Renal Flashcards
What percentage of CO do kidneys receive?
20-25%
Autoregulation occurs with MAP between…
…50-150 mmHg
Kidney Responsibilities
- Water conservation
- Electrolyte homeostasis
- Acid-base balance
- Neurohumoral/ hormonal functions
- Waste filtration
Precursors to Renal Disease
- DM
- HTN
- Family history
- > 65 y/o
Of the blood that the kidneys receive for CO, where is the majority of it directed?
Outer Cortex
What is Glomerular Filtration Rate (GFR)?
Measurement of volume filtered through glomerular capillaries and into Bowman’s capsule per unit of time
What is the best measure of renal function?
GFR
What do we (mostly) use for GFR measurements?
- Creatinine clearance (most practical & inexpensive)
- Direct measurement of clearance: Creatinine and Inulin
Normal GFR
90 to 140 mL/min/1.73m2
GFR varies with…
- gender
- body weight
- age
GFR decreases…
…1% per year after age 20 (10% per decade after 30)
When the GFR decreases to ______, we start to see clinical manifestations.
GFR < 15 mL/min/1.73m2
% of normal kidney function: Stage 1
90% or more
% of normal kidney function: Stage 2
60-89%
% of normal kidney function: Stage 3
30-59%
% of normal kidney function: Stage 4
15-29%
% of normal kidney function: Stage 5
< 15%
Creatinine Clearance
- Most reliable measure for clinically assessing overall kidney function (GFR)
- Endogenous marker of renal filtration
- Produced at constant rate
- Freely filtered- not reabsorbed**
- Normal = 110-150 mL/min
Most reliable measure for clinically assessing overall kidney function (GFR)?
Creatinine Clearance
Serum Creatinine
- Creatinine is product of muscle metabolism
- Serum creatinine directly r/t body muscle mass
- Can be used to reliably estimate GFR in non-critically ill patient
- rate of creatinine production and its Vd can be abnormal in critcally ill pts
- 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 ↓ from 100 mL/min to 10 mL/min, serum creatinine values do not ↑ for ~ 1 wk
Blood Urea Nitrogen (BUN)
- Directly r/t protein catabolism, inversely r/t GFR
- Sometimes used, but not ideal
- Results potentially misleading d/t:
- Dietary intake (high or low protein)
- Co-existing disease (GI bleeding, febrile illness)
- Intravascular fluid volume (dehydration)
- Can see increase in BUN despite normal GFR in situations above
- Normal = 10-20 mg/dL
- Despite extraneous variables: BUN > 50 mg/dL usually reflect ↓GFR/ impaired renal function
- BUN not elevated in kidney dz until GFR ↓to almost 75% of normal
Renal tubular dysfunction
Kidneys do not produce appropriately concentrated urine in presence of a physiologic stimulus for release of ADH
Renal Tubular Function and Integrity: Concentration
- Assessed by measuring urine concentrating ability
- Urine specific gravity > 1.018 = renal tubules adequately able to concentrate urine
Renal Tubular Function and Integrity: Protein
- Presence of protein may reflect renal tubule damage–why we use this as a measure of renal tubular function
-
Proteinuria- relatively common (5%-10% of adults)
- Transient: associated w/ fever, CHF, seizures, pancreatitis, exercise
- Persistent: generally implies renal dz
Patients without renal disease can excrete up to ______ mg of protein per day (greater amounts may be present with exercise).
150 mg
What amount of protein in the urine is considered abnormal and indicative of servere glomerular damage?
> 750 mg/day
Renal Tubular Function and Integrity:
Fractional Excretion of Sodium (FENA)
- Measure of percentage of filtered Na+ excreted in urine
- Useful to distinguish hypovolemia and renal injury (differentiate b/t prerenal and renal causes of azotemia)
- FENA > 2% (or urine Na+ concentration > 40 mEq/L) reflects ↓ ability of renal tubules to conserve Na+ and is consistent w/ tubular dysfunction
- FENA < 1% (or urine Na+ excretion < 20 mEq/L) occurs when normally functioning tubules are conserving Na+ and is suggestive of prerenal azotemia
Renal Tubular Function and Integrity: Urinalysis
- Useful for renal tubular dysfunction and urinary tract disease
- Detects presence of:
- Protein
- Glucose
- Acetoacetate
- Blood
- Leukocytes
- Urine pH & solute concentrations (specific gravity) determined
- Microscopy used to identify cells, casts, microorganisms, crystals
Microhematuria found in U/A may reflect what?
- Glomerulonephritis
- Renal calculi
- CA of the GU tract
RBC casts found in U/A may reflect what?
Acute glomerulonephritis
WBC casts found in U/A may reflect what?
Pyelonephritis
Acute Kidney Injury (AKI) is characterized by…
- Deterioration of renal function- hrs to days
- Failure to excrete waste products
- Failure to maintain fluid & electrolyte homeostasis
Diagnosis of AKI
- Increase in serum creatinine > 0.3 mg/ dL in 48 hrs or > 50% increase over 7 days
- Acute drop in urine: < 0.5 mL/kg/h for > 6 hrs (oliguria)
- Severe injury: UO < 100 mL/day
- Diagnostic biomarkers & urinalysis
S&S of AKI
- Generalized malaise
- Fluid overload
- dyspnea
- edema
- HTN
- Nausea
- Confusion
- Hematuria
- ** Caution: encephalopathy, coma, seizures, death
AKI Definition: Society of Thoracic Surgeons
new dialysis
OR
rise in serum creatinine >2 mg/dL,
50% increase in serum creatinine
AKI Definition: The Acute Dialysis Quality Initiative Group
Creatinine rise of:
50% as “risk”
100% “injury”
200% “failure”
(RIFLE criteria)
AKI Definition: Acute Kidney Injury Network
1.5X or 0.3 mg/dL creatinine rise w/in 48-hr period
OR
> 6hrs of oliguria (modified RIFLE)
AKI Definition:
Kidney Disease Improving Global Outcomes
(KDIGO)
↑ in serum creat at least 0.3 mg/dL w/in 48 hrs
OR
↑ in serum creat 1.5X baseline w/in prior 7 days
OR
UOP < 0.5 mL/kg/h X 6 hrs
KDIGO definiton of AKI
Creatinine Criteria
Stage 1
Cr 1.5-1.9X baseline
OR
Cr increase >0.3 mg/dL
KDIGO definiton of AKI
Creatinine Criteria
Stage 2
Cr 2-2.9X baseline
KDIGO definiton of AKI
Creatinine Criteria
Stage 3
Cr > 3X baseline
OR
Cr > 4 mg/dL
OR
Initiation of Dialysis
KDIGO definiton of AKI
Urine Output Criteria
Stage 1
< 0.5 mL/kg/hr X 6-12 hrs
KDIGO definiton of AKI
Urine Output Criteria
Stage 2
< 0.5 mL/kg/hr for > 12 hrs
KDIGO definiton of AKI
Urine Output Criteria
Stage 3
< 0.3 mL/kg/hr for > 24 hrs
OR
Anuria > 12 hrs
AKI Etiology
- 5%-7% of hospitalized patients
- Associated w/ other systemic disease/ clinical conditions/ drugs/ interventional therapy
AKI Causes: Prerenal
Hypoperfusion
Hemorrhage, GI fluid loss, Trauma, Surgery, Burns, Cardiogenic shock, Sepsis, Hepatic failure, Aortic or renal artery clamping, Thromboembolism
AKI Causes: Intrarenal (intrinsic)
Underlying renal causes
Ischemia
Nephrotoxins
Acute glomerulonephritis, Vasculitis, Interstitial nephritis (drug allergy, infiltrative diseases), Acute tubular necrosis, Ischemia, Nephrotoxic drugs (aminoglycosides, nonsteroidal anti-inflammatory drugs), Solvents (carbon tetrachloride, ethylene glycol), Heavy metals (mercury, cisplatin), Radiographic contrast dyes, Myoglobinuria, Intratubular crystals (uric acid, oxalate)
AKI Causes: Postrenal
- Urinary collecting system obstruction
- Nephrolithiasis, BPH, Clot retention, Bladder CA*
Azotemia Definition
Condition marked by abnormally high serum concentrations of nitrogen-containing compounds such as BUN & creatinine and is hallmark of AKI, regardless of cause.
Prerenal Azotemia
- ½ of hospital-acquired cases
- Pre-existing CHF, liver dysfunction, septic shock
- Reduced RBF d/t ↓ in PP
- Hypovolemia & blood loss
- Rapidly reversible if underlying cause treated
- Untreated: = ischemia-induced acute tubular necrosis
- Elderly susceptible: hypovolemia/ renovascular disease
- Assess volume status, hemodynamics, drug therapy
- Blood and urine specimens (Refer to Stoelting’s 22.5)
What is the hallmark of AKI?
Azotemia
Intrinsic Azotemia
- Categorized according to site of injury
- Glomerulus
- Renal tubules- ischemia or nephrotoxins
- Interstitium
- Renal vasculature
- Ischemic AKI typically reversible, but…
- Irreversible cortical necrosis occurs if severe or prolonged ischemia
- Reperfusion: influx of inflammatory cells/ cytokines/ oxygen free radicals
Postrenal Azotemia
- Urinary outflow tracts are obstructed (prostatic hyperplasia, prostate/cervical CA)
- May occur at any level of collecting system
- Recovery inversely r/t duration of obstruction
- Treatment: percutaneous nephrostomy
Risk Factors for Periop Renal Failure
- Pre-existing renal dx
- Advanced age
- CHF
- PVD
- DM
- Emergency surgery
- Major surgery (aortic aneurysm repair)
Iatrogenic Risk Factors for Periop Renal Failure
- Inadequate fluid replacement
- Hypotension
- Delayed treatment of sepsis
- Nephrotoxic drugs
Complications of AKI: Neuro
- Confusion
- Somnolence
- Asterixis
- Seizures
- Polyneuropathy r/t build up of protein & amino acids
Complications of AKI: CV
- Systemic HTN
- CHF
- Pulmonary edema r/t Na+ & H2O retention
- Dysrhythmias
-
Uremic pericarditis
- may be asymptomatic or have chest pain and cardiac tamponade
- LVH
- Inc CO
- accelerated CAD, PVD
Complications of AKI: Heme
- Anemia (when creat. clearance falls below 30 mL/min)
- Coagulopathy
- Hct 20-30% common d/t hemodilution & ↓ erythropoietin
- ↑ r/f bleeding d/t uremia-induced platelet dysfunction
- decreased platelet aggregation and adhesiveness
Complications of AKI: Metabolic
- Hyperkalemia and metabolic acidosis
- Hyperphos & hypocalc
- Hypoalbuminemia
Complications of AKI: GI
- Anorexia, N/V
- Ileus
- Gastroparesis
- GI bleeding
Complications of AKI: Infection
- Respiratory & urinary tracts and sites where breaks in normal anatomic barriers have occurred
- Impaired immune response– white cell function are impaired in pts w/ kidney failure
Management of AKI
- No specific treatment modalities
- Treatment aims:
- Limit further injury
- Correct fluid/electrolyte/acid-base derangements
- Reverse underlying causes of injury (hypovolemia, hypotension, low CO, sepsis)
- Maintain MAP > 65 or (no evidence supporting outcomes w/ supraphysiologic values)
- Fluid resuscitation (goal-directed therapy) & vasopressor therapy (norepi/vasopressin)
- Diuretics not advised
- Alkalinization of urine w/ sodium bicarb (rhabdo); reduces incidence of contrast-induced nephropathy
- Dialysis- mainstay for severe AKI
Indications for Dialysis in Management of AKI
Dialysis- mainstay for severe AKI:
- Volume overload
- Hyperkalemia
- Severe metabolic acidosis
- Symptomatic uremia
- Overdose w/ dialyzable drug – day of surgery/ day before
AKI Prognosis
- Hospital acquired AKI is poor
- Mortality > 20%
- Dialysis- mortality rates > 50%
- Full recovery from AKI- 15%
- Retain a degree of stable renal insufficiency- 5%
- Continued deterioration throughout life- 5%
AKI Management of Anesthesia/Principles that guide anesthetic management
- High M&M
- Only life-saving surgery
- Principles that guide anesthetic management:
- Maintain adequate systemic BP & CO
- Avoid further renal insults – hypovolemia, hypoxia, nephrotoxins
- Invasive hemodynamic monitoring – ABGs & Lytes
- Consider initiation of post-op dialysis if in stable condition
- Caution w/ diuretics
Chronic Kidney Disease: Defined
Estimated GFR <60 mL/min/1.73m2 for 3 months or more
In the US, what is responsible for CKD?
DM & HTN responsible for 2/3 of all cases
(also glomerulonephritis, polycystic kidney disease)
Clinical manifestations of CKD are due to:
- Inability to:
- Excrete waste
- Regulate fluid and electrolyte balance
- Secrete hormones
CKD Incidence and Etiology
- •U.S. Renal Data System of the NIH (2012)-
- 636,000 individuals with ESRD
- Prevalence continues- aging population/ increased survival
- Incidence varies by race & ethnicity (African American, Native Americans, Hispanics)
- Genetic variables + disparities in healthcare access
Diagnosis of CKD
- Diverse signs, non-specific complaints (fatigue, malaise, anorexia)
- Diagnosis made during routine testing
Serum creatinine level &
urinary sediment analysis
Progression of CKD:
Intrarenal hemodynamic changes likely responsible.
- Glomerular HTN
- Glomerular hyperfiltration & permeability changes
- Glomerulosclerosis
Progression of CKD:
Management
- Reduce systemic & glomerular HTN:
- ACEI’s & ARBs
- Moderate protein restriction
- Control BG
- Hyperlipidemia - statin therapy advised
- Smoking cessation
Adaptation
- Patients w/ CKD remain relatively asymptomatic until RF is < 10% of normal
- 3 stages of adaptation:
- GFR ↓ w/ ↑ in creat & urea
- Serum K ↑ (normal until GFR approaches 10% of normal)
- Na+ homeostasis and regulation of ECF (volume overload/ volume depletion)
Describe the balance of Na+ in CKD
Sodium balance remains fairly intact, but the system can be overwhelmed by abrupt increases or decreases in sodium intake.
Increase Na+ intake = volume overload
Decrease Na+ intake = volume depletion
What is uremic syndrome?
- Inability to excrete uremic toxins, secrete, regulate
- BUN useful clinical indicator of severity & response to therapy
- Serum creatinine poor clinical indicator
S&S of uremic syndrome
- N/V, Anorexia
- Pruritus
- Anemia, Fatigue
- Coagulopathy
Treatment of uremic syndrome
dietary protein restriction + dialysis
Describe renal osteodystrophy
- Secondary hyperparathyroidism & ↓ Vit D production – impairs intestinal absorption of Ca
- Hypocalcemia stimulates PTH secretion – leads to bone resorption to restore serum Ca concentrations
- As GFR ↓, phosphate clearance ↓ = ↑ serum phosphate/ ↓ Ca
Renal osteodystrophy treatment
- Restrict dietary phosphate
- oral Ca and Vit D supplements
-
antacids to bind phos in GI tract (avoid mag & aluminum)
- If medical therapies fail- subtotal parathyroidectomy
-
antacids to bind phos in GI tract (avoid mag & aluminum)
CKD Complications: Anemia
- Likely responsible for symptoms of fatigue, weakness, low exercise tolerance
- Normochromic & normocytic d/t decreased erythropoietin
- Excess parathyroid hormone (by replacing bone marrow with fibrous tissue)
Anemia Treatment
- Erythropoietin or darbepoetin
- Avoid blood transfusions
- Iron
CKD Complications: Uremic Bleeding
- ↑ tendency to bleed & persistent anemia (despite normal platelet count and normal PT/PTT)
- Bleeding time: best correlates w/ tendency to bleed
- Hemorrhagic episodes: significant source of morbidity
Treatment for uremic bleeding
- Desmopressin: ↑ factor 8-vWF complex (present w/in 2-4 hrs & lasts 6-8 hrs)
- Conjugated estrogens (onset approx. 6 hrs & lasts 14-21 days)
- Erythropoietin: enhances platelet aggregation & ↑ platelet counts
CKD: Neurologic Changes
- Initial symptoms may be mild
- impaired abstract thinking, insomnia, irritability
- As dz progresses- significant changes:
- seizures, obtundations, uremic encephalopathy, coma
- Advanced RF:
- BLE symmetric mixed motor and sensory polyneuropathy & weakness
CKD: Neurologic Changes Treatment
HD may be helpful
CKD: CV Changes
-
Systemic HTN- contributes to CHF, CAD, CVD
- Uncontrolled HTN speeds dz progression
- Pathogenesis- retention of Na & water + RAAS activation = intravascular volume expansion
- Dyslipidemias
- Silent MI
- Uremic pericarditis
CKD: CV Changes Treatment
- Dialysis- d/t hypervolemia & uremic pericarditis
- Increase dosage of antihypertensives
- Tamponade- prompt drainage of effusion
Management of CKD
- BP control: ACEI & ARBs (1st line), diuretics, Ca channel blockers, aldosterone antagonists
-
Nutrition
- Protein restriction (0.6 g/kg/day)
- Phos restriction 600–800 mg/ day
- Sodium restriction (< 1500-2000 mg/day)
- Advanced dz- alkali salts
- Vitamin D
- Long-term: euglycemia
-
Anemia: Benefits vs risks
- Erythropoietin (target Hb range 10-11.5 g/ dL)
-
Renal Replacement Therapy
- Advised when GFR 10 mL/min/1.73 m2
- Effective dialysis = greater survival
Management of Anesthesia: Pre-op
-
Preop Eval
- Renal function stable? –trends in serum creat.
- Blood volume status before & after dialysis
- VS
- BG management
- BP (ACE-I and ARBs often withheld day of surgery)
- Serum K should not exceed 5.5 mEq/ L day of surgery
- Anemia
- Coagulopathy
- Gastric aspiration prophylaxis (dose adjustment)
- Dialysis w/in 24 hrs preceding elective surgery
Management of Anesthesia: Induction
- Safe w/ most IV induction drugs – concern is accumulation of active metabolites
- ESRD pts- respond as if they are hypovolemic
- Uremia & antihypertensives – result in hypotension
- Attenuated SNS activity impairs compensatory peripheral vasoconstriction (exaggerated hypotension)
- Exaggerated CNS effects – uremia induced
- May induce w/ succinylcholine if K is <5.5
Management of Anesthesia: Maintenance
- Balanced approach – VA’s or TIVA, MR’s, opioids
- VA’s: good control of HTN & decrease dose of MR’s, but depress CO
- Sevo sometimes avoided (fluoride nephrotoxicity/ compound A), but no evidence of increased risk
-
Muscle relaxants – slow excretion of vec, roc/cisatra independent of renal function
- ↓ initial dose and base subsequent doses on TOF
-
Opioids:
- morphine & meperidine –> morphine-6-glucoronide & normeperidine (neurotoxic compounds) that rely on renal clearance. Hydromorphone active metabolite (hydromorphone-3-glucoronide) may accumulate in CKD.
Management of Anesthesia: Maintenance
Fluid Management & UOP
- May benefit from preop hydration (500 mL) if…
- Do not require HD or W/out renal dz undergoing surgery w/ high incidence of post-op RF
- Caution – LR or K-containing fluids
- UOP – 0.5 mL/kg/h
- Diuretics not advised in absence of fluid replacement
- HD dependent – narrow margin of safety
Management of Anesthesia: Maintenance
Monitoring
Monitoring
-
Avoid:
- Venipuncture in nondominant arm & upper part of dominant arm
- Radial and ulnar cannulation (same may be said of brachial and axillary)
-
Considerations:
- Femoral cannulation: r/f infection
- DP or PT arteries: inconvenient/difficult to access
- Arterial pressure & ABG will not be accurate if on same extremity as AV fistula
- Venous pressure monitoring: may be helpful, CVC access may be difficult
- TEE
- Dialysis catheters may be used. Use aseptic techniqu, aspirate heparin, heparin after d/c of use
Management of Anesthesia: Maintenance
Associated Concerns
- Positioning – prone to bruising, sloughing/ protect vulnerable nerves
-
Protect fistulas
- NO BP cuff on arm w/ fistula
- If possible, maintain intra-op access to arm w/ fistula
Management of Anesthesia: Maintenance
Regional Anesthesia
Regional Anesthesia
- Neuraxial may be considered
- Considerations:
- Sympathetic block T4-T10- may improve renal function vs platelet dysfunction, residual heparin, Must maintain adequate intravascular fluid volume
- Brachial plexus block – assess for presence of uremic neuropathies
- Metabolic acidosis - may decrease seizure threshold in response to LAs
Management of Anesthesia: Maintenance–
Reversal
- Reversal – Renal excretion 50% of clearance of neostigmine, prolonged effect
- “Recurarization” is unlikely
- Sugammadex: not recommended in low creatinine clearance (< 30 mL/min) or RRT
Management of Anesthesia: Post-op
- Skeletal muscle weakness: from residual neuromuscular blockade or… antibiotics, acidosis, electrolyte imbalance
- Caution w/ parenteral opioids – respiratory depression
- Avoid NSAIDs
- Continuous ECG monitoring
- Supplemental O2
- Check electrolytes, BUN/creat, HCT
- Bleeding- uremic coagulopathy
Renal Transplantation
- Reserved for pts w/ ESRD on long-term RRT
- Common causes of ESRD:
- Systemic HTN
- DM
- Glomerulonephritis
- Cadaver donor – can be preserved for 48 hrs
- Preop - match HLA antigens and ABO blood groups
- Immunosuppressive therapy instituted
Renal Transplant: Management of Anesthesia
General Anesthesia
- RA and GA successful – GA more common
- Minimize decrease in CO – promote renal perfusion
- High-normal BP is required
- Cisatracurium is often drug of choice
- CVP is useful
- Mannitol (osmotic diuretic)
- Albumin administration is helpful
- Release of vascular clamps – be aware of hypotension & cv arrest
Renal Transplant: Management of Anesthesia
Regional Anesthesia
- Advantages – No ETT & muscle relaxants
- Advantage negated if need to supplement RA with IV anesthetics
- BP control may be more difficult
- Controversial in presence of abnormal coagulation
Renal Transplant: Management of Anesthesia
Post-op Complications
- Acute immunologic rejection – almost immediate
- Delayed signs of graft rejection – fever, local tenderness, decreased UOP
- Treatment:
- High dose corticosteroids & antilymphocyte globulin
- Monoclonal antibodies
- Tacrolimus
- Mycophenolate mofetil
- Dialysis may be required
- Opportunistic infections
Renal Transplant: Management of Anesthesia
Anesthesia Considerations (other)
Anesthesia Considerations
- Often elderly
- Co-existing CV dz
- Co-existing DM
- Consider side effects of immunosuppressant drugs
- HTN, low seizure threshold, anemia, thrombocytopenia
- Consider drugs excreted by kidneys
- Avoid drugs that are nephrotoxic or dependent on renal clearance
- Minimize decreases in RBF
Induction agents depend significantly on renal elimination
Phenobarbital
Thiopental
Muscle relaxants that depend significantly on renal elimination
Gallamine
Metocurine
Pancuronium
Vecuronium
Cholinesterase inhibitors that depend significantly on renal elimination
Edrophonium
Neostigmine
Cardiovascular drugs that depend significantly on renal elimination
Atropine
Digoxin
Glycopyrrolate
Hydralazine
Milrinone
Antimicrobials that depend significantly on renal elimination
Aminoglycosides
Cephalosporins
Penicillins
Sulfonamides
Vancomycin
Analgesics that depend significantly on renal elimination
Codeine
Meperidine
Morphine
Target Hb range for CKD
10-11.5 g/dL