NP33 Nephrology

Acute Kidney Injury

Essential Med Notes 2015

Acute Kidney Injury

Definition
abrupt decline in renal function leading to increased nitrogenous waste products normally
excreted by the kidney
formerly known as Acute Renal Failure
Clinical Features
azotemia (increased BUN, Cr)
abnormal urine volume: formally <0.5 ml/kg/h for >6 h but can manifest as anuria, oliguria, or
polyuria
AKI

Prerenal

Disordered Autoregulation
NSAIDs
ACEI/ARBs
Calcineurin inhibitors
(cyclosporine, tacrolimus)
Hypercalcemia

Renal

Hypovolemia

Absolute
Hemorrhage
GI loss
Skin loss
Renal loss

Postrenal (especially if solitary kidney)

Neurogenic

Effective
Low cardiac
output
Cirrhosis
Sepsis
3rd spacing

Vascular
Vasculitis
Malignant HTN
Thrombotic microangiopathy
Cholesterol emboli
Large vessel disease

Glomerular
GN

Interstitial
AIN

Anatomic
Ureter
Bladder
Urethra

Tubular
ATN

Figure 18. Approach to AKI

Approach to AKI
Investigations
blood work: CBC, electrolytes, Cr, urea (think prerenal if increase in urea is relatively greater
than increase in Cr), Ca2+, PO43 urine volume, C&S, R&M: sediment, casts, crystals
urinary indices: electrolytes, osmolality
fluid challenge (e.g. fluid bolus to rule out most prerenal causes)
imaging: abdo U/S (assess kidney size, hydronephrosis, postrenal obstruction)
indications for renal biopsy
diagnosis is not certain
prerenal azotemia or ATN is unlikely
oliguria persists >4 wk
Treatment
1. preliminary measures
prerenal
correct prerenal factors: optimize volume status and cardiac performance using fluids
that will stay in the plasma subcompartment (NS, albumin, blood/plasma), hold ACEI/
ARB (gently rehydrate when needed, e.g. CHF)
renal
address reversible renal causes: discontinue nephrotoxic drugs, treat infection, and
optimize electrolytes
postrenal
consider obstruction: structural (stones, strictures) vs. functional (neuropathy)
treat with Foley catheter, indwelling bladder catheter, nephrostomy, stenting
2. treat complications
fluid overload
NaCl restriction
high dose loop diuretics
hyperkalemia (refer to Approach to Hyperkalemia, NP12)

The 2 most common causes of acute

kidney injury in hospitalized patients are
prerenal azotemia and ATN; remember
that prerenal failure can lead to ATN

Clues to Prerenal Etiology

Clinical: Decreased BP, increased HR,
and orthostatic HR and BP changes
Increased [urea] >> Increased [Cr]
Urine [Na+] <10-20 mEq/L
Urine osmolality >500 mOsm/kg
Fractional excretion of Na+ <1%
Clues to Renal Etiology
Appropriate clinical context
Urinalysis positive for casts:
Pigmented granular ATN
WBC AIN
RBC GN
Clues to Postrenal Etiology
Known solitary kidney
Older man
Recent retroperitoneal surgery
Anuria
Palpable bladder
U/S shows hydronephrosis

Differentiating Prerenal from ATN

Prerenal

ATN

Urinalysis

Normal

RBC, pigmented
granular casts

Urine [Na+]

<20

>40 mEq/L

Urine[Na+]/[Cr] <20

>40

Urine osmolality >500

<350 mOsm/kgH2O

FeNa

>1%

<1

Drugs Implicated in Prerenal Azotemia

Diuretics
NSAIDs
ACEI/ARBs

Indications for Dialysis

(refractory to medical therapy)
AE IOU
Acidosis
Electrolyte imbalance (K+)
Intoxication
Overload (fluid)
Uremic encephalopathy, pericarditis,
urea >35-50 mM