AKI Clinical Manifestations
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Clinically, AKI may progress through phases: oliguric, diuretic & recovery.
CKD may develop if patient doesn't recover from AKI
RIFLE classification - standardizes the diagnosis of AKI
R - Risk
I - Injury
F - Failure
L - Loss
E - End-stage kidney disease
AKI & Hyperkalemia
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, Hyperkalemia is one of the most serious complications in AKI because it
can cause life-threatening cardiac dysrhythmias
Both insulin and sodium bicarbonate serve as a temporary measure for
treatment of hyperkalemia by promoting a shift of potassium into the cells,
but potassium will eventually be released
Calcium gluconate raises the threshold at which dysrhythmias will occur,
serving to temporarily stabilize the myocardium
Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually
remove potassium from the body
Never give this drug to a patient with a paralytic ileus because bowel
necrosis can occur.
AKI Clinical Manifestations - Recovery Phase
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May take up to 12 months for kidney function to stabilize
Begins when the GFR increases, allowing the BUN and serum creatinine
levels to plateau and then decrease.
The outcome of AKI is influenced by the patient's overall health, the
severity of kidney failure, and the number and type of complications
Treatment for CKD-MBD (mineral and bone disorder)
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Phosphate not restricted until patient requires renal replacement therapy
Phosphate intake restricted to less than 1000 mg/day
Phosphate binders
-Calcium acetate (PhosLo)
-Calcium carbonate (Caltrate): bind phosphate in bowel and in
excretement
-Sevelamer hydrochloride (Renagel): lowers cholesterol and LDL levels
Phosphate binders should be administered with each meal. Side effect:
constipation
, Supplementing Vitamin D:
-Calcitrol (Rocaltrol)
-Serum phosphate level must be lowered before calcium or vitamin D is
administered
Controlling secondary hyperparathyroidism:
-Calcimimetic agents: Cinacalcet (Sensipar) increase sensitivity of calcium
receptors in parathyroid glands
-Subtotal parathyroidectomy
AKI Nutritional Therapy
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Maintain adequate caloric intake - prevent further breakdown of body
protein for energy purposes
Restrict sodium - prevent edema, HTN and HF
Increase dietary fat - pt needs to receive at least 30-40% of total calories
from fat
Enteral nutrition - if unable to maintain adequate oral intake
AKI - Indications for Renal Placement Therapy (RRT)
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The most common indications for RRT in AKI are
1. volume overload, resulting in compromised cardiac and/or pulmonary
status;
2. elevated serum potassium level;
3. metabolic acidosis (serum bicarbonate level less than 15 mEq/L [15
mmol/L]);
4. BUN level greater than 120 mg/dL (43 mmol/L);
5. significant change in mental status; and
6. pericarditis, pericardial effusion, or cardiac tamponade.
Peritoneal dialysis (PD) - not frequently used
Intermittent hemodialysis (HD) - at intervals of 4 hours either daily, every
Give this one a try later!
Clinically, AKI may progress through phases: oliguric, diuretic & recovery.
CKD may develop if patient doesn't recover from AKI
RIFLE classification - standardizes the diagnosis of AKI
R - Risk
I - Injury
F - Failure
L - Loss
E - End-stage kidney disease
AKI & Hyperkalemia
Give this one a try later!
, Hyperkalemia is one of the most serious complications in AKI because it
can cause life-threatening cardiac dysrhythmias
Both insulin and sodium bicarbonate serve as a temporary measure for
treatment of hyperkalemia by promoting a shift of potassium into the cells,
but potassium will eventually be released
Calcium gluconate raises the threshold at which dysrhythmias will occur,
serving to temporarily stabilize the myocardium
Only sodium polystyrene sulfonate (Kayexalate) and dialysis actually
remove potassium from the body
Never give this drug to a patient with a paralytic ileus because bowel
necrosis can occur.
AKI Clinical Manifestations - Recovery Phase
Give this one a try later!
May take up to 12 months for kidney function to stabilize
Begins when the GFR increases, allowing the BUN and serum creatinine
levels to plateau and then decrease.
The outcome of AKI is influenced by the patient's overall health, the
severity of kidney failure, and the number and type of complications
Treatment for CKD-MBD (mineral and bone disorder)
Give this one a try later!
Phosphate not restricted until patient requires renal replacement therapy
Phosphate intake restricted to less than 1000 mg/day
Phosphate binders
-Calcium acetate (PhosLo)
-Calcium carbonate (Caltrate): bind phosphate in bowel and in
excretement
-Sevelamer hydrochloride (Renagel): lowers cholesterol and LDL levels
Phosphate binders should be administered with each meal. Side effect:
constipation
, Supplementing Vitamin D:
-Calcitrol (Rocaltrol)
-Serum phosphate level must be lowered before calcium or vitamin D is
administered
Controlling secondary hyperparathyroidism:
-Calcimimetic agents: Cinacalcet (Sensipar) increase sensitivity of calcium
receptors in parathyroid glands
-Subtotal parathyroidectomy
AKI Nutritional Therapy
Give this one a try later!
Maintain adequate caloric intake - prevent further breakdown of body
protein for energy purposes
Restrict sodium - prevent edema, HTN and HF
Increase dietary fat - pt needs to receive at least 30-40% of total calories
from fat
Enteral nutrition - if unable to maintain adequate oral intake
AKI - Indications for Renal Placement Therapy (RRT)
Give this one a try later!
The most common indications for RRT in AKI are
1. volume overload, resulting in compromised cardiac and/or pulmonary
status;
2. elevated serum potassium level;
3. metabolic acidosis (serum bicarbonate level less than 15 mEq/L [15
mmol/L]);
4. BUN level greater than 120 mg/dL (43 mmol/L);
5. significant change in mental status; and
6. pericarditis, pericardial effusion, or cardiac tamponade.
Peritoneal dialysis (PD) - not frequently used
Intermittent hemodialysis (HD) - at intervals of 4 hours either daily, every
