protein binding may result in higher free fractions
hydromorphone dosage trend and CKD
decrease dosage as ESRD gets worse
CKD and ketamine
8% of administered ketamine is metabolized by liver forming norketamine (non active). norketamine is then hydroxylated into a water soluble metabolite excreted by the kidney. most clinicians believe that dose modification for ketamine is not required.
gabapentinoids (gabapentin, pregabalin) and CKD
do not undergo hepatic metabolism and are excreted solely by the kidney. a reduction of 50% of dose for each 50% decline in GFR or creatinine clearance and increasing the time interval between each dose is advised.
inhalation agents and renal: isoflurane
decreases BP (dose dependent)
inhalation agents and renal: desflurane
with increased HR, may maintain greater degree of CO and therefore renal perfusion
inhalation agents and renal: sevoflurane
free fluoride ion metabolite. was more pronounced and only proven with methoxyflurane (and >5 mac hours) and clear evidence has not been established with sevoflurane
compound A
CO2 absorbents containing some line degrade sevoflurane resulting in production of vinyl ether compound called compound A.
risk for compound A is dependent on (3)
duration of exposure
FGF rate
concentration of sevo (mac hours)
AMSORB
replaces soda lime
is non caustic and can be disposed of in domestic waste
no production of compound A even when desiccated and low flows with sevo are safe
propofol
dose not adversely effect renal tubular function
may be an extra hepatic site of propofol disposition (along with liver and small intestine glucoronidation)
prolonged infusions may result in green urine due to presence of phenolic metabolites (discoloration does not affect renal function)
propofol infusion syndrome can result in renal failure secondary to
rhabdomyolysis
myoglobinuria
hypotension
metabolic acidosis
succinylcholine
can be used carefully. metabolism is catalyzed by pseudocholinesterase to yield nontoxic succinic acid and choline. .5mEq/L transient increase in K can be exaggerated in patient with renal failure.
okay if patient has receive HD within 24h and has normal K
metabolic precursor of succinc acid and choline and where its excreted
succinylmonocholine is excreted via the kidneys
DOA of muscle relaxants my be _______ in patients with renal failure
prolonged
sugammadex
cyclodextrin molecule that inactivates aminosteroidal NMB’s, resultant sugammadex NMB complex is excreted by the kidney. in patient with severe renal impairment, cyclodextrin complexes can accumulate. insufficient data of what long term exposure to the complexes means
sodium nitroprusside
cyanide is an intermediate in the metabolism of sodium nitroprusside, with thiocyanate being the final metabolic end product
half life of thiocyanate
normally >4d, and is prolonged in patients with renal failure
s/sx of thiocyanate levels >10mg/100mL
hypoxia, nausea, tinnitus, muscle spasm, disorientation, and psychosis
thiocyanate toxicity associated with
long term infusions (usually >6d)
albumin
may be protective by maintaining renal perfusion, binding of endogenous toxins and nephrotoxic drugs, and preventing oxidative damage
hetastarch/dextran
associated with AKI secondary to breakdown of synthetic carbohydrates to degradation products that cause direct tubular injury and plugging of tubules. worsened by decreased renal perfusion
dopaminergics
dopamine and fenoldapam (selective D1 agonist) dilate afferent and efferent arterioles and increase renal perfusion
anti dopaminergics
(metoclopramide, phenothiazines, droperidol) may impair renal response to dopamine
renal pathophysiology requiring surgery (4)
renal cell carcinoma
renal dysplasia
PKD (polycystic kidney disease)
wilms tumor
renal cell carcinoma
most common renal malignancy
originates in lining of proximal tubular
refractory to chemo or radiation
surgical resection is often curative
renal cell carcinoma triad
hematuria, flank pain, renal mass.
renal cell carcinoma extensions would be found
5-10%, the tumor extends into renal vein and IVC and RA. may then require CPB.
renal dysplasia
malformation of tubules during fetal development (modern family girl)
kidney consists of irregular cysts of varying sizes
dx often made in utero by US
may also have ureteropelvic function obstruction and vesicoureteral reflux
linked to genetic mutation and illicit drug use by mother
bilateral is incompatible with survival
about 90% of patients will have contralateral hypertrophy by adulthood for compensation
renal dysplasia can lead to (3)
CKD, HD, transplant
polycystic kidney disease (PKD)
inherited (dominant or recessive), massive engagement of kidneys with compromised renal function.
cysts can also occur on other organs (liver, pancreas, spleen)
painful due to distention of cysts and stretching of fascia.
hemorrhage, rupture, or infection exacerbate this pain
non functioning fluid filled cysts that range in size from microscopic to mass effect producing size
most cases progress to bilateral disease by adulthood
complications of PKD (4)
HTN d/t activation of RAAS
cyst infections
bleeding
decline in renal function
PDK tx
sx management
HD
transplant
wilms tumor (nephroblastoma)
often presents unilaterally and a painless, palpable abdominal mass.
can be associated with congenital/genetic malformations
most common malignant renal tumor in children
requires resection and possible chemo
capacity for rapid growth
where would wilms tumor likely metastasize to
lungs
wilms tumor tx
resection and possibly chemo
stages of wilms tumor, stage 1:
43% of classes, limited to kidney and is completely excised
stages of wilms tumor, stage 2:
23% of vases, tumor extends beyond the kidney but is completely excised
stages of wilms tumor, stage 3:
20% of vases, inoperable primary tumor or lymph node metastasis
stages of wilms tumor, stage 4:
lymph node metastases outside of abdominopelvic region
stages of wilms tumor, stage 5:
bilateral renal involvement
total nephrectomy
renal artery and vein are ligated and then it involves removal of the kidney, ipsilateral adrenal gland, peirnephric fat, and surrounding fascia. other kidney needs to be functional
partial nephrectomy
nephron sparing surgery, considered for patients with solitary functional kidney, small lesions (<4cm), or bilateral tumors, or for patents with increased risk because of other diseases, such as DM or HTN
how are nephrectomies performed
open, lap, and/or robotic
nephrectomy pre surgery considerations (4)
flank mass, HTN (on antihypertensives), US and CT, biopsy and dx
nephrectomy anesthesia plan of care
premedicaiton
inhalation induction if pedes
BP control (hyper dynamic, volume and pressors plausible)
PIV x 2, aline, CVC placed by surgeon if used for chemo or by anesthesia for IV immunosuppression medication
anesthesia considerations for nephrectomy
standard risk assessment ID smoking and age risk factors note any preexisting renal dysfunction many are anemic, get CBC and type/cross BMP to assess K regional anesthesia includes blockage of nerve roots T8-L3 ERRAS opioid sparing
PTH increased _______ in exhange for _________
Ca reabsorption in exchange for phosphate
where is aldosterone secreted from
adrenal cortex, causes reabsorption of Na
