20 - AKI Flashcards
AKI vs CKD
AKI = Acute Decline in Kidney Function
we look at
Serum Creatinine +/- Urine Output
CKD
renal dysfunction for 3+ months
Preventable & Non-Preventable
Risk Factors for AKI
Not Preventable
CKD / >75yo
Peripheral Vascular Dz / HF / Liver Disease / Diabetes
- *Preventable**
- *Nephrotoxins** = NSAIDs / AminoGlycosides
- Hypo*Tension = HypoVolemia / Cardiac Disease
- *Sepsis**
Causes of PRE-RENAL AKI
IVF Volume Depletion
hypovolemia / hemorrhage / GI losses / Urinary Losses
Cirrhosis / HF / sepsis / vasodilators
- *Reduced Cardiac Output**
- HypoTension / HF / MI / Drugs = CCBs*
Vascular Obstruction
BILATERAL renal artery stenosis
Renal A-fferent Arteriol Vasoconstriction = NSAIDs / Vasopressors / TAC+CSA
VVVV
all leads to
Decreased Renal Blood flow –> ↑SCr
Pre-Renal AKI
Diagnosis & Evaluation
History
Dehydration / Diarrhea / Diuresis
Physical Exam
Orthostatic Hypotension + TACHYcardia
Labs:
BUN:SCr >20 // USG > 1.015
Urine >500 mOsm/L // Urine Na Conc < 20
FENa < 1%
Diagnostic Challenge
Post-Renal AKI
is NOT likely without what?
complaints of
URINARY FREQUENCY
or
BLADDER FULLNESS
Diagnosisng PRE-RENAL AKI
History & Physical Exam
“EASY WAY”
Is the patient HypoVolemic (dry) ?
Low BP // HIGH HR
Dry oral mucosa
Poor Skin Turgor
Dry Underarms
FLUID CHALLENGE
Used for WHAT & how is it done?
If OVERT HypoVolemia….
Give bolus fluid +/- start maintenance IV fluids
VVV
if SCr significantly IMPROVES = PRE-RENAL AKI
- if it does not:*
- *AKI = likely intrinsic**
FENa of 1-2%
means WHAT?
- EITHER*
- *Pre-Renal** or Intrinsic
Limitations:
Only Accurate in OLIGURIC AKI (UOP<400-500 mL/d)
will be FALSELY HIGH in patients on Diuretics
FENa of >2%
means WHAT?
INTRINSIC
Renal Disease
Limitations:
Only Accurate in _OLIGURIC AK_I (UOP <400-500mL/d)
will be FALSELY HIGH in patients on Diuretics
if on DIURETICS & >2%** –> **use FEUrea
FENa of <1%
means WHAT?
PRE-RENAL AKI
Limitations:
Only Accurate in OLIGURIC AKI (UOP <400-500mL/d)
will be FALSELY HIGH in patients on Diuretics
- *if FENa is LOW despite being on DIURETICS**
- *likely PRE-RENAL AKI**
FEUrea of 50-65%%
Means WHAT?
&
When do we use FEUrea?
INTRINSIC AKI
Used when taking DIURETICS
because FENA will be FALSELY ELEVATED
FEUrea of <35%
Means WHAT?
&
When do we use FEUrea?
PRE-RENAL AKI
Used when taking DIURETICS
because FENa will be FALSELY ELEVATED
Intrinsic Renal Disease
Causes
GlomeruloNephropathy = GNs
damage to glomerulus generally due to AUTOIMMUNE disease
since it acts a a filter –> allows PROTEINS –> tubules
Characteristic Finding is PROTEINURIA
Also:
Tubular Nephropathy
Most commonly - ATN (Acute Tubular Necrosis)
also AIN (Acute Interstitial Nephritis)
- *Nephrotic Range Proteinuria**
- *Typically Caused by? & range?**
Intrinsic AKI from GNs (glomerulonephropathies)
By definition:
- *Urine Protein** > 3.5 gm/d
- normal is <80 mg/d for 24 hr sample*
Typically done with:
24 Urine collection (gold standard but difficult)
Random = Spot
Protein to Creatinine Ratio
Nephrotic Syndome
From what & Features?
NOT a disease, but a Group of Signs + Symptoms
seen in patients with
NEPHROTIC RANGE PROTEINURIA (Intinsic AKI)
Hallmark features
FACIAL EDEMA** + **FROTHY URINE
Loss of Antithrombin –> risk of DVTs & PEs
Loss of LMW complements + ABs –> increased risk of INFECTION
Increased:
Cholesterol / LDL / VLDL / TGs
Treatment Approach for GNs
Intrinsic AKI
IMMUNOSUPRESSIVE THERAPY
Also, Supportive Therapy for:
Proteinuria / Clots / Edema
+
HYPERlipidemia + HT
Treatment for PROTEINURIA
Nephrotic Range Proteinurea –> Intrinsic AKI
ACE** or **ARB
may reduce proteinuria by up to 40-50%
also improved with salt restriction
a rise of 10-20% in SCr –> should NOT cause cessation of treatment
Causes:
INDUCED E-fferent Vasodilation
AC-E
ACE-I / ARB
MoA for Proteinuria
caused by Glomerulonephopathies = GNs –> Intrinsic AKI
Induced E-ferrent VasoDilation
AC-E
Opens up –> Exit Arteries
VVV
Reduction in Arteriolar Pressure
VVV
less Protein Filtration –> INCREASE SCr
Which Type of Tubular Nephropathy?
UNCOMMON
AUTOIMMUNE RELATED
Caused by:
DRUG ALLERGY - 75%
or SLE / Sarcoidosis
May present with
STERILEPURIEA
rash / fever / eosinophilia
AIN
Acute Interstitial Nephropathy
cause of
INTRINSIC RENAL DISEASE
Which Type of Tubular Nephropathy?
Due to:
Prolonged or Severe PRE-RENAL AKI –> ischemia
Results in the:
Necrosis of the tubules –> MUDDY BROWN granular CASTS
ATN
Acute Tubular Necrosis
cause of
INTRINSIC RENAL DISEASE
MOST COMMON CAUSE of AKI
Goals + Mangement
of INTRINSIC AKI
Goal:
prevent progression of AKI & need for Dialysis
Management:
Removal of cause if possible / known
IMS if autoimmune
Prevent HypoTension & HypoVolemia
AVOID Nephrotoxins
EDEMA
Management & Values
SODIUM RESTRICTION
to PREVENT edema: < 2gm/d
- If SIGNIFICANT Edema:*
- *Sodium Restriction to 1-1.5gm/d**
- *Loop Diuretis**
Monitor Weight Daily
with goal loss of 1 kg/day
Indications for DIALYSIS
Starting dialysis EARLIER
in the course of renal failure
does NOT improve Outcomes
A E I O U
Metabolic Acidosis pH <7.1
Electrolytes: K > 6.5 or rapidly rising K
Intoxication
Refractory Fluid Overload
Uremia - ConfUsion
Pathogenesis of AKI
from POST-RENAL Obstruction
Interstitial Damage to Kidneys
INCREASED RISK of:
UTIs** + **PYELONEPHRITIS
