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CPR 2018 Renal Acute Kidney Injury Jefferson
CPR 2018 Renal Acute Kidney Injury Jefferson
A.Pre-renal uremia
B.ATN 2nd
rhabdomyolysis
C.Dead (cardio-renal)
D.Obstruction
Acute Kidney Injury
Why do we care?
– Accumulation of uremic toxins (GI symptoms, neurological
(seizures, encephalopathy)
– Volume overload
– Hyperkalemia (arrythmias)
– Progressive acidosis
– Accumulation of medications
How much urine is enough….oliguria?
Definitions
Oliguria: < 500mls/day
Anuria: < 50mls /day
A. AKI
Team Question: Is this AKI?
B. CKD
43 year old Boeing engineer
presents to primary care
physician with fatigue.
Labs:
Na Cl BUN
136 100 78
K HCO3
5.3 18 8.0
Urine output
– oliguria denotes AKI
Potentially reversible
Clinical Case: AKI and acute pancreatitis
Ucreat: 35 mg/dl
Uosm: 560 mOsm/kg
Team Question: What is the most likely
diagnosis of her AKI?
A.Pre-renal uremia
B.Acute tubular
necrosis (ATN)
C.Acute interstitial
nephritis
D.Acute obstruction
Differential diagnosis of Acute Kidney Injury
Pre-Renal
Renal
Post-Renal
Post-Renal: Obstruction Hydronephrosis
Pre-renal uremia
“a good kidney looking at a bad world”
Na, H2O
High BUN + urea
– Pre-renal (diuretics)
– Other Causes
• High protein intake/TPN
• Catabolism
• Drugs (steroids, tetracyclines)
• Gastro-intestinal hemorrhage
Low Creatinine
– Muscle mass
Urine electrolytes are the best marker for
impaired renal perfusion (pre-renal)
Normal Sodium Reabsorption
65% 5-7%
18,000mmol 1000mmol
GFR 180L/d
25,000mmol
Na filtered 2-5%
450mmol
20-25%
6000mmol
Angiotensin II
SNS
↓GFR 14mls/min
= 20L/d
2800 mmol
Na filtered Aldosterone
ADH
RAAS
(aldo)
ADH
Low perfusion states leading to low UNa
Peripheral
Hypovolemia Cardiogenic Renovascular
vasodilation
Clinical
• Oliguric AKI in setting advanced cirrhosis
• UNa < 10, benign urine sediment, no USS or pathological abnormalities
• Unresponsive to IV fluid challenge.
Mechanism
• Renal vasoconstriction
• Peripheral vasodilatation & shunting
Precipitating Factors
– GI bleed, XS diuresis, infection (SBP), paracentesis
Treatment
– IV Albumin
– Midodrine (α1 agonist) + octreotide (inhibits endogenous vasodilators)
– Liver transplant
NSAID and ACEI are common causes of AKI
- in setting of decreased renal perfusion
Rx underlying cause
– Volume expansion (normal saline)
– Cardiac support etc.
Pre-Renal
Renal
Post-Renal
Causes of Acute Kidney Injury
Arterial injury
Vascular Atheroembolism
Vasculitis
Pre-Renal
Glomerular Glomerulonephritis
Renal
Tubular ATN
Post-Renal
Acute interstitial
Interstitial nephritis
Frequency of Hospital acquired AKI
50%
40%
30%
20%
10%
0%
l n ar
TN a it o l N IN
A ren cu PG A
e - ruc s R
r t Va
P bs
O
Toxic Injury
Exogenous
– Drugs (gentamicin, amphotericin, NSAID, cisplatin, others)
– Toxins (heavy metals, herbs, radiocontrast, solvents)
Endogenous
– Heme pigments (rhabdomyolysis)
– Uric acid (tumor lysis syndrome)
Radiocontrast induced nephropathy
Risk Factors
– Renal impairment (eGFR < 30)
– Diabetes
– CHF
– Volume depletion
Prevention
– Avoid procedure (if possible)
– Limit amount of IV contrast
– IV fluids (saline / NaHCO3)
– N-acetylcysteine Only IV, Not oral contrast as above!
ATN: Rhabdomyolysis
Causes
– Trauma / crush injury (“found down”)
– Seizures
– Drugs (statins, cocaine, others)
– Electrolytes (hypoK, hypoPO4)
Therapy
– Aggressive volume resuscitation
– ?alkaline diuresis
– Rx electrolyte abnormalities
How do we differentiate ATN from Pre-renal
Uremia
How do we differentiate ATN from Pre-renal
Uremia
Acute Tubular
Pre-Renal Uremia
Necrosis
Urine Sodium (mEq/L) <10 >20
(Urine Chloride) (<15) (>20)
Fractional Excretion
<1% >2%
Sodium (FeNa)
Prevent complications
– Volume control
– Dosing medications appropriately
– Avoiding further nephrotoxic agents (e.g contrast, antibiotics)
Supportive Care
Acute Dialysis
– Hyperkalemia
– Symptomatic Uremia
– Volume Overload
– Metabolic Acidosis
– Pericardial Rub
Causes of Acute Kidney Injury
Arterial injury
Vascular Atheroembolism
Vasculitis
Pre-Renal
Glomerular Glomerulonephritis
Renal
Tubular ATN
Post-Renal
Acute interstitial
Interstitial nephritis
Renal Atheroembolism
Clinical Features
– AKI
– Digital infarcts
– Livedo reticularis
– Hypocomplementemia
– Peripheral eosinophilia
Management
– ACEI
– Statins
– Avoidance of
anticoagulation
Acute (Allergic) Interstitial Nephritis (AIN)
Drugs
– Antibiotics (penicillins; rifampin;
ciprofloxacin; sulfonamides)
– Others (NSAID; omeprazole;
allopurinol…..)
Clinical Features
– Fever, rash, eosinophilia (< 50%)
– Oliguria, microhematuria, UTP<1g
– Urine eos (low predictive value)
Therapy
– Stop offending agent
– + / - steroids
How much pee is in a swimming pool?
Methods
Measure concentration of artificial sweetener
acesulfame potassium (ACE K) in 31 pools
in two Canadian Cities (Univ of Alberta)
Results
Estimate that a 110,000 gallon pool would
contain 7 gallons of urine
2. Tubuloglomerular feedback
Failure to reabsorb NaCl in PCT
activation of TGF and GFR
Why does tubular injury lead to a decrease in
GFR
2. Tubuloglomerular feedback
Failure to reabsorb NaCl in PCT activation of TGF
and GFR
1. Clown: Dead
2. CKD
3. Pre-renal uremia