Chapter 24 Drugs for Kidney Failure
Pharmacotherapy:
 Attempts to manage cause of dysfunction:
o Diuretics to increase urine output
o Cardiovascular drugs to treat hypertension or heart failure
o Dietary management:
 Restriction of protein, reduction of sodium, potassium, phosphorus,
magnesium
Diuretics site of action:
Mannitol and Acetazolamide work in proximal loop
Loop diuretics works in the loop of Henle
Thiazide diuretics works in the distal loop
Spironolactone works in the collecting duct
Loop Diuretics
 Prototype: Furosemide (Lasix)
 MOA: to block reabsorption of sodium and chloride in loop of Henle
 Primary use: to reduce edema associated with heart, hepatic cirrhosis, or renal failure
 Check the patient’s serum potassium levels before administering the drug.
 Adverse effects: potential electrolyte imbalances, the most important of which is
hypokalemia.
 Hypovolemia may cause orthostatic hypotension and syncope. Ototoxicity is rare but
may result in permanent hearing deficit.
 Contraindications: severe fluid or electrolyte depletion.
 Because hypokalemia may cause dysrhythmias in patients taking cardiac glycosides,
combination therapy with digoxin must be carefully monitored.
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Concurrent use with corticosteroids, amphotericin B, or other potassium-depleting
drugs can result in hypokalemia.
Furosemide may diminish the hypoglycemic effects of sulfonylureas and insulin.
Thiazide Diuretics
 Prototype: Hydrochlorothiazide (Microzide)
 MOA: to block Na+ reabsorption and increase potassium and water excretion
 Primary use: to treat mild to moderate hypertension. Also indicated to reduce edema
associated with heart, hepatic, and renal failure
 When hydrochlorothiazide blocks this reabsorption, more Na+ is sent into the urine.
 The most common adverse effects are potential electrolyte imbalances due to loss of
excessive K+ and Na+.
 patients are usually instructed to increase their potassium intake as a precaution
 Hypokalemia caused by hydrochlorothiazide may increase digoxin toxicity
 Ginkgo biloba may produce a paradoxical increase in blood pressure.
 most commonly prescribed class of diuretics
 Increased risk of lithium toxicity when taking thiazide diuretics
Potassium-Sparing Diurestics
 Prototype: Spironolactone (Aldactone)
 MOA: either by blocking sodium or by blocking aldosterone, the hormone that controls
renal reabsorption of sodium and potassium
 Primary Use: to treat mild HTN, often in combination with other antihypertensives. It
may be used to reduce edema associated with CKD or liver disease, and it is effective in
slowing the progression of heart failure
 Advantage: diuresis without affecting blood potassium levels
 When aldosterone is blocked by spironolactone, Na+ and water excretion is increased
and the body retains more potassium
 Adverse effect: hyperkalemia may develop
 Aspirin and other salicylates may increase potassium levels, which can lead to
spironolactone toxicity.
 hawthorn may result in additive hypotensive effects.
 Limit potassium intake and avoid use of potassium-based salt substitutes
Miscellaneous Diuretics—Carbonic Anhydrase Inhibitors
 Example: acetazolamide (Diamox)
 MOA: to inhibit formation of carbonic acid
 Primary use: to decrease intraocular fluid pressure in patients with open-angle
glaucoma
 Adverse effects: allergic reaction (contain sulfa), fluid and electrolyte imbalances
Miscellaneous Diuretics—Osmotic Diuretics
 Example: mannitol (Osmitrol)
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MOA: inhibits carbonic anhydrase
Primary use: to reduce intracranial pressure due to cerebral edema
Also used to maintain urine flow in prolonged surgery, acute renal failure, or severe
renal hypoperfusion
o Can worsen edema; used with caution
Chapter 25 Drugs for Fluid Balance, Electrolyte, and Acid–Base Disorders
Osmolality
 Dependent on number of dissolved solutes in 1 kg (1 L) of fluid
o Usually sodium, glucose, or urea
 Normal osmolality is 275–295 mOsm/kg
Osmosis
 Movement of water from area of low osmolality to areas of high osmolality
 Hypertonic intravenous fluid
o Water moves from interstitial space to plasma
 Hypotonic intravenous fluid
o Water moves from plasma to interstitial space
 Isotonic intravenous fluid
o No fluid shift
Intravenous Fluid Therapy
 Replaces fluids and electrolytes
o Crystalloids used to replace fluids and promote urine output
o Colloids rapidly expand plasma volume, increasing osmotic preasure
 Causes of water and electrolyte loss
o Gastrointestinal fluid loss, vomiting, diarrhea, laxatives, suctioning
o Perspiration, burns, hemorrhage, excessive diuresis, ketoacidosis
Fluid Replacement Agents—Colloids
 Prototype: dextran 40 (Gentran 40, L M D, others)
 MOA: to raise oncotic pressure of blood; expands plasma volume within minutes of
administration
 Primary use: as fluid replacement with hypovolemic shock from hemorrhage, surgery,
severe burns
 acts by raising the osmotic pressure of the blood, thereby causing fluid to move from
the interstitial spaces of the tissues to the intravascular space (blood).
 Emergency administration may be given 1.2 to 2.4 g/min.
 Nonemergency administration should be infused no faster than 240 m g/min.
 Discard unused portions once opened because dextran contains no preservatives.
 Vital signs should be monitored continuously
 Fluid overload can lead to HTN = cardiac arrest or stroke
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ELECTROLYTES:
Sodium:
 Essential for maintaining osmolality, water balance, acid–base balance
 Sodium movement is link between water retention, blood volume, and blood pressure
 Regulated by kidneys and aldosterone
Hypernatremia:
 Sodium level above 145 mEq/L
 Most commonly caused by kidney disease
 Sodium accumulates:
o Decreased excretion
o High net water loss (watery diarrhea, fever, burns)
o High doses of corticosteroids or estrogens
 Signs and symptoms:
o Thirst, fatigue, weakness, muscle twitching
o Convulsions, altered mental status, decreased level of consciousness
 Treatment:
o low-salt diet
o Acute hypernatremia treated with hypotonic intravenous fluids (if hypovolemic)
or diuretics (if hypervolemic
Hyponatremia:
 Sodium level below 135 mEq/L
 Causes:
o excessive dilution of plasma
 Excess antidiuretic hormone (A D H) secretion
 Excessive administration of hypotonic intravenous solution
o Vomiting, diarrhea, gastrointestinal suctioning, diuretic use
 Signs and symptoms:
o Early symptoms
 Nausea, vomiting, anorexia, abdominal cramping
o Later signs
 Altered neurologic function such as confusion, lethargy, convulsions,
coma, muscle twitching, tremors
 Treatment:
o Hyponatremia caused by excessive dilution
 Treat with loop diuretics to cause an isotonic diuresis
o Hyponatremia caused by sodium loss
 Treat with oral sodium chloride or intravenous fluids containing salt
 Normal saline
 Lactated Ringer’s
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Prototype: sodium chloride (Nacl)
MOA: as electrolyte/ sodium supplement
Primary use: to treat hyponatremia when serum levels fall below 130m E q/L
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Adverse effects: hypernatremia and pulmonary edema
Contraindications: This drug should not be administered to patients with hypernatremia,
heart failure, or impaired kidney function
administered for hyponatremia when serum levels fall below 130 mEq/L.
When serum sodium falls below 115 mEq/L, a highly concentrated (9% NaCl) solution
may be infused
Teach patients to drink water or balanced sports drinks to replenish lost fluids and
electrolytes
Potassium:
 Essential for proper nerve and muscle function
 Maintaining acid–base balance
 Influenced by aldosterone
o For each sodium ion reabsorbed, one potassium ion secreted into renal tubules
 Imbalances can be serious, even fatal
Hyperkalemia:
 Potassium level above 5 mEq/L
 Causes:
o high consumption of potassium-rich food, dietary supplements
o Risk with patient taking potassium-sparing diuretics
o Accumulates when renal disease causes decreased excretion
 Signs and Symptoms:
o Most serious are dysrhythmias and heart block
o Other symptoms are muscle twitching, fatigue, paresthesias, dyspnea, cramping,
and diarrhea
 Treatment:
o Restrict dietary sources
o Decrease dose of potassium-sparing diuretics
o Administer glucose and insulin
o Administer calcium to counteract potassium toxicity on heart
o Administer polystyrene sulfonate (Kayexalate) and sorbitol to decrease
potassium levels
Hypokalemia:
 Potassium level below 3.5 mEq/L
 Causes:
o High doses of loop diuretics (furosemide)
o Strenuous muscle activity (long distance running in hot weather)
o Severe vomiting or diarrhea (gastroenteritis, food poisoning)
 Signs and symptoms:
o Neurons and muscle fibers most sensitive to potassium loss
o Muscle weakness, lethargy, anorexia, dysrhythmias, cardiac arrest
 Treatment:
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o Mild: increase dietary intake (banana/day, dried apricots, figs, dates, etc.).
o Severe: give oral or parenteral potassium supplements
Prototype: potassium chloride (KCl)
MOA: as electrolyte/potassium supplement
Primary use: to treat hypokalemia
Adverse effects: GI irritation, hyperkalemia; contraindicated in patients with chronic
renal failure or those taking potassium-sparing diuretic
When given IV, potassium must be administered slowly, since bolus injections can
overload the heart and cause cardiac arrest.
Never administer IV push
Hyperkalemia may occur if the patient takes potassium supplements concurrently with
potassium-sparing diuretics.
Overdose treatment:
o IV administration of 10% dextrose solution containing 10–20 units of regular
insulin.
o Sodium bicarbonate may be infused to correct acidosis.
o Polystyrene sulfonate may be administered to enhance potassium elimination.
Acid-Base Balance
 Acidosis is excess acid (pH below 7.35)
 Alkalosis is excess base (pH above 7.45)
Acidosis
Alkalosis
Respiratory Origins of Acidosis
Respiratory Origins of Alkalosis
Hypoventilation or shallow breathing
Airway constriction
Damage to respiratory center in medulla
Hyperventilation due to asthma, anxiety, or high
altitude
Metabolic Origins of Acidosis
Metabolic Origins of Alkalosis
Severe diarrhea
Kidney failure
Diabetes mellitus
Excess alcohol ingestion
Starvation
Constipation for prolonged periods
Ingestion of excess sodium bicarbonate
Diuretics that cause potassium depletion
Severe vomiting
Acidosis:
 May be respiratory
o Causes: hypoventilation, airway constriction, damage to respiratory center
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May be metabolic
o Causes: diarrhea, kidney failure, diabetes, excess alcohol, starvation
Symptoms affect central nervous system
o Lethargy, confusion, coma
o Deep, rapid respirations in attempt to blow off excess acid
Goal to quickly reverse effects of excess acid in blood
Administration of sodium bicarbonate infusion
Acid–Base Agents
 Prototype: sodium bicarbonate
 MOA: to decrease p H of body fluids
 Primary use: treatment of acidosis
 Adverse effect: metabolic alkalosis caused by receiving too much bicarbonate ion and
hypokalemia
 Give oral sodium bicarbonate 2 to 3 hours before or after meals and other medications.
 Contraindications: Patients who are vomiting or have continuous GI suctioning (may be
in metabolic alkalosis state)
Alkalosis:
 May be respiratory
o Cause: hyperventilation due to asthma, anxiety, high altitude
 May be metabolic
o Prolonged constipation, excess sodium bicarbonate, diuretics that cause
potassium depletion, severe vomiting, and continuous suctioning.
 Symptoms are due to central nervous system stimulation
o Nervousness, hyperactive reflexes, convulsions
o Slow, shallow respirations in attempt to retain acid
 Treatment:
o Administration of ammonium chloride (severe cases)
o Administration of sodium chloride with potassium chloride (mild cases)
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