Acute Kidney Injury

Question 1

Acute Kidney Injury

Answer 1

Rapid loss of kidney function
Elevates serum creatinine
Decreases urine output/oliguria
Potentially reversible
Severity levels:
-Mild
-Azotemia

Question 2

Azotemia

Answer 2

An accumulation of nitrogenous waste products like urea nitrogen, creatinine in the blood

Question 3

AKI can develop…

Answer 3

over hours or days with progressive elevations of BUN, creatinine, and potassium with or without a reduction in urine output

Question 4

Prerenal

Answer 4

Causes are factors external to the kidneys that reduce renal blood flow
-severe dehydration
-heart failure
-decreased CO
Decreases glomerular filtration rate
Causes oliguria
Autoregulatory mechanisms attempt to preserve blood flow

Question 5

Intrarenal

Answer 5

Causes include conditions that cause direct damage to kidney tissue
Potentially reversible as long as basement membrane is not destroyed

Question 6

Intrarenal results from:

Answer 6

Prolonged ischemia
Nephrotoxins
Hemoglobin released from hemolyzed RBCs
Myoglobin released from necrotic muscle cells

Question 7

Acute tubular necrosis (ATN)

Answer 7

Intrarenal
Results from ischemia, nephrotoxins, or sepsis
Severe ischemia causes disruption in basement membrane
Nephrotoxic agents cause necrosis of tubular epithelial cells
Potentially reversible

Question 8

Postrenal causes

Answer 8

Benign prostatic hyperplasia
Prostate cancer
Calculi
Trauma
Extrarenal tumors

Question 9

Postrenal causes include

Answer 9

mechanical obstruction in the outflow of urine

Question 10

What is hydronephrosis?

Answer 10

Kidney dilation as a result from bilateral ureteral obstruction
Increases hydrostatic pressure
Tubular blockage results in progressive decline in kidney function

Question 11

RIFLE Classification

Answer 11

Used to describe the stages of AKI
Standardizes the diagnosis of AKI
Risk
Injury
Failure
Loss
End-stage kidney disease

Question 12

R

Answer 12

Risk

First stage of AKI where GFR is decreased by 25%

Question 13

I

Answer 13

Injury

Second stage where GFR is decreased by 50% and then increases in severity to the final or third stage

Question 14

F

Answer 14

Failure
GFR is decreased by 75%
Two outcome variables are L and E

Question 15

L

Answer 15

Loss
Outcome from failure and decreased GFR
Complete failure of kidneys

Question 16

E

Answer 16

End stage kidney disease
Outcome from failure and decreased GFR
Complete failure of kidneys

Question 17

Oliguric Phase

Answer 17

Urinary changes
-Output less than 400mL/day
-Occurs within 1-7 days after injury
-Lasts 10-14 days
-Urinalysis may show casts, RBCs, WBCs
Fixed urine specific gravity and osmolality
-Fixed plasma osmolality
-Proteinuria if glomerular dysfunction

Question 18

Oliguric phase: Fluid Volume

Answer 18

Hypovolemia may exacerbate AKI
W/ decreased urine output, fluid retention occurs
-neck veins distended
-bounding pulse
-edema
-hypertension
Fluid overload can lead to HF, pulmonary edema, and pericardial/pleural effusions

Question 19

Oliguric phase clinical manifestations

Answer 19

Fluid volume
Metabolic acidosis
Sodium balance
Potassium excess
Hematologic disorders
Waste product accumulation
Neurologic disorders

Question 20

Oliguric phase: Metabolic Acidosis

Answer 20

Serum bicarbonate level decreases
Severe acidosis develops
-Kussmaul respirations

Bicarbonate is used to buffer hydrogen ions because kidneys cannot synthesize ammonia which is needed for hydrogen ion excretion

Question 21

Oliguric phase: Sodium Balance

Answer 21

Increased excretion of sodium
Hyponatremia can lead to cerebral edema

Damaged tubules cannot conserve sodium. Uncontrolled hyponatremia or water excess can lead to cerebral edema

Question 22

Oliguric phase: Potassium Excess

Answer 22

ECG changes

Levels may increase because kidney’s normal ability to excrete potassium is impaired. Massive tissue trama and damaged cells release additional K and ECF.

Question 23

How does hyperkalemia cause changes in the ECG?

Answer 23

Peaked T waves
Widening of the QRS complex
ST segment depression

Question 24

Oliguric phase: Hematologic Disorders

Answer 24

Leukocytosis

Question 25

Oliguric phase: Waste product accumulation

Answer 25

Elevated BUN and serum creatinine levels

Question 26

Urea

Answer 26

end product of protein metabolism

Question 27

Creatinine

Answer 27

end product of endogenous muscle metabolism

Question 28

Diuretic phase clinical manifestations

Answer 28

Daily urine output is 1-3 L
May reach 5 L or more
Monitor for hyponatremia, hypokalemia, and dehydration

Question 29

Recovery phase clinical manifestations

Answer 29

May take up to 12 months for kidney function to stabilize
Begins when GFR increases, allowing BUN and creatinine to plateau then decrease
Improvements occur in first 1-2 weeks

Question 30

Diagnostic studies

Answer 30

Thorough history
Serum creatinine
Urinalysis
Kidney ultrasonography
Renal scan
CT scan
Renal biopsy

Question 31

Collaborative care

Answer 31

Ensure adequate intravascular volume and cardiac output
-IV/oral fluids based on urine output
-Loop diuretics
-Osmotic diuretics
Therapies for hyperkalemia

Question 32

Nutritional therapy

Answer 32

Maintain adequate caloric intake
Restrict sodium K
Increase dietary fat
Enteral nutrition

Question 33

Health promotion

Answer 33

Identify and monitor populations at high risk
Control exposure to nephrotoxic drugs and industrial chemicals
Prevent prolonged episodes of hypotension and hypovolemia

Question 34

Gerontologic considerations for being more susceptible to AKI

Answer 34

Polypharmacy (5+ prescribed drugs a day)
Hypotension
Diuretic therapy
Aminoglycoside therapy
Obstructive disorders
Surgery
Infection