Classification	GFR Criteria	Urine Output Criteria
Risk	Serum creatinine increased 1.5 times	Less than 0.5 ml/kg/hr for 6 hours
Injury	Serum creatinine increased 2 times	Less than 0.5 ml/kg/hr for 12 hours
Failure	Serum creatinine increased 3 times or greater than 355 μmol/L or mg/dl when there was an acute rise of greater than 44 μmol/L or mg/dl	Less than 0.3 ml/kg/hr for 24 hours or anuria for 12 hours
Loss	Persistent acute renal failure: complete loss of kidney function for longer than 4 weeks
End-stage renal disease	End-stage renal disease for longer than 3 months

Table 6-2 CAUSES OF ACUTE RENAL FAILURE

Prerenal (Decreased Renal Perfusion)	Intrarenal (Parenchymal Damage; Acute Tubular Necrosis)	Postrenal (Obstruction)
*Hypovolemia* • GI losses • Hemorrhage • Third-space (interstitial) losses (burns, peritonitis) • Dehydration from diuretic use *Hepatorenal syndromeEdema-forming conditions* • Right ventricular failure • Cirrhosis • Nephrotic syndrome Renal vascular disorders** • Renal artery stenosis • Renal artery thrombosis • Renal vein thrombosis

Prerenal (Decreased Renal Perfusion)

Intrarenal (Parenchymal Damage; Acute Tubular Necrosis)

Postrenal (Obstruction)

Hypovolemia

• GI losses

• Hemorrhage

• Third-space (interstitial) losses (burns, peritonitis)

• Dehydration from diuretic use

Hepatorenal syndromeEdema-forming conditions

• Right ventricular failure

• Cirrhosis

• Nephrotic syndrome

Renal vascular disorders

• Renal artery stenosis

• Renal artery thrombosis

• Renal vein thrombosis

Nephrotoxic Agents

• Antibiotics (aminoglycosides, sulfonamides, methicillin)

• Diuretics (e.g., furosemide)

• Nonsteroidal anti-inflammatory drugs (e.g., ibuprofen)

• Contrast media

• Heavy metals (e.g., lead, gold, mercury)

Organic solvents (e.g., carbon tetrachloride, ethylene glycol)Infection (gram-negative sepsis), pancreatitis, peritonitis transfusion reaction (hemolysis)

• Rhabdomyolysis with myoglobinuria (severe muscle injury)

• Trauma

• Exertion

• Seizures

Glomerular diseases

• Poststreptococcal glomerulonephritis

• IgA nephropathy (e.g., Berger disease)

• Lupus glomerulonephritis

• Serum sickness

• Ischemic injury

CalculiTumorBenign prostatic hypertrophyNecrotizing papillitisUrethral stricturesBlood clotsRetroperitoneal fibrosis

GI, gastrointestinal; IgA, immunoglobulin A; IV, intravenous.

Prerenal failure, or azotemia, is the result of decreased blood flow to the kidneys. The events leading to prerenal insults cause decreased renal vascular perfusion and may be associated with systemic hypoperfusion. If treated promptly, this form of ARF/AKI is readily reversible. Chronic heart failure, drugs such as nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitors, volume loss, or sequestration and shock states (especially septic shock) all may lead to reduced renal perfusion. If not managed aggressively, parenchymal (intrarenal) involvement, or acute tubular necrosis (ATN), can result. Intrarenal damage may result from a mean arterial pressure less than75 mm Hg. Autoregulation fails; the sympathetic response increases and, with the action of the renin-angiotensin system, results in severe constriction of the afferent arteriole. Glomerular blood flow and hydrostatic pressure are reduced, and the GFR decreases. The amount of cellular damage depends on the duration of ischemia: mild damage (less than 25 minutes), moderate/severe damage (40 to 60 minutes), and irreversible damage (may occur within 60 to 90 minutes).

The most common cause of ARF/AKI is ATN. ATN may be the result of nephrotoxic injury, a prolonged reduction in renal perfusion (ischemic injury), or pigmenturia (myoglobinuria and hemoglobinuria). Prolonged renal hypoperfusion due to shock, particularly septic shock, is a common cause of ATN. Renal ischemia may potentiate the injury produced by nephrotoxins. Toxic ATN, caused by nephrotoxic agents (aminoglycoside antibiotics, radiographic contrast agents), is an insult or injury to the tubular cell. Thrombotic occlusion, malignant hypertension, emboli, thrombotic thrombocytopenic purpura (TTP), hemolytic-uremic syndrome (HUS), and vasculitis can all result in ATN.

6-1 RESEARCH BRIEF

Conclusion: N-acetylcysteine (e.g., Mucomyst) is more renoprotective than hydration alone for management of contrast-induced nephropathy. Theophylline may also reduce risk for contrast-induced nephropathy, although the detected association was not significant. The data support the administration of N-acetylcysteine prophylaxis, particularly in high-risk patients, given its low cost, availability, and few side effects. Not all agents analyzed had beneficial effects—fenoldopam, furosemide, mannitol, and the combination of furosemide, dopamine, and mannitol had odds ratios greater than 1.

From Kelly AM. Meta-analysis: effectiveness of drugs for preventing contrast-induced nephropathy. Ann Intern Med 148:284–294, 2008.

ATN is characterized by tubular cell necrosis, cast formation, and tubular obstruction caused by casts and cellular debris. Therapy is focused on maintenance of renal perfusion pressure, administering renal vasodilators to restore blood flow, and promoting diuresis to “wash out” the intratubular debris. Sometimes ATN is nonoliguric. Oliguria may occur with both toxic ATN and ischemic ATN. Common nephrotoxic agents are found in Table 6-3.

Table 6-3 COMMON NEPHROTOXIC AGENTS

Drugs	X-ray Contrast Media
*Antineoplastics* Methotrexate Cisplatin *Antibiotics* Cephalosporins Aminoglycosides Tetracycline *Nonsteroidal anti-inflammatory drugs* Ibuprofen Ketorolac	*Biologic substances* Myoglobin Tumor products *Chemicals* Ethylene glycol Pesticides Organic solvents *Heavy metals* Lead Mercury Gold

Postrenal failure is the least common cause of ARF/AKI and may be either intrarenal (within the kidney) or extrarenal (outside the kidney in another area of the elimination tract) obstruction. Intrarenal obstruction is often due to crystal deposition caused by medications (e.g., acyclovir, indinavir, sulfonamides, methotrexate) or endogenous substances (oxalate, uric acid). Extrarenal obstruction may be related to bladder outlet problems (prostate and urethral obstruction) or stones, clots, pus, tumor, fibrosis, or ligation of or papilla within the ureters.

Fluid, electrolyte, and acid-base disorders that occur with ARF include hypervolemia, hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, and metabolic acidosis (Table 6-4). Phosphate levels rise because of impaired excretion of phosphorus by the renal tubules with continued gastrointestinal (GI) absorption. Hypocalcemia results from the lack of active vitamin D, which is activated by the kidney, which would otherwise stimulate absorption of calcium from the GI tract, or high phosphate levels, which inhibit absorption of calcium. Hypocalcemia triggers the parathyroid glands to secrete parathyroid hormone (PTH), which mobilizes calcium from the bone into the blood. Hypermagnesemia is generally moderate (2 to 4 mg/dl) and is rarely symptomatic unless the patient receives magnesium-containing antacids (e.g., Maalox, Milk of Magnesia).

Table 6-4 ALTERED ELECTROLYTE BALANCE IN ACUTE RENAL FAILURE (ARF)

Condition/Cause	Nursing Implications
*Hyperkalemia*
Decreased ability to excrete K⁺; K⁺ release with catabolism	• Monitor ECG for tall and peaked T waves, loss of P waves, prolonged PR interval, widened QRS when K⁺ is greater than 6.5 mEq/L. Cardiac arrest is more likely seen with K⁺ greater than 7.5 mEq/L. • Monitor serum K⁺ levels for values greater than 5 mEq/L. • Monitor patient for such indicators as paresthesias, muscle weakness or flaccidity, and HR less than 60 beats/min. • Teach patient and significant others the indicators of hyperkalemia and the importance of notifying nurse promptly if they occur. • Provide a list of foods high in potassium (see Box 1-5), and stress the importance of avoiding these foods. • Implement the following to help minimize the cellular release of potassium: • Ensure that patient consumes only the amount of protein prescribed by physician; enforce sound infection control techniques to minimize risk of infection; and treat fevers promptly. Catabolism of protein, which occurs in these situations, causes potassium to be released from the tissues. • Ensure that patient consumes the allotted amounts of carbohydrates, and limit strenuous patient activity as prescribed, both of which will spare protein. • Be aware that hyperkalemia can be a fatal complication, especially during the oliguric phase of ARF, because of its adverse effect on cardiac status. Keep emergency supplies (i.e., manual resuscitator, crash cart, emergency drug tray) readily available. • For more information, see Fluid and Electrolyte Imbalances: Hyperkalemia, p. 37.
*Hypokalemia*
Prolonged, inadequate oral intake; use of potassium-losing diuretics without proper replacement; excessive loss from vomiting, diarrhea, or gastric or intestinal suctioning	• Monitor ECG for prolonged PR interval, flattened or inverted. • T wave, depressed ST segment, presence of U wave, and ventricular dysrhythmias; ECG changes are more likely to occur at serum K⁺ levels less than 3 mEq/L. • Be alert to serum K⁺ less than 3.5 mEq/L. • Monitor patient for muscle weakness, soft and flabby muscles, paresthesias, decreased bowel sounds, ileus, weak and irregular pulse, and distant heart sounds. • Neuromuscular symptoms are seen at serum levels of approximately 2.5 mEq/L. • Teach patient and significant others the indicators of hypokalemia and the importance of notifying nurse promptly if they occur. • Provide a list of foods high in potassium (see Box 1-5), and assist with planning menus that incorporate them. • Administer potassium-sparing diuretics (e.g., spironolactone, triamterene) as prescribed. • Administer oral or IV potassium supplements as prescribed; for oral route, administer with at least 4 oz water or juice to minimize gastric irritation. • For more information, see Fluid and Electrolyte Imbalance: Hypokalemia, p. 37.
*Hypernatremia*
Kidneys’ inability to excrete excess sodium; decreased water intake; increased water losses via osmotic diuresis; excessive parenteral administration of sodium-containing solutions (e.g., sodium bicarbonate, 3% sodium chloride)	• Monitor serum sodium levels for serum Na⁺ greater than 147 mEq/L. • Monitor VS and I&O hourly; weigh patient daily. • Be alert to dry mucous membranes, flushed skin, firm and rubbery tissue turgor, hyperthermia, oliguria, or anuria. • Assess sensorium for restlessness and agitation; institute seizure precautions as indicated. • Administer prescribed IV replacement fluids. • Administer diuretics as prescribed. • For more information, see Fluid and Electrolyte Imbalance: Hypernatremia, p. 37.
*Hyponatremia*
Loss through vomiting, diarrhea, profuse diaphoresis; use of potent diuretics; salt-losing nephropathies; administration of large amount of sodium-free IV fluids (may be associated with fluid volume excess or postobstructive diuresis)	• Monitor for serum Na⁺ less than 137 mEq/L. • Monitor I&O hourly; record weight daily for trend. • Assess patient for abdominal cramps, diarrhea, nausea, dizziness when changing position, postural hypotension, cold and clammy skin, and apprehension. • Provide parenteral replacement therapy as prescribed. • Institute a safe environment for individuals with altered LOC. • For more information, see Fluid and Electrolyte Imbalance: Hyponatremia, p. 46.
*Hypocalcemia*
Poor absorption of dietary calcium; precipitation of calcium out of the tissues in the presence of elevated phosphorus level; inadequate absorption and utilization of calcium occurring with lack of conversion of vitamin D to its usable form	• Monitor for serum Ca²⁺ less than 8.5 mg/dl. • Monitor for numbness and tingling around the mouth, muscle twitching, facial twitching, and tonic muscle spasms. • Assess for Trousseau sign (carpopedal spasm) and Chvostek sign (spasm of lip and cheek). • Administer calcium and vitamin D supplements as prescribed. • Reinforce the necessity of taking these medications as prescribed. • Teach patient and significant others the indicators of hypocalcemia. • Teach the importance of continued medical follow-up to check serum Ca²⁺ levels. • For more information, see Fluid and Electrolyte Imbalance: Hypocalcemia, p. 57.
*Hyperphosphatemia*
Abnormal retention of phosphates caused by the kidneys’ inability to excrete excess phosphorus	• Monitor for serum phosphate greater than 4.5 g/dl. • Although most foods contain generous amounts of phosphate, those especially high in phosphate include beef, pork, dried beans, dried mature peas, and dairy products (see Box 1-6). Monitor patient’s diet accordingly. • Administer phosphate binders as prescribed. Assess for constipation, which may result from use of phosphate binders. • Teach patient and significant others the relationship between calcium and phosphate levels in the body. • Emphasize that maintaining good phosphate control and calcium balance may help control itching and prevent future problems with bone disease. • Reinforce the need for follow-up visits to check serum phosphate levels. • For more information, see Fluid and Electrolyte Imbalance: Hyperphosphatemia, p. 67.
*Hypermagnesemia*
Administration of magnesium-containing medications to patients with impaired renal function	• Monitor serum Mg²⁺ levels greater than 2.5 mEq/L. • Assess for diaphoresis, flushing, hypotension, drowsiness, weak-to-absent DTRs, bradycardia, lethargy, and respiratory impairment. • Teach the above indicators to patient and significant others. • Avoid giving medications that contain magnesium (see Box 1-7). Emphasize to patient that such medications should not be taken without physician’s approval. • For more information, see Fluid and Electrolyte Imbalance: Hypermagnesemia, p. 73.
*Metabolic Acidosis*
Kidneys’ inability to excrete excess acid produced by normal metabolic processes; marked tissue trauma, infection, and diarrhea may contribute to a more rapid development of acidosis (often associated with K⁺ greater than 5 mEq/L)	• Monitor for HCO₃⁻ less than 22 mEq/L and pH less than 7.35. • Monitor I&O, LOC, and VS. • Be alert to Kussmaul respirations, SOB, anorexia, headache, nausea, vomiting, weakness, apathy, fatigue, and coma. • Institute seizure precautions in the presence of altered LOC. • Administer IV fluids and bicarbonate as prescribed. • Teach patient the importance of dietary restrictions, particularly of protein, and of maintaining adequate carbohydrate intake to prevent worsening acidosis. • Stress that patient should report to physician increased temperature and other signs of infection. • Teach patient the importance of taking sodium bicarbonate as prescribed and of maintaining dialysis schedule (both hemodialysis and peritoneal dialysis help correct acidosis). • For more information, see Acid-Base Imbalances, Chronic Metabolic Acidosis, p. 20.
*Uremia*
Failure of the kidneys to excrete urea, creatinine, uric acid, and other metabolic waste products	• Monitor patient for chronic fatigue, insomnia, anorexia, vomiting, metallic taste in the mouth, pruritus, increased bleeding tendency, muscular twitching, involuntary leg movements, decreasing attention span, anemia, muscle wasting, and weakness. • Teach patient and significant others that the indicators of uremia develop gradually and are very subtle. Explain the importance of notifying nurse of sudden worsening of the symptoms that may be present. • Monitor and record dietary intake of protein, potassium, and sodium. • Use lotions and oils to lubricate patient’s skin and relieve drying and cracking. • Provide oral hygiene at frequent intervals, using a soft-bristle toothbrush and mouthwash, to help combat patient’s thirst and the metallic taste caused by uremia. Chewing gum and hard candy also may help alleviate thirst and the unpleasant taste. • Encourage isometric exercises and short walks, if patient is able, to help maintain patient’s muscle strength and tone, especially in the legs. • Teach significant others that because of patient’s decreasing concentration level, they should communicate with patient by using simple and direct statements. • Teach patient to maintain good nutrition by ingesting the allotted amounts of carbohydrates and high-biologic value protein to support cell rebuilding and decrease waste products from protein breakdown. • Explain that profuse bleeding can occur with uremia and that knives, scissors, and other sharp instruments should be used with caution. • Stress that OTC medications such as aspirin and ibuprofen may enhance bleeding tendency. • Emphasize the importance of follow-up visits to evaluate the progression of uremia. • Stress the dialysis schedule should be maintained to decrease the symptoms of uremia and correct many of the metabolic abnormalities that occur.

ARF, acute renal failure; Ca²⁺, calcium; DTR, deep tendon reflex; ECG, electrocardiogram; HCO₃⁻, bicarbonate; HR, heart rate; I&O, intake and output; IV, intravenous; K⁺, potassium; LOC, level of consciousness; Mg²⁺, magnesium; Na⁺, sodium; OTC, over-the-counter; SOB, shortness of breath; VS, vital signs.

There are three identifiable stages/phases of ARF:

1. Oliguric phase: A drop in the 24-hour urinary output to less than 400 ml lasting approximately 7 to 14 days. About 30% of patients have nonoliguric renal failure.

2. Diuretic phase: A doubling of the urinary output from the previous 24-hour total. During this phase the patient may produce as much as 3 to 5 L of urine in 24 hours.

3. Recovery phase: A return to a normal 24-hour volume (1500 to 1800 ml). Usually, renal function continues to improve and may take 6 months to 1 year from the initial insult to return to baseline functional status.

Chronic illness (e.g., hypertension, diabetes, cardiomyopathy, peripheral vascular disease), recent infections or sepsis (e.g., streptococcal), recent episodes of hypotension (e.g., major bleeding, septic shock, major surgery), exposure to nephrotoxins (e.g., carbon tetrachloride, diuretics, aminoglycoside antibiotics, contrast media), recent blood transfusion, urinary tract disorders, toxemia of pregnancy or abortion, recent severe muscle damage (e.g., rhabdomyolysis with myoglobinuria), crush injury, and burn trauma

Prerenal presentation

• Oliguric or nonoliguric

• Urinary sodium (Na⁺) less than 20 mEq/L

• Elevated specific gravity

• Increased urine osmolality

• Normal or mildly abnormal sediment with the presence of hyaline and granular casts

• Elevated plasma BUN/creatinine ratio (greater than 20:1)

Intrarenal presentation

• Oliguric or nonoliguric

• Urinary Na⁺ greater than 20 mEq/L

• Low specific gravity

• Decreased urinary osmolality

• Markedly abnormal sediment with red blood cell (RBC) casts and cellular debris in the urine

• Decreased plasma BUN/creatinine ratio (10:1)

• Most common cause of ARF/AKI

Postrenal presentation

• Urinary chemical indices are ineffective in determining postrenal failure

• Likely oliguric but may be nonoliguric

• Normal or mildly abnormal sediment (hematuria, pyuria, and crystals)

• Often associated with urinary tract or pelvic cancer

• Often associated with renal/ureteral calculi

Vital signs

• BP may be elevated in states of fluid volume excess or decreased in states of fluid volume deficit.

• Heart rate (HR) may be increased or decreased with abnormal rhythms based on fluid and electrolyte abnormalities.

• Weight may be increased or decreased based on fluid volume status.

• Temperature: May be hyperthermic or hypothermic if patient is septic

Palpation

• Edema (scale 0 to 4+): extremities and sacrum

• Muscle tenderness

• Suprapubic tenderness or distention

• Flank tenderness

Auscultation

• S₃ and S₄ gallops indicative of heart failure

• Pericardial friction rub

• Tachycardia or dysrhythmias

• Pulsus paradoxus in the presence of fluid volume excess

• Crackles

• Bruits over the renal arteries indicative of renovascular disease

Screening labwork

Blood and urine studies will determine the level of renal dysfunction and can provide clues to the cause of ARF/AKI.

• BUN and creatinine: Elevations indicative of renal impairment

• GFR: Most reliable estimation of renal function using 24-hour creatinine clearance or laboratory estimation, which is part of renal panel in most laboratories

• Electrolyte levels: Elevated or decreased potassium, phosphorus, magnesium, sodium

• Urinalysis: Presence of sediment including tubular epithelial cells, debris, casts, protein, RBC casts, or myoglobin

• Urinary sodium: Prerenal disease results in urinary sodium levels less than 10 mEq/L

• CBC and coagulation studies (PT, PTT): Evaluate for hematologic complications.

• Arterial blood gas (ABG) values: Evaluate for metabolic acidosis associated with ARF/AKI.

Diagnostic Tests For Acute Renal Failure (ARF)/Acute Kidney Injury (AKI)

Test	Purpose	Abnormal Findings
Ultrasonography	Provides general appearance, size and scarring	Small scarred kidneys Renal mass Kidney stones Hydronephrosis
Radionuclide renal scan	Evaluate renal perfusion	Renal thromboemboli Tumors or cysts Asymmetry of blood flow
Magnetic resonance imaging	More specific in detecting renal masses and vessel malformations	Tumors or cysts Vessel malformation
Retrograde or antegrade pyelography	Diagnose partial or complete obstruction	Ureteric or ureteral stenosis or obstruction
Renal angiography	Evaluate renal vessels	Thrombotic, stenotic lesions in the main renal vessels
Renal biopsy	Determine intrarenal pathology	Acute glomerulonephritis, vasculitis, or interstitial nephritis
*Blood Studies*
Complete blood count (CBC) Hemoglobin (Hgb) Hematocrit (Hct) RBC count (RBCs) WBC count (WBCs)	Assess for anemia, inflammation, and infection; assists with differential diagnosis of septic cause of ARF/AKI	Decreased RBCs, Hgb, or Hct reflects anemia or recent blood loss.
Coagulation profile Prothrombin time (PT) with international normalized ratio (INR) Partial thromboplastin time (PTT)	Assess for the presence of bleeding or clotting and disseminated intravascular coagulation (DIC)	Decreased PT with low INR promotes clotting; elevation promotes bleeding.
Blood urea nitrogen (BUN) Creatinine Estimated glomerular filtration rate (eGFR)	Assess for the severity of renal dysfunction	Elevation indicates renal dysfunction. Creatinine may be markedly elevated in the presence of massive skeletal muscle injury (e.g., multiple trauma, crush injuries). BUN is influenced by hydration, catabolism, GI bleeding, infection fever, and corticosteroid therapy. The eGFR in ARF/AKI is usually less than 50 ml/min.
Electrolytes Potassium (K⁺) Sodium (Na⁺) Calcium (Ca²⁺) Magnesium (Mg²⁺)	Assess for abnormalities associated with ARF/AKI	Increase or decrease in K⁺ may cause arrhythmias. Elevated Na⁺ may indicate dehydration. Decreased Na⁺ may indicate fluid retention. Low Mg²⁺ or Ca²⁺ may cause dysrhythmias.
Arterial blood gases (ABGs)	Assess for the presence of metabolic acidosis	Low PaCO₂ and plasma pH values reflect metabolic acidosis.
Urinalysis	Assess for the presence of sediment	Presence of sediment containing tubular epithelial cells, cellular debris, and tubular casts supports diagnosis of ARF/AKI. Increased protein and many RBC casts are common in intrarenal disease. Sediment is normal in prerenal causes. Large amounts of myoglobin may be present in severe skeletal muscle injury or rhabdomyolysis
Urinary sodium	Differentiate prerenal from intrarenal cause	Urinary Na⁺ is less than 20 mEq/L in prerenal causes. Urinary Na⁺ is more than 20 mEq/L in intrarenal causes.

Collaborative management

Care priorities for all arf/aki pathologies

The major priorities for all patients with ARF/AKI regardless of etiology are the assessment of the contributing causes of the initial injury, identification of the clinical course with an emphasis on comorbidities, assessment of volume status, and prevention of further deterioration in renal function (Table 6-5).

Table 6-5 MANAGEMENT CONSIDERATIONS: ACUTE RENAL FAILURE (ARF)/ACUTE KIDNEY INJURY (AKI)

Treatment	Rationale
Volume replacement for dehydration	Replacement solutions include free water plus electrolytes lost through urine, wounds, drainage tubes, diarrhea, and vomiting. Usually losses are replaced on a volume-for-volume basis. Maintenance fluid approximately 1500 ml/24 hr. With moderate fluid deficit (5% weight loss), at least 2400 ml/24 hr. Severe deficit (more than 5% weight loss) requires replacement of at least 3000 ml/24 hr.
Forced alkaline diuresis	Use of mannitol or sodium bicarbonate solution to manage pigmenturia (myoglobinuria, hemoglobinuria) due to rhabdomyolysis or severe crush or skeletal muscle injury. In addition, aggressive volume replacement to maintain renal perfusion pressure and reduce cast formation leading to renal tubular obstruction.
Diuretics (furosemide, bumetanide, torsemide, ethacrynic acid)	Decrease filtrate reabsorption and enhance water excretion. Use only after adequate hydration to increase urine output or in an attempt to prevent onset of oliguria. If volume overload is present, they are used to prevent pulmonary edema. Osmotic diuretics such as mannitol may be used to increase intravascular volume, promote renal blood flow, increase glomerular filtration rate, and stimulate urinary output. See Table 6-7.
Dopamine	Controversial treatment: Low doses usually less than 2 mcg/kg/min used to stimulate dopaminergic receptors, encourage renal vasodilatation, and promote renal blood flow. Studies have shown that this approach is ineffective if the patient remains oliguric. Doses of 3-10 mcg/kg/min are used to stimulate beta₁ receptors resulting in improved BP, cardiac output, and urine output. Doses greater than 10 mcg/kg/min may cause damaging renal vasoconstriction. May increase urine output in critically ill patients, but it neither prevents nor improves ARF. Increased diuresis may actually increase the risk of ARF in normovolemic and hypovolemic patients. Potentially detrimental effect of dopamine on splanchnic oxygen uptake Decreased GI motility Diminished respiratory drive
Nesiritide	Synthetic BNP (brain natruretic peptide), which results in vasodilatation, natriuresis, diuresis, and decreased renin-angiotensin activity, resulting in lower pulmonary artery occlusive pressure, decreased systemic vascular resistance, and increased cardiac output and cardiac index. Used to manage heart failure associated with prerenal azotemia. Increased cardiac output augments renal perfusion. Meta-analyses have revealed there is increased mortality and increased renal dysfunction with use of nesiritide compared to other medications.
Management of hyperkalemia	Intravenous calcium gluconate 10% or calcium chloride 10% (1 g of calcium chloride does not provide an equivalent dose to 1 g gluconate) (immediate onset) infusion of glucose, insulin, bicarbonate (20- to 60-minute onset) Inhaled albuterol (30- to 60-minute onset), sodium polystyrene sulfonate (Kayexalate) with sorbitol enema (1- to 4-hour onset). Hemodialysis (1- to 3-hour onset) may be used for control of elevated potassium.
Removal or discontinuation of toxin	Agents such as aminoglycoside antibiotics or angiotensin-converting enzyme (ACE) inhibitors used for blood pressure control and heart failure prevention; and nonsteroidal anti-inflammatory drugs (NSAIDs) used for pain management, must be discontinued or removed.
Prevention of contrast-induced nephropathy	Hydration, oral or IV Mucomyst (N-acetylcysteine) may be used before sending borderline or patients with renal insufficiency for radiologic procedures requiring contrast media. Aggressive hydration and possible IV mannitol after the procedure may also assist in clearing contrast from the patient. Intravenous fenoldopam (e.g., Corlopam) is no longer recommended in this setting.
Renal replacement therapy	Maintain homeostasis (see Continuous Renal Replacement Therapies, p. 603).
Nutrition therapy	Diet high in carbohydrates and with catabolic patients, essential and nonessential amino acids to prevent endogenous protein catabolism and muscle breakdown; low in sodium for individuals who retain sodium and water, high in sodium for those who have lost large volumes of sodium and water as a result of diuresis or other body drainage; low in potassium if the patient is retaining potassium; and if not catabolic, low in protein to maintain daily requirements while minimizing increases in azotemia. Nutrition is delivered via oral, enteral, or total parenteral nutrition (TPN). (See Box 1-4 for a list of foods high in sodium and Box 1-5 for a list of foods high in potassiums.)
Hematologic problems	Packed RBCs are given to maintain Hct. Anemia caused by decreased erythropoietin, low-grade GI bleeding from mucosal ulceration, blood drawing, and shortened life of the RBCs. Erythropoietin is used for primary prevention and treatment of anemia. Prolonged bleeding time is caused by decreased platelet adhesiveness.
Pharmacotherapy	Antihypertensives (see Table 5-22): phosphate binders (calcium carbonate antacids, calcium acetate) to bind phosphorus and control hyperphosphatemia and hypermagnesemia are given with meals. Sodium bicarbonate is given to control metabolic acidosis and promote the shift of potassium back into the cells. Water-soluble vitamin supplements are given to patients on dialytic therapy.
Relief of obstruction	Achieved via catheterization with indwelling urinary catheter or nephrostomy tube, or ureteral stent to relieve obstruction prior to surgical intervention or lithotripsy to disintegrate stones.