Renal Failure: Section Six Genitourinary and Gynecologic Systems

SECTION SIX Genitourinary and Gynecologic Systems
83
Renal Failure
Allan B. Wolfson
KEY CONCEPTS RENAL FAILURE

• T he causes of acute kidney injury (AKI) can be classified as prerenal, post-
The evaluation of renal disease in the emergency department (ED)
renal, and intrinsic renal disorders. Abrupt cessation of glomerular filtration
requires an approach that incorporates the urinalysis, serum and urine
typically results in a rise of the serum creatinine level of 1 to 2 mg/dL per
chemical determinations, and renal imaging studies. This approach
day.
assesses the degree of renal dysfunction and establishes the foundation
• Management of AKI is directed first at potentially lethal complications such
for distinguishing acute kidney injury (AKI) from chronic kidney dis-
as hyperkalemia or volume overload and then at reversal of the underlying
ease (CKD).
cause of renal dysfunction. It is important to avoid any further hemody-
namic or toxic insults to the kidneys.
• Patients with acute or chronic kidney disease have a limited ability to ACUTE KIDNEY INJURY
handle fluid and solute loads and have altered metabolism of many drugs.
Foundations
Therefore, the patient’s impaired renal function must be considered when
The hallmark of AKI (formerly termed acute renal failure [ARF]) is
fluid is administered or drugs are prescribed.
progressive azotemia, which commonly is accompanied by a wide
• The most rapidly lethal complication of acute and chronic kidney disease is
range of other disturbances, depending on the severity and duration
hyperkalemia.
of renal dysfunction. These include metabolic derangements (e.g.,
• The most common problems with vascular access devices used for hemo-
metabolic acidosis, hyperkalemia), disturbances of body fluid balance
dialysis are thrombosis, hemorrhage, and infection. Access infection often
(particularly volume overload), and a variety of effects on almost every
presents as fever without an obvious source and, if suspected, appropriate
organ system (Box 83.1).
IV antibiotics should be administered presumptively while awaiting blood
The causes of AKI are divided into those that decrease renal blood
culture results.
flow (prerenal), produce a renal parenchymal insult (intrarenal), or
• Peritoneal dialysis–associated peritonitis typically presents with cloudi-
obstruct urine flow (obstructive, or postrenal). Identification of a pre-
ness of the peritoneal dialysis effluent. The diagnosis is made by a positive
renal or postrenal cause of AKI generally makes it possible to initiate
Gram stain or finding of more than 100 WBC/mm3 in the effluent, with at
specific corrective therapy; if these two broad categories of AKI can
least 50% polys. It is generally treated on an outpatient basis with intraper-
be excluded, an intrarenal cause is implicated. The renal parenchymal
itoneal antibiotics self-administered by the patient.
causes of AKI can be usefully subdivided into those primarily affecting
• Chest pain in the dialysis patient should be presumed initially to be due to
the glomeruli, intrarenal vasculature, or renal interstitium. The term
acute coronary syndrome, although other potentially serious causes may
acute tubular necrosis denotes another broad category of intrinsic renal
also be responsible. Serum troponin levels tend to be elevated in patients
failure that cannot be attributed to a specific glomerular, vascular, or
with poor renal function, but patients with myocardial infarction show the
interstitial cause (Fig. 83.1).
typical temporal pattern of rise and fall of troponin levels.
Renal failure can lead to numerous other systemic and organ-specific
• Hypotension in patients with chronic kidney disease (CKD) may be caused
effects. Uremia impairs host defenses, particularly leukocyte function,
by infection but may also be the result of rapid fluid removal during dial-
and infection is a significant cause of morbidity and mortality in AKI.
ysis. This often responds readily to fluid administration. Pericardial tam-
Pericarditis, which has a prevalence of 10% to 20% in dialyzed patients
ponade is another cause of hypotension that should be considered for
with CKD, also may occur in patients with AKI. Urgent dialysis is indi-
these patients.
cated when there is associated pericardial effusion and tamponade.
• Altered mental status is most commonly due to causes similar to those
Neurologic abnormalities in AKI may be precipitated by electrolyte
seen in patients without renal disease but is sometimes the result of over-
abnormalities, medications, or uremia. Anorexia, nausea, vomiting, gas-
rapid shifts in intravascular fluid and solutes during dialysis, termed dis-
tritis, and pancreatitis also are associated with AKI and significant gas-
equilibrium syndrome.
trointestinal (GI) hemorrhage is seen in about 10% of patients.
1163
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1164 PART III Emergency Medicine by System
Impaired erythropoiesis, shortened red blood cell (RBC) survival, between AKI and CKD often is difficult, especially if prior records and
hemolysis, hemodilution, and GI blood loss all play a role in the normo- laboratory results are not available. The finding of small kidneys on
cytic normochromic anemia that usually accompanies AKI. Although abdominal imaging or bone changes of secondary hyperparathyroid-
mild thrombocytopenia may be present, it is the qualitative defect in ism on hand films demonstrating abnormal calcifications suggests that
platelet function thought to be caused by the effect of circulating ure- the renal failure is chronic. Anemia, hypocalcemia, and hyperphospha-
mic toxins that contributes to these patients’ bleeding tendencies. temia, however, should not be relied on to identify patients who have
CKD because these abnormalities can develop rapidly in AKI.
Clinical Features In evaluating the patient with azotemia, the emergency clinician
When the presence of azotemia or renal failure has been discovered, uses history, physical examination, and laboratory studies to seek
the first consideration in the ED evaluation should be the possibility of clues to the cause and to identify signs and symptoms of uremia, vol-
potentially life-threatening complications (e.g., hyperkalemia, pulmo- ume overload, or other complications of renal failure. In attempting
nary edema). Assuming that these have been satisfactorily ruled out, to identify the cause, the general strategy is to rule out prerenal and
the next step is to determine whether the condition represents AKI postrenal causes before considering the many intrinsic renal causes.
or is the result of preexisting renal disease. The clinical distinction First, potential sources of volume loss and causes of decreased cardiac
output are sought in the history, and the patient should be questioned
about lightheadedness, bleeding, GI fluid loss, abnormal polyuria,
BOX 83.1 Clinical Features of Acute Kidney or symptoms of congestive heart failure (CHF). In men, a history
Injury of nocturia, frequency, hesitancy, or decreased urinary stream sug-
gests prostatic obstruction. A history of lower tract symptoms or of
Cardiovascular
abdominal or pelvic tumor in either gender is sought, as is a history
Pulmonary edema
of kidney stones or chronic urinary tract infection (UTI). A history of
Arrhythmia
acute anuria, defined as the production of less than 100 mL of urine/
Hypertension
day, is most often the result of high-grade urinary tract obstruction,
Pericarditis
although it also may accompany severe volume depletion, severe
Pericardial effusion
acute glomerulonephritis, cortical necrosis, or bilateral renal vascu-
Myocardial infarction
lar occlusion. Intermittent anuria, on the other hand, is characteris-
Pulmonary embolism
tic of obstructive disease. Medication use and possible exposure to
Metabolic radiographic contrast agents or other exogenous toxins are other key
Hyponatremia components of the history. A history of hypertension, dark-colored
Hyperkalemia urine, rash, fever, or arthritis suggests intrinsic renal disease or a mul-
Acidosis tisystem disorder.
Hypocalcemia The physical examination focuses on signs of volume depletion,
Hyperphosphatemia such as tachycardia and decreased skin turgor. Documented short-term
Hypermagnesemia changes in body weight also offer a valuable clue in assessing volume
Hyperuricemia status, particularly in patients who are chronically ill. Volume overload
Neurologic
Asterixis Azotemia
Neuromuscular irritability
Mental status changes
Somnolence
History, physical exam,
Coma serum chemistries
Seizures
Gastrointestinal
Correct prerenal azotemia Improves
Nausea
Vomiting
Gastritis
Gastroduodenal ulcer Rule out obstruction Improves
Gastrointestinal bleeding
Pancreatitis
Malnutrition Intrinsic renal disease
Hematologic
Anemia Urinalysis
Hemorrhagic diathesis Urine electrolytes
Infectious
Pneumonia
Vascular Glomerular AIN ATN
Septicemia (vasculitis) (glomerulonephritis)
Urinary tract infection
Wound infection Fig. 83.1 Evaluation of azotemia. AIN, Acute interstitial nephritis; ATN,
acute tubular necrosis.
CHAPTER 83 Renal Failure 1165
is suggested by findings of jugular vein distention and the presence of Patients who have CHF or cirrhosis form an important subset
rales or peripheral edema. of those with prerenal azotemia. These patients often are sodium-
A distended bladder is percussible when it contains at least 150 mL overloaded and water-overloaded, yet the effective intra-arterial vol-
of urine, and the dome is palpable abdominally when the bladder con- ume is decreased. Administration of diuretics has the potential to
tains 500 mL. Ultrasonography can be used to detect bladder distention decrease intravascular volume further, resulting in decreased glomer-
or postvoid residual volume if there is a question of urinary retention. ular filtration and prerenal azotemia. For some patients with advanced
A prostate examination in men and pelvic examination in women are CHF or hepatic disease, a state of chronic, stable, prerenal azotemia
also necessary components of the examination. The presence of rash, may be the best achievable compromise between symptomatic volume
purpura, pallor, or petechiae on skin examination may be noted, as is overload and severe renal hypoperfusion.
arthritis, musculoskeletal tenderness, and findings suggestive of infec- Glomerular perfusion also may be decreased in patients with
tion or malignancy. normal intravascular volume and normal renal blood flow who take
angiotensin-converting enzyme (ACE) inhibitors or, more commonly,
Differential Diagnosis prostaglandin inhibitors. All nonsteroidal antiinflammatory drugs
The management of AKI requires a systematic approach to the poten- (NSAIDs), including aspirin, inhibit prostaglandin synthesis. Renal
tial underlying causes. Once prerenal and postrenal causes are consid- vasodilator prostaglandins are critical in maintaining glomerular per-
ered, the diagnostic and management strategies focus on the intrarenal fusion in patients with conditions such as CHF, chronic renal insuffi-
pathologies. ciency, and cirrhosis, in which elevated circulating levels of renin and
angiotensin II decrease renal blood flow and GFR. In this setting, a
Prerenal Azotemia decrease in the production of vasodilator prostaglandins may result
Decreased renal perfusion that is sufficient to cause a decrease in in acute intrarenal hemodynamic changes and a reversible decrease
the glomerular filtration rate (GFR) results in azotemia. The possible in renal function. This phenomenon also is seen with the selective
causes are grouped into entities causing intravascular volume deple- cyclooxygenase-2 inhibitor class of NSAIDs. Other risk factors include
tion, volume redistribution, or decreased cardiac output (Box 83.2). advanced age, diuretic use, renovascular disease, and diabetes. This
Patients who have preexisting renal disease are particularly sensitive to entity is distinct from other renal complications of NSAIDs such as
the effects of diminished renal perfusion. interstitial nephritis and papillary necrosis.
Prerenal azotemia is characterized by increased urine specific grav-
ity, a blood urea nitrogen (BUN) to creatinine ratio generally between Postrenal (Obstructive) Acute Kidney Injury
10:1 and 20:1, urine sodium concentration less than 20 mEq/dL, and Obstruction is an eminently reversible cause of AKI and should be
fractional excretion of sodium (FENa) less than 1%. The condition considered in every patient with newly discovered azotemia or wors-
generally can be corrected readily by expanding extracellular fluid vol- ening renal function. Obstruction may occur at any level of the uri-
ume, augmenting cardiac output, or discontinuing vasodilating anti- nary tract but usually is caused by prostatic hypertrophy or functional
hypertensive drugs. However, severe prolonged prerenal azotemia can bladder neck obstruction (e.g., secondary to medication side effects
result in acute tubular necrosis (ATN). or neurogenic bladder; Box 83.3). Intrarenal obstruction may result
from the intratubular precipitation of uric acid crystals (e.g., with
tumor lysis), oxalic acid (as in ethylene glycol ingestion), phosphates,
BOX 83.2 Causes of Prerenal Azotemia myeloma proteins, methotrexate, sulfadiazine, acyclovir, or indinavir.
Bilateral ureteral obstruction (or obstruction of the ureter of a soli-
Volume Loss tary kidney) may be caused by retroperitoneal fibrosis, tumor, surgical
Gastrointestinal—vomiting, diarrhea, nasogastric drainage complications (such as inadvertent ligation of the ureter), stones, or
Renal—diuresis
Blood loss
Insensible losses
BOX 83.3 Causes of Postrenal Renal Failure
Third-space sequestration
Pancreatitis Intrarenal and Ureteral Causes
Peritonitis Kidney stones
Trauma Sloughed papillas
Burns Bilateral ureteral compression related to malignancy or benign gynecologic
causes
Cardiac Causes Retroperitoneal fibrosis
Myocardial infarction Uric acid, oxalic acid, or phosphate crystal precipitation
Valvular disease Sulfonamide, methotrexate, acyclovir, or indinavir precipitation
Cardiomyopathy
Decreased effective arterial volume Bladder
Antihypertensive medication Kidney stone
Nitrates Blood clot
Prostatic hypertrophy
Neurogenic Causes Bladder carcinoma
Sepsis Neurogenic bladder
Anaphylaxis
Hypoalbuminemia Urethra
Nephrotic syndrome Phimosis
Liver disease Stricture
blood clots. A sudden deterioration in renal function in the setting of testing to identify the cause of acute glomerulonephritis is not indi-
diabetes mellitus, analgesic nephropathy, or sickle cell disease suggests cated in the ED setting and is more appropriately performed as part of
papillary necrosis. an inpatient evaluation.
Acute Interstitial Nephritis. Acute interstitial nephritis (AIN) is
Intrinsic Acute Kidney Injury usually precipitated by drug exposure or by infection. Drug-induced
Of the specific intrarenal disorders that cause AKI, glomerulonephritis, AIN is poorly understood, but the absence of a clear relationship to the
interstitial nephritis, and abnormalities of the intrarenal vasculature dose, and recurrence of the syndrome on rechallenge with the offending
are amenable to specific therapy and are important to consider as pos- agent, suggests that an immunologic mechanism is responsible. The
sible causes. These entities are responsible for only 5% to 10% of cases most commonly incriminated drugs are the penicillins, diuretics, and
of AKI in adult inpatients; most cases are caused by ATN. In adults in NSAIDs. AIN has been reported in association with bacterial, fungal,
whom AKI develops outside the hospital, the incidence of glomerular, protozoan, and rickettsial infections.
interstitial, and small vessel disease is much greater. In children, these Patients with AIN typically have rash, fever, eosinophilia, and eosin-
entities account for approximately 50% of the cases of AKI (Box 83.4). ophiluria, but it is common for one or more of these cardinal signs to
Acute Glomerulonephritis. This may represent a primary renal be absent. Pyuria, gross or microscopic hematuria, and mild protein-
process or may be the manifestation of any of a wide range of uria are observed in some cases. A definite diagnosis sometimes can be
other disease entities (see Box 83.4). Patients may have dark urine, made only on renal biopsy. Treatment of AIN is directed at removing
hypertension, edema, or CHF (secondary to volume overload) or the presumed cause; infections should be treated and offending drugs
may be completely asymptomatic, in which case the diagnosis rests discontinued. Renal function generally returns to baseline over several
on an incidental finding on urinalysis. The hematuria associated with weeks, although chronic renal failure has been reported to occur.
glomerular disease may be microscopic or gross and may be persistent Intrarenal Vascular Disease of the Kidney. This can be classified
or intermittent. Proteinuria, although often in the range of 500 mg/day according to the size of the vessel that is affected. Disorders such
to 3 g/day, is not uncommonly in the nephrotic range, defined as 3.5 g/ as renal arterial thrombosis or embolism, which affect large blood
day or more. The presence of hematuria, proteinuria, or red cell casts vessels, must be bilateral—or affect a single functioning kidney—to
is highly suggestive of glomerulonephritis. Conversely, the absence produce AKI. Whether to attribute such cases of AKI to a prerenal or
of red cell casts, proteinuria, and hematuria essentially excludes intrarenal vascular cause is a matter of semantics. The most common
glomerulonephritis as the cause of AKI. cause of thrombosis probably is trauma; thrombosis also may occur
The specific diagnosis of acute glomerulonephritis caused by pri- after angiography or may be secondary to aortic or renal arterial
mary renal disease often is ultimately made by renal biopsy. However, dissection. Renal atheroembolism is thought to occur commonly, at
when glomerulonephritis is secondary to a systemic disease such as least on a microscopic level, after arteriography but it is an uncommon
systemic lupus erythematosus, the clinical signs and symptoms and cause of AKI. Similarly, patients with chronic atrial fibrillation or
results of laboratory assessment aid considerably in narrowing the infective endocarditis may experience embolization of the kidney
scope of the differential diagnosis. As a rule, extensive laboratory but rarely develop AKI as a result. Renal arterial embolism can
BOX 83.4 Intrinsic Renal Diseases That Cause Acute Kidney Injury
Vascular Diseases Other postinfectious glomerulonephritis
Large-Vessel Diseases Rapidly progressive glomerulonephritis
Renal artery thrombosis or stenosis
Renal vein thrombosis Tubulointerstitial Diseases and Conditions
Atheroembolic disease Drugs (many)
Toxins (e.g., heavy metals, ethylene glycol)
Small-and Medium-Sized Vessel Diseases Infections
Scleroderma Multiple myeloma
Malignant hypertension
Hemolytic uremic syndrome Acute Tubular Necrosis
Thrombotic thrombocytopenic purpura Ischemia
HIV-associated microangiopathy Shock
Sepsis
Glomerular Diseases Severe prerenal azotemia
Systemic Diseases
Systemic lupus erythematosus Nephrotoxins
Infective endocarditis Antibiotics
Systemic vasculitis (e.g., periarteritis nodosa, Wegener granulomatosis) Radiographic contrast agents
Henoch-Schönlein purpura Myoglobinuria
HIV-associated nephropathy Hemoglobinuria
Essential mixed cryoglobulinemia
Goodpasture syndrome Other Diseases and Conditions
Severe liver disease
Primary Renal Diseases Allergic reactions
Poststreptococcal glomerulonephritis NSAIDs
HIV, Human immunodeficiency virus; NSAIDs, nonsteroidal antiinflammatory drugs.
cause acute renal infarction, generally manifested by sudden flank, ATN is common in postoperative patients, although not all cases
back, chest, or upper abdominal pain. Urinary findings, including can be attributed to intraoperative hypotension or hemorrhage. Con-
hematuria, are variable. The diagnosis usually is made by renal flow comitant sepsis, increased age, preexisting renal disease, and other
scanning or arteriography. comorbid conditions are associated with a worse outcome.
Several diseases that affect the smaller intrarenal vessels can cause Recently, it has been noted that patients hospitalized for coronavi-
AKI (see Box 83.4). Patients whose disease is severe enough to cause rus disease 2019 (COVID-19) may develop AKI during the course of
AKI also are generally found to have hypertension, microangiopathic their illness, particularly when intensive care is required. The mech-
hemolytic anemia, and other systemic and organ-specific manifesta- anism is likely to be multifactorial, including hypovolemia, cardiac
tions. Infection with Escherichia coli O157:H7 has emerged as a major dysfunction, exposure to nephrotoxins, and direct renal endothelial
cause of hemolytic uremic syndrome, an important cause of AKI in damage related to viremia, immune dysfunction, or hypercoagulability.
children. Patients may initially present with proteinuria early in the course; AKI
Patients with scleroderma (systemic sclerosis) may have so-called is felt to be a marker of the severity of disease. Treatment is supportive,
scleroderma renal crisis, characterized by malignant hypertension and with careful management of fluid balance and optimization of renal
rapidly progressive renal failure. Whereas vasculitis associated with glo- perfusion. More severe cases require hemodialysis or other forms of
merular capillary inflammation typically causes gross or microscopic renal replacement therapy.14
hematuria and the formation of red cell casts, vascular involvement of Nephrotoxins constitute the other major cause of ATN. Among the
the medium-sized vessels, such as that produced by scleroderma, often most prominent of these are the endogenous pigments myoglobin and
spares the preglomerular vessels and tends not to produce an active hemoglobin, associated with rhabdomyolysis (Box 83.5). Hypotension
urine sediment. Extrarenal manifestations (e.g., rash, fever, arthritis, secondary to fluid loss into damaged muscle is thought to worsen the
pulmonary symptoms) are usually evident. effects of myoglobinuria on the renal tubule, as does acidemia. Hemo-
For malignant hypertension, both as a separate entity and as a part lysis, resulting in the release of hemoglobin into the circulation and
of scleroderma renal crisis, appropriate treatment can produce remis- hemoglobinuria, can cause ATN but usually only in the presence of
sion of AKI. Patients with malignant hypertension have been reported coexisting dehydration, acidosis, or other causes of decreased renal
to recover renal function after aggressive antihypertensive therapy, perfusion. ATN may be associated with the hemolysis of as little as 100
with temporary maintenance on dialysis if necessary. In patients with mL of blood.
scleroderma renal crisis, specific therapy with ACE inhibitors has been ATN associated with rhabdomyolysis is often oliguric; it is char-
shown to result in improvement in renal function in a significant pro- acterized by rapid increases in the serum creatinine, potassium,
portion of cases. phosphorus, and uric acid levels. Creatine released from muscle is
Acute Tubular Necrosis. ATN refers to a generally reversible metabolized to creatinine, which may result in serum creatinine level
deterioration of kidney function associated with a variety of renal increases of more than 2 mg/dL/day, in contrast to the increase of 0.5
insults. Oliguria may or may not be a feature. The diagnosis is made to 1.0 mg/dL/day typically seen in other forms of AKI. The BUN/cre-
after prerenal and postrenal causes of ARF and disorders of glomeruli, atinine ratio often is less than 10 : 1. Intracellular potassium released
interstitium, and intrarenal vasculature have been excluded. In a from damaged muscle may raise the serum potassium level by 1 to
few disorders, these discrete categories overlap. For example, AKI 2 mEq/L in several hours. Likewise, phosphate released from mus-
associated with multiple myeloma or ethylene glycol toxicity is cle may cause dramatic increases in the serum phosphate level. Uric
associated with intrarenal obstruction and interstitial disease, as well acid, produced by the metabolism of purines released from damaged
as a probable direct toxic effect on the renal tubule itself. muscle, may accumulate to levels high enough to cause acute uric
The most common precipitant of ATN is renal ischemia occurring acid nephropathy.
during surgery or after trauma and sepsis. The remainder of cases
occur in the setting of medical illness, usually as a result of the admin-
istration of a nephrotoxic aminoglycoside antibiotic or in association BOX 83.5 Causes of Pigment-Induced
with rhabdomyolysis. Multiple causes can be identified in some cases; Acute Kidney Injury
in others, a definitive cause cannot be established.
Rhabdomyolysis and myoglobinuria
Decreased renal perfusion results in a continuum of renal dys-
Crush injury
function that ranges from transient prerenal azotemia at one extreme
Compartment syndrome
to ATN at the other. Early during the period of renal ischemia, renal
Electrical injury
function can be restored completely by restoring renal blood flow but,
Myonecrosis from coma or immobilization
at some point, continued hypoperfusion results in renal dysfunction
Acute arterial occlusion
unresponsive to volume repletion, and ATN supervenes. ATN may
Vigorous exertion
occur in the absence of frank hypotension; even modest renal ischemia
Status epilepticus
may result in ATN in susceptible persons. Individual susceptibility to
Hyperthermia/heat stress
ATN may be related to the balance of prostaglandin-mediated vaso-
Metabolic myopathy
pressor and vasodilatory influences on the renal vasculature.
Drugs/toxins
Postischemic ATN can occur in the setting of volume loss from the
Hypokalemia
GI tract (upper or lower), skin, or kidneys or can result from severe
Hypophosphatemia
hemorrhage or major burns. Heat stroke commonly is associated with
Hemoglobinuria
the development of ATN, which is thought to result from a combina-
Acute hemolysis
tion of volume loss, hyperpyrexia, and rhabdomyolysis. Another cause
Transfusion reaction
of ATN is hyperglycemic hyperosmolar syndrome, which can be asso-
Drugs/toxins
ciated with loss of as much as 25% of total body water. ATN also is seen
Infections
in the setting of cardiogenic shock, sepsis, and third spacing of fluids in
pancreatitis and peritonitis. G6PD, Glucose-6-phosphate dehydrogenase; RBCs, red blood cells.
Urine dipstick testing yields a positive result for heme in, at most, calcium, phosphorus, and magnesium determinations), electrocardio-
50% of patients with rhabdomyolysis, because myoglobin is rapidly gram (ECG), and chest radiograph help establish the patient’s baseline
cleared from the serum and may therefore be undetectable in the urine status and provide information about possible complications.
at the time of presentation. Thus, a negative result on urine dipstick
testing does not rule out the diagnosis. Serum creatine kinase (CK) Urine Volume
is cleared much more slowly, so measurement of serum CK levels is a Urine flow does not diminish until the GFR is sharply decreased; thus,
more sensitive test. urine volume is a poor indicator of renal dysfunction. Oliguria, defined
Antibiotics are commonly implicated in the development of ATN, as a urine volume of 100 to 400 mL/24 hr, may be seen with prerenal
with aminoglycosides being the most commonly associated. Higher (blood flow–dependent), intrinsic (intrarenal), or postrenal (obstruc-
doses and longer duration of therapy are associated with higher serum tive) causes of AKI. Although uncommon, alternating oliguria and
drug levels, leading to greater accumulation of drug in the renal anuria (the latter defined as less than 100 mL/24 hr), is a classic indica-
parenchyma and a greater likelihood of nephrotoxicity. Increased age, tor of intermittent obstruction, which occurs as urine collects behind
impaired renal function, dehydration, and exposure to other nephro- an obstructing stone or tumor and then is allowed to flow past as the
toxins are additional risk factors. Once-daily administration of a some- obstructing material shifts position.
what higher dose is associated with less nephrotoxicity but has equal
antimicrobial effectiveness. Urinalysis
Aminoglycoside-induced ATN typically has a gradual onset. Clini- The standard urinalysis consists of dipstick screening for heme pig-
cally significant renal dysfunction usually occurs only after several days ment, protein, glucose, ketones, pH, leukocyte esterase, and nitrite and
and often after more than 1 week of therapy. However, renal failure can microscopic examination of a spun specimen of freshly voided urine
develop as late as 10 days after a drug has been discontinued, an obser- and should be performed on all patients with AKI. Dipstick testing for
vation that appears to be explained by the prolonged tissue half-life heme and protein can provide important information related to renal
characteristic of these agents. Renal function returns to normal after function.
an average of 6 weeks, but the condition occasionally progresses to per- Heme. The dipstick detects free hemoglobin from lysed RBCs (or
manent renal injury. myoglobin) and the hemoglobin inside RBCs but is more sensitive to
Radiographic contrast agents have long been considered a common free hemoglobin. Although as few as three RBCs/high-power field (hpf)
cause of hospital-acquired renal insufficiency. AKI associated with can be detected, on any given sample the dipstick may fail to identify
these agents has been defined as an increase in serum creatinine level of 10% to 15% of patients who are otherwise found to have microscopic
25% or an increase of 0.5 mg/dL over baseline, with a temporal relation hematuria, typically defined as more than three RBCs/hpf. A positive
to contrast medium administration and in the absence of other iden- result on dipstick testing should prompt microscopic examination of
tifiable causes. Cases have been noted after any procedure involving the urine. If red cells are seen, the diagnosis of hematuria is confirmed,
intravascular administration of contrast material. though a level of two to three RBCs/hpf is commonly accepted as
Radiocontrast-associated AKI presents on a spectrum ranging normal. If the dipstick result is positive but findings on microscopic
from asymptomatic nonoliguric renal insufficiency to severe renal fail- examination are negative, pigmenturia (myoglobin or free hemoglobin)
ure requiring dialysis. Most cases are mild, however, likely due at least is suspected.
partially to the broad criteria by which the entity has been defined.1-3 Protein. The dipstick test for protein, which uses the color change
Typically, an increase in the serum creatinine level is noted within 3 of tetrabromophenol blue, can detect protein at concentrations of
days of exposure, with a return to normal levels within 10 to 14 days. 10 to 15 mg/dL but does not yield reliably positive results until the
The most important risk factor for radiocontrast agent–induced concentration is greater than 30 mg/dL. Moreover, the relation between
AKI is preexisting renal insufficiency. Diabetes mellitus, multiple color intensity and protein concentration is only approximate. The
myeloma, age older than 60 years, and volume depletion are also asso- dipstick reagent is three to five times more sensitive to albumin than to
ciated with greater risk. Diabetic patients with a serum creatinine level globulins and immunoglobulin light chains (e.g., Bence Jones protein),
less than 1.5 mg/dL appear to be at lower risk than those whose serum an important limitation. False-positive results are caused by alkaline
creatinine level is more than 1.5 mg/dL. Importantly, large doses and urine, hematuria, or prolonged immersion of the dipstick in the urine.
repeated doses of contrast material are associated with increased risk False-negative results are seen with dilute urine. After dipstick testing
of ATN, particularly if a second study is performed within 72 hours of has been completed, the sediment from a spun urine specimen is
the first. examined under the microscope.
Volume depletion is an independent risk factor for contrast Casts are formed from urinary Tamm-Horsfall protein—a product
nephropathy, and aggressive volume expansion before contrast expo- of the tubular epithelial cells that gels at low pH and high concentration
sure appears to have a protective effect.4 Modest volumes of intrave- and when mixed with albumin—or from red cells, tubular cells, or cel-
nous normal saline (3 mL/kg over 1 hour, followed by 1.5 mL/kg/hr for lular debris in the urine. The composition of a cast reflects the contents
4 hours after contrast exposure) appear to be effective in decreasing the of the tubule. Casts are classified according to their appearance or con-
likelihood of nephrotoxicity. Sodium bicarbonate does not appear to stituents (e.g., hyaline, red cell, white cell, granular, or fatty casts). Hya-
offer an advantage over normal saline, and the weight of evidence does line casts, those that are devoid of contents, are seen with dehydration,
not favor a beneficial effect of administering oral N-acetylcysteine as after exercise, or in association with glomerular proteinuria. Red cell
part of the treatment regimen.5 casts indicate glomerular hematuria, as seen in glomerulonephritis;
the presence of even a few red cell casts is significant. White cell casts
Diagnostic Testing imply the presence of renal parenchymal inflammation. Granular casts
Laboratory evaluation of renal dysfunction begins with a dipstick are composed of cellular remnants and debris. Fatty casts, like oval fat
and microscopic urinalysis and measurement of urine output. BUN, bodies, generally are associated with heavy proteinuria and nephrotic
serum creatinine, urine sodium, and FENa levels are determined to syndrome.
help evaluate renal function and provide clues about the cause of AKI. Microscopic examination of the urinary sediment can be helpful
A complete blood count, serum electrolyte panel (expanded to include in establishing the cause of AKI. A sediment without formed elements
or with only hyaline casts is characteristic of prerenal azotemia or particularly if the renal injury is mild and some capability to retain
obstruction. Red cell casts suggest glomerulonephritis or vasculitis. sodium has been preserved. Thus, intermediate values for urine sodium
Fatty casts also suggest glomerular disease. In ATN, the urinary sedi- concentration and FENa are of little help in differentiating between
ment commonly shows granular casts and renal tubular epithelial cells. the two conditions. The administration of mannitol or a loop diuretic
Large numbers of polymorphonuclear leukocytes are observed in inter- within the several hours preceding urine collection also may make
stitial nephritis, papillary necrosis, and pyelonephritis. Eosinophil- interpretation of urine values difficult because the urinary sodium
containing casts, appreciated only after staining of the sediment, are level will tend to be higher and the urine less concentrated, causing the
typical of allergic interstitial nephritis. Uric acid crystals suggest uric results in prerenal azotemia to resemble those in intrinsic renal failure.
acid nephropathy but are extremely nonspecific; oxalic acid or hippuric In glomerulonephritis, the urinary indices generally reflect intact
acid crystals may be seen in cases of ethylene glycol ingestion. tubular sodium handling, but the diagnosis is more accurately made
by urine microscopy. In obstructive uropathy, the values of the urinary
Serum and Urine Chemical Analysis indices depend on the duration of obstruction and cannot be relied on
Creatinine and Blood Urea Nitrogen. The normal range for the to indicate the presence or absence of obstruction.
serum creatinine level extends from 0.5 mg/dL in thin people to 1.5
mg/dL in muscular persons. Spurious elevations (up to 2 mg/dL) Renal Imaging
can be caused by acetoacetate, which cross-reacts with creatinine in Renal imaging is often helpful in the evaluation of the patient with
some commonly used assays, and by certain medications (such as kidney dysfunction, particularly when obstruction is suspected. Com-
trimethoprim and cimetidine) that reversibly inhibit tubular creatinine puted tomography (CT) scanning provides an anatomic image of the
secretion, causing a modest elevation of the serum creatinine despite urinary tract but does not provide an evaluation of renal function. The
a normal GFR. Serum creatinine concentration is a function of the classic CT findings of obstruction are kidneys that are normal to large
amount of creatinine entering the blood from muscle, its volume of in size, and demonstration of hydronephrosis or hydroureter. Since
distribution, and its rate of excretion. Because the first two are usually contrast-enhanced CT subjects the kidneys of an already azotemic
constant, changes in the serum creatinine concentration generally patient to the risk of an additional potential insult from the contrast
reflect changes in GFR. The creatinine clearance is commonly estimated agent, ultrasonography and noncontrast CT are much preferred for
by the Cockcroft-Gault equation: patients with preexisting renal insufficiency (Fig. 83.2).
Computed Tomography. Noncontrast CT may be useful in
Creatinine clearance (mL/min) = ([140–age] × weight) evaluating some azotemic patients. Hydronephrosis can be recognized
⁄(72 × serum creatinine) without the use of contrast material. Often, dilated ureters can also be
(× 0.85 if female) seen without contrast enhancement, and the level of obstruction can be
determined. The cause of obstruction (e.g., bilateral stones, lymphoma,
Under steady-state conditions, if the GFR is halved, the serum cre- retroperitoneal hemorrhage, metastatic cancer, retroperitoneal fibrosis)
atinine doubles. Abrupt cessation of glomerular filtration causes the often can also be delineated. Occasionally, bilateral ureteral obstruction
serum creatinine level to rise by 1 to 2 mg/dL per day. Thus, a daily produced by malignancy or retroperitoneal fibrosis may not cause
increment of less than 1 mg/dL suggests that at least some renal func- detectable proximal dilation of the urinary tract. When noninvasive
tion has been preserved. Rhabdomyolysis releases creatine into the studies yield negative results, the diagnosis of obstruction can be made
plasma and may cause the serum creatinine level to increase by more by retrograde pyelography or antegrade pyelography performed via a
than 2 mg/dL per day. The BUN level also rises with renal dysfunction percutaneous nephrostomy.
but is also influenced by many extrarenal factors. Increased protein Ultrasonography. Ultrasonography is a safe and reasonably reliable
intake, GI bleeding, and the catabolic effects of fever, trauma, infec- method for excluding obstruction as a cause of AKI. The normal kidney
tion, and drugs such as tetracycline and corticosteroids all increase shows an echo-free renal parenchyma surrounding the echogenic central
protein turnover and result in increased hepatic urea production and
increased BUN levels. Conversely, the BUN level tends to be decreased
in patients with liver failure or protein malnutrition.
When glomerular filtrate has been formed, renal urea clearance
is largely a function of flow rate. Urea clearance is thus decreased in
patients with prerenal azotemia or acute obstruction, despite preserva-
tion of tubular function. In such cases, the BUN/creatinine ratio usu-
ally is greater than the normal value of 10:1, whereas this ratio usually
is not markedly increased in cases of uncomplicated intrinsic AKI.
Urine Sodium and Fractional Excretion of Sodium. Normally, urine
sodium concentration parallels sodium intake. A low urine sodium
concentration thus indicates not only intact tubular reabsorptive
function but also the presence of a stimulus to conserve sodium.
The urine sodium concentration, as well as the FENa, an additional
measure of tubular sodium handling, helps distinguish between the
two most common causes of AKI, prerenal azotemia and ATN.
Measurement of urinary indices can be helpful in oliguric patients.
An oliguric patient with a urine sodium concentration less than 20
mEq/L and FENa less than 1% is likely to have prerenal azotemia,
whereas a urine sodium concentration more than 40 mEq/L and FENa
more than 1% suggest ATN. Values in patients with prerenal azote- Fig. 83.2 CT scan of bilateral hydronephrotic kidneys without IV contrast
mia overlap somewhat with those in patients with nonoliguric ATN, medium.
urothelium of the renal pelvis and calices. The sonographic appearance Treatment of postrenal AKI consists of relief of the obstruction. In
of the kidney in obstruction is that of an enlarged, central, sonolucent the absence of infection, full renal recovery is possible, even after 1 to 2
area that spreads the normal central echo densities. A similar pattern weeks of total obstruction, although the serum creatinine level may not
may be produced by renal cysts, but without associated ureteral dilation. return to baseline for several weeks. Because the onset of irreversible
Dilation of the collecting system generally is apparent within 24 to 36 loss of renal function with obstruction appears to be gradual, a few
hours of the onset of obstruction, but obstruction may not be evident in days’ delay in diagnosis generally is considered acceptable. Still, com-
patients who are evaluated early in the development of obstructive AKI. mon sense dictates that obstructions should be detected and relieved
promptly.
Diagnosis When prerenal and postrenal factors have been ruled out, the chal-
Prerenal azotemia is suspected in the setting of volume loss, volume lenge is to identify the cause of intrinsic renal AKI, keeping in mind
redistribution, or decreased effective renal perfusion. It typically the multitude of known possible causes (see Box 83.4). The differential
is associated with a normal urinalysis, high BUN/creatinine ratio, diagnosis can often be significantly narrowed by considering the clini-
increased urine osmolality, urine sodium concentration less than 20 cal setting and physical and laboratory findings. The clinical picture is
mEq/L, and FENa less than 1%. A rapid response to volume repletion often most consistent with the broad category of ATN.
also is characteristic. Patients who have oliguric AKI have a significantly higher mortality
Urethral or bladder neck obstruction is documented by the find- rate and much greater risk of complications than those who are not
ing of significant amounts of residual urine in the bladder by cathe- oliguric. The difference in prognosis may simply reflect a more severe
terization or ultrasound examination after the patient has voided or renal insult in patients who are oliguric, however, and it is not clear that
attempted to void spontaneously. An important point is that the abil- interventions aimed at converting oliguric to nonoliguric AKI have a
ity to void does not rule out obstruction. In fact, the urine volume in beneficial effect on renal function or mortality. Nevertheless, because
the presence of obstruction may range from zero to several liters per nonoliguric patients are easier to manage, an attempt to increase urine
day. Flank pain is likewise an insensitive marker for obstruction. Urine flow is warranted.
indices and the BUN/creatinine ratio tend not to be helpful, although The use of loop diuretics or mannitol often is effective in increas-
an increase in the latter is common in obstruction. A renal parenchy- ing urine flow when intravascular volume deficits have been corrected.
mal disorder often can be diagnosed by its manifestations on micro- Furosemide has not been shown to shorten the clinical course or affect
scopic urinalysis or by associated extrarenal manifestations (e.g., with mortality. Mannitol appears to be most useful when given at the time
multisystem disease) or clinical setting (e.g., recent exposure to a new of, or shortly after, the renal insult; the recommended adult dose is 12.5
medication). The absence of evidence of prerenal or postrenal causes in to 25 g, intravenous (IV). If urine output does not increase, further
a patient with AKI may be taken as presumptive evidence of an intra- doses may cause hyperosmolality and clinically significant intravascu-
renal parenchymal process. Among these, the possibility of an acute or lar volume overload in patients with impaired renal function. Dopa-
ongoing vascular insult should be kept in mind because timely inter- mine also has been used in an effort to increase urine output, but it has
vention can be important in preserving ultimate renal function. not been proven effective.
Certain specific considerations apply to toxin- induced ATN.
Management Pigment-induced ATN may be prevented by avoidance of hemolysis
ED management of AKI is directed at reversing decreases in GFR and and muscle injury and correction of the factors (e.g., dehydration,
urine output (if possible) while minimizing further hemodynamic and acidemia) known to predispose patients with pigmenturia to the
toxic insults, maintaining normal fluid and electrolyte balance, and development of renal failure. When hemolysis or rhabdomyolysis has
managing other complications of AKI, as required. Because renal fail- occurred, treatment is directed at eliminating the cause and preventing
ure alters the metabolism and action of many drugs, often in ways that the development of renal failure.
are not predictable, great care should be exercised in prescribing all Mannitol has been shown to prevent AKI in experimental mod-
medications. Easy access to online sources that provide guidelines for els of myoglobinuria, presumably by inducing osmotic diuresis and
drug dosages in renal failure, and readily available consultation with a decreasing intratubular deposition of pigment. Furosemide, on the
hospital pharmacist are of great help for this purpose. other hand, has not consistently shown a beneficial effect. Other stud-
After ensuring that the vital signs are adequate and the patient is ies have suggested that myoglobin precipitates in an acidic urine but
in no immediate danger from volume or metabolic derangements, the not in an alkaline urine. Thus, aggressive volume repletion, alkalini-
next step is to correct prerenal and postrenal factors, if any are iden- zation, and mannitol infusion have traditionally been recommended
tified. Intravascular volume is repleted in hypovolemic patients and after crush injuries to reduce the likelihood or severity of AKI. How-
maintained in euvolemic patients by matching input to measured and ever, there is good evidence that aggressive volume resuscitation alone
insensible output. Inadequate cardiac output is augmented when pos- is equally effective. When AKI has occurred, management is similar
sible. Postrenal or obstructive AKI is treated by restoration of normal to that for other forms of AKI, but early dialysis may be required to
urine outflow. Bladder outlet obstruction may be relieved by passage of control rapidly developing hyperkalemia, hyperphosphatemia, and
a Foley catheter, whereas upper tract obstruction may require percuta- hyperuricemia.
neous nephrostomy. Patients who have radiocontrast agent–induced ATN usually require
Renal insufficiency secondary to NSAIDs generally is revers- only supportive therapy. A more significant aspect of ED management
ible after withdrawal of the causative agent. For patients who are at is identifying patients who are at risk when contrast studies are being
increased risk but require treatment with NSAIDs, a short-acting considered. BUN and serum creatinine levels should be checked before
preparation (e.g., ibuprofen) should be prescribed and follow-up mon- contrast exposure in patient with risk factors, such as older age, dia-
itoring of renal function and the serum potassium level should begin betes, volume depletion, and underlying renal disease. Patients at risk
within days rather than weeks. If renal function is unchanged after a should be volume-repleted (if not contraindicated) before undergoing
short course of treatment, adverse effects from continuing therapy are the study, the administered dose of contrast agent should be kept as low
unlikely, although other potential mechanisms for the development of as possible, and multiple exposures to contrast should be avoided, as
renal dysfunction (e.g., interstitial nephritis) should be kept in mind. should concomitant use of other nephrotoxins.4
In addition to general measures aimed at minimizing decreases in phosphorus level usually ranges from 6 to 8 mg/dL but may be much
GFR and increasing urine output, an important component of the man- higher with rhabdomyolysis or in catabolic states. A calcium-phosphate
agement of AKI is the prevention or control of systemic complications. product greater than 70 mg2/dL2 may result in metastatic soft tissue
Of particular significance in this regard are metabolic derangements calcification. Hyperphosphatemia often is treated with oral calcium-
(e.g., hyperkalemia, hypocalcemia, hyperphosphatemia, metabolic aci- based antacids that bind ingested phosphate in the gut.
dosis) and complications of volume overload (e.g., hypertension, CHF). Acids produced in normal metabolic processes accumulate in AKI
and are buffered in part by serum bicarbonate, resulting in a decrease
Hyperkalemia and Other Metabolic Derangements in the serum bicarbonate level and a high anion gap metabolic aci-
Hyperkalemia. The most common metabolic cause of death in dosis. Compensatory hyperventilation may be mistakenly attributed
patients with AKI results from an inability to excrete endogenous and to primary cardiac failure or volume overload. The metabolic acido-
exogenous potassium loads. In oliguric patients, the serum potassium sis associated with AKI usually is mild, and treatment generally is not
level typically increases by 0.3 to 0.5 mEq/L per day, but greater increases necessary if the serum bicarbonate level is greater than 10 mEq/L.
occur in catabolic, septic, or traumatized patients and in the presence of Overzealous correction may result in hypokalemia, hypocalcemia, or
acidosis or exogenous potassium loads from diet or medication. This is of volume overload.
particular concern in patients with rhabdomyolysis and associated AKI. Hypermagnesemia. This may complicate AKI when patients
Hyperkalemia results in serious disturbances in cardiac electro- are given magnesium-containing antacids or laxatives. Thus, these
physiology that may culminate in cardiac arrest. Calcium chloride products, as well as magnesium itself (e.g., when given for preeclampsia
is considered the second choice agent given its irritating effect when or for treatment of arrhythmia or wheezing), should be avoided in the
administered parentally. Hyperkalemia is essentially asymptomatic setting of AKI.
until major manifestations of cardiotoxicity appear. Accordingly, Disturbances of Volume Regulation. These can be expected to occur
detection of hyperkalemia is a primary consideration in these patients. in most patients with AKI. Some nonoliguric patients excrete enough
Electrocardiographic changes correlate only roughly with the serum salt and water to produce intravascular volume depletion if adequate
potassium level. Mild hyperkalemia (serum potassium < 6.0 mEq/L) fluid replacement is not provided. Volume depletion prolongs recovery
may be cautiously observed without specific treatment while all exog- from AKI. Much more commonly, AKI is complicated by volume
enous sources of potassium are eliminated. If the serum potassium overload because sodium and water excretion may be inadequate to
level is greater than 6.5 mEq/L, and particularly if electrocardiographic match even modest intakes. Volume overload is largely responsible for
changes are present, urgent intervention is necessary. the hypertension often seen in those with AKI and commonly leads to
When cardiotoxicity must be reversed immediately (e.g., when CHF and pulmonary edema. Iatrogenic volume overload is particularly
there is hemodynamic compromise), IV calcium (10 mL of 10% cal- common and can be prevented only by careful attention to fluid intake
cium gluconate infused over 2 minutes, repeated after 5 minutes if and output, with prudent estimates of insensible loss. Volume overload
necessary) is the treatment of choice. Calcium directly antagonizes can be treated with diuretics or intravenous nitroglycerin while
the membrane effects of hyperkalemia. IV insulin, given with glucose preparations are being made to initiate dialysis.
to prevent hypoglycemia, temporarily shifts potassium to the intra-
cellular space. The safety and efficacy of β-agonists in hyperkalemic Disposition
patients have been well documented; like insulin, inhaled albuterol Patients with new-onset severe AKI should be hospitalized. If nephrol-
(in a dose of 10–20 mg for adult patients; for pediatric patients, a fixed ogy consultation and dialysis facilities are not available, transfer to
dose should be given based on patient weight [<25 kg: 2.5 mg, 25 to 50 another institution is advisable once volume and metabolic abnormal-
kg: 5 mg, >50 kg: 10 mg]) causes potassium to move into cells, thereby ities have been controlled and the patient is hemodynamically stable.
controlling hyperkalemia for 2 hours or more. Bicarbonate appears to Decisions regarding dialysis generally are made by the nephrology
be less effective in shifting potassium into cells than once thought. It consultant and take into account many factors, including laboratory
should be used with caution in patients with renal failure because of its test abnormalities and the presence or absence of signs and symptoms
potential to cause volume overload and provoke hypocalcemic tetany of uremia (e.g., nausea, vomiting, change in mental status). Many
or seizures. Sodium polystyrene sulfonate (Kayexalate), a potassium- nephrologists choose to initiate dialysis when the BUN level exceeds
binding ion exchange resin, has long been administered with sorbitol 100 mg/dL or the serum creatinine level exceeds 10 mg/dL. Intractable
to promote elimination of potassium from the body, but it is no longer volume overload and life-threatening hyperkalemia are the two most
considered to be effective or free of adverse effects.6 More recently, common indications for emergency dialysis.
other nonabsorbable cation exchangers such as patiromer and sodium
zirconium cyclosilicate have been used to control hyperkalemia in CHRONIC KIDNEY DISEASE
patients with renal failure, but they have not been evaluated in patients
who present with acute hyperkalemia.7 Foundations
Hypocalcemia. Hypocalcemia is a common feature of AKI that CKD denotes kidney damage or decreased renal function for 3 months
can develop rapidly after its onset. Vitamin D–dependent intestinal or longer and is characterized by irreversible nephron loss and scar-
absorption of calcium is decreased in AKI because of decreased renal ring. Chronic renal insufficiency, which denotes a condition in which
synthesis of 1,25- dihydroxyvitamin D. Another factor promoting the GFR has been moderately reduced but not to a degree sufficient to
hypocalcemia is the complexing of calcium with retained phosphate. cause clear-cut clinical symptoms, has been replaced by an indication
Rhabdomyolysis- associated AKI, in particular, is often associated of the degree to which the GFR is reduced. End-stage renal disease, now
with the deposition of complexed calcium in muscle and other tissues. termed kidney failure, describes a condition in which renal function has
Asymptomatic hypocalcemia requires no immediate treatment, but diminished to a low level and in which serious, life-threatening mani-
subtle or frank tetany should be treated with IV calcium (10–20 mL of festations can be expected to occur without dialysis or transplantation.
10% calcium gluconate infused over several minutes). At this stage, the kidneys often are shrunken and diffusely scarred to
Hyperphosphatemia. Hyperphosphatemia resulting from decreased such a degree that it may be impossible to make an etiologic diagnosis,
renal elimination of phosphate is another common feature. The serum even on pathologic examination.
The causes of CKD are numerous; their relative frequency depends Barring renal transplantation, CKD is an essentially irreversible
primarily on the population studied. As with AKI, they can be conve- condition generally characterized by a relentless decrease in renal
niently classified as prerenal (vascular), intrinsic renal (glomerular and function. The most common problems requiring emergent interven-
tubulointerstitial), or postrenal (obstructive; Box 83.6). Glomerular dis- tion are severe hyperkalemia and symptomatic volume overload. In
ease accounts for approximately one-third to half of the cases of CKD; in the patient with CKD who has an acute problem, the focus should be
the United States, diabetic nephropathy forms the largest group of these. on the identification and treatment of an intercurrent illness that has
Hypertensive nephrosclerosis is another important cause, particularly caused clinical decompensation, with the goal of returning the patient
among blacks, in whom it may be the cause of 25% or more of cases of to a stable, chronically compensated status.
CKD. Among children and adolescents, reflux nephropathy is the most
common cause of CKD. Renal failure related to IV drug use or human Pathophysiology
immunodeficiency virus disease is a major consideration in some pop- Progressive loss of renal function eventually results in a recognizable
ulations. Clues to other specific causes may be gained from elements of syndrome termed uremia. Clinical manifestations do not generally
the history, physical examination, and laboratory and imaging studies. appear, however, until the GFR has been reduced to approximately
Although determining the underlying cause of CKD can permit the 15% to 20% of normal. As the patient becomes unable to excrete an
underlying disease to be treated and can lead to some improvement in ingested salt or water load promptly, the external balance of sodium
renal function in some cases, this is the exception rather than the rule. and water is affected; volume overload or hypernatremia or hypona-
tremia may result. Inability to concentrate the urine is an early man-
ifestation of renal insufficiency and may be manifested as nocturia.
BOX 83.6 Major Causes of Chronic Kidney Potassium homeostasis is likewise disrupted, and a relatively small
Disease potassium load may lead to dangerous hyperkalemia. The acid-base
balance is affected because the kidney fails to clear the daily metabolic
Vascular Causes
acid load owing to a decreased ability to excrete ammonium and phos-
Renal arterial disease
phate; the result is a non–anion gap acidosis in the earlier stages of
Hypertensive nephrosclerosis
CKD and a superimposed anion gap acidosis as the GFR decreases fur-
Glomerular Causes ther. Calcium and phosphate metabolism is affected as well; retention
Primary Glomerulopathies of phosphate and progressive loss of the kidney’s capacity to synthe-
Focal sclerosing glomerulonephritis (GN) size 1,25-dihydroxycholecalciferol, the active form of vitamin D, lead
Membranoproliferative GN to hypocalcemia, secondary hyperparathyroidism, and eventually the
Membranous GN development of renal osteodystrophy.
Crescentic GN Nitrogenous byproducts of protein catabolism retained in the blood
IgA nephropathy are the presumed cause of many of the diverse abnormalities of organ
function in renal failure. Most patients with CKD show decreased glu-
Secondary Glomerulopathies cose tolerance, although it is rarely severe enough to require treatment
Diabetic nephropathy unless the medical history includes established diabetes. In the latter
Collagen vascular disease case, insulin or other hypoglycemic therapy may need to be continued,
Amyloidosis but generally at a lower dosage than required before the onset of renal
Postinfectious failure because the normal kidney has a major role in insulin degra-
HIV nephropathy dation. Alterations in lipid metabolism result in elevated low-density
lipoprotein levels and hypertriglyceridemia in many patients with
Tubulointerstitial Causes CKD.
Nephrotoxins
Analgesic nephropathy Clinical Features
Hypercalcemia or nephrocalcinosis Uremia has specific effects on a variety of organ systems. Many of these
Multiple myeloma manifestations are relieved by dialysis, but others are not. A number
Reflux nephropathy have been attributed in some degree to the retention of nitrogenous
Sickle nephropathy wastes and to derangements in vitamin D and parathyroid hormone
Chronic pyelonephritis metabolism.
Tuberculosis
Cardiovascular System
Obstructive Causes The cardiovascular system is perhaps most dramatically affected in
Nephrolithiasis CKD. Many of the manifestations can be attributed to the effects of
Ureteral tuberculosis chronic volume overload, anemia, hyperlipidemia, alterations in
Retroperitoneal fibrosis calcium and phosphorus metabolism, and volume-and hormone-
Retroperitoneal tumor mediated hypertension. Pericarditis, with or without pericardial fluid
Prostatic obstruction accumulation, also is common in CKD, particularly among patients
Congenital abnormalities who have not undergone dialysis.8
Hereditary Causes Pulmonary Effects
Polycystic kidney disease
Uremic pleuritis, with or without associated pleural fluid collections,
Alport syndrome
may develop in some patients. So-called “uremic lung,” often mani-
Medullary cystic disease
fested radiographically by bat wing perihilar infiltrates, represents
HIV, Human immunodeficiency virus; IgA, immunoglobulin A. pulmonary edema and is almost always caused by volume overload
or myocardial dysfunction. Noninflammatory pleural effusion caused several overlapping varieties of bone disease that can cause bone pain
by volume overload also is fairly common. Of special importance in or frank fractures. Patients with CKD generally are treated with long-
the ED evaluation is that the radiographic appearance in pulmonary term oral calcium and vitamin D in an effort to prevent secondary
edema may at times be misleading, simulating an infectious lobar infil- hyperparathyroidism and uremic osteodystrophy. Occasional patients
trate or even assuming a nodular appearance in some cases. will have a poor response to therapy and require parathyroidectomy. A
specific type of arthritis caused by the deposition of calcium hydroxy-
Neurologic Features apatite or calcium oxalate crystals in joints is seen in some patients,
Neurologic dysfunction is common in those with advanced uremia as are periarticular calcium deposition, spontaneous tendon rupture,
and may manifest as lethargy, somnolence, difficulty concentrating, or myopathy, and carpal tunnel syndrome.
frank alteration in mental status. Seizures may occur, although causes
other than uremia alone must be ruled out. Uremic encephalopathy Immunologic Considerations
commonly manifests with hiccups, asterixis, or myoclonic twitching. Uremic patients have long been noted to have an increased susceptibil-
The latter should not be confused with tetany caused by hypocalcemia, ity to infection due to alteration of both humoral and cellular immu-
which also is common in untreated CKD patients. In the peripheral nity. The relative importance of each in the pathogenesis of infection
nervous system, uremia often causes cramps and a distal sensorimotor in renal failure is not completely clear, but defects in cellular immunity
neuropathy. appear to be more significant clinically. Although patients with renal
failure should be considered to be immunocompromised, most infec-
Gastrointestinal System tions in patients with CKD are caused by common pathogens rather
Anorexia and nausea are nearly constant features of uremia. These GI than opportunistic organisms.
manifestations are caused by the accumulation of nitrogenous wastes
that correlate roughly with the BUN level and may be relieved even in Hematologic Effects
the undialyzed patient by introduction of a low-protein diet. A pronounced normochromic normocytic anemia, with a hemato-
crit value commonly in the range of 18% to 25%, is nearly universal
Dermatologic Features in those with untreated CKD, except among patients with polycystic
The skin of patients with CKD has a characteristic yellowish tinge. Ure- disease. It is caused primarily by the kidneys’ decreased production of
mic frost, the result of the deposition of urea from evaporated sweat erythropoietin, a hormone that stimulates red cell production by the
on the skin, is a classic finding that, like so-called uremic fetor, is seen bone marrow. Other contributing factors are increased red cell hemo-
only rarely now with the widespread use of dialysis (Fig. 83.3). Diffuse lysis, nutritional deficiencies, and increased bleeding secondary to
pruritus is often a major source of discomfort for the patient with CKD; platelet dysfunction.
in some cases, it may be caused by calcium deposition in the skin sec- Although the platelet number generally is normal in uremia, the
ondary to derangements in calcium metabolism. bleeding time is prolonged because of defective platelet adhesiveness
The use of gadolinium-based contrast agents for magnetic reso- and activation. Numerous ecchymoses, seen in many patients with
nance imaging has been associated with the development of nephro- CKD, are a common manifestation.
genic systemic fibrosis, a potentially fatal disorder that occurs in
patients with moderate-to-severe chronic kidney failure. Differential Diagnosis
Patients with CKD commonly present with nonspecific complaints
Musculoskeletal System that are often of insidious onset, such as generalized weakness, poor
The complex disturbances of calcium and phosphate metabolism in appetite, or deterioration of mental functioning. However, because
CKD result in renal osteodystrophy, a clinical entity encompassing CKD can affect all organ systems, a number of life-threatening con-
ditions, including hyperkalemia and myocardial infarction, are in the
differential, and a comprehensive evaluation is generally indicated.
In patients without an established diagnosis of CKD, the first consider-
ation is to determine that the renal failure is chronic rather than acute. An
explicit history to that effect, obtained from previous medical records or
from the patient or family, provides the most straightforward and reliable
confirmation, as does the presence of a dialysis access device on physical
examination. If such a history is unavailable, the finding of bilaterally small
kidneys, readily detected by plain abdominal radiography or ultrasonogra-
phy, constitutes equally good evidence. However, the converse is not nec-
essarily true—a finding of normal-sized or large kidneys does not rule out
CKD. In such cases, additional diagnostic steps are required to establish
the diagnosis. A convincing history of the long-standing presence of the
presenting symptoms or of symptoms, such as nocturia, may be helpful in
suggesting chronicity, as may a history of familial kidney disease, such as
polycystic kidney disease or Alport syndrome.
Laboratory abnormalities such as anemia, acidosis, hyperuricemia,
hypocalcemia, and hyperphosphatemia can occur in patients with
acute kidney failure as early as 10 days after onset. Although urinary
findings likewise tend not to be helpful, the presence of broad waxy
casts on microscopic examination is suggestive of chronic disease,
Fig. 83.3 Uremic frost. Note the fine white powder on the skin of this whereas the finding of an active sediment (e.g., red cell casts) is good
patient with kidney failure. evidence for an acute process.
Although as a rule chronic kidney failure is irreversible and slowly disease. Stone disease, retroperitoneal fibrosis, and even rarer entities
progressive, an essential component of the ED evaluation is to exclude such as ureteral tuberculosis also should not be overlooked.
the possibility of potentially reversible factors (in effect, ruling out Finally, treatment of the underlying disorder that has caused the
“acute on chronic” renal failure) and to ensure that treatable causes of CKD can occasionally result in the return of some renal function, most
CKD—disorders that if treated might allow for some return of renal notably in cases of myeloma kidney, some forms of secondary glomer-
function—have not been overlooked. These potentially reversible ulonephritis, and severe hypertensive disease. Although this consider-
factors and treatable causes of CKD are important to keep in mind ation relates to long-term care and follow-up, it is appropriate that ED
because they represent the only potential opportunity to reverse the management address this issue to ensure that appropriate evaluation
patient’s disease rather than simply to manage its results (Box 83.7). and disposition are arranged.
Primary among superimposed reversible factors are those that lead
to decreased renal perfusion. Of these, the most common is volume Diagnostic Testing
depletion. Regardless of the initiating cause, the process is exacerbated Diagnostic testing for CKD generally follows the principles outlined
by the diseased kidney’s impaired ability to conserve sodium and con- for AKI (see earlier section “Acute Kidney Injury: Diagnostic Testing”),
centrate the urine appropriately. Decreased renal perfusion caused though prerenal causes are of concern mostly as exacerbating factors in
by cardiac dysfunction of any cause is another extremely common patients with CKD.
and potentially reversible factor. An uncommonly encountered but
important vascular cause of reversible deterioration of renal function Management
is scleroderma renal crisis, a syndrome of accelerated hypertension and CKD patients are susceptible to infection, bleeding, and the numerous
severe vasoconstriction in patients with underlying scleroderma that other complications associated with renal failure, as well as those that
can be reversed by timely treatment with ACE inhibitors. Increased may be associated with the underlying causative disorder. Moreover,
catabolism caused by infection, trauma, surgery, corticosteroids, or GI these patients are more vulnerable to the effects of any intercurrent ill-
bleeding is another reversible factor that often is responsible for wors- ness or trauma. Those who are maintained with chronic hemodialysis
ening azotemia and the development of uremic symptoms. or peritoneal dialysis are subject to potential complications from the
Drugs and toxins constitute another important group of reversible dialysis therapy itself.
factors. Not only may these agents exacerbate renal insufficiency by Patients with CKD also are uniquely susceptible to iatrogenic
causing intravascular volume depletion (diuretics), decreased renal illness. First, they are less able to handle fluid and solute loads than
perfusion (antihypertensive agents), or increased catabolism (tetra- normal persons. Just as important, the presence of renal failure sig-
cycline), they also can cause ATN (aminoglycosides, rhabdomyoly- nificantly alters the metabolism and action of many drugs, often in
sis), AIN (many drugs), or inhibition of renal prostaglandin synthesis ways that are not predictable (Box 83.8). Thus, the dose and schedule
(NSAIDs). Particularly noteworthy is the dramatic decrease in renal of every agent administered, even those that are apparently innocu-
function produced when an ACE inhibitor is administered to a patient ous, such as antacids, laxatives, antiemetics, or multivitamin prepara-
with renal insufficiency caused by bilateral renal artery stenosis or tions, should be carefully considered, and the hospital pharmacist or
renal artery stenosis in a solitary kidney. other dependable resource consulted. In general, consultation with the
Postrenal reversible factors also are important because of their fre- patient’s nephrologist is recommended on completion of the initial ED
quency, particularly obstructive disease in the older male patient and evaluation because management and follow-up monitoring after the
reflux nephropathy in the child. Papillary necrosis should remain a patient has left the ED are often complex.
consideration in the diabetic patient and the patient with sickle cell In the United States, most patients with advancing CKD eventually
will require dialysis, but several true emergencies may develop in the
patient with CKD before chronic dialysis has been instituted. Specific
BOX 83.7 Reversible Factors and Treatable diagnostic and therapeutic considerations apply to the management of
Causes of Chronic Kidney Disease these conditions, regardless of whether they occur in dialyzed or undi-
alyzed patients.
Reversible Factors
Hypovolemia Hyperkalemia
Congestive heart failure Potentially the most rapidly lethal complication of CKD is severe
Pericardial tamponade hyperkalemia. As a rule, this condition is clinically silent until it causes
Severe hypertension
Catabolic state, protein loads
Nephrotoxic agents BOX 83.8 Mechanisms of Drug Toxicity
Obstructive disease in Renal Failure
Reflux disease
Excessive drug level
Treatable Causes Impaired renal excretion of drug
Renal artery stenosis Impaired renal excretion of active metabolite
Malignant hypertension Impaired hepatic metabolism
Acute interstitial nephritis Increased sensitivity to drug
Hypercalcemic nephropathy Changes in protein binding
Multiple myeloma Changes in volume of distribution
Vasculitis (e.g., systemic lupus erythematosus, Wegener granulomatosis, Changes in target organ sensitivity
polyarteritis nodosa) Metabolic loads administered with drug
Obstructive nephropathy Misinterpretation of measured serum drug level (i.e., change in therapeutic
Reflux nephropathy range)
potentially life-threatening manifestations. Accordingly, hyperkale- diagnosis is not always straightforward. A history of increasing dys-
mia must be looked for in every patient with CKD. These patients can pnea on exertion or paroxysmal nocturnal dyspnea may be suggestive,
become severely hyperkalemic when required to handle even modest but the physical examination may not reveal the expected signs of CHF,
exogenous and endogenous potassium loads; moreover, even drugs that and even chest radiography may be deceptive. Recent weight gain or
have only minimal effects on the serum potassium level in normal per- a body weight considerably over dry weight (typically >5 pounds) is
sons, such as β-blockers and ACE inhibitors, can cause hyperkalemia in the most reliable clue and, in the absence of convincing evidence of
these patients. There is concern that the use of succinylcholine in patients another cause for dyspnea, volume overload should be assumed to be
with CKD has the potential to cause rapid deterioration in patients who the cause.
are already hyperkalemic, although this appears to be rare. Treatment of pulmonary edema in the patient with CKD is of neces-
An ECG should be obtained whenever hyperkalemia is a possibility sity somewhat different from that in other patients. Arrangements for
and, if signs of hyperkalemia are noted, appropriate therapy should be initiation of dialysis should be made as soon as possible because it is
started immediately, even before laboratory confirmation of a high serum the most rapidly effective means to decrease intravascular volume in
potassium level. Electrocardiographic changes may be completely absent, the absence of renal function. Other immediate measures should be
even when hyperkalemia is severe; thus, a normal ECG does not preclude instituted in the meantime. Although such measures may occasionally
the need for laboratory confirmation of a normal serum potassium level. prove to be effective enough to avoid dialysis temporarily in patients
A potassium level of 6 mEq/L should be considered potentially dangerous, who possess some residual renal function, it should nevertheless be
even though many patients with CKD chronically tolerate levels somewhat anticipated that the response to even extremely aggressive medical
above this threshold, without electrocardiographic changes. A patient with therapy, short of dialysis, will be inadequate.
CKD who is in cardiac arrest should be assumed to be hyperkalemic and The CKD patient with pulmonary edema is placed in the sitting
treated accordingly while the usual resuscitative measures are taken. See position, and high-flow oxygen is administered by mask. The use of
earlier (“Acute Kidney Injury: Management”) and Table 83.1. continuous or bilevel positive airway pressure (CPAP or BiPAP) is a
In patients who still retain some renal function, the most effective useful adjunct for patients with CKD, as it is for patients without renal
way to treat hyperkalemia in patients with CKI may be to administer failure. Sublingual nitroglycerin can be administered immediately
an IV diuretic such as furosemide (if the patient is not hypovolemic) and functions rapidly to reduce preload and afterload; an IV infusion
and to provide volume, if necessary. Large doses of diuretic may be beginning at 10 to 20 μg/min can be initiated promptly and titrated to
necessary for a satisfactory diuresis to be induced. In light of the poten- effect. Diuretics are not expected to be helpful unless the patient has
tial for ototoxicity with the use of loop-active diuretics, these drugs retained a significant level of renal function.
should be administered by slow infusion rather than by bolus and may
be contraindicated in patients who also are receiving other potentially Infection
ototoxic agents. During the course of any of these therapeutic inter- Because infection is a major contributor to morbidity and mortality
ventions, the electrocardiographic and serum potassium levels must be among patients with CKD, the possibility of serious infection should
monitored frequently. be entertained, even when the expected classic findings are not all pres-
ent. For example, bacteremia may manifest with fever alone, just as in
Pulmonary Edema other patients with impaired immunity. Patients with pneumonia may
Perhaps the most common ED problem in patients with CKD is have only vague dyspnea or malaise, symptoms that may be attributed
pulmonary edema secondary to volume overload. Surprisingly, the to volume overload or uremia. Thus, all diagnostic possibilities should
TABLE 83.1 Treatment of Hyperkalemia

Agent or Modality Dose and Regimen Onset/Duration of Action Mechanism of Action Comments
Calcium gluconate (10%) 10 mL IV (may repeat × 2 prn 1–5 min/≈1 hr Antagonizes membrane Monitoring of ECG required; do
every 5–10 min) effects of K not mix with HCO3−
Beware—hypercalcemia
Albuterol 10–20 mg (nebulized) by 30 min/2 hr or more Intracellular movement of K Relatively free of significant
inhalation side effects; tachycardia
Glucose and insulin 10–20 units regular insulin/ 30 min/while infusion continued Intracellular movement of K Beware—hyperglycemia,
100 g glucose hypoglycemia
Infused volume may be
decreased by giving D10W,
D20W, or D50W
Sodium bicarbonate 150 mEq/L IV infusion (rate Approximately 10–15 min/1–2 hr Possible intracellular Most effective with organic
variable) movement of K acidosis
Dialysis HD, PD Minutes/while continued Removal of K from blood HD may remove 50 mEq/hr
Beware—K rebound
PD may remove 15 mEq/hr
IV diuretics (IV fluid if patient Furosemide 40–80 mg IV 15 minutes/while diuresis Urinary K excretion Only in patients with some
is hypovolemic) continued (depending on renal residual renal function
function)
D10W, 10% dextrose in water; D20W, 20% dextrose in water; D50W, 50% dextrose in water; ECG, electrocardiogram; HD, hemodialysis; IV, intrave-
nous; PD, peritoneal dialysis; PO, orally.
be pursued, and empirical broad-spectrum antibiotic coverage often is without the intermittent rapid shifts of solute typical of hemodialysis.
advisable until infection has been ruled out in the hospital. Bacteremia Medications such as insulin and antibiotics can be administered via
resulting from vascular access infection is common in patients under- the intraperitoneal (IP) route, allowing smoother absorption and more
going hemodialysis, as is peritonitis in patients undergoing peritoneal stable blood levels. The main disadvantage of peritoneal dialysis is a
dialysis. significant incidence of bacterial peritonitis, which is usually readily
A UTI can occur even in patients with minimal urine output or treatable.
those with long-standing renal failure. Urinary stasis is undoubtedly Indications for Dialysis. The decision to initiate chronic dialysis in
a predisposing factor. However, asymptomatic pyuria is common in the patient with CKD generally is made by the patient’s nephrologist
these patients and is not necessarily indicative of infection. For patients in the setting of a gradually decreasing GFR and progressive
with symptoms, urine culture is helpful in guiding treatment decisions. manifestations of renal failure. The absolute value of the BUN or serum
An upper UTI associated with a clinical picture typical of pyelone- creatinine level generally is used only as a rough guide to determine
phritis or renal colic is unusual, but when seen it is often in patients when chronic dialysis should be instituted. The provision of vascular or
with polycystic kidney disease and requires parenteral treatment. A peritoneal access usually has been arranged weeks to months before the
clinical diagnosis can be made presumptively in the ED, but invasive anticipated initiation of dialysis to allow the access site to mature and to
measures sometimes are necessary to document infection and guide minimize any mechanical complications of the procedure.
therapy. For infected cysts, lipid-soluble antibiotics (e.g., ciprofloxacin, For patients who come to the ED with AKI, however, as well as for
trimethoprim-sulfamethoxazole) offer the best antibiotic penetration, patients with CKD in whom acute problems have developed, the emer-
although surgical intervention for these infections sometimes becomes gency clinician must be prepared to make the decision to arrange for
necessary. emergent dialysis (Box 83.9). How urgently dialysis must be initiated
depends not only on the severity and acuteness of the presenting prob-
Dialysis lem, but also on the availability of technical facilities and trained dial-
Dialysis can normalize fluid balance, correct electrolyte and other sol- ysis personnel and the effectiveness of available temporizing measures
ute abnormalities, and remove uremic toxins or drugs from the circu- for the problem at hand.
lation when the patient’s kidneys are unable to do so. Dialysis also can The most common problem requiring emergent dialysis, particu-
reverse some uremic symptoms, but generally to a lesser degree, and larly in the patient with CKD, is pulmonary edema secondary to vol-
permit better long-term control of hypertension, anemia, and renal ume overload. In general, the inciting cause is over-ingestion of fluid
osteodystrophy. and salt in excess of the patient’s greatly diminished renal excretory
The two major dialysis modalities are hemodialysis and perito- capacity. Despite the effectiveness of temporizing measures, many of
neal dialysis. Each is based on a technique whereby the patient’s blood these patients require immediate dialysis—emergency hemodialysis or,
comes into contact with a semipermeable membrane, on the other in the case of the patient maintained on peritoneal dialysis, intensifica-
side of which is a specially constituted balanced physiologic solution. tion of the usual dialysis regimen.
Water and solutes diffuse across the membrane by moving along con- A related problem that may require emergent, or at least urgent,
centration and osmotic gradients, effectively normalizing the blood’s dialysis is malignant hypertension, particularly when associated with
composition. hypertensive encephalopathy or cardiovascular decompensation.
Hemodialysis. This requires special access to the patient’s Because hypertension in patients with renal failure is commonly
circulation, generally through a surgically created arteriovenous fistula volume-dependent, correction of volume overload, even if not appar-
or an implanted artificial graft or through a surgically placed tunneled ent clinically, is a central component of therapy. Temporizing measures
catheter. The vascular access site must be treated with care because such as the administration of IV nitroglycerin often permit hyperten-
hemodialysis cannot be performed without it. Careless manipulation sion to be controlled sufficiently for dialysis to be delayed for several
or puncture can cause bleeding, infection, or thrombosis, which may hours. However, in many cases, hypertension and associated symptoms
result in loss of the access. The involved arm should not be used for are difficult to control until dialysis permits the volume overload to
blood pressure determinations and a tourniquet should not be applied. be corrected. Because blood pressure often is dramatically responsive
In general, blood is drawn and IV lines are established in other loca- to reduction of circulating volume, other antihypertensive agents with
tions. In exceptional circumstances, if no other site is available and it more prolonged effects should be withheld until after dialysis to avoid
is essential to obtain blood samples quickly, the fistula or graft may hypotension after circulating volume has been acutely reduced.
be used, but with precautions. A tourniquet is not applied, the area is Severe hyperkalemia is another common indication for emergent
cleansed scrupulously before the puncture, and extreme care is taken or urgent dialysis, particularly in the patient with AKI who is hyper-
not to puncture the back wall of the access. After the puncture, firm catabolic. In the patient with CKD, hyperkalemia usually is caused by
but nonocclusive pressure is applied for at least 10 minutes. The pres- excessive potassium intake, but endogenous causes such as hemolysis
ence of a thrill before and after the procedure is documented. Similar or rhabdomyolysis should also be kept in mind. The available tempo-
precautions are taken in the exceptional cases in which the fistula or rizing measures can be used to control the serum potassium level, but
graft must be used for IV access. If this is done, an automated infusion dialysis remains the most effective means of removing potassium from
pump is essential to control the infusion rate into these relatively high-
pressure blood vessels.
Peritoneal Dialysis. In peritoneal dialysis, the patient’s peritoneum BOX 83.9 Indications for Emergency Dialysis
functions as the dialysis membrane. Dialysate is infused through
• Pulmonary edema
a surgically implanted Silastic catheter (Tenckhoff catheter) that
• Severe uncontrollable hypertension
penetrates the lower abdominal wall. Fluid exchanges are generally
• Hyperkalemia
performed several times daily, typically by the patient at home.
• Other severe electrolyte or acid-base disturbances
As compared with hemodialysis, peritoneal dialysis offers the
• Some overdoses
theoretical advantages of greater patient independence, avoidance of
• Pericarditis (possibly)
anticoagulation, and smoother control of volume and hypertension,
the body. For rapid control of the serum potassium level, hemodialysis occlude and possibly cause thrombosis of the vessel by compressing it
leads to high clearance rates and is preferred to peritoneal dialysis. too vigorously, and the presence of a thrill immediately after the pro-
Other severe electrolyte and acid- base disturbances, including cedure should be documented in the chart. It may be necessary to keep
diabetic ketoacidosis, may sometimes necessitate emergent dialysis. the patient in the ED for a time to ensure that bleeding does not recur.
Occasional patients with renal failure and severe hypercalcemia uncon- Recurrent bleeding, especially from an aneurysm or a pseudoaneu-
trollable by other modalities (e.g., patients with multiple myeloma rysm, is best evaluated by a vascular surgeon.
causing both renal failure and hypercalcemia) may require dialysis. The Similarly, if the patient reports that the thrill in the access has been
occasional patient with renal failure in whom severe hypermagnese- lost, a vascular surgeon is consulted immediately. Although thrombo-
mia develops after inappropriate therapy or magnesium ingestion may lytic agents are generally used, definitive treatment is usually surgical
require immediate dialysis to reverse life-threatening paralysis or car- revision. The access device should not be forcefully manipulated or
diac dysrhythmia. Severe metabolic acidosis in the setting of renal fail- irrigated because rupture of the vessel or venous embolization may
ure is another indication for emergent dialysis, particularly if volume result.
overload or hypocalcemia (with the risk of tetany and convulsions) Infection of the vascular access can result in persistent or recurrent
precludes the administration of bicarbonate. bacteremia, as well as loss of the access. Infection appears to be a conse-
A related situation is one in which a patient with renal failure has quence of contamination at the time of puncture for dialysis, and most
taken an overdose or inadvertently been administered medication that infections are caused by staphylococci typical of skin flora. Infections
is ordinarily cleared by the kidneys. If the agent is adequately dialyz- are more likely to occur in grafts than in native fistulas. The signs and
able and its continued presence in the circulation poses a significant symptoms of an access infection—redness, warmth, and tenderness
risk to the patient, immediate dialysis can be lifesaving. An example over the site—often are obvious, but in many cases localizing findings
is the ingestion of methanol or ethylene glycol by a dialysis patient. are absent and the patient has only a fever or a history of recurrent
Similarly, ill-advised use of magnesium- containing cathartics or episodes of fever and documented bacteremia. For this reason, it is
phosphate-containing enemas by patients with CKD can lead to dan- common practice to obtain blood cultures for all patients on hemo-
gerous hypermagnesemia and hyperphosphatemia and may necessitate dialysis who have a fever without an obvious source of infection and
urgent dialysis. to treat them presumptively for an abscess infection. A careful search
The serum creatinine and BUN levels themselves are not consid- for other sources of infection should be performed before an abscess
ered definitive indications for dialysis. A creatinine level of 10 mg/dL infection is assumed to be the cause. Infections such as odontogenic
or BUN level of 100 mg/dL often is used as a guideline for beginning abscess, extremity cellulitis (particularly in diabetics), and perirectal
chronic dialysis in the patient with progressive renal failure. In dia- abscess can easily be missed.
lyzed patients, however, the serum creatinine level often is considerably Although some nephrologists prefer to admit all dialysis patients
greater than 10 mg/dL but is a reflection of total body muscle mass with fever to the hospital, management of these patients on an out-
more than of the adequacy of dialysis. The BUN level is a somewhat patient basis often is possible, provided that they otherwise feel well
better indicator; in well-dialyzed persons, it generally is in the range and do not appear to be septic and provided that they can care for
of 50 to 80 mg/dL and is more than 100 mg/dL in less well-dialyzed themselves at home and return promptly if their condition worsens.
patients. Neither blood level, however, correlates more than roughly This course is made possible by the fact that they can be loaded with
with uremic symptoms, even in undialyzed patients, or has any direct IV antibiotics that dependably maintain adequate blood levels until
bearing on how urgently dialysis should be initiated. the next scheduled dialysis treatment, at which time the culture and
The occurrence of uremic symptoms or signs such as nausea, vom- sensitivity test results can be checked and therapy adjusted accord-
iting, lethargy, or twitching indicates a need for dialysis but does not ingly. IV vancomycin, 1 to 1.5 g, given as a single loading dose, is the
necessitate immediate initiation of dialysis unless symptoms are severe. drug of choice in this case because most abscess infections are staph-
Pericarditis, even in the absence of cardiac tamponade, often is consid- ylococcal and because this drug is only minimally hemodialyzable
ered an indication for urgent dialysis, but pericarditis can also occur and needs to be given only every 4 to 7 days in the chronic dialysis
in well-dialyzed CKD patients. In a previously undialyzed patient with patient. If a gram-negative infection also is thought to be likely, as in
progressive renal insufficiency, the appearance of pericarditis indicates a patient who has had recent episodes of gram-negative bacteremia,
that it is time to initiate dialysis, although not necessarily on an emer- a loading dose of a second drug (e.g., a third-generation cephalo-
gency basis. sporin or aminoglycoside) also can be administered. Patients can be
reloaded with these drugs at the end of their next hemodialysis ses-
COMPLICATIONS OF DIALYSIS sion if culture results prove to be positive.
A number of complications can be manifested after dialysis has been Non–Vascular Access–Related Complications of Dialysis
initiated. The hemodialysis procedure itself, which entails invasion of the vascu-
lature, anticoagulation, and significant shifts of fluid and solutes, often
Hemodialysis is associated with acute complications such as hypotension, shortness
Vascular Access–Related Complications of breath, chest pain, and neurologic abnormalities.
The performance of hemodialysis depends on reliable vascular access, Hypotension. Hypotension that occurs after dialysis is usually the
and it is the vascular access device that is responsible for the compli- result of an acute reduction in circulating intravascular volume and
cations of dialysis that most often require evaluation in the ED setting. failure of the patient’s homeostatic mechanisms to compensate for
These problems must be attended to promptly to minimize the risk of it. Because hemodialysis is episodic, each treatment must remove
losing the patient’s dialysis lifeline. the excess fluid that has accumulated over the period since the last
Bleeding from the dialysis puncture site can occur hours after a dialysis (generally, 2–3 days), and patients often are relatively volume-
hemodialysis treatment, either spontaneously or after inadvertent overloaded at the beginning of each treatment. With rapid removal of
minor trauma to the site. Such bleeding can usually be stopped by extracellular fluid, there is inadequate time for transcellular fluid shifts
applying firm pressure to the access site. Care should be taken not to to replace intravascular volume. Antihypertensive medications that are
dialysis patients, is unusual. The latter, although reported occasionally

BOX 83.10 Differential Diagnosis of
in the past, has been all but eliminated by improved dialysis monitor-
Hypotension in Hemodialysis Patients ing equipment and safety mechanisms.
Hypovolemia Two additional entities in the differential diagnosis for hypotension
Excessive fluid removal are of particular importance in the patient with CKD—acute pericar-
Hemorrhage dial tamponade and severe, life-threatening hyperkalemia. Acute peri-
Septicemia cardial tamponade may be the result of sudden pericardial hemorrhage
Cardiogenic shock or sudden worsening of a formerly compensated pericardial effusion
Dysrhythmia after acute correction of elevated preload. The clinical features of tam-
Pericardial tamponade ponade in the dialysis patient are similar to those in other populations,
Myocardial infarction but the common preexistence of cardiomegaly may make the chest film
Myocardial or valvular dysfunction difficult to interpret unless it shows the typical water bottle shape and a
Electrolyte disorders definite increase in heart size from previous examinations.
Hyperkalemia or hypokalemia Similarly, an elevated central venous pressure is of little use in
Hypercalcemia or hypocalcemia differentiating tamponade from underlying right-sided heart failure.
Hypermagnesemia Even the finding of pericardial fluid on bedside ultrasonographic
Vascular instability examination, although suggestive, is not proof that tamponade is
Drug-related present, because many dialysis patients chronically have pericardial
Dialysate-related effusions that do not cause hemodynamic compromise. The ultraso-
Autonomic neuropathy nographic demonstration of right ventricular diastolic collapse is more
Excessive access arteriovenous flow specific. A definitive diagnosis of tamponade depends on the direct
Anaphylactoid reaction demonstration of equal pressures in the right and left atria on cardiac
Air embolism catheterization.
Emergency pericardiocentesis must occasionally be performed in
the ED to relieve acute tamponade, but there often is enough time
required when the patient is in a volume-expanded state, particularly for the patient to be transported to the catheterization suite or oper-
β-blockers, can contribute to the hypotension when intravascular ating room for safer and more definitive therapy in a controlled set-
volume is normalized. ting. If immediate pericardiocentesis is believed to be necessary, the
Most episodes of hypotension that occur during hemodialysis emergency clinician should not hesitate to perform this potentially
resolve spontaneously or can be readily managed by a decrease in lifesaving procedure, despite the many potential complications and
blood flow rate or by infusion of small volumes of saline (to cause tran- increased risk of bleeding in patients with CKD. Similarly, in the case
sient volume expansion) or hypertonic solutions (to reverse transient of a dialysis patient who is in cardiac arrest, pericardiocentesis gen-
acute hypo-osmolality). Patients with significant hypotension who do erally should be attempted if initial resuscitative efforts have not been
not respond to these maneuvers often are brought to the ED for fur- successful.
ther evaluation. Patients on dialysis with persistent hypotension should Severe life-threatening hyperkalemia, although unusual in a dia-
be considered to be at risk for acute myocardial infarction, acute dys- lyzed patient, can occur in the presence of underlying catabolic illness
rhythmias, and sepsis (Box 83.10). or with a prolonged period of hypotension and low flow. Patients who
Acute blood loss is another consideration when a hemodialysis are hyperkalemic can have profoundly slow heart rates, particularly if
patient presents with hypotension, symptomatic angina, or CHF. Dial- they have been treated with β-blockers or calcium channel blockers. If
ysis patients are commonly treated with epoetin or darbepoetin to a dialysis patient is in cardiac arrest, it should be assumed that hyperka-
prevent severe anemia; untreated patients typically have low baseline lemia is present, and IV calcium should be given immediately.
hemoglobin levels. Serum levels of clotting factors are normal in CKD, Shortness of Breath. Shortness of breath in dialysis patients generally
but patients are routinely anticoagulated for each hemodialysis treat- is caused by volume overload. In the patient who becomes short of
ment and, although transient thrombocytopenia may occur during breath while being dialyzed, however, other causes must be sought—
the dialysis procedure, the qualitative platelet defect characteristic of primarily sudden cardiac failure, pericardial tamponade, pleural
renal failure is an important factor in bleeding that continues beyond effusion, or pleural hemorrhage. Air embolism and anaphylactoid
the peridialytic period. This abnormality is only partially reversed by reactions are unusual causes. Pneumonia or underlying reactive airway
dialysis but can be corrected by the administration of desmopressin disease may be responsible.
(DDAVP), which increases the release of factor VIII–von Willebrand Chest Pain. Cardiovascular disease is a leading cause of death in
factor polymers from vascular endothelium. DDAVP has been used patients with CKD, and most episodes of chest pain occurring during
successfully to normalize the bleeding time in preparation for surgery dialysis are likely to be ischemic in origin. Most dialysis patients have
in patients with CKD.9 Cryoprecipitate and conjugated estrogen both risk factors for coronary artery disease, related to CKD itself or to the
have been shown to produce similar effects for a longer period. underlying condition that led to renal failure, and many have well-
Overt bleeding from the GI tract, often caused by angiodysplasia or documented coronary artery disease. CKD is commonly associated
peptic ulcer disease, is common and can be dramatic. Occult hemor- with hypertension, hyperlipidemia, carbohydrate intolerance, and
rhage in other locations, however, can present a diagnostic challenge disturbances of calcium and phosphorus metabolism. In addition,
because symptoms and signs of volume loss tend to be overshadowed dialysis patients may be anemic, and many are chronically volume-
by local manifestations of bleeding into a closed space. Spontaneous overloaded. During hemodialysis, these underlying factors may be
retroperitoneal or pleural hemorrhage may manifest with flank pain or added to acute physiologic stresses such as transient hypotension and
with chest pain and shortness of breath, respectively. hypoxemia, which often are associated with the dialysis procedure,
Acute pulmonary embolism and acute air embolism are two less thereby increasing myocardial oxygen demand while decreasing
likely possibilities. The former, although it does occur occasionally in oxygen delivery.
In evaluating presumed ischemic chest pain in a patient with CKD,

BOX 83.11 Differential Diagnosis of Altered
reversible precipitants should be considered. It should be determined
whether increasing anemia, poorly controlled hypertension, or uncor-
Mental Status in Dialysis Patients
rected volume overload are factors, particularly when a patient whose Structural Conditions
angina has been stable begins to experience more frequent or more Cerebrovascular accident (particularly hemorrhage)
severe anginal episodes. Patients who repeatedly experience chest pain Subdural hematoma
during dialysis are candidates for a complete cardiac evaluation. Dial- Intracerebral abscess
ysis patients who have repeated ED visits for chest pain should have a Brain tumor
coordinated strategy developed by their nephrologist and cardiologist
to set guidelines regarding further admissions. Metabolic Conditions
The presence of renal failure and its associated electrolyte and acid- Disequilibrium syndrome
base disturbances does not obscure the usual electrocardiographic Uremia
changes of angina or acute myocardial infarction. The pattern of change Drug effects
of serum cardiac enzyme levels with acute infarction also is not altered Meningitis
by CKD, although the baseline level of these enzymes may be higher Hypertensive encephalopathy
than in the general population.10-12 Troponin appears to perform best Hypotension
as a marker of infarction in patients with CKD.10-12 Treatment of isch- Postictal state
emic chest pain is the same as for other populations. Hypernatremia or hyponatremia
Among nonischemic causes of chest pain, pericarditis should Hypercalcemia
always be a consideration, even in the well-dialyzed patient. The pre- Hypermagnesemia
sentation is essentially the same as in nonrenal patients; fever, a friction Hypoglycemia
rub, or atrial dysrhythmias may be associated findings. Signs of peri- Severe hyperglycemia
cardial effusion or early tamponade should be sought by bedside ultra- Hypoxemia
sonography. Indomethacin often is effective in relieving pain, but some Dialysis dementia
patients eventually require further measures, such as pericardiocen-
tesis with corticosteroid instillation or pericardial stripping. Patients
with pericarditis may require more frequent or intensified dialysis continued presence of a foreign body—the Tenckhoff catheter—in the
because pericarditis is thought to be a marker for inadequate dialysis.8 peritoneal cavity. Occasionally, when an episode of peritonitis responds
Neurologic Dysfunction. Neurologic symptoms during or poorly to antimicrobial therapy or when a patient has repeated epi-
immediately after hemodialysis may be caused by disequilibrium sodes of peritonitis caused by the same organism, the catheter must be
syndrome, a constellation of symptoms and signs thought to result removed and the patient sustained with hemodialysis until the infec-
from rapid changes in body fluid composition and osmolality during tion is completely cleared and a new catheter can be placed. Repeated
hemodialysis. It usually occurs only in patients with high BUN levels infections carry the risk of permanently altering peritoneal permea-
who are just starting hemodialysis and does not occur with peritoneal bility or effective surface area and necessitating a permanent switch to
dialysis. Typically, patients have headache, dizziness, nausea, vomiting, hemodialysis.
and muscle cramps, but in more severe cases features may include Peritonitis in patients who are on peritoneal dialysis is presumably
altered mental status, seizures, or coma. Symptoms resolve over several caused by inadvertent bacterial contamination of the dialysate or tub-
hours as fluid and solutes are redistributed across cell membranes. ing during an exchange or by extension of an infection of the exit site
Altered mental status in the CKD patient should not be attributed or subcutaneous tunnel into the peritoneal cavity. Most cases of perito-
to disequilibrium syndrome unless other causes have been ruled out nitis are caused by Staphylococcus aureus or Staphylococcus epidermidis,
(Box 83.11), particularly when symptoms persist, fluctuate, or worsen and most of the remainder (≈30%) by gram-negative enteric organ-
during a reasonable period of observation. Likewise, when seizures isms.13 Fungal infections are uncommon but generally are refractory to
occur during dialysis, they should not be attributed to disequilibrium medical therapy and are often considered as an indication for catheter
syndrome without considering other potentially serious causes, even in removal. Polymicrobial infection suggests direct contamination from
patients who have had seizures in the past. Any new focal neurologic the GI tract and mandates a search for the site of perforation or fistula,
abnormality requires an immediate head CT scan to detect intracra- although such a source is identified in only a minority of cases. No
nial hemorrhage. Similarly, if fever or other evidence of infection is organism is identified in approximately 10% to 20% of cases of perito-
present, meningitis should be a serious consideration. Other consid- neal dialysis–associated peritonitis.
erations include hyperglycemia and hypoglycemia, especially in the The diagnosis of peritonitis usually is made by the patient when a
diabetic patient, as well as electrolyte abnormalities, hypoxic states, cloudy dialysis effluent is noted, corresponding with the appearance of
hypotension, and other toxic or metabolic causes. The acute treatment white blood cells (WBCs) in the dialysate. Peritonitis is often accompa-
of seizures in patients with CKD is essentially the same as for other nied by nonspecific abdominal pain, malaise, or fever. When a patient
populations. has fever or abdominal symptoms, even in the absence of cloudy fluid,
it is advisable to consider peritonitis and check the fluid, because early
Peritoneal Dialysis peritonitis may manifest in an atypical manner. In more severe cases,
As with hemodialysis, most of the complications of peritoneal dialy- peritonitis is accompanied by nausea, vomiting, severe pain, and hypo-
sis are related to the dialysis access device, in this case the peritoneal tension, necessitating hospitalization and consideration of the possibil-
catheter. In contrast to hemodialysis, however, the dialytic process in ity of acute surgical disease.
peritoneal dialysis occasions few immediate difficulties. In the ED setting, the diagnosis of peritonitis is confirmed by the
Peritonitis is the most common complication of peritoneal dialysis. finding of more than 100 WBCs/mm3 in the peritoneal fluid, with
Fortunately, it is generally much less severe than other types of peri- more than 50% neutrophils, or by a positive result on Gram stain. A
tonitis and can be treated readily on an outpatient basis, despite the sample of fluid is obtained for analysis. If a specialized dialysis nurse
is available to obtain the fluid, this may be preferable. If not, the fluid brownish or fecal material in the peritoneal drainage should suggest a
is obtained through the use of sterile technique. Fluid is sent for cell ruptured viscus until proven otherwise and immediate surgical consul-
count and differential, Gram staining, and culture, with the use of tation should be sought. Detection of a localized tenderness, palpable
blood culture bottles. mass, or incarcerated hernia on physical examination can be extremely
Peritoneal dialysis–associated peritonitis is treated with an initial helpful in making the diagnosis. Plain abdominal radiography or
intraperitoneal (IP) loading dose of antibiotic, followed by a 10-to abdominal CT may be useful for demonstrating the presence of ileus,
14-day course of IP antibiotics self-administered by the patient on an but pneumoperitoneum may reflect only the introduction of air during
outpatient basis. After the diagnosis has been confirmed, consultation a recent fluid exchange rather than a perforated viscus.
with the patient’s nephrologist or dialysis nurse specialist is indicated Infection of the catheter exit site or tunnel is another relatively com-
to determine antibiotic therapy and to plan for outpatient management mon problem for which the patient on chronic peritoneal dialysis may
and follow-up evaluation or, occasionally, if peritonitis is severe or seek care in the ED. These infections tend to be caused by typical skin
outpatient management is precluded by psychosocial considerations, flora and manifest with local signs of infection. Although not serious
for hospitalization. A common treatment regimen is a loading dose of in themselves, exit site infections may lead to infection of the subcuta-
vancomycin, 15 to 30 mg/kg IP, followed by further IP doses every 4 to neous tunnel, which can cause repeated episodes of peritonitis and may
7 days, plus ceftazidime or cefepime, 1 g IP, or gentamicin, 0.6 mg/kg ultimately necessitate removal of the catheter. Any visible exudate is
IP. The last two regimens are given as a loading dose followed by main- cultured and Gram-stained and therapy with an oral antibiotic such as
tenance doses administered IP once daily at the time of an exchange.13 cephalexin or dicloxacillin is started, pending the results of culture and
Heparin, 500 to 1000 units, may also be added to each liter of dialysate sensitivity testing. The patient is instructed to cleanse the site meticu-
for the first few days of treatment to help reduce the formation of fibrin lously several times a day using povidone-iodine or peroxide solution.
strands that may obstruct the catheter. Patients should be seen by the Tunnel infections can be difficult to detect on physical examina-
dialysis nurse in 24 to 48 hours for assessment of the response to ther- tion and may be suspected only after the patient has several bouts of
apy and adjustment of antibiotic therapy as necessary after review of peritonitis caused by the same organism. As with other closed space
the results of culture and sensitivity testing. infections, tunnel infections tend to be difficult to eradicate unless the
Catheter contamination or leaks from the catheter, tubing, or dialy- tunnel is partially unroofed and drained.
sate bag should be managed in the same fashion as for frank peritonitis. Patients maintained on peritoneal dialysis also may come to the ED
The site and cause of leakage are identified, and damaged elements are with positional or mechanical problems with the site, of which the most
promptly replaced. Occasionally, with leakage of peritoneal fluid from common is failure of the dialysate to drain completely at the time of
around the catheter, surgical correction of the underlying problem will an exchange. Occasionally this problem is caused simply by kinking
be necessary. or inadvertent clamping of the external catheter or tubing. More often,
Patients who have severe abdominal pain, vomiting, ileus, chills or however, it is the result of catheter obstruction by fibrinous debris or
high fever, or hypotension require hospital admission and manage- kinking or migration of the catheter within the peritoneal cavity, often
ment. Likewise, patients with severe underlying illness and those who associated with constipation. Catheter position is best assessed by a CT
cannot reliably perform exchanges or administer antibiotics at home scan of the abdomen. Specific intervention may be guided by a contrast
also require inpatient management. Dialysis exchanges are continued catheterogram. Fibrinolytic agents have been used successfully to open
on the same schedule. The inpatient antibiotic regimen is essentially occluded catheters, but surgical intervention for catheter replacement
the same as for outpatients. often is required. Severe metabolic disturbances are much less common
Perhaps the most serious potential pitfall in caring for the patient among patients on peritoneal dialysis than patients on hemodialysis,
maintained on peritoneal dialysis with abdominal pain or other signs because in the former group dialysis is being performed essentially
of peritonitis is to overlook other serious intra-abdominal conditions continuously and the blood remains in near-equilibrium with the dial-
whose presentation may mimic that of peritonitis. Patients on perito- ysate. However, significant disturbances do occasionally occur, usually
neal dialysis are at increased risk for abdominal wall or inguinal hernia in association with hypercatabolic states, major dietary indiscretions,
because of chronically increased intra-abdominal pressures; previous or significant GI fluid loss. One derangement that occurs occasion-
abdominal surgery also places them at risk for hernia, as well as for ally in diabetic patients undergoing peritoneal dialysis is a syndrome
obstruction secondary to adhesions. The manifestations of serious of severe hyperglycemia—sometimes even despite continuation of the
disorders unrelated to dialysis (e.g., acute appendicitis, diverticulitis, usual insulin dose—that results from absorption of glucose from the
cholecystitis, acute pancreatitis, ischemic bowel, perforated viscus, or hyperosmolar dialysate, with associated nonspecific symptoms of mal-
spontaneous bacterial peritonitis in patients with chronic liver disease) aise, weakness, and headache. Although glucose levels may be as high as
also may be attributed to ordinary peritoneal dialysis–associated peri- 1500 mg/dL in these patients, they cannot undergo an osmotic diuresis
tonitis, with the potential for disastrous consequences. The accessi- and remain clinically euvolemic. Correction of hyperglycemia must be
bility of the peritoneal fluid for examination may prove to be helpful undertaken carefully to avoid causing rapid osmolar and volume shifts.
in documenting the presence of an inflammatory process, but it also The references for this chapter can be found online at ExpertConsult.
has the potential to mislead ED investigation of its cause. A finding of com.
REFERENCES 8. Rehman KA, Betanco J, Xu B, et al. Uremic pericarditis, pericardial
effusion, and constrictive pericarditis in end-stage renal disease: insights
1. Rudnick MR, Leonberg-Yoo AK, Litt HI, et al. The controversy of and pathophysiology. Clin Cardiol. 2017;40:839–846.
contrast-induced nephropathy with intravenous contrast: what is the risk? 9. Kim JH, Baek CH, Min JY, et al. Desmopressin improves platelet function
Am J Kidney Dis. 2020;75:105–113. in ureic patients taking antiplatelet agents who require emergency invasive
2. Luk L, Steinman J, Newhouse JH. Intravenous contrast-induced procedures. Ann Hematol. 2015;94:1457–1461.
nephropathy—the rise and fall of a threatening idea. Adv Chronic Kidney 10. Twerenbold R, Wildi K, Jaeger C, et al. Optimal cutoff levels of more
Dis. 2017;24:169–175. sensitive cardiac troponin assays for the early diagnosis of myocardial
3. Hinson JS, Ehmann MR, Fine DM, et al. Risk of acute kidney injury infarction in patients with renal dysfunction. Circulation. 2015;131:
after intravenous contrast media administration. Ann Emerg Med. 2041–2050.
2017;69:577–586. 11. Miller-Hodges E, Anand A, Shah ASV, et al. High-sensitivity cardiac
4. Mehran R, Dangas GD, Weisbord SD. Contrast-associated acute kidney troponin and the risk stratification of patients with renal impairment
injury. N Engl J Med. 2019;380:2146–2155. presenting with suspected acute coronary syndrome. Circulation.
5. Weisbord SD, Gallagher M, Jneid H, et al. Outcomes after angiography with 2018;137:425–435.
sodium bicarbonate and acetylcysteine. N Engl J Med. 2018;378:603–614. 12. Huang HL, Zhu S, Wang WQ, et al. Diagnosis of acute myocardial
6. Hagan AE, Farrington CA, Wall GC, Belz MM. Sodium polystyrene infarction in hemodialysis patients with high-sensitivity cardiac troponin
sulfonate for the treatment of acute hyperkalemia: a retrospective study. T assay. Arch Pathol Lab Med. 2016;140:75–80.
Clin Nephrol. 2016;85:38–43. 13. Li PK, Szeto CC, Piraino B, et al. ISPD Peritonitis Recommendations:
7. Meaney CJ, Beccari MV, Yang Y, Zhao J. Systematic review and 2016 update on prevention and treatment. Perit Dial Int. 2016;36:
meta‐analysis of patiromer and sodium zirconium cyclosilicate: a new 481–508.
armamentarium for the treatment of hyperkalemia. Pharmacotherapy. 14. Ronco C, Reis T, Husain-Syed F. Management of acute kidney injury in
2017;37:401–411. patients with COVID-19. Lancet Respir Med. 2020;8:738–742.
C H A P T E R 8 3 : Q U E S T I O N S A N D A N S W E R S
1. Of the following choices, which is the correct match between type 3. What is the most common cause of nontraumatic hematuria?
of urine cast and pathologic condition? a. Carcinoma of the kidney or bladder
a. Fatty casts—glomerulonephritis b. Cystitis
b. Granular casts—renal parenchymal infection c. Kidney stones
c. Hyaline casts—dehydration, exercise d. Prostatic hyperplasia
d. Red cell casts—nephrotic syndrome e. Transfusion reaction
e. White cell casts—acute tubular necrosis (ATN) Answer: c. In descending frequency, the most common causes are
Answer: c. Hyaline casts are associated with dehydration, exer- kidney stones, lower urinary tract infection (UTI), benign prostatic
cise, and glomerular proteinuria. The following are the other correct hypertrophy (BPH), carcinoma of the kidney or bladder, urethritis, and
associations: glomerulonephritis.
• Fatty casts—nephrotic syndrome 4. A 53-year-old man presents with painless gross hematuria. His only
• Red cell casts—glomerulonephritis past medical history is an aortic valve replacement for which he
• White cell casts—renal parenchymal infection takes warfarin. The physical examination is nonfocal. Laboratory
• Granular casts—ATN evaluation is remarkable for a normal chemistry panel and blood
2. A 34-year-old man with chronic kidney disease has missed his count, too numerous to count (TNTC) red blood cells (RBCs) on
last two hemodialysis treatments and presents with generalized urinalysis, and international normalized ratio (INR) of 1.8. What is
fatigue and dyspnea on exertion. Vital signs include a blood the next indicated step?
pressure of 165/94 mm Hg but are otherwise normal. Room air a. Admission and observation
Sao2 is 94% at rest. A portable chest x-ray shows vascular con- b. Parenteral vitamin K
gestion. Which of the following is an indication for immediate c. Reassurance
dialysis? d. Renal imaging
a. Blood urea nitrogen (BUN) level of 87 mg/dL and serum creati- e. Withholding warfarin (Coumadin) for 3 days
nine level of 10.6 mg/dL Answer: d. When hematuria is associated with anticoagulant use,
b. Serum calcium level of 6.8 mg/dL and serum albumin level of underlying disease can be identified in a significant proportion of
3.0 g/dL patients.
c. Serum potassium level of 7.6 mEq/L (not hemolyzed) 5. A 33-year-old woman presents with mild nonfocal abdominal
d. Serum sodium level of 124 mEq/L pain and subjective fever. Her past medical history is significant
e. Serum troponin level of 0.08 ng/mL for hypertension-induced renal failure, for which she is on peri-
Answer: c. Severe hyperkalemia is an indication for immediate dial- toneal dialysis (PD). The physical examination is remarkable for
ysis in this patient. An ECG should be obtained stat to determine the a temperature of 38°C (100.4°F), blood pressure 190/110 mm
degree of cardiotoxicity, and immediate medical treatment for hyper- Hg, and mild nonfocal abdominal pain. Slightly cloudy perito-
kalemia should be given while awaiting initiation of dialysis. Abnor- neal fluid is aspirated from the PD catheter and sent for analysis.
malities of the serum sodium or calcium level can generally be treated Which of the following statements regarding this patient’s condi-
without hemodialysis. A minimal troponin level elevation may be seen tion is correct?
in patients with chronic kidney disease, but does not generally require a. A peritoneal fluid white blood cell (WBC) count >50/mm3 is
specific treatment without other signs of cardiac ischemia; dialysis is diagnostic.
not required. b. Intravenous antibiotics should be started empirically.
1180.e1
1180.e2 PART III Emergency Medicine by System
C H A P T E R 8 3 : Q U E S T I O N S A N D A N S W E R S — c o n t ’ d
c. Most cases are due to Staphylococcus. in 20% of cases. A polymicrobial infection warrants GI evaluation for
d. No organism is identified in 50% of cases. possible perforation or intra-abdominal abscess. A PD fluid count
e. Polymicrobial infections suggest sample contamination. >100 cells/mm3, with a neutrophil count >50% or positive Gram stain,
Answer: c. Most PD-associated cases of peritonitis are due to Staphylo- is considered confirmatory. Treatment is typically with intraperitoneal
coccus aureus or Staphylococcus epidermidis. No organism is identified antibiotics given for a 10-to 14-day course.

Renal Failure: Section Six Genitourinary and Gynecologic Systems

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Renal Failure: Section Six Genitourinary and Gynecologic Systems

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SECTION SIX Genitourinary and Gynecologic Systems

KEY CONCEPTS RENAL FAILURE

HIV, Human immunodeficiency virus; NSAIDs, nonsteroidal antiinflammatory drugs.

TABLE 83.1 Treatment of Hyperkalemia

dialysis patients, is unusual. The latter, although reported occasionally

In evaluating presumed ischemic chest pain in a patient with CKD,

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