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73 Cards in this Set

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Azotemia
containing containing
compounds, such as urea, creatinine, various compounds, such as urea, creatinine, various
body waste compounds, and other nitrogen body waste compounds, and other nitrogen rich compounds in the blood related to rich compounds in the blood related to
insufficient filtering of blood by the kidneys insufficient filtering of blood by the kidneys
Uremia
Nitrogenous wastes + symptoms (Nausea, vomitting,disorientation, seizure, coma, death)
Epidemology of Acute Renal Failure (ARF)
Prevalence
– Healthy population - Very low ~ 0.02%
– Hospitalized patient - ~7%
– Chronic kidney disease - Increased risk ~ 13%
– Critically ill patients - Up to 23%
Mortality
– 35 - 80% in hospitalized patients
ARF is an independent risk factor for death
Acute Renal Failure Outcomes
90% of individuals who survive recover enough renal function to live normal lives
50% of them are left with some deficits
5% do not recover renal function and require renal replacement therapy or transplantation
5% have progressive deterioration after initial recovery
Risk factors for Acute renal failure
Dehydration
Pharmacologic agents
Contrast media
Nephrotoxic drugs
Chemotherapy, NSAIDs, ACE-I, ARBs, Antimicrobials
> 60 yo
Male
Acute infection
Heart failure
Respiratory failure
Trauma
Rhabdomyolysis
Blood vessel thrombosis
Acute Renal Failure definition
Decrease in glomerular filtration rate (GFR) occurring over hours to days (< 2-4 weeks)
Chronic Renal Failure
presence of proteinuria or reduced GFR (e.g. GFR < 90 ml/min) for at least 3 months
Commonly used criteria used to diagnose ARF
Absolute serum creatinine (SCr) value
Change in SCr value over time
Urine output decrease
RIFLE criteria
Risk — 1.5-fold increase in the serum creatinine or GFR decrease by 25 percent or urine output <0.5 mL/kg per hour for six hours
Injury — Twofold increase in the serum creatinine or GFR decrease by 50 percent or urine output <0.5 mL/kg per hour for 12 hours
Failure — Threefold increase in the serum creatinine or GFR decrease by 75 percent or urine output of <0.5 mL/kg per hour for 24 hours, or anuria for 12 hours
Loss — Complete loss of kidney function (eg, need for renal replacement therapy) for more than four weeks
ESRD — Complete loss of kidney function (eg, need for renal replacement therapy) for more than three months
Etiologies for Acute Renal Failure
Pre-Renal (Most common)
Decreased renal perfusion
Intrinsic
Structural damage to the kidney
Postrenal
Post kidney urine flow obstruction
Normal renal hemodynamics in the afferent arteriole
Tone is controlled by vasodilators (PGE, PGI2)
Normal renal hemodynamics in the efferent arteriole
Tone is controlled by vasoconstrictors (Angiotensin II, Norepinephrine)
Functional Renal Failure
Decreased GFR and hydrostatic pressure at the level of the glomerulus
Decreased blood flow to the kidney decreases GFR
Alteration in afferent/efferent arteriole tone
No structural damage, readily reversible with increased blood flow
Overlaps with causes of prerenal dysfunction
Decline in GFR secondary to reduced hydrostatic pressure
Afferent arteriole vasoconstriction
Efferent arteriole vasodilation
Causes of Functional Renal Failure
Reduced effective blood volume
CHF, Cirrhosis, Pulmonary HTN, Hypoalbuminemia (proteins increase osmotic pressure. Decreased intervascular volume - Can’t deliver enough volume to the kidneys)
Renovascular disease
Renal artery stenosis (- Inhibits the ability of the arteries to flex so no vasoconstriction or vasodilation)
Drugs
ACE-I
ARB
Hepatorenal syndrome (HRS)
Development of renal failure in patients with advanced liver failure (acute or chronic) in the absence of any identifiable causes of renal pathology
Type I
Rapidly progressive
SCr doubling or >2.5mg/dL in less than 2 weeks
Type II
Slow progressive renal insufficiency
HRS Pathogenic Mechanisms
HRS Treatment Options
Vasoactive agents - )(Need to vasoconstrict the splanchnich blood supply) Vasopressin and vasopressin analogues (Improves pressure and flow to the kidney)
Octreotide + Midodrine
Norepinephrine
Treatments that don't work for HRS
Dopamine
Fenoldopam
Diuretics
Arginine Vasopressin
For the treatment of HRS:
Receptors
V1a – vasoconstriction of vascular smooth muscle
V2 – mediates osmoregulation and water retention
V3 – Affect corticotropin secretion

Splanchnic vasculature has large number of V1 receptors
V1 effects increase effective arterial blood volume and suppress activation of the RAAS and SNS, reversing vasoconstriction and increase renal perfusion
HRS Treatment Options
Vasoactive agents - )(Need to vasoconstrict the splanchnich blood supply) Vasopressin and vasopressin analogues (Improves pressure and flow to the kidney)
Octreotide + Midodrine
Norepinephrine
Treatments that don't work for HRS
Dopamine
Fenoldopam
Diuretics
Arginine Vasopressin
For the treatment of HRS:
Receptors
V1a – vasoconstriction of vascular smooth muscle
V2 – mediates osmoregulation and water retention
V3 – Affect corticotropin secretion

Splanchnic vasculature has large number of V1 receptors
V1 effects increase effective arterial blood volume and suppress activation of the RAAS and SNS, reversing vasoconstriction and increase renal perfusion
Vassopressin
Retrospective evaluation of 43 patients
Response
Complete - decrease in SCr to ≤ 1.5 mg/dL
Partial - 50% decrease in SCr to a value >1.5 mg/dl
Vassopressin
Retrospective evaluation of 43 patients
Response
Complete - decrease in SCr to ≤ 1.5 mg/dL
Partial - 50% decrease in SCr to a value >1.5 mg/dl
Vassopressin
Retrospective evaluation of 43 patients
Response
Complete - decrease in SCr to ≤ 1.5 mg/dL
Partial - 50% decrease in SCr to a value >1.5 mg/dl
Drug-Induced Functional ARF
NSAIDS: Effect afferent arteriole tone
The rest Effect Efferent arteriole tone
Prerenal ARF
Hypoperfusion of the renal parenchyma (e.g. nephrons)

Caused by
Low effective blood volume
Hypotension
Hemmorrhage
Dehydration
Hypoalbuminemia
Diuretic therapy
Renal artery occlusion
Prerenal Compensation
Activation of
Sympathetic nervous system
Renin-angiotensin-aldosterone
Antidiuretic hormone
Which causes
Thirst
Increased fluid intake
Sodium and water retention
Functional/Pre-renal Failure Presentation
Increased Scr
Oliguria (< 500 ml urine per day)
Decreased FENa (< 1%)
Normal urine sediment, no RBC or WBC
High BUN/SCr ratio
Intrinsic ARF
Kidney damage
Renal vasculature
Glomeruli
Tubules
Interstitium
Renal Vascular Damage
Renal artery thrombosis
Renal vasculitis
Hypertensive emergency
Hemolytic uremic syndrome (HUS)
Thrombotic thrombocytopenic purpura (TTP)
Glomerular Damage
Low incidence ~ 5% of ARF
Systemic lupus erythematosus - rheumatologic diseases
Poststreptococcal glomerulonephritis - bacterial toxins
Antiglomerular basement membrane disease - Autoimmune
Acute tubular necrosis (ATN)
Causes
85% of all intrinsic ARF
The tubule of the kidney has high oxygen demand, so it is very sensitive to low oxygen states

Causes
Ischemia (decreased flow to the kidney for an extended period of time so not enough O2 Supplied to the tubules)
Hypotension or vasoconstriction
Extended pre-renal state
Toxins
Contrast dye, heavy metals, drugs (e.g. aminoglycosides, amphotericin, etc)
Myoglobin, hemoglobin, uric acid
Acute tubular necrosis (ATN)
Mechanism
Tubular cells die and slough off into the tubular lumen causing increase tubular pressure and decreased GFR
Kidneys lose their ability to concentrate urine
Prolonged exposure to ischemia or toxins cause tubular cells to die
If ischemia/toxins removed before complete necrosis occurs
2-3 week maintenance phase followed by 2-3 week recovery phase where cells regenerate
(2-4 weeks to regenerate once ATN is treated)
Drug Induced ATN
Rhabdomyolysis induced ATN
Rhabdomyolysis - statin drugs are associated with this condition
Breakdown of skeletal muscle fibers, which leads to the release of potentially nephrotoxic intracellular contents into the circulation (e.g. Myoglobinuria)

Mechanisms of Rhabdomyolysis induced ARF
renal vasoconstriction
heme-mediated proximal tubular epithelial cell toxicity (via peroxidation)
intratubular cast formation

Common causes
Statins, trauma, etc.

Urine color
heme-pigment urine
Interstitial Damage
Immunologic response (monocytes, macrophages, B cells, T cells)
Widespread inflammation and edema of tissues surrounding nephrons/tubules
Acute interstitial nephritis (Common culprits)
Drugs
Penicillins, ciprofloxacin, sulfonamides
Infections
Viral, bacteria, fungus, other
Intrinsic Renal Failure Presentation
Oliguric or non-oliguric (urine > 500 ml/day)
Dilute appearing urine or discolored urine ( due to inability to concentration)
Casts and cellular debris
Urinary RBC or WBC
Higher FENa than pre-renal (>1 because body isn’t able to reabsorb Na+ as well)
Lower BUN/SCr ratio compared to pre-renal
Postrenal ARF
Obstruction between the tubule and urethra
Bladder outlet obstruction
Prostate hypertrophy or cancer
Neurogenic bladder or anticholinergic medications
Improper foley placement
Ureteral
Nephrolithiasis, blood clots, physical compression
Renal pelvis or tubules
Nephrolithiasis, oxalate, drugs
Drugs – Indinavir, sulfa, acyclovir, uric acid
Drug Induced Postrenal ARF
Acyclovir
Topiramate
Methotrexate
Indinavir
Trimethoprim/Sulfamethoxazole
Anticholinergic medications
Cocaine
Post-renal Presentation
Increased SCr
Urine output will depend on extent of obstruction
Urine crystals – can see precipitates
Cellular debris – not usually casts unless long term
Variable FENa and BUN/SCr ratio
Patient Assessment
Past medical history
Patient weight, edema
Urine labs
Radiographic tests (e.g. ultrasound, CT)
Current medications
Recent procedures
Acute Renal Failure Assessment Summary
SCr values vs. GFR in ARF
SCr values lag behind what is actually going on in the kidney

A patient suffers a pre-renal ARF due to trauma or infection
GFR plunges but SCr slowly builds up
During recovery GFR improves but the SCr underestimates improvement due to lag in removal
Renal Function Assessment in ARF
Cockcroft-Gault and MDRD
Overestimate renal function when worsening
Underestimate renal function when improving
Urine output over last 4 hours
Abrupt decline or increase suggests change in renal function
Does not evaluate quality of urine produced
Solute content, waste, electrolytes, acids/bases
Goals/approach to ARF
1. Prevent ARF if possible
2. Minimize further renal damage
3. Provide supportive measures until kidney function returns
Prevention of ARF
Specifically targeted patients
Chronic kidney disease
Elderly
Comorbid conditions

Recommendations
Daily fluid intake (~ 2 L/day) to avoid dehydration
Identify medications that put patients at risk
Chemotherapy, Contrast dye, aminoglycosides, etc.
Treatment of ARF
Goals of therapy
Minimize insult to kidney
Shorten time to renal function recovery
Restore renal function to baseline function

No pharmacologic therapy to date has been shown to reverse the decline or accelerate recovery of renal function
General Treatment Approach for ARF
Pre-Renal (flow issue)
Hemodynamic support
Volume replacement (increase volume = increase pressure)
Interstitial damage
Removal of inciting agent
Immunosuppressive therapy (e.g. steroids) (in)
Postrenal
Remove obstruction (Identify drugs that can cause crystallization in the urine)
Supportive therapy for ARF
All patients need supportive therapy
Fluids for prerenal ARF (250 ml – 2 liter boluses, then maintenance rate 75-200 ml/hr)
Blood pressure control (hypo and hypertension)
Electrolyte balance
Cardiac support if heart failure
Antibiotic therapy for infection
Removal of medications that decrease renal blood flow
Etc.
Electrolyte Balance Issues in ARF
Hypernatremia
No more than 3g/day of sodium intake
Hyperkalemia
potassium is 90% renally eliminated
Hyperkalemia can lead to cardiac arrhythmias
Reduce potassium intake
Magnesium
Phosphorus
Acute Hyperkalemia
Serum potassium > 6 mmol/L
Life threatening
Treatment
Calcium chloride
Sodium bicarbonate
Insulin + Dextrose
Albuterol nebs
Furosemide
Kayexalate
Dialysis
Diuretics for Fluid Management
Diuretic resistance
Poor response to administered diuretics
Reduced secretion of diuretics into tubular fluid due to renal dysfunction
Excessive sodium intake can override a diuretics ability to eliminate sodium
Patients with ATN have a reduced number of functioning nephrons on which the diuretic can exert action
Proteinuria: high amounts of protein in the tubules binds the diuretic
Overcoming Diuretic Resistance
Continuous infusions (e.g. furosemide)
Combining diuretic classes
Furosemide + metolazone
Provides synergistic effects
Use of Diuretics in ARF
Not shown to affect the course or outcome of patients with ARF
May be useful for:
Volume overload in early ARF
Oliguric ATN in ICU patients
May combine loop with thiazide
Avoid potassium sparing agents!
Effect of Dopamine on ARF patient outcomes
Increases urine output, but does not decrease mortality or the need for RRT
Artificial kidney - dialysis
Used in patients who cannot be managed by supportive therapy alone
Useful for managing
Uremia
Metabolic acidosis
Hyperkalemia and other electrolyte imbalances
Excess fluid retention
Accumulation of renally cleared medications
Indications for Renal Replacement Therapy (RRT) in ARF
A – Acid-base abnormalities
E – Electrolyte imbalance
I – Intoxications
O – Fluid Overload
U - Uremia
SCr value - SCr does not dictate when to give dialysis
Urinary Output - also does not dictate when to give dialysis
Renal Replacement Therapy for ARF
Intermittent Hemodialysis
~ 4 hour treatments (4 hours that day then more the next day)

Continuous Renal Replacement Therapy
Continuous (e.g. 24 hour) treatment (24 hour a day dialysis can be safer, gentler, and continuously monitored)
Comparative recovery from the different types of ARF
Contrast Induced Nephropathy (CIN)
Contrast agents used in patients with decreased renal function can cause ARF

Accounts for ~12% of hospital acquired ARF
IV Contrast Agent use
Radiography
Interventional cardiology
CT scans
Etc.
Mechanisms for CIN
When comparing contrast agents
The lower the osmolarity, the less toxic the agent and the less ionized the better.
Selected Risk Factors for CIN
Pre-existing renal dysfunction
Diabetic renal disease
Dehydration
Heart failure
EF < 40%
Concurrent nephrotoxins
High volume of contrast
Age
Hyper or hypotension
Anemia
Use of Fluids in Prevention of CIN
Contrast toxicity can occur within minutes, so interventions need to start prior to contrast administration

Fluids
Dilute contrast media
Prevent renal vasoconstriction
Help avoid tubular obstruction

Fluid choice
Encourage oral fluid intake
0.9% NaCl is superior to D5W or 0.45% NaCl
Example: 0.9% NaCl 1 ml/kg/hr 12 hrs before and after contrast or 0.9% 500-1000 ml bolus over 1-2 hrs prior to contrast
This is the best, most important thing that can be done.
Use N-Acetylcysteine (NAC) in the prevention of CIN
N-Acetylcysteine (NAC)
Antioxidant
Free radical scavenger
Dose
600-1200 mg q12h starting 24 hrs before contrast and continue 24hrs post contrast (4 doses)
IV and PO dosing protocols with varying dosing schedules
Must also give IV hydration!
This is a good option.
Use of Sodium bicarbonate in the prevention of CIN
Sodium bicarbonate
hypothesis that contrast injury is from free radicals generated within the acid environment of the renal medulla
By increasing medullary pH, bicarbonate might protect from oxidant injury by slowing Haber-Weiss radical production (Fe3+ + O2- → Fe2+ + O2; Fe2+ + H2O2 → Fe3+ + OH + OH–)
bicarbonate scavenges peroxynitrite and other reactive species generated from nitric oxide
Sodium bicarbonate dose
3 ml/kg/hr x 1 hour before contrast administration followed by an infusion of 1 ml/kg/hr x 6 hours postcontrast
Bicarb can slow down free radical generation and provides fluid hydration to the patient
Use of Fenoldopam in the prevention of CIN
This is NOT a currently recommended therapy for prevention of CIN due to mixed study results.

Fenaldopam is a DA1 Agonist which should increase renal blood flow, increase GFR, increase natiuresis, increase diuresis and inhibits Na/K exchange
What is the most beneficial combination therapy for the prevention of CIN?
Bicarbonate plus NAC
Glycemic Control in the prevention of CIN
Maintaining blood glucose 80-110 mg/dL vs. 180-200 mg/dL in surgical ICU patients