lecture 9: Renal Flashcards
pathophysiology review
Protein metabolism results in ATP and NH3 (ammonia) -> Liver processes ammonia into Urea -> travels to the kidneys for urinary excretion -> BUN result from PROTEIN metabolism, Cr result from MUSCLE breakdown
BUN: 7-20
Cr: 0.6-1.2
Extra-Renal Causes of Increases in BUN (5)
Catabolic states
Steroids
Burns
Tetracycline abx
Low flow states
Extra-Renal Causes of Increases in Creatinine (2)
Increased Muscle mass
Increased Muscle breakdown
Extra-Renal Causes of Decreases in BUN (1)
Liver failure
- Can no longer turn ammonia into BUN
Extra-Renal Causes of Decreases in Creatinine (1)
Decreased muscle mass
Acute Kidney Injury (AKI)
- AKI occurs in up to ___ to ___ of hospitalized patients and in up to ___ of ICU patients.
- Mortality rate between ___-___% patients treated with _______ ________ _______.
- Greater than ____% survivors of severe AKI are _______ of dialysis by discharge.
- what is the hallmark sign of AKI? term? what is sometimes considered a better marker d/t being relatively unaffected by metabolic factors?
- AKI occurs in up to 15% to 18% of hospitalized patients and in up to 66% of ICU patients.
- Mortality rate between 50% and 60% patients treated with renal replacement therapy (RRT)
- Greater than 80% survivors of severe AKI are independent of dialysis by discharge.
- Hallmark decrease GFR and accumulation of BUN and serum creatinine
—- Termed “azotemia” (means high levels of nitrogenous compounds)
—- Serum creatinine is sometimes considered a better marker because relatively unaffected by metabolic factors
Acute Kidney Injury definition (3)
Increase in Serum Creatinine of >0.3mg/dl within 48 hours
Increase serum creatinine of >1.5 mg/dL times baseline in 7 days
Urine volume <0.5mL/kg/hr for >6hr
RIFLE Classification: Grades AKI
Risk (>1.5mg/dL Cr)
Injury (>2mg/dL Cr)
Failure (>3mg/dL Cr)
Loss (persistent AKF>4weeks)
End-stage kidney disease
Urine Output Patterns (3)
what is this NOT?
Oliguria (< 400 mL/d)
Nonoliguria (> 400 mL/d)
Anuria (< 100 mL/d)
NOT Diagnostic criteria
Pre-Renal Kidney injury (2)
- Changes in the blood flow to the kidney
- Evidence of preserved tubular function
Causes of Prerenal AKI (2)
Hypo perfusion
Renal artery stenosis (Very rare)
Resulting Pathophysiology of Prerenal AKI
- what?
- drugs that interfere with auto-regulation include? (3)
- what does prerenal AKI change?
Disruption in the Renin–angiotensin–aldosterone cascade
- Drugs that interfere with auto-regulation include:
—–NSAIDs
—–ACE inhibitors, ARBs
- Changes urinary composition and volume follow predictable pattern
Pre-renal Labs (3)
Concentrated urine
FE Ur (Fractional excretion of Urea)
FE Na (Fractional excretion of Sodium)
What does this mean?: The percentage of Na or Urea in the urine as it relates to the concentrations in the blood
Labs changes during Pre-renal Failure
- BUN
- GFR
-BUN/CR
BUN will increase at a higher rate than Creatinine
This indicates a low glomerular filtration rate
Both BUN and Creatinine will not filter out as quickly a result of decreased GFR
BUN, however, once filtered out, will be reabsorbed back into the blood in low flow states
This results in a higher BUN:Cr ratio
- Normal may be 15:1
- May increase to 30:1. (ie. BUN is 60, Creatinine is 4)
Intrarenal AKI (4) catergorized according to?
Categorized according to anatomical compartment:
- Glomerular
- Vascular
- Interstitial
- Tubular*
Glomerular (2)
Acute glomerulonephritis
Immune complex–mediated causes
Interstitial (1)
Acute allergic interstitial nephritis
Vascular (2)
- Malignant hypertension
- Microangiopathic processes
Tubular (Acute tubular necrosis in most cases) (2)
- Obstructive or prolonged ischemia
- Drug intoxication
Postrenal AKI
- about ____% of hospital cases
- caused by?
- etiologies include: 3
About 10% hospital cases
Caused by any obstruction in flow of urine from collecting ducts in kidneys to external urethral orifice
Etiologies include
- Ureteral obstruction (ie, stones)
- Urethral blockage (ie, strictures)
- Extrinsic source (ie, tumor)
Pathophysiology: Post-renal AKI (5)
- Congestion causes retrograde pressure.
- Slows tubular fluid flow and lowers GFR
- Increased reabsorption Na+, water, and urea
- Dilated collecting ducts that compress nephrons
- Dysfunction concentrating and diluting mechanism
Acute Tubular Necrosis (2)
what?
____% of AKI cases seen in the ICU
- A type of Intra-renal failure caused by Pre-renal
- 76% of AKI cases seen in the ICU
Diagnosis of AKI: History and Physical
1) history that indicates ______
2) history of any disease that affect ______ ______: (3)
3) _____ status
1) History that indicates hypoperfusion
2) History of any diseases that affect the renal system:
- Renal artery stenosis
- Lupus or vasculitis
- Abdominal tumors
3) Fluid status
ATN phase 1
phase?
onset?
injury ->?
Phase: onset phase
- Onset hours to days (treatment aimed at preventing damage)
- Injury -> signs and symptoms
ATN phase 2
phase:
s/sx (8)
interventions (5)
Phase: ATN
1) Signs and Symptoms
- <400ml/day, low GFR, BUN/Cr, Neuro changes/confusion, itching, fluid retention, metabolic Acidosis
- Electrolyte imbalances, concentrated urine (>1.020)
2) Interventions:
- Limit protein consumption, survey for hyperkalemia, BP monitoring, assess lung sounds
- Dialysis
ATN phase 3
phase:?
s/sx: (5)
interventions: (2)
Phase: Diuretic phase
- lasts 1-3 weeks
1) S/S:
- Slight increase in GFR
- improved MS
- osmotic diuresis (Urine grav <1.020)
- hypotension
- hypokalemia
2) Interventions:
- Track I/O’s
- replace fluid and electrolytes
ATN phase 4
phase:?
s/sx (2)
interventions (2)
Phase: Recovery phase
- several months to a year
1) S/S:
- 1-2L/day urine
- labs normalize
2) Interventions:
- Track I/O’s
- replace fluid and electrolytes
Treatment of AKI (13)
1) correct? (4)
2) treat?
3) what is something to consider between?
4) avoid what types of medications?
5) restrict what in anuric patients?
6) monitor?
7) what type of medication does NOT work?
8) what medication has no influence on the outcome of oliguric AKI
9) know the status of?
10) don’t overload with what?
11) what needs to be done to keep the patient alive?
12) what 2 factors influence survival and recovery?
1) Correct life-threatening problem
- Hypoxemia, hypotension, hyperkalemia, acidosis (malperfusion)
2) Treat underlying cause
3) Fluids vs Diuretics (issues with flow -> CHF -> diuretics)
4) Avoid nephrotoxins- VANCOMYCIN
5) Restrict K+ in anuric patients-
6) I&O, Daily electrolytes and waste products
7) Low dose dopamine doesn’t work
8) Diuretics have no influence on the outcome of oliguric AKI (If it doesn’t work, they won’t respond)
10) Know the volume status- ie. Dry or overloaded?
11) Don’t overload with protein
12) Keep them alive- correct underlying problems
13) Age and co-morbidities influence survival and recover
Common Nephrotoxins
1) _______________ -> what type of medications?
- 10-20% of patients
- onset delayed, 5-10 days after onset treatment
- where do you want to keep the MAP?
2) ________ ________ _________
- may not be as big of a problem as we once thought
- occurs within ___to__ hours and peaks within __to__ days
- ____ _____ patients
- how do you reduce risk of developing it? (4)
Aminoglycosides – Gentamycin, Vancomycin
- 10% to 20% of patients
- Onset delayed, 5 to 10 days after onset treatment
- KEEP MAP 65+
Contrast-induced nephropathy (CIN)
- May not be as big of a problem as we once thought
- Occurs within 24 to 48 hours and peaks within 5 to 7 days
- High-risk patients
- Reduce risk: fluid administration (1L), using low or iso-osmolar nonionic contrast or CO2, N-acetylcysteine (NAC) - mucomist, alkalinize urine - bicarb to help with metabolic acidosis
Contrast Induced Nephropathy (2)
1) Contrast has always been linked to worsening nephropathy
2) Recent studies suggest that this may not be the case
- Studies involved retrospective audit of patients with nephropathy who received IV contrast
- In practice, most still treat contrast as a nephrotoxic agent
Urinary Values (5)
Urine tests helpful in diagnosing etiology
Urine sodium, osmolality, and specific gravity
Fractional excretion of Na+
Fractional excretion urea nitrogen
Sedimentation
Diagnostic Studies (3)
1) Renal ultrasonography
- R/O obstruction
2) CT and MRI
- Evaluate for masses or vascular disorders
3) Renal biopsy
Chronic Kidney Failure
what (2)
leads to? (1)
Slow, progressive, irreversible deterioration of renal function
Kidney’s inability to eliminate waste products and maintain fluid and electrolyte balances
Leads to end-stage renal disease (ESRD)
ESRD (3)
Currently, more than 52,000 dialysis and renal transplant recipients in the United States
24% higher in men than in women
Incidence in African American 3.7 times higher than in white population
CKD Causes
1) two most common?
2) other common causes (5)
Two most common:
1) Diabetes (54%) - mgmt c/ meds
2) Hypertension (33%)
Other common causes include
1) Glomerulonephritis
2) Interstitial nephritis
3) Genetic disorders
4) Hepatorenal syndrome
5) Microangiopathic
Pathophysiology of ESRD (3)
1) common morphological features (3)
2) ______ ______ theory (3)
3) possible mediators include (2)
1) Common morphological features
- Fibrosis
- loss of native renal cells
- infiltration
2) Intact nephron theory
- Hyperfiltration response non-diseased nephrons
- Eventually reach maximal filtration
- May accelerate loss of nephrons
3) Possible mediators include
- Hypoxia
- angiotensin
Proteinuria
1) result of (2)
2) _______ _______ ______ is reabsorbed and stored where?
- causes?
- results in (2)
3) very strong predictor of what?
1) Result of glomerular hypertension and abnormal glomerular permeability
2) Abnormally filtered protein is reabsorbed and stored intracellularly
- Causes production of pro-inflammatory cytokines
- Results in scarring and fibrosis
3) Very strong predictor of chronic kidney disease progression
tip:
- should never have protein (can induce damage to nephron)
- powerlifters -> normal find
Preventing the Progression
1) _______ insults accelerates the loss of?
2) include: (7)
1) Secondary insults accelerate loss of nephrons.
2) Include:
- Hypovolemia
- Nephrotoxic agents
- Urinary obstruction and infections
- NSAIDs
- Hyperglycemia
- Hypertension
- Hyperlipidemia
Management of Renal Failure (3)
1) Manage fluid balance changes
- Treat hypovolemia
- Prevent hypervolemia
2) Use diuretics
- Furosemide, mannitol, thiazide diuretics
3) Dialysis or ultrafiltration
Manage acid–base alterations (2)
- Metabolic acidosis
- IV sodium bicarbonate
Manage cardiovascular alterations (3)
1) Hypertension
- Be aware of risk for Hypotension during dialysis
2) Hyperkalemia
3) Pericarditis
Managing pulmonary alterations (4)
- Pulmonary edema
- Pleural effusions
- pneumonitis
- pulmonary infections
Managing gastrointestinal alterations (4)
- GI bleeding
- Anorexia, nausea and vomiting, diarrhea, GERD
- Stomatitis
- Constipation
Managing neuromuscular alterations (3)
- Sleep disturbances, muscle irritability
- Peripheral neuropathies
- Seizures
Managing hematological alterations (1)
Increased bleeding tendency
Management of alterations in drug elimination (1)
Adjust dosages according to GFR
Management of skeletal alteration includes loss of bone density and formation of calcium phosphate crystals (4)
- Regulate phosphate.
- Maintain calcium levels.
- Treat vitamin D deficiency.
- Control metabolic acidosis.
Managing of integumentary alterations include dryness, pruritus, uremic frost, ecchymosis, and purpura (2)
- Meticulous skin care
- Prevent skin breakdown
Managing alterations in dietary intake (2)
- Restrict fluid, sodium, potassium, and phosphate
- High calorie, moderate protein restrictions
Managing alterations in psychosocial functioning
?
ECG Changes in Hyper-kalemia (3)
1) Peaked T-waves, prolonged PR interval, depressed ST segment
2) Lost P-waves
3) Widened QRS complex
Anemia in ESRD
1) causes include: (4)
2) mgmt: (2)
Causes include:
- Erythropoietin deficiency
- Decreased RBC survival time
- Blood loss
- Other
Management:
- Administer iron and human erythropoietin.
- Blood products
CAPD- Continuous Ambulatory Peritoneal Dialysis
pros: 3
cons: 2
Pro’s
Ambulatory
Can be done while sleeping
Gentle relative to HD
Con’s
Risk of infection*
Requires high level of adherence
AKI Management during hemodynamic instability via Continuous Renal Replacement Therapy
1) NEVER?
2) after ESRD reaches stage ____ -> what occurs?
- avoid ______
- administer?
1) NEVER draw blood or take blood pressures on a limb with a graft/fistula
2) *After ESRD reaches stage 3- Vein preservation strategies should be employed
- Avoid subclavian veins
- Administer IV medications appropriately
Continuous Renal Replacement Therapy - CRRT
1) requires?
2) what is the process?
3) provides _____ ______ at a rate around ? -> removes more ______ + more gentle if?
- slower rates allow?
4) how long does each cartridge last for?
5) removes more _____ than?
1) Requires “leur lock” dialysis access catheter (Quinton/groin or Permacath/subclavian)
2) Uses Diffusion to remove solute
- Solutes move across a semipermeable membrane
3) Provides continuous dialysis at a rate around 150ml/min -> removes more solute + more gentle if hemodynamically unstable
- Slower rate allows more control over fluid volume
4) Each cartridge lasts 48 hours
5) Removes more solute than conventional dialysis
