Resident Grand Rounds

Series Editor: Mark A. Perazella, MD, FACP

Acute Renal Failure in the Hospital:

Diagnosis and Management
Sri Yarlagadda, MD
Mark A. Perazella, MD, FACP

A 69-year-old man with a history of coronary artery disease, hypertension, and stage 3 chronic kidney disease presented to
the emergency department with acute onset of chest pain, dyspnea, and dizziness. The patient was hypotensive (68/36 mm Hg)
with clinical evidence of pulmonary edema. Electrocardiogram revealed an acute anterior wall myocardial infarction. The patient
underwent emergent cardiac catheterization during which an intra-aortic balloon pump (IABP) was placed for management of
cardiogenic shock. Two coronary artery stents were placed and 380 mL of low-osmolar contrast were administered. Blood
pressure improved over the next 24 hours and the IABP was removed. Urine output declined to less than 400 mL/day and the
serum creatinine concentration increased from a baseline of 1.5 mg/dL to 6.8 mg/dL over 4 days. Serum potassium concentration increased to 6.8 mEq/L. The patient became anorexic with nausea and vomiting. Uremic symptoms and metabolic abnormalities developed, and acute hemodialysis was initiated.

cute renal failure (ARF) frequently complicates the course of hospitalized patients. The
incidence of hospital-acquired ARF is between
4.9% and 7%.1,2 ARF occurs commonly in the
intensive care unit, with an incidence up to 20% in this
setting.3 In contrast, the incidence of communityacquired ARF is 0.9%.4 Despite technical advances in
the management of ARF over the past 50 years, mortality rates remain unchanged at 50%.5 Hospital-based
clinicians should be familiar with the diagnosis and
management of this renal disorder.

DEFINITION AND CLASSIFICATION

The term acute renal failure describes an abrupt decline in kidney function. There is no consensus on the
definition of ARF; most definitions are based on absolute
or relative changes in serum creatinine concentration.6
An absolute increase in serum creatinine concentration
by 0.5 or 1.0 mg/dL or a relative increase of 25% to
100% occurring over 24 to 72 hours is considered consistent with ARF. A multidisciplinary group convened in a
consensus conference (the Acute Dialysis Quality Initiative [ADQI]) used both evidence and expert opinion
to define and classify ARF. Based on this meeting, the
ADQI group proposed the RIFLE system, which classifies
ARF into 3 categories according to severity and 2 cate-

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gories according to clinical outcome (Table 1).7 Although serum creatinine concentration is commonly
used to assess renal function and to estimate ARF severity,
a precise correlation between changes in creatinine concentration and glomerular filtration rate (GFR) does not
exist. The non-steady state conditions that prevail in ARF
make estimation of GFR using standard formulas inaccurate, often overestimating true GFR.8
ARF is also classified based on urine output: anuric
(< 100 mL/d), oliguric (100399 mL/d), and nonoliguric (> 400 mL/d). Anuria usually reflects either complete urinary tract obstruction or a vascular catastrophe
complicated by cortical necrosis.
ETIOLOGY
The causes of ARF traditionally have been divided
into 3 major categories based on pathophysiology: prerenal, intrinsic renal, and postrenal (Table 2). Prerenal
etiologies are the most common, accounting for 30% to
60% of all cases of ARF.4 Prerenal azotemia results from
either an absolute or relative decrease in blood volume

Dr. Yarlagadda is a fellow in nephrology, and Dr. Perazella is an associate

professor of medicine, and director of the Nephrology Fellowship Program;
both are at the Yale University School of Medicine, New Haven, CT.

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Table 1. RIFLE Classification of Acute Renal Failure (ARF)

TAKE HOME POINTS

The causes of acute renal failure (ARF) are classified as prerenal, intrinsic renal, and postrenal.
Prerenal azotemia results from an absolute or relative decrease in blood volume or altered intrarenal
hemodynamics, decreasing renal perfusion without
causing cellular injury.
The most common form of intrinsic renal failure is
acute tubular necrosis, which most frequently is
caused by ischemia, toxins, and urinary crystals.
Diagnosis of ARF requires thorough review of the
hospital record, evaluation of volume status, and performance of pertinent laboratory and imaging tests.
Intrinsic renal failure is considered after prerenal
and postrenal causes have been excluded and clinical
data point to a structural problem within the kidneys.
Management of ARF entails correction of prerenal
and postrenal diseases; optimal therapy of metabolic,
uremic, and volume-related complications; and renal
replacement therapy for severe renal insufficiency.

or altered intrarenal hemodynamics, decreasing renal

perfusion without cellular injury. It is rapidly reversible
if the hemodynamic insult is corrected. If the insult is
sustained, overt cellular injury results (ie, acute tubular
necrosis [ATN]) with transition from prerenal to intrinsic ARF. Postrenal ARF is less common in the hospital
setting, accounting for between 1% and 10% of cases of
hospital-acquired ARF, and is characterized by structural or functional obstruction of the urinary tract. Obstruction occurs at any level from the renal pelvis to the
urethra; either complete or partial obstruction can
cause ARF. Postrenal causes should be quickly recognized and treated because recovery of renal function is
inversely related to the duration of obstruction.9
Intrinsic renal failure is considered after prerenal and
postrenal causes have been excluded and clinical data
point to a structural problem within the kidneys. Intrinsic
renal diseases are characterized according to the primary
site of injury, including the vasculature, glomerulus,
tubules, and interstitium. The most common form of
hospital-acquired intrinsic renal failure is ATN. This
term is misleading because there is a spectrum of tubular
dysfunction that may or may not result in tubular necrosis. The most common causes of ATN are ischemia, exogenous toxins (drugs and radiocontrast agents), endogenous toxins (heme pigments and toxic light chains), and
natural or drug-induced urinary crystals.

52 Hospital Physician March 2006

Glomerular
Filtration Rate

Urine Output
Criteria

Risk

SCr increased 1.5 times

< 0.5 mL/kg/h for 6 h

Injury

SCr increased 2.0 times

< 0.5 mL/h for 12 h

Failure

SCr increased 3.0 times

< 0.3 mL/kg/h for 24 h

or anuria for 12 h

Loss

Persistent ARF; complete

loss of kidney function
for longer than 4 wk

End stage

ESRD persisting longer

than 3 mo

ESRD = end stage renal disease; SCr = serum creatinine.

DIAGNOSIS
A comprehensive history with detailed review of the
hospital medical record, physical examination, and basic
laboratory tests correctly identifies hospital-acquired
ARF. Diagnosis requires knowledge of the natural history of various causes of ARF and a systematic approach to
evaluating renal insufficiency by excluding and correcting both prerenal and postrenal causes.
History
In the hospital, patients develop excessive fluid losses from diarrhea, ostomy losses, or high urine output.
These losses are compounded by limited fluid intake
prior to the recognition of ARF. Obstruction, especially
from urinary retention, is common and reduces urine
output. The presence of urine output does not exclude partial urinary tract obstruction as a cause of
ARF. Bone pain in an elderly patient might suggest
multiple myeloma as a cause of ARF.
Review of the hospital record for recent intake/output data, trends in body weights, episodes of hypotension (especially requiring vasopressors), evidence of
sepsis, use of radiocontrast for procedures, and administration of any number of nephrotoxic medications is
critical. Invasive vascular procedures, including both
percutaneous and open operative interventions, should
be assessed for their temporal relationship to ARF. The
operative report of any surgical procedure should be
scrutinized to identify hypotension, blood loss, and administration of potential nephrotoxins.
Physical Examination
Evaluation of intravascular volume status in hospitalized patients is important to assess for prerenal ARF. The
examination should include measurement of blood pressure and heart rate, including orthostatic readings, and

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assessment for pulsus paradoxus. Other required evaluations include assessment of mucosal hydration and skin
turgor and assessment for the presence of edema (pretibial in ambulatory patients, sacral in bedridden patients),
jugular venous distension, lung crackles, and an S3 cardiac gallop. Equally important are signs of coexistent comorbidities, such as congestive heart failure, cirrhosis,
nephrosis, and vascular disease. The presence of a diffuse
rash, livedo reticularis with skin mottling, or palpable
purpura suggest renal and vascular injury. Suprapubic
fullness indicates a postrenal cause of ARF. Limb ischemia suggests the possibility of underlying rhabdomyolysis.
Laboratory Testing
Blood tests. Measurement of serum blood urea
nitrogen (BUN) and creatinine concentration, electrolytes, calcium, and phosphate is an integral part of the
diagnosis of hospital-acquired ARF and management
of its associated complications. The trends in BUN and
serum creatinine concentrations help define the severity and course of ARF. Metabolic disturbances such as
hyperkalemia and hyperphosphatemia accompanied by
an elevated creatine kinase level suggest rhabdomyolysis. Hypercalcemia can point to a malignant condition
such as multiple myeloma; similarly, hyperuricemia indicates tumor lysis syndrome. Abnormal transaminase
levels suggest congestive heart failure or liver disease;
elevated bilirubin levels may represent hemolysis or
hepatic disease.
Anemia in the presence of schistocytes and thrombocytopenia should raise suspicion for a thrombotic
microangiopathy (hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, antiphospholipid
antibody syndrome), endocarditis, and disseminated
intravascular coagulation. Eosinophilia may be seen
with acute interstitial nephritis (AIN) and atheroembolic renal disease. Finding a monoclonal protein in
the serum suggests multiple myeloma. Positive blood
cultures can point to an endovascular infection with an
associated acute immune complexassociated glomerulonephritis. The utility of serologic tests such as hepatitis serology and measurement of antinuclear antibody, complement, and antineutrophil cytoplasmic
antibody levels depend upon clinical suspicion.
Urine studies. Routine urinalysis consists of dipstick
testing, which provides information about urine concentration and detects protein, ketones, glucose, leukocyte esterase, bilirubin, and blood. In the absence of
red blood cells (RBC), heme-positive urine suggests
the presence of heme protein from either myoglobin
(rhabdomyolysis) or hemoglobin (hemolysis).
Microscopic examination of the spun urine sedi-

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Table 2. Common Causes of Hospital-Acquired Acute Renal

Failure
Prerenal
True volume depletion: nausea/vomiting, hemorrhage, burns, diarrhea/
ostomy output, diuretics
Effective volume depletion: congestive heart failure, hepatorenal syndrome, sepsis/third spacing of fluids, pancreatitis
Intrinsic
Ischemic acute tubular necrosis: shock from any cause, vasopressors
Nephrotoxic acute tubular necrosis
Medications: aminoglycosides, amphotericin B, radiocontrast
agents, osmotic agents, crystal-forming agents, acyclic nucleotide phosphonates, zoledronate/pamidronate, oral sodium
phosphate solution
Endogenous toxins: light chains, heme pigments, uric acid
Vascular injury: renal cholesterol emboli (atheroemboli)
Postrenal
Retroperitoneal obstruction: hematoma, cancer
Bladder outlet obstruction: structural, functional

ment is essential in the evaluation of ARF. The sediment should be closely inspected for cellular elements,
casts, and crystals. RBCs indicate bleeding along the
urogenital tract if the cells are monomorphic (normal
appearing) or glomerular injury if the cells are dysmorphic. Renal tubular epithelial (RTE) cells suggest tubular injury, while white blood cells (WBC) suggest infection or renal inflammation. RTE cell casts and granular
casts typically represent renal tubular injury (Figure 1).
RBC casts confirm glomerular injury, while WBC casts
suggest either intrarenal infection or AIN. Uric acid
crystals in the urine of a patient with ARF suggest the
possibility of tumor lysis syndrome. Urine crystals associated with medications (acyclovir, indinavir, sulfadiazine)
point to drug-associated crystal nephropathy.
Urine chemistries can also provide useful information to classify the cause of ARF (Table 3). These tests
must be interpreted in conjunction with clinical assessment of the patient and other serum and urine test
results.
Diagnostic Imaging
Renal ultrasound is both sensitive (90%) and specific
(90%) in diagnosing urinary tract obstruction. Hydronephrosis, which reflects dilatation of the renal pelvis and
ureters, is readily seen on ultrasound (Figure 2). Ultrasound also provides information about renal size and
echogenicity and cortical thickness. The absence of
hydronephrosis does not always exclude obstruction,
especially in the setting of acute obstruction (< 72 h),

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Figure 1. A granular cast is noted in the urine of a patient

with acute tubular necrosis. This finding represents tubular
injury with sloughing of cells into the urine. (Image courtesy
of Mark A. Perazella, MD.)

retroperitoneal fibrosis, or severe hypovolemia. Computed tomography scan without radiocontrast is also useful in the diagnosis of urinary obstruction (Figure 2). Its
advantage over ultrasound is enhanced sensitivity in visualizing the various etiologies of obstruction, such as
stones, retroperitoneal disease, and malignancy.
Renal Biopsy
Renal biopsy is rarely required in the work-up of
ARF. When a primary renal disease other than ischemic or toxic ATN is suspected, renal biopsy may
establish the diagnosis. Common indications include
unexplained ARF, suspicion of acute glomerulonephritis or lupus nephritis, protracted renal dysfunction in
patients suspected for AIN, and ARF that fails to improve after 6 to 8 weeks (due to potentially irreversible
causes such as cholesterol emboli [Figure 3] and cortical necrosis). In a prospective study of patients with
ARF, renal histology altered management in 75% of
cases.10 Because the risks associated with renal biopsy
are low (< 1%), this diagnostic procedure should be
used in the appropriate setting to evaluate ARF.11
MANAGEMENT
The initial care of patients with ARF should focus
on reversing the underlying cause (prerenal and postrenal) and correcting fluid, electrolyte, and acid-base
imbalances (Table 4). Every effort should be made to
prevent further kidney injury and to provide supportive care (including dialysis), until recovery occurs.

54 Hospital Physician March 2006

Fluids
An important goal of patient management is maintaining euvolemia. Careful physical examination and,
when appropriate, invasive monitoring is vital to this
process. Achieving appropriate fluid balance involves
2 conflicting goals: providing sufficient volume to ensure
adequate renal perfusion and avoiding volume overload
with resulting pulmonary congestion. Attention to all
sources of fluid intake and output, including surgical
drains, nasogastric suction, diarrhea, and insensible losses is required. There is no substitute for daily weights.
Rapid restoration of intravascular volume may reverse prerenal azotemia and prevent ischemic damage.
Crystalloid solutions are often the best fluid choice. In
situations of increased vascular permeability, colloid
solutions may provide enhanced restoration of intravascular volume. Albumin therapy should be restricted to
situations where synthetic colloids cannot be used.12 Of
the synthetic colloids, hydroxyethyl starch (HES) solutions with low in vivo molecular weight (HES, 200/0.5)
demonstrate the best risk/benefit ratio,13 but these
should be avoided in patients with underlying kidney
disease due to enhanced risk of ARF.
Vasoactive Agents
If hypotension persists despite adequate fluid replacement, vasopressors are indicated. However, intrarenal vasoconstriction develops with these drugs and
may negate the hemodynamic benefit of increased
blood pressure. Norepinephrine reduces renal blood
flow in normal humans but improves renal blood flow
and augments urine output and GFR in patients with
septic shock.14 Vasopressin also increases urine output
and GFR in patients with septic shock.15 Inotropic
agents such as dobutamine increase cardiac output
and augment renal blood flow in patients with systolic
dysfunction and ARF.
Low-dose dopamine (0.50.2 g/kg body weight) is
commonly used to increase urine output in oliguric patients. Several studies have demonstrated that dopamine
does not promote renal recovery or reduce mortality1618 and is associated with tachyarrhythmias, pulmonary shunting, and gut or digital necrosis.19 Dopamine should not be employed in the treatment of ARF.
Diuretics
Diuretics are often required to treat ARF when volume overload develops. Loop diuretics (furosemide,
ethacrynic acid, torsemide) diminish active transport
and energy requirements in the thick ascending limb.
Although a favorable diuretic response occurs with these

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Table 3. Diagnostic Clues to the Etiology of Acute Renal Failure

Urine
Osmolality,
mOsm/kg

Urine
Sediment

BUN/ Cr
Ratio

Urine
Dipstick

Urine Na,
mmol/L

FE Na, %

FE Urea, %

Prerenal

> 500

Bland or
hyaline casts

> 20

No proteinuria

< 20

<1

< 35

Intrinsic

< 450

RBCs, WBCs,
cellular casts

< 20

++ Proteinuria

> 40

>1

> 50

Postrenal

< 450

Bland, RBCs,
crystals

< 20

No proteinuria

> 40

>1

BUN = blood urea nitrogen; Cr = creatinine; FE = fractional excretion; RBCs = red blood cells; WBCs = white blood cells.

Figure 2. (A) Dilated renal calyces on ultrasound scan indicative of hydrenephrosis. This ultrasound finding is highly specific for
renal obstruction. (B) Dilated renal calyces on computed tomography scan indicative of hydronephrosis. This finding is also highly specific for renal obstruction. (Images courtesy of Mark A. Perazella, MD.)

drugs when administered within the first 24 hours of

onset of oliguria, this effect does not translate into
enhanced renal recovery or a mortality benefit. In a
prospective study of loop diuretics in ARF, no significant
difference in renal recovery, requirement for dialysis, or
death was observed.20 In another study, diuretics were
associated with nonrecovery of renal function and
increased risk of death in critically-ill patients.21 Other
diuretics such as mannitol are used in limited clinical situations such as rhabdomyolysis with myoglobinuric ARF.
Thiazide diuretics may increase urine output when combined with loop diuretics. Thus, diuretics should be used
only in ARF for management of volume with no expectation that these agents improve outcomes.
Metabolic Management
Acidosis. Metabolic acidosis in ARF can be explained

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largely by (1) reduced renal excretion of acid and several organic and inorganic anions and (2) excessive acid
production via catabolism. Correction of metabolic acidosis enhances response to vasopressors, improves cardiac contractility, ameliorates bone injury due to acid
buffering, and reduces catabolism. Bicarbonate containing intravenous fluids correct acidosis, but proper use is required to limit excess volume repletion and
minimize symptoms of hypocalcemia. Depending on
the serum sodium concentration, sodium bicarbonate
(50150 mEq) can be added to a liter of either 5% dextrose in water or 0.45% normal saline to make an isotonic solution. Oral bicarbonate or bicarbonate precursors (citrate) are preferable in patients able to take pills
or a liquid preparation. The goal is to correct the serum bicarbonate to approximately 22 mEq/L, depending on respiratory status and arterial pH.

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Table 4. Strategies for Management of Acute Renal Failure

Exclude urinary tract obstruction by utilizing clinical suspicion,
assessment of postvoid urine residual, and renal ultrasonography
Evaluate for the presence of a prerenal state
If evidence of intravascular depletion is present, restore intravascular
volume
Always consider the possibility of intrarenal causes that require early
diagnosis
Discontinue all potential nephrotoxins or drugs associated with acute
interstitial nephritis
Search for and treat acute uremic complications such as hyperkalemia, hyponatremia, acidosis, and volume overload
Optimize nutritional status and avoid foods high in potassium and
phosphorus

Figure 3. Kidney biopsy specimen showing atheroemboli and

cholesterol clefts surrounded by fibrin within the blood vessel lumen. This histology explains the etiology of protracted
renal failure. (Image courtesy of Mark A. Perazella, MD.)

Hyponatremia. Hyponatremia is the most common

electrolyte abnormality in oliguric renal failure and usually is the result of excess water in the setting of reduced
renal free water clearance. Sources of free water in hospitalized patients are hypotonic solutions (5% dextrose,
0.45% normal saline), parenteral medications administered in 5% dextrose, or excessive amounts of hypotonic fluid with enteral or parenteral feeds. Restriction of
these types of fluid often minimizes worsening of hyponatremia and allows slow correction.
Hyperkalemia. Hyperkalemia is the most serious
electrolyte abnormality associated with ARF. Cardiac
toxicity as manifested by several forms of arrhythmia is
a life-threatening complication. Serum potassium concentrations greater than 6.0 to 6.5 mEq/L require
rapid therapy. The electromechanical effects of hyperkalemia are potentiated by hypocalcemia, acidosis, and
certain medications. The ECG, which measures the
summation of these effects, should be examined in
concert with serum potassium concentration. The earliest change is peaked T waves, followed by shortening
of the QT interval and flattening of P waves, which
eventually disappear. Later, QRS complex widening,
prolongation of the QT interval, and ultimately a sine
wave pattern develop.
Therapy is based on stabilization of excitable membranes, rapid reduction in serum potassium concentration utilizing cellular shift, and removal of potassium
from the body (Table 5). Along with these interventions, limited potassium intake is an obvious therapy.
Hyperphosphatemia and hypocalcemia. Impaired
renal function limits phosphate excretion and pro-

56 Hospital Physician March 2006

Dose drugs appropriately according to estimated renal clearance

using glomerular filtration rate estimation formulas, recognizing
their limitations in the setting of acute renal failure
Initiate renal replacement therapy before uremic, metabolic, or
volume-related complications develop

motes hyperphosphatemia. Cell release of phosphate in

certain settings (rhabdomyolysis, tumor lysis syndrome,
and hemolysis) exacerbates hyperphosphatemia. Severe
hyperphosphatemia can cause hypocalcemia and soft
tissue calcium and phosphate deposition as well as
impair renal function. Hypocalcemia is often asymptomatic, although tetany can develop with overly aggressive correction of acidosis.
Treatment of hyperphosphatemia is based on reducing gastrointestinal absorption. Reduced dietary
phosphate (including parenteral nutrition) and oral
phosphate binders with meals are the mainstay of treatment. Phosphate-containing bowel-cleansing regimens should be avoided. Hypocalcemia rarely requires
therapy in the absence of symptoms of tetany. If symptoms develop, intravenous calcium gluconate should
be administered to acutely improve symptoms, followed by oral calcium carbonate to correct the calcium
to the lower limit of normal.
Renal Replacement Therapy
Multiple modalities of renal replacement therapy
(RRT) are available to manage ARF, including intermittent hemodialysis (IHD), peritoneal dialysis (PD), continuous renal replacement therapy (CRRT), and new
hybrid therapies such as sustained low efficiency dialysis. Despite 4 decades of experience with RRT in ARF,
there are no strict guidelines on the appropriate indications for initiation of therapy, the most appropriate
modality, and the optimal dose of dialysis. Despite the
absence of solid evidence, there is general consensus

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regarding some of these issues. Treatment should be

initiated before uremic, metabolic, and volume-related
complications occur.22 Commencement of RRT is
appropriate for volume overload that is unresponsive to
diuretics, hyperkalemia and metabolic acidosis, refractory to conservative measures, and pericarditis or
encephalopathy due to uremia. Strict laboratory values
per se are not an indication for initiation of RRT,
although a low threshold develops when the BUN level
exceeds 100 mg/dL.
Until CRRT emerged as a form of therapy, IHD, and
less commonly, acute PD were utilized for severe ARF.
The advantages of CRRT over IHD include more precise fluid, electrolyte, and metabolic control; increased
hemodynamic stability; and the ability to administer
unlimited nutritional support. The disadvantages of
CRRT include requirements for prolonged anticoagulation, patient immobilization, and sophisticated nursing
surveillance. PD is utilized in hypotensive patients where
CRRT is unavailable. Although CRRT is often considered to be superior to IHD, studies have not demonstrated a significant difference in patient outcomes.23 However, CRRT is preferable in patients with cerebral
edema, liver failure, severe lactic acidosis, and profound
hypotension. Sustained low efficiency dialysis has
promise as a hybrid therapy that combines the advantages of both continuous and intermittent therapies.

Table 5. Treatment of Hyperkalemia

Stabilize excitable tissues (cardiac and neuromuscular):
Calcium gluconate (10% solution), 10 to 20 mL given as an
intravenous bolus
Calcium chloride (10% solution), 5 mL given as an intravenous
bolus
Each may be repeated every 5 min if the electrocardiogram
appearance does not improve. Calcium gluconate should be
mixed in 100 mL of 5% dextrose and infused over 10 to 20 min
if the patient has been treated with digoxin.
Shift potassium into cells:
Regular insulin, 10 U plus 50 mL of 50% dextrose given as an
intravenous bolus, followed by 10% dextrose at 50 mL/min until
definitive therapy is instituted. Check glucose levels at 1 to 2 h
intervals.
Albuterol (5 mg/mL concentration), 10 to 20 mg nebulized over
approximately 10 min
Terbutaline, 7 g/kg administered via subcutaneous injection
Combination therapy of insulin/dextrose and nebulized albuterol
Remove potassium from the body:
Acute hemodialysis (low potassium dialysate) to remove potassium in patients with severe renal insufficiency
Sodium polystyrene sulfonate, 15 to 30 g plus 15 to 30 mL of
sorbitol administered orally or rectally (without sorbitol)

PROGNOSIS
Given its diverse causes, the long-term effects of
ARF are unknown. Progressive kidney dysfunction is
commonly observed after severe ARF.24 Irreversible
ARF occurs in 5% of cases and approaches 16% in the
elderly.25 When ARF is severe enough to necessitate
RRT, hospital mortality exceeds 50%.26

4.

5.

6.

CONCLUSION
Hospitalized patients may develop ARF from various
etiologies, although ATN is the most common cause.
Rapid diagnosis utilizing history, chart review, physical
examination, and laboratory data enhances the chances
for renal recovery. Appropriate management of ARF
and its complications is required to improve patient outcome. ARF that requires RRT is associated with inHP
creased mortality.

7.

8.

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