Renal Flashcards
1
Q
What are some functions of the kidneys?
A
Responsibilities/ contributions:
- Water conservation
- Electrolyte homeostasis
- osmolality (via ADH action on DCT)
- regulation of Na, K, Cl, Hco3, H, Ca through various ionic channels through the nephron
- Acid-base balance
- Neurohumoral/ hormonal functions
- hormones involved with: fluid homeostasis, bone metabolism and hematopoiesis
- Waste filtration
- excretion of end products of metabolism nd drugs
- Regulation of vitamin D production
- Red blood cell production via erythropoietin
2
Q
What is the nephron?
A
-
fundamental unit of the kidney
- Composed of a vascular network close to a series of tubules with distinct physiologic functions that empty into collecting ducts to form urine.
- Approximately 1 million nephrons in the normal kidney.
- Receive about 20% of the cardiac output and are responsible for 7% of total body oxygen consumption
Nephron Anatomy:
- Bowman’s capsule: participates in filtration of blood; creates urinary space
- Glomerulus: tuft of capillaries; filters plasma to produce glomerular filtrate
-
PCT: reabsorption of water, ions, organic nutrients
- system begins with proximal convoluted tubule
- high-density of mitochondria and extensive surface area of apical and basilar cell membranes mark the renal tubule and high energy requireent
- 80% of energy is for Na/K ATP ase which maintains the osmotic gradient needed for resorption of filtered molecules
- even though high energy demand, tubule system supplied by only 10-15% RBF. This is the key etiology behind acute tubular necrosis after hypotensive events
-
LOH (thin & thick): reabsorption of water and sodium & chloride ions
- proximal tubule leads to thinner epithelium of descending thin loop of henle
- then turn 180 degrees to ascending loop of henle
- 80% of nephrons begin in cortex and have short loops of henle that only go to outer medulla
- remaining 20% juxtamedullary nephrons start at corticomedullary junction and have more elongated loops of henle that go to the most distal extent of medulla
-
DCT: secretion of ions, acids, drugs, toxins; variable reabsorption of water, sodium ions, calcium ions
- have juxtaglomerular apparatus that comprised of specialized epithelial cells called macula densa
- essential for maintenance of BP
-
CD: variable reabsorption of water. reabsorption or secretion of sodium , potassium, hydrogen and bicarb ions
- empties ultrafiltrate into renal pelvis and then ureters
3
Q
What controls blood flow through the kidneys?
A
- Autoregulatory mechanisms control renal blood flow within a broad range of pressures to maintain a stable GFR. (50-150)
- Factors and diseases might disrupt renal autoregulation, leading to ischemia and kidney injury. These include:
- hypertension,
- kidney disease,
- major surgery,
- Reduced renal blood flow leads to renal hypoxia, inflammation, and fibrosis, which induce microvascular dysfunction in hemodynamic compromised conditions
- Kidney disease can result from disturbances of within
- vascular,
- glomerular
- tubular components.
- Knowledge of these factors is important to anesthesia providers to limit decrements in renal function during the perioperative period.
4
Q
What is GFR? Normal ranges?
A
GFR: measurement of volume filtered through the glomerular capillaries and into the Bowman’s capsule per unit of time
- Considered best indicator of renal function
- Based on patient size/gender/weight/age
- GFR can be calculated from timed urine volume measurements
-
Calculation of creatinine clearance is a less accurate method to evaluate GFR
- Cockcroft-Gault Equation – typically underestimates GFR by 10 - 20%
- Ranges
-
Normal: 90 - 140 mL/min
- Decreases with age
- about 10%/decade after age 30
- Decreases with age
- Abnormal: < 60 mL/min – start altering anesthesia medications
-
Failure: < 15 mL/min
- a/w uremic symptoms and may require dialysis
-
Normal: 90 - 140 mL/min
5
Q
What is creatinine clearance?
A
assessment of renal function (GFR, BUN, CrCl)
- Specific test for GFR – most reliable assessment tool for renal FCN (however GFR is best indicator of renal function?!)
- Measures ability of glomeruli to excrete creatinine
- Normal: 95 – 150 ml’s/min
- Mild dysfunction: 50 – 80 ml’s/min
- Moderate dysfunction: < 25 ml’s/min
- Anephric: < 10 ml’s/min
6
Q
What is creatinine?
A
- Creatinine is product of muscle metabolism
- creatine is product of muscle metabolism that is nonenzymatically converted to creatinine
- rate of creatinine production, and volume of distribution, may be abnormal in critically ill patients
- single serum creatinine measurement often not accurately reflect GFR in physiological disequilibrium of AKI
- Serum creatinine directly r/t body muscle mass
- creatinine is generally neither secreted nor reabsorbed in kidney
- amount that appears in urine in specified time interval refects amount filtered at glomerulus.
- Can be used to reliably estimate GFR in non-critically ill patient
- Normal (reflects differences in skeletal muscle mass):
- Men- 0.8-1.3 mg/dL
- Women- 0.6-1.0 mg/dL
- Slow to reflect acute changes in renal function
- Ex. if acute injury occurs and GFR decreases from 100 mL/min to 10 mL/min, serum creatinine values do not increase for about a week
7
Q
What is BUN?
A
assessment of renal function (GFR, BUN, CrCl)
Blood Urea Nitrogen
- Primary source is liver (protein catabolism)
- BUNdirectly related to protein catabolism and inversely related to GFR
- Not a reliable indicator of GFR (unless protein catabolism is normal and constant)
- 40-50% passively reabsorbed by renal tubule
- Hypovolemia increases this
- Influenced by:
- dietary intake
- coexisting dx
- intravascular fluid volume
Values:
- Normal 10 -20 mg/dL
- 20 – 40 mg/dL: dehydration, high catabolism, decreased GFR
- > 50 mg/dL indicate impairment of renal function
-
Increased BUN with normal serum creatine suggests nonrenal cause
- high protein diet
- GI bleed
- dehydration
- febrile illness
- BUN concentrations higher than 50 mg/dL usually indicate decreased GFR
8
Q
What is fractional excretion of sodium measuring?
A
Assessment of tubular function along with urinalaysis
- Fractional Excretion of Sodium- measure of percentage of filtered sodium that is excreted in urine
- shows renal tubule function
- FENa is a measure of sodium clearance as a percentage of creatine clearance.
- calculated by simultaneous samples of blood and urine collection
- FENa is measure of % filtered sodium excreted in urine. filtered sodium dvidied by GFR
- Useful to distinguish hypovolemia and renal injury (ie acute tubular necrosis)
- FENA > 2% (or urine sodium concentration > 40 mEq/L) reflects decreased ability of the renal tubules to conserve sodium and is consistent with tubular dysfunction
- acute tubular necrosis causes impairment in concentrating ability of nephrons, therefore Na and water will be lost in the urine
- FENA < 1% (or urine sodium excretion < 20 mEq/L occurs when normally functioning tubules are conserving sodium
- in dehydration, nephrons are trying to conserve Na and water, therefor less is in the urine
9
Q
What are the stages of CKD? Manifestations?
A
- 5 GROUPS
- Stage 1 GFR >90- kidney damage with normal kidney function
- Stage 2 GFR 60-89mL/min- kidney damage with mild loss kidney function
- Stage 3 GFR 30-59mL/min
- Stage 4 GFR 15-29 mL/min
- Stage 5 GFR <15 mL/min
Manifestations of reduced GFR not seen until 50% normal
- GFR 30% normal, moderate renal insufficiency ensues
- patients remain asymptomatic withonly biochemical evidence of decline GFR (urea/cr increase)
- further workup reveals symptoms such as nocturia, anemia, loss of energy, decreased appetite, abnormalities in calcium and phos metabolism
- As GFR decreases further- severe renal insufficiency
- profound clinical manifestation uremia and biochemical abnormlaities (academia, volume overload, neuro, cardiac and respiratory manifestations
- GFR 5-10% need renal replacement therapy
10
Q
What is measured in a urinanalysis?
A
Urinalysis- index of kidney’s concnetrating ability, specifically renal tubular function
- Specific gravity
- Measures solutes in urine
- Kidney’s ability to excrete concentrate/dilute urine
- Normal 1.003 to 1.008 (> 1.018 indicates reasonable function)
- dx of renal tubular dysfunction is established by demonstarting kidneys to not produce adequately concentrated urine
- Proteinuria- common and present in 5-10% of adults
- > 150 mg/day- can be normal
- greater amounts can be present after strenuous exercise of standing for several hours
- > 750 mg/day indicates sever glomerular damage
- More likely to develop AKI
- transient proteinuria may be associated with fever, CHF, seizure activity, pancreatitis, and heavy exercise
- persistent proteinuria generally connotes significant renal disease
- > 150 mg/day- can be normal
- Microscope
- RBC (bleeding), WBC (infection), Casts (disease of nephron) or crystals (metabolism)
11
Q
Sevo use in renal dysfuntion?
A
- 3-5% biodegradation
- Inorganic fluoride ions
- Fl ions the same or higher than enflurane
- Can be > 50 μmol/L
- not associated with clinically significant renal dysfunction
- Increased NAG (β – N – acetylglucosaminidase)
- Intracellular indicator of acute proximal renal tubular injury
- BUN and plasma creatinine did not change
- CO2 absorbers with potassium or sodium hydroxide
- Base-catalyzed degradation
- Vinyl ether compound called Compound A
- Renal PCT injury in rats
- increased compound A with increased respiratory gas temperature, low flow anesthesia, dry barium hydroxide absorbent (baralyme)
- Barium hydroxide > soda lime
- alkali such as barium hydroxide lime or soda lime (but not calcium hydroxide) can degrade sevo
- No renal failure noted in low flow or closed- circuit anesthesia
12
Q
Succinylcholine use in renal failure?
A
- Hyperkalemia
- 0.5 -1 mEq/dl increase in potassium
- potassium rise is generally well tolerated in patients with chronically elevated serum potassium levels
- want K <5.5 if considering succinylcholine admin
- Renal failure patients are no more susceptible to exaggerated response to succinylcholine than normal patients
- Infusions problematic
- Succinylmonocholine- weakly active metabolite that is excreted by kidney
- Weaker neuromuscular blocker with longer duration of action
- 0.5 -1 mEq/dl increase in potassium
- Conflicting reports of plasma cholinesterase activity in renal failure
13
Q
Atracurium use in renal failure?
A
- Hofmann elimination and ester hydrolysis
- OK in renal failure patients
- Laudanosine metabolite (30% renal)
- Plasma ½ life same in both normal and renal failure patients
-
may cause seizures in experimental animals and can accumulate with repeated dosing or continuous infusion
- however, not been realized in ICU patients with renal failure receiving prolonged infusions
14
Q
Cisatracurium use in renal failure?
A
- Hofmann elimination (77% of elimination)
- OK in renal failure patient
- 16% renally eliminated
- 4-5x’s as potent as atracurium so less laudanosine metabolites
15
Q
Impact of anesthesia on renal function?
A
- all generl anesthetics decrease GFR and intraoperative urine flow d/t decreased CO and BP
- iInjury more common with:
- preexisting renal disease
- nephrotoxic injury
- hypovolemia
- combination of these factors which exacerbate renal dysfunction
*
16
Q
Vecuronium use in renal failure?
A
- Metabolized in liver to 3 different metabolites
- 3-OH vecuronium has 80% potency of vecuronium
- can accumulate in anephric patients receiving continuous infusion
- Approximately 30 - 40% excreted unchanged by the kidney
- Single dose fine, but multiple doses/infusions may require adjustment
-
DOA of vec prolonged as result of reduced plasma clearance and increased elimination half life
- incubating dose lasts 50% longer in patients with ESRD
-
DOA of vec prolonged as result of reduced plasma clearance and increased elimination half life
17
Q
Rocuronium use in renal failure?
A
- Primarily eliminated by the liver and excreted in the bile
- NO active metabolites
- Approximately 30% excreted unchanged by the kidney
- Single dose fine, but multiple doses/infusions may require adjustment
- conflicting results
18
Q
Cholinesterase inhibitor use in renal failure?
A
- Neostigmine, pyridostigmine, physostigmine, & edrophonium
- Renal excretion accounts for 50 – 75% of the drugs
- Renal failure decreases plasma clearance as much, if not more than, the long- acting neuromuscular blocking drugs
- prolonged duration of action in ESRD due to heavy reliance on renal excretion
- anticholinergic agent atropine and glyco, used in conjunction with anticholinesterases, are similarly excreted by kidney
- no dose alternation of anticholinesterase is required when antagnoizing NMB in patients with reduced renal function
19
Q
Sugammadex use in ESRD?
A
- 75% of dose is eliminated through the urine
- Clearance approaches GFR
- With substantial renal impairment, clearance of sugammadex/rocuronium complex was decreased and elimination ½ life was increased
- reversal of NMB by sugammadex is still as timely and effective in these patients as in healthy controls
- Dialysis is inconstant in removing suggammadex
- Do not use if creatinine clearance < 30 ml/hr
20
Q
Propofol use in renal disorders?
A
- Clearance exceeds hepatic blood flow (extra hepatic sites)
- undergoes extensive rapid hepatic biotransformation to inactive metabolites which are renally excreted
- Metabolites excreted in urine
- Renal dysfunction does not alter clearance
- no prolongation of effects of propofol in renal dysfunction
- NO change in dosing
21
Q
Precedex use in renal failure?
A
- Sedation and anxiolysis
- Extensive hepatic metabolism (methyl and glucuronide)
- Extensive renal excretion of metabolites
- Reduce dosage in patients with renal insufficiency
- longer lasting sedative effect in subjects with renal impairment
- most likely explanation is decreased protein binding of preceded in patients with renal dysfunction
22
Q
Midazolam use in renal dysfunction?
A
- Elimination ½ time, Vd, and clearance not altered
- NO change in bolus dosing; may need to decrease infusion
- use cautiously in renal impairment
- Metabolite: 1-hydroxymidazolam is about ½ as potent as midazolam
- Rapidly conjugated to 1-hydroxymidazolam glucuronide (60-80%) and cleared by kidney
- May accumulate in kidney failure
- benzos as a group are highly protein bound. CKD increases free fraction of benzos in plasma due to low protein.
23
Q
What is acute kidney injury? characterization? occurence? causes?
what does preop AKI increase?
A
- Characterized by:
- Deterioration of renal function- hours to days
- Failure to excrete waste products
- Failure to maintain fluid & electrolyte homeostasis
- Occurs:
- All hospitalized - 5%
- Critically ill – 8 - 10%
- Postoperative AKI
- General – 1%
- Cardiothoracic & vascular - 30%
- The causes of AKI are classically divided into
- prerenal,- results from hemodynamic or endocrine factors that impair renal perfusion
- intrarenal (or intrinsic), and
- postrenal- from urinary tract obstruction
- Preoperative AKI increases:
- hospitalization,
- mortality, and
- morbidity
24
Q
DIagnosis/Classficiation of AKI?
A
- Classifications:
- RIFLE criteria (Risk- Injury-Failure-Loss-End-Stage)
- Acute Kidney Injury Network
- Kidney Disease: Improving Global Outcomes (KDIGO)
- combines both RIFLE and AKIN criteria
- Based on
- Increase of serum creatinine of 0.3 mg/dL over 48 hours
- Increase of serum creatinine > 50% over 7 days
- Acute drop of UOP to < 0.5 mL/kg/hr for > 6 hours
- Anuria < 100 ml/day – sign of severe injury
-
Increased appreciation for AKI since development of KDIGO criteria.
- Even mild changes in kidney function seem to be associated with short and longterm adverse outcomes
25
Q
Various etiologies of AKI?
A
- Prerenal- hypoperfusion
-
from stoelting 22.4
- hemorrhage
- GI fluid loss
- trauma
- surgery
- burn
- cardiogenic shock
- sepsis
- hepatic failure
- aortic/renal artery clamping
- thromboembolism
-
from stoelting 22.4
- Intrarenal (intrinsic)- underlying renal causes, ischemia, nephrotoxins
-
ATN most common @75%
- ischemia, nephrotoxic drugs, solvent,s heavy metals, contrast dye
- acute glomerulonephritis
- vasculitis
- interstitial nephritis
-
ATN most common @75%
- Postrenal- urinary collecting system obstruction
- nephrolithisasis
- BPH
- Clot retention
- bladder carcinoma
26
Q
Risk factors for AKI development perioperatively?
Iatrogenic risk factors?
A
Risk Factors for Perioperative Renal Failure (Stoelting’s 22.6)
- Pre-existing renal dx
- Advanced age
- CHF
- PVD
- DM
- Emergency surgery
- Major surgery (aortic aneurysm repair)
- cardiac, vascular, major abdominal surgery at increased risk for renal dysfuntion
Iatrogenic Risk Factors
- Inadequate fluid replacement
- Hypotension
- Delayed treatment of sepsis
- Nephrotoxic drugs
27
Q
Neuro and Cardiac AKI Complications?
A
Neurologic:
- confusion,
- asterixis,
- somnolence,
- seizures,
- polyneuropathy r/t build up of protein & amino acids
- autonomic and peripheral neuropathies
Cardio:
- systemic HTN,
- RAAS activation lead to HTN
- CHF,
- increased cardiac demand r/t anemia and HTN makes CKD patients prone to congestive heart failure
- pulmonary edema r/t sodium & water retention;
- increased permeability of alveolar-capillary membrane predispose to pulmonary edema
- dysrhythmias,
- due to deposition of Ca in conduction system
- uremic pericarditis
- may present with CP, cardiac tamponade or may be asymptomatic
- accelerated CAD and PVD
- CO _increases_ in kidney failure to maintain oxygen delivery due to decreased blood-oxygen carrying capacity
28
Q
Hematologic complications of AKI?
A
- anemia
- Almost always present when CrCl <30 mL/min
-
Generally 6-8 g/dL due to decreased erythropoietin
- difficult to maintain >9 even with transfusions
- coagulopathy
- HCT 20-30% common d/t hemodilution & decreased erythropoietin
- increased risk of bleeding d/t uremia-induced platelet dysfunction
- decreased Plt Factor III as well as decreased PLT adhesiveness and aggregation
-
wbc function impaired
- susceptible to infections
29
Q
Metabolic complications of AKI?
A
- metabolic acidosis
- failure to excrete nonvolatile acids produce increased anion gap metabolic acidosis
- hyperkalemia
- potentially lethal consequence
- occurs in pt with CrCl <5 mL/min but also develops rapidly in patients with higher clearances in setting of large potassium loads (trauma, hemolysis, infection, K administration)
- hyperphosphatemia
- hypocalcemia
- r/t resistance of PTH
- decreased intestinal absorption Ca and hyperphosphatemia-associated calcium deposition into bone
- symptoms hypocalcemia rarely develop unless pt is alkalotic
- hypoalbuminemia
- d/t anorexia, protein restriction, dialysis
- hypermagnesemia
- usually mild
- hyperuricemia
- Hyponatremia
- d/t water and sodium retnetion
30
Q
GI effects of AKI complications?
A
- anorexia
- N & V
- ileus
- gastroparesis
- secondary to kidney-disease associated autnomic neuropathy may predispose to perioperative aspiration
- GI bleeding
- hypersecretion gastric acid leads to peptic ulceration and GI hemorrhage in 10-30% patients
- increased incidence hep B and C- associated with hepatic dysfunction
45
Q
Where do carbonic anydrase inhibitors work?
A
Proximal convoluted tubule
ex- acetazolamide
- Carbonic anhydrase inhibitors are drugs that inhibit carbonic anhydrase
- net effect of these agents is of Na and HCO3, which would otherwise have been reabsorbed, remain in urine and results in alkaline diuresis
- patient may develop metabolic acidsois when taking these
- compensatory process in tubules accommodate effects of carbonic anhydrase inhibitors, so their long-term use rarely causes a problem
- useful agents in contraction alkalosis from aggressive diuresis with loop diuretics
- Can reduce CO2 and improve PaO2 with little accompanying change in pH
-
Uses:
- morning sickness
- open-angle glaucoma
- increase respiratory drive in patients with central sleep apnea
46
Q
Where do osmotic diuretics work?
USES? SE?
A
Proximal convoluted tubule
ex mannitol
- mannitol is freely filtered at glomerulus, but poorly reabsorbed by renal tubule
- causes osmotic diuresis
- water-permeable segments of proximal tubule and loop of henle, fluid reabsorption occurs and filtered mannitol is concentrated
- eventually, oncotic pressure in tubular fluid resists further fluid reabsorption
- mannitol draws water from cells into plasma and increases RBF
- USES:
- Increase ICP
- AKI prophylaxis in kidney transplantation
- no evidence to support mannitol is effective for prevention or treatment of AKI nepropathy outside of kidney transplant
-
SE**
- hypochloremia
- intracellular increase K and H
- circulatory overload with hemodilution and pulmonary edema
- hyperkalemic metabolic acidosis
- CNS depression
- severe hyponatremia requiring hemodialysis
47
Q
What are loop diuretics?
A
work on thick ascending limb of Henle loop
- Ex- furosemide, bumetanide, torsemide
- inhibits electroneutral transporter, preventing salt reabsorption from occurring
- allow large salt load to pass to distal convoluted tubule
- first line therapy for treatment of acute decompensated CHF
52
Q
What are distal (collecting duct) acting diuretics? eXAMPLES?
MOA?
A
- K-sparing diuretics and competitive aldosterone antagonists
- Ex- spironolactone, eplerenone
- usually, mineralocorticoid hormone, aldosterone, is released by body in response to angiotensin II or hyperkalemia
- aldosterone stimulates Na reabsortpiona nd K excretion in collecting duct
- inhibition of aldosterone causes mild natriuresis and K retention
- aldosterone stimulates Na reabsortpiona nd K excretion in collecting duct
- Use
- primarily for K sparing diuresis (in pt with volume overload receiving digitalis or hypokalemic alkalosis)
- treatment of secondary hyperaldosteronism
- ie cirrhosis, ascites
