51
Acute Kidney Injury and
Chronic Kidney Disease
Hazel A. Dennison
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Acid-Base Balance Elimination
Adherence Fluids and Electrolytes
Coping Nutrition
LEARNING OUTCOMES
1. Outline criteria used to classify acute kidney injury using 6. Explain the conservative interprofessional care and related
the acronym RIFLE (Risk, Injury, Failure, Loss, End-stage nursing management of the patient with chronic kidney
renal disease). disease.
2. Relate the clinical course of acute kidney injury. 7. Distinguish among renal replacement therapy options for
3. Explain the interprofessional and nursing management of a persons with end-stage renal disease.
patient with acute kidney injury. 8. Compare and contrast nursing interventions for patients on
4. Define chronic kidney disease and delineate its 5 stages peritoneal dialysis and hemodialysis.
based on the glomerular filtration rate. 9. Discuss the role of nurses in managing patients who receive
5. Identify risk factors for chronic kidney disease. a kidney transplant.
KEY TERMS
acute kidney injury (AKI) CKD mineral and bone disorder (CKD-MBD)
acute tubular necrosis (ATN) continuous ambulatory peritoneal dialysis (CAPD)
anuria continuous renal replacement therapy (CRRT)
arteriovenous fistula (AVF) dialysis
arteriovenous grafts (AVGs) end-stage renal disease (ESRD)
automated peritoneal dialysis (APD) hemodialysis (HD)
azotemia peritoneal dialysis (PD)
chronic kidney disease (CKD) uremia
Kidney failure, also called renal failure, is the partial or com-
plete impairment of kidney function. It results in the inability to
ACUTE KIDNEY INJURY
excrete metabolic waste products and water. Kidney failure con- Acute kidney injury (AKI) is the term used to encompass the
tributes to problems with all body systems. Patients have prob- entire scope of the syndrome, ranging from a slight deterio-
lems with fluid, electrolyte, and acid-base imbalance. Adhering ration in kidney function to severe impairment. AKI is char-
to diet therapy and the treatment plan can be challenging. The acterized by a rapid loss of kidney function with or without
patient must deal with changes in lifestyle, occupation, family decreased urine output. This loss is accompanied by progres-
relationships, and self-image that can lead to withdrawal and sive increases in blood urea nitrogen (BUN), creatinine, and
depression. The patient grieves the loss of kidney function and potassium. The severity of dysfunction can range from a small
independence. increase in serum creatinine or reduction in urine output to
We classify kidney failure as acute or chronic (Table 51.1). the development of azotemia, an accumulation of nitrogenous
Acute kidney injury (AKI) has a rapid onset. Chronic kidney waste products (urea nitrogen, creatinine) in the blood.
disease (CKD) is gradual with a progressive decline in kidney AKI can develop over hours or days. Although AKI is poten-
function. tially reversible, it has a high mortality rate.1 AKI usually affects
1232
, CHAPTER 51 Acute Kidney Injury and Chronic Kidney Disease 1233
people with other life-threatening problems (Table 51.2).2 It leads to decreased glomerular perfusion and filtration of the
often follows severe, prolonged hypotension, hypovolemia, or kidneys.
exposure to a nephrotoxic agent. Hospitalized patients develop It is important to distinguish prerenal oliguria from the oli-
AKI at a high rate (1 in 5) and have a high mortality rate. When guria of intrarenal AKI. In prerenal oliguria there is no damage
AKI develops in an intensive care unit (ICU) patient, the mor- to the kidney tissue (parenchyma). The oliguria is caused by a
tality rate can be as high as 80%.2 decrease in circulating blood volume (e.g., severe dehydration,
heart failure [HF], decreased cardiac output). Prerenal oliguria
Etiology and Pathophysiology
The causes of AKI are multiple and complex. We categorize Prerenal Intrarenal Postrenal
them as prerenal, intrarenal (or intrinsic), and postrenal causes
(Table 51.2 and Fig. 51.1).
Prerenal
Prerenal causes are factors that reduce systemic circulation,
causing decreased renal blood flow. The decrease in blood flow
TABLE 51.1 Comparison of AKI and CKD
AKI CKD
Onset Sudden Gradual, often over
many years
Most common cause Acute tubular necrosis Diabetic nephropathy
Diagnostic criteria Acute reduction in urine GFR <60 mL/min/1.73
output m2 for >3 months
AND/OR AND/OR
↑ Serum creatinine Kidney damage >3
months
Reversibility Potentially Progressive and
irreversible
Main cause of death Infection CVD
Fig. 51.1 Prerenal, intrarenal, and postrenal causes of AKI.
TABLE 51.2 Common Causes of AKI
Prerenal Intrarenal Postrenal
Decreased Cardiac Output Interstitial Nephritis • BPH
• Cardiogenic shock • Allergies: antibiotics (sulfonamides, rifampin), NSAIDs, ACE inhibitors • Bladder cancer
• Dysrhythmias • Infections: bacterial (acute pyelonephritis), viral (Epstein-Barr), fungal • Calculi formation
• HF (candidiasis) • Neuromuscular disorders
• MI • Prostate cancer
Nephrotoxic Injury • Spinal cord disease
Decreased Peripheral Vascular • Chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride • Strictures
Resistance • Contrast media • Trauma (back, pelvis, perineum)
• Anaphylaxis • Drugs: aminoglycosides (gentamicin, amikacin), amphotericin B
• Neurologic injury • Hemolytic blood transfusion reaction
• Septic shock • Severe crush injury
Decreased Renovascular Blood Other
Flow • Acute glomerulonephritis
• Bilateral renal vein thrombosis • Malignant hypertension
• Embolism • Prolonged prerenal ischemia
• Hepatorenal syndrome • Systemic lupus erythematosus
• Renal artery thrombosis • Thrombotic disorders
• Toxemia of pregnancy
Hypovolemia
• Burns
• Dehydration
• Excessive diuresis
• GI losses (diarrhea, vomiting)
• Hemorrhage
• Hypoalbuminemia
,1234 SECTION 10 Problems of Urinary Function
is readily reversible with proper treatment.3 With a decrease major surgery, shock, blood transfusion reaction, muscle injury
in circulating blood volume, autoregulatory mechanisms that from trauma, and prolonged hypotension. ATN is potentially
increase angiotensin II, aldosterone, norepinephrine, and antid- reversible if the basement membrane is not destroyed and the
iuretic hormone try to preserve blood flow to essential organs. tubular epithelium regenerates.
Prerenal azotemia results in decreased sodium excretion (less
than 20 mEq/L), increased sodium and water retention, and Postrenal
decreased urine output. Prerenal problems can contribute to Postrenal causes of AKI involve mechanical obstruction in
intrarenal AKI. If decreased perfusion persists for an extended the outflow of urine. With the flow of urine obstructed, urine
time, the kidneys lose their ability to compensate and damage to refluxes into the renal pelvis, impairing kidney function. The
kidney tissue occurs (intrarenal damage). most common postrenal causes are benign prostatic hyper-
plasia (BPH), prostate cancer, stones, trauma, and extrarenal
Intrarenal tumors. Bilateral ureteral obstruction leads to hydronephrosis
Intrarenal causes of AKI (Table 51.2) include problems that cause (kidney dilation), increase in hydrostatic pressure, and tubular
direct damage to the kidney tissue, resulting in impaired neph- blockage, resulting in a progressive decline in kidney function.
ron function. The damage from intrarenal causes usually results If bilateral obstruction is relieved within 48 hours of onset, com-
from prolonged ischemia, nephrotoxins (e.g., aminoglycosides, plete recovery is likely. Prolonged obstruction can lead to tubu-
contrast media), hemoglobin released from hemolyzed red blood lar atrophy and irreversible kidney fibrosis. Postrenal causes of
cells (RBCs), or myoglobin released from necrotic muscle cells. AKI account for less than 10% of AKI cases.3
Nephrotoxins can cause obstruction of intrarenal structures
by crystallizing or causing damage to the epithelial cells of the Clinical Manifestations
tubules. Hemoglobin and myoglobin can block the tubules and Prerenal and postrenal AKI that has not caused intrarenal dam-
cause renal vasoconstriction. Kidney diseases, such as acute glo- age usually resolves quickly with treatment. When tissue dam-
merulonephritis and systemic lupus erythematosus (SLE), may age occurs from either prerenal or postrenal causes, or when
cause AKI. damage occurs directly as with intrarenal causes, AKI has a
Acute tubular necrosis (ATN) is the most common intra- prolonged course. Clinically, AKI may progress through phases:
renal cause of AKI in hospitalized patients. It can result from oliguric, diuretic, and recovery. When a patient does not recover
ischemia, nephrotoxins, or sepsis. Ischemic and nephrotoxic from AKI, CKD may develop.
ATN causes 90% of intrarenal AKI cases.3 Severe kidney isch- The RIFLE classification describes the stages of AKI (Table
emia causes a disruption in the basement membrane and patchy 51.3). Risk, the first stage of AKI, is followed by Injury, which is
destruction of the tubular epithelium. Nephrotoxic agents cause the second stage. Then AKI increases in severity to the last, or
necrosis of tubular epithelial cells, which slough off and plug the third, stage, Failure. The 2 outcome variables are Loss and End-
tubules. Other risk factors for ATN while in the hospital include stage renal disease.3
TABLE 51.3 Diagnostic Criteria
RIFLE Classification for Acute Kidney Injury
Stage GFR Criteria Urine Output Criteria Clinical Example
Risk Serum creatinine increased × 1.5 Urine output <0.5 mL/kg/hr for • 68-year-old patient with type 2 diabetes, hypertension,
OR 6 hr CAD, CKD
GFR decreased by 25% • Scheduled for emergency coronary artery bypass graft
• Serum creatinine is 1.8 mg/dL (increased), weight 60 kg
• Calculated GFR is 35 mL/min/1.73 m2
• Has stage 3b CKD
Injury Serum creatinine increased × 2 Urine output <0.5 mL/kg/hr for • During surgery, hypotensive for a sustained period
OR 12 hr • Diagnosed with acute tubular necrosis
GFR decreased by 50% • After surgery: serum creatinine is 3.6 mg/dL, urine output
reduced to 28 mL/hr
Failure Serum creatinine increased × 3 Urine output <0.3 mL/kg/hr for • 72 hr after surgery, develops ventilator-associated pneumo-
OR 24 hr (oliguria) nia and sepsis while in ICU
GFR decreased by 75% OR • Serum creatinine rises to 5.2 mg/dL, urine output drops to
OR Anuria for 12 hr 10 mL/hr
Serum creatinine >4 mg/dL with acute • BP remains low despite dopamine therapy
rise ≥0.5 mg/dL
Loss Persistent acute kidney failure. — • Starts on continuous venovenous hemodialysis
Complete loss of kidney function • After 3 weeks of therapy has a cardiopulmonary arrest and
>4 weeks does not survive
End-stage renal Complete loss of kidney function — —
disease >3 months
, CHAPTER 51 Acute Kidney Injury and Chronic Kidney Disease 1235
Oliguric Phase potassium is impaired. The risk for hyperkalemia increases if
Next, we will discuss the most common manifestations of AKI. AKI is caused by massive tissue trauma because the damaged
Urinary changes. The most common initial manifestation cells release potassium into the extracellular fluid (ECF).
of AKI is oliguria, a reduction in urine output to less than 400 Bleeding and blood transfusions may cause cellular destruction,
mL/day. It usually occurs within 1 to 7 days of the injury to the releasing more potassium into the ECF. Metabolic acidosis
kidneys. If the cause is ischemia, oliguria often occurs within 24 worsens hyperkalemia as hydrogen ions enter the cells, and
hours. When nephrotoxic drugs are involved, the onset may be potassium is driven out of the cells into the ECF.
delayed for as long as 1 week. This phase lasts on average 10 to While patients with hyperkalemia are often asymptomatic,
14 days. It can last months in some cases. The longer the oliguric some may have weakness with severe hyperkalemia. Acute or
phase lasts, the poorer the prognosis for complete recovery of rapid development of hyperkalemia may result in electrocar-
kidney function.1 diogram (ECG) changes (see Fig. 17.14). These changes include
Nonoliguric AKI has a urine output greater than 400 mL/ peaked T waves, widening of the QRS complex, and ST seg-
day. About 50% of patients will be nonoliguric. This makes their ment depression.4 Because cardiac muscle is intolerant of acute
initial diagnosis more difficult.2 increases in potassium, emergency treatment of hyperkalemia
While changes in urine output often do not correspond to is needed.
changes in glomerular filtration rate (GFR), they can help us Hematologic problems. Several hematologic problems occur
determine the cause of AKI. For example, anuria (no urine in patients with AKI. Hospital-acquired AKI often occurs in
output) is usually seen with urinary tract obstruction. Oliguria patients who have multiorgan failure. Leukocytosis is often
often occurs with prerenal causes. Nonoliguric AKI occurs with present. The most common cause of death in AKI is infection.
acute interstitial nephritis and ATN.2 The most common sites of infection are the urinary and
A urinalysis may show casts, RBCs, and white blood cells respiratory systems.
(WBCs). Casts form from mucoprotein impressions of the Waste product accumulation. The kidneys are the
necrotic renal tubular epithelial cells, which slough into the main excretory organs for urea (an end product of protein
tubules. The specific gravity may be fixed at around 1.010, with metabolism) and creatinine (an end product of endogenous
urine osmolality at about 300 mOsm/kg (300 mmol/kg). This is muscle metabolism). BUN and serum creatinine levels are
the same specific gravity and osmolality of plasma, thus reflect- increased in kidney disease. An increased BUN level also can be
ing tubular damage and the loss of concentrating ability by the caused by dehydration, corticosteroids, or catabolism resulting
kidney. Proteinuria may be present if AKI is related to glomeru- from infections, fever, severe injury, or GI bleeding. The best
lar membrane dysfunction. serum indicator of AKI is creatinine because it is not affected
Fluid volume. Hypovolemia (volume depletion) has the by other factors.
potential to worsen all forms of AKI. Fluid replacement is often Neurologic problems. Neurologic changes can occur as the
enough to treat many forms of AKI, especially prerenal causes. nitrogenous waste products accumulate in the brain and other
When urine output decreases, fluid retention occurs. The nervous tissue. The manifestations can be as mild as fatigue and
severity of the manifestations depends on the extent of the fluid difficulty concentrating and escalate to seizures, stupor, and
overload. In the case of reduced urine output (anuria, oliguria), coma.
the neck veins may become distended with a bounding pulse.
Edema and hypertension may develop. Fluid overload can Diuretic Phase
eventually lead to HF, pulmonary edema, and pericardial and During the diuretic phase of AKI, daily urine output is usually
pleural effusions. around 1 to 3 L. It may reach 5 L or more. The nephrons are
Metabolic acidosis. In the normal kidney, excess hydrogen still not fully functional even as urine output increases. The high
ions are excreted to keep a physiologic balance of the blood urine volume is caused by osmotic diuresis from the high urea
pH. Impaired kidneys cannot excrete hydrogen ions or the concentration in the glomerular filtrate and the inability of the
acid products of metabolism. Serum bicarbonate (HCO3−) tubules to concentrate the urine. In this phase, the kidneys have
production decreases from defective reabsorption and recovered their ability to excrete wastes but not to concentrate
regeneration of HCO3− ions. Serum HCO3− is depleted through the urine. Hypovolemia and hypotension can occur from mas-
buffering of acidic hydrogen ions and metabolic end products. sive fluid losses.
The patient with severe acidosis may develop rapid, deep Patients who had an oliguric phase will have greater diure-
respirations to try to compensate by increasing CO2 exhalation. sis as kidney function returns. Large losses of fluid and electro-
Sodium balance. Damaged tubules cannot conserve sodium. lytes require us to monitor for hyponatremia, hypokalemia, and
Urinary sodium excretion may increase, resulting in normal or dehydration. The diuretic phase may last 1 to 3 weeks. Near the
below-normal levels of serum sodium. Excess sodium intake is end of this phase, the patient’s acid-base, electrolyte, and waste
avoided because it can lead to volume expansion, hypertension, product (BUN, creatinine) values stabilize.
and HF. Uncontrolled hyponatremia or water excess can lead to
cerebral edema. Recovery Phase
Potassium excess. The kidneys normally excrete 80% to The recovery phase begins when the GFR increases, allowing the
90% of the body’s potassium. In AKI the serum potassium BUN and serum creatinine levels to decrease. Major improve-
level increases because the kidney’s normal ability to excrete ments occur in the first 1 to 2 weeks of this phase. It may take
Acute Kidney Injury and
Chronic Kidney Disease
Hazel A. Dennison
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Acid-Base Balance Elimination
Adherence Fluids and Electrolytes
Coping Nutrition
LEARNING OUTCOMES
1. Outline criteria used to classify acute kidney injury using 6. Explain the conservative interprofessional care and related
the acronym RIFLE (Risk, Injury, Failure, Loss, End-stage nursing management of the patient with chronic kidney
renal disease). disease.
2. Relate the clinical course of acute kidney injury. 7. Distinguish among renal replacement therapy options for
3. Explain the interprofessional and nursing management of a persons with end-stage renal disease.
patient with acute kidney injury. 8. Compare and contrast nursing interventions for patients on
4. Define chronic kidney disease and delineate its 5 stages peritoneal dialysis and hemodialysis.
based on the glomerular filtration rate. 9. Discuss the role of nurses in managing patients who receive
5. Identify risk factors for chronic kidney disease. a kidney transplant.
KEY TERMS
acute kidney injury (AKI) CKD mineral and bone disorder (CKD-MBD)
acute tubular necrosis (ATN) continuous ambulatory peritoneal dialysis (CAPD)
anuria continuous renal replacement therapy (CRRT)
arteriovenous fistula (AVF) dialysis
arteriovenous grafts (AVGs) end-stage renal disease (ESRD)
automated peritoneal dialysis (APD) hemodialysis (HD)
azotemia peritoneal dialysis (PD)
chronic kidney disease (CKD) uremia
Kidney failure, also called renal failure, is the partial or com-
plete impairment of kidney function. It results in the inability to
ACUTE KIDNEY INJURY
excrete metabolic waste products and water. Kidney failure con- Acute kidney injury (AKI) is the term used to encompass the
tributes to problems with all body systems. Patients have prob- entire scope of the syndrome, ranging from a slight deterio-
lems with fluid, electrolyte, and acid-base imbalance. Adhering ration in kidney function to severe impairment. AKI is char-
to diet therapy and the treatment plan can be challenging. The acterized by a rapid loss of kidney function with or without
patient must deal with changes in lifestyle, occupation, family decreased urine output. This loss is accompanied by progres-
relationships, and self-image that can lead to withdrawal and sive increases in blood urea nitrogen (BUN), creatinine, and
depression. The patient grieves the loss of kidney function and potassium. The severity of dysfunction can range from a small
independence. increase in serum creatinine or reduction in urine output to
We classify kidney failure as acute or chronic (Table 51.1). the development of azotemia, an accumulation of nitrogenous
Acute kidney injury (AKI) has a rapid onset. Chronic kidney waste products (urea nitrogen, creatinine) in the blood.
disease (CKD) is gradual with a progressive decline in kidney AKI can develop over hours or days. Although AKI is poten-
function. tially reversible, it has a high mortality rate.1 AKI usually affects
1232
, CHAPTER 51 Acute Kidney Injury and Chronic Kidney Disease 1233
people with other life-threatening problems (Table 51.2).2 It leads to decreased glomerular perfusion and filtration of the
often follows severe, prolonged hypotension, hypovolemia, or kidneys.
exposure to a nephrotoxic agent. Hospitalized patients develop It is important to distinguish prerenal oliguria from the oli-
AKI at a high rate (1 in 5) and have a high mortality rate. When guria of intrarenal AKI. In prerenal oliguria there is no damage
AKI develops in an intensive care unit (ICU) patient, the mor- to the kidney tissue (parenchyma). The oliguria is caused by a
tality rate can be as high as 80%.2 decrease in circulating blood volume (e.g., severe dehydration,
heart failure [HF], decreased cardiac output). Prerenal oliguria
Etiology and Pathophysiology
The causes of AKI are multiple and complex. We categorize Prerenal Intrarenal Postrenal
them as prerenal, intrarenal (or intrinsic), and postrenal causes
(Table 51.2 and Fig. 51.1).
Prerenal
Prerenal causes are factors that reduce systemic circulation,
causing decreased renal blood flow. The decrease in blood flow
TABLE 51.1 Comparison of AKI and CKD
AKI CKD
Onset Sudden Gradual, often over
many years
Most common cause Acute tubular necrosis Diabetic nephropathy
Diagnostic criteria Acute reduction in urine GFR <60 mL/min/1.73
output m2 for >3 months
AND/OR AND/OR
↑ Serum creatinine Kidney damage >3
months
Reversibility Potentially Progressive and
irreversible
Main cause of death Infection CVD
Fig. 51.1 Prerenal, intrarenal, and postrenal causes of AKI.
TABLE 51.2 Common Causes of AKI
Prerenal Intrarenal Postrenal
Decreased Cardiac Output Interstitial Nephritis • BPH
• Cardiogenic shock • Allergies: antibiotics (sulfonamides, rifampin), NSAIDs, ACE inhibitors • Bladder cancer
• Dysrhythmias • Infections: bacterial (acute pyelonephritis), viral (Epstein-Barr), fungal • Calculi formation
• HF (candidiasis) • Neuromuscular disorders
• MI • Prostate cancer
Nephrotoxic Injury • Spinal cord disease
Decreased Peripheral Vascular • Chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride • Strictures
Resistance • Contrast media • Trauma (back, pelvis, perineum)
• Anaphylaxis • Drugs: aminoglycosides (gentamicin, amikacin), amphotericin B
• Neurologic injury • Hemolytic blood transfusion reaction
• Septic shock • Severe crush injury
Decreased Renovascular Blood Other
Flow • Acute glomerulonephritis
• Bilateral renal vein thrombosis • Malignant hypertension
• Embolism • Prolonged prerenal ischemia
• Hepatorenal syndrome • Systemic lupus erythematosus
• Renal artery thrombosis • Thrombotic disorders
• Toxemia of pregnancy
Hypovolemia
• Burns
• Dehydration
• Excessive diuresis
• GI losses (diarrhea, vomiting)
• Hemorrhage
• Hypoalbuminemia
,1234 SECTION 10 Problems of Urinary Function
is readily reversible with proper treatment.3 With a decrease major surgery, shock, blood transfusion reaction, muscle injury
in circulating blood volume, autoregulatory mechanisms that from trauma, and prolonged hypotension. ATN is potentially
increase angiotensin II, aldosterone, norepinephrine, and antid- reversible if the basement membrane is not destroyed and the
iuretic hormone try to preserve blood flow to essential organs. tubular epithelium regenerates.
Prerenal azotemia results in decreased sodium excretion (less
than 20 mEq/L), increased sodium and water retention, and Postrenal
decreased urine output. Prerenal problems can contribute to Postrenal causes of AKI involve mechanical obstruction in
intrarenal AKI. If decreased perfusion persists for an extended the outflow of urine. With the flow of urine obstructed, urine
time, the kidneys lose their ability to compensate and damage to refluxes into the renal pelvis, impairing kidney function. The
kidney tissue occurs (intrarenal damage). most common postrenal causes are benign prostatic hyper-
plasia (BPH), prostate cancer, stones, trauma, and extrarenal
Intrarenal tumors. Bilateral ureteral obstruction leads to hydronephrosis
Intrarenal causes of AKI (Table 51.2) include problems that cause (kidney dilation), increase in hydrostatic pressure, and tubular
direct damage to the kidney tissue, resulting in impaired neph- blockage, resulting in a progressive decline in kidney function.
ron function. The damage from intrarenal causes usually results If bilateral obstruction is relieved within 48 hours of onset, com-
from prolonged ischemia, nephrotoxins (e.g., aminoglycosides, plete recovery is likely. Prolonged obstruction can lead to tubu-
contrast media), hemoglobin released from hemolyzed red blood lar atrophy and irreversible kidney fibrosis. Postrenal causes of
cells (RBCs), or myoglobin released from necrotic muscle cells. AKI account for less than 10% of AKI cases.3
Nephrotoxins can cause obstruction of intrarenal structures
by crystallizing or causing damage to the epithelial cells of the Clinical Manifestations
tubules. Hemoglobin and myoglobin can block the tubules and Prerenal and postrenal AKI that has not caused intrarenal dam-
cause renal vasoconstriction. Kidney diseases, such as acute glo- age usually resolves quickly with treatment. When tissue dam-
merulonephritis and systemic lupus erythematosus (SLE), may age occurs from either prerenal or postrenal causes, or when
cause AKI. damage occurs directly as with intrarenal causes, AKI has a
Acute tubular necrosis (ATN) is the most common intra- prolonged course. Clinically, AKI may progress through phases:
renal cause of AKI in hospitalized patients. It can result from oliguric, diuretic, and recovery. When a patient does not recover
ischemia, nephrotoxins, or sepsis. Ischemic and nephrotoxic from AKI, CKD may develop.
ATN causes 90% of intrarenal AKI cases.3 Severe kidney isch- The RIFLE classification describes the stages of AKI (Table
emia causes a disruption in the basement membrane and patchy 51.3). Risk, the first stage of AKI, is followed by Injury, which is
destruction of the tubular epithelium. Nephrotoxic agents cause the second stage. Then AKI increases in severity to the last, or
necrosis of tubular epithelial cells, which slough off and plug the third, stage, Failure. The 2 outcome variables are Loss and End-
tubules. Other risk factors for ATN while in the hospital include stage renal disease.3
TABLE 51.3 Diagnostic Criteria
RIFLE Classification for Acute Kidney Injury
Stage GFR Criteria Urine Output Criteria Clinical Example
Risk Serum creatinine increased × 1.5 Urine output <0.5 mL/kg/hr for • 68-year-old patient with type 2 diabetes, hypertension,
OR 6 hr CAD, CKD
GFR decreased by 25% • Scheduled for emergency coronary artery bypass graft
• Serum creatinine is 1.8 mg/dL (increased), weight 60 kg
• Calculated GFR is 35 mL/min/1.73 m2
• Has stage 3b CKD
Injury Serum creatinine increased × 2 Urine output <0.5 mL/kg/hr for • During surgery, hypotensive for a sustained period
OR 12 hr • Diagnosed with acute tubular necrosis
GFR decreased by 50% • After surgery: serum creatinine is 3.6 mg/dL, urine output
reduced to 28 mL/hr
Failure Serum creatinine increased × 3 Urine output <0.3 mL/kg/hr for • 72 hr after surgery, develops ventilator-associated pneumo-
OR 24 hr (oliguria) nia and sepsis while in ICU
GFR decreased by 75% OR • Serum creatinine rises to 5.2 mg/dL, urine output drops to
OR Anuria for 12 hr 10 mL/hr
Serum creatinine >4 mg/dL with acute • BP remains low despite dopamine therapy
rise ≥0.5 mg/dL
Loss Persistent acute kidney failure. — • Starts on continuous venovenous hemodialysis
Complete loss of kidney function • After 3 weeks of therapy has a cardiopulmonary arrest and
>4 weeks does not survive
End-stage renal Complete loss of kidney function — —
disease >3 months
, CHAPTER 51 Acute Kidney Injury and Chronic Kidney Disease 1235
Oliguric Phase potassium is impaired. The risk for hyperkalemia increases if
Next, we will discuss the most common manifestations of AKI. AKI is caused by massive tissue trauma because the damaged
Urinary changes. The most common initial manifestation cells release potassium into the extracellular fluid (ECF).
of AKI is oliguria, a reduction in urine output to less than 400 Bleeding and blood transfusions may cause cellular destruction,
mL/day. It usually occurs within 1 to 7 days of the injury to the releasing more potassium into the ECF. Metabolic acidosis
kidneys. If the cause is ischemia, oliguria often occurs within 24 worsens hyperkalemia as hydrogen ions enter the cells, and
hours. When nephrotoxic drugs are involved, the onset may be potassium is driven out of the cells into the ECF.
delayed for as long as 1 week. This phase lasts on average 10 to While patients with hyperkalemia are often asymptomatic,
14 days. It can last months in some cases. The longer the oliguric some may have weakness with severe hyperkalemia. Acute or
phase lasts, the poorer the prognosis for complete recovery of rapid development of hyperkalemia may result in electrocar-
kidney function.1 diogram (ECG) changes (see Fig. 17.14). These changes include
Nonoliguric AKI has a urine output greater than 400 mL/ peaked T waves, widening of the QRS complex, and ST seg-
day. About 50% of patients will be nonoliguric. This makes their ment depression.4 Because cardiac muscle is intolerant of acute
initial diagnosis more difficult.2 increases in potassium, emergency treatment of hyperkalemia
While changes in urine output often do not correspond to is needed.
changes in glomerular filtration rate (GFR), they can help us Hematologic problems. Several hematologic problems occur
determine the cause of AKI. For example, anuria (no urine in patients with AKI. Hospital-acquired AKI often occurs in
output) is usually seen with urinary tract obstruction. Oliguria patients who have multiorgan failure. Leukocytosis is often
often occurs with prerenal causes. Nonoliguric AKI occurs with present. The most common cause of death in AKI is infection.
acute interstitial nephritis and ATN.2 The most common sites of infection are the urinary and
A urinalysis may show casts, RBCs, and white blood cells respiratory systems.
(WBCs). Casts form from mucoprotein impressions of the Waste product accumulation. The kidneys are the
necrotic renal tubular epithelial cells, which slough into the main excretory organs for urea (an end product of protein
tubules. The specific gravity may be fixed at around 1.010, with metabolism) and creatinine (an end product of endogenous
urine osmolality at about 300 mOsm/kg (300 mmol/kg). This is muscle metabolism). BUN and serum creatinine levels are
the same specific gravity and osmolality of plasma, thus reflect- increased in kidney disease. An increased BUN level also can be
ing tubular damage and the loss of concentrating ability by the caused by dehydration, corticosteroids, or catabolism resulting
kidney. Proteinuria may be present if AKI is related to glomeru- from infections, fever, severe injury, or GI bleeding. The best
lar membrane dysfunction. serum indicator of AKI is creatinine because it is not affected
Fluid volume. Hypovolemia (volume depletion) has the by other factors.
potential to worsen all forms of AKI. Fluid replacement is often Neurologic problems. Neurologic changes can occur as the
enough to treat many forms of AKI, especially prerenal causes. nitrogenous waste products accumulate in the brain and other
When urine output decreases, fluid retention occurs. The nervous tissue. The manifestations can be as mild as fatigue and
severity of the manifestations depends on the extent of the fluid difficulty concentrating and escalate to seizures, stupor, and
overload. In the case of reduced urine output (anuria, oliguria), coma.
the neck veins may become distended with a bounding pulse.
Edema and hypertension may develop. Fluid overload can Diuretic Phase
eventually lead to HF, pulmonary edema, and pericardial and During the diuretic phase of AKI, daily urine output is usually
pleural effusions. around 1 to 3 L. It may reach 5 L or more. The nephrons are
Metabolic acidosis. In the normal kidney, excess hydrogen still not fully functional even as urine output increases. The high
ions are excreted to keep a physiologic balance of the blood urine volume is caused by osmotic diuresis from the high urea
pH. Impaired kidneys cannot excrete hydrogen ions or the concentration in the glomerular filtrate and the inability of the
acid products of metabolism. Serum bicarbonate (HCO3−) tubules to concentrate the urine. In this phase, the kidneys have
production decreases from defective reabsorption and recovered their ability to excrete wastes but not to concentrate
regeneration of HCO3− ions. Serum HCO3− is depleted through the urine. Hypovolemia and hypotension can occur from mas-
buffering of acidic hydrogen ions and metabolic end products. sive fluid losses.
The patient with severe acidosis may develop rapid, deep Patients who had an oliguric phase will have greater diure-
respirations to try to compensate by increasing CO2 exhalation. sis as kidney function returns. Large losses of fluid and electro-
Sodium balance. Damaged tubules cannot conserve sodium. lytes require us to monitor for hyponatremia, hypokalemia, and
Urinary sodium excretion may increase, resulting in normal or dehydration. The diuretic phase may last 1 to 3 weeks. Near the
below-normal levels of serum sodium. Excess sodium intake is end of this phase, the patient’s acid-base, electrolyte, and waste
avoided because it can lead to volume expansion, hypertension, product (BUN, creatinine) values stabilize.
and HF. Uncontrolled hyponatremia or water excess can lead to
cerebral edema. Recovery Phase
Potassium excess. The kidneys normally excrete 80% to The recovery phase begins when the GFR increases, allowing the
90% of the body’s potassium. In AKI the serum potassium BUN and serum creatinine levels to decrease. Major improve-
level increases because the kidney’s normal ability to excrete ments occur in the first 1 to 2 weeks of this phase. It may take
