ARF
a
condition in which a previously normal serum creatinine rises by 0.5 mg/dL, or
an absolute increase in serum creatinine of >1 mg/dL in a patient
with previous chronic kidney disease (CKD).
In
the clinical setting, ARF is classified in a variety of ways. Classifying ARF
by daily urine output can be useful. Anuria is defined as a urine output of <50
mL/d, oliguria is when the daily urine output is 50 to 450 mL/d, and
nonoliguria occurs when the patient can make >450 mL of urine per
day.
EPIDEMIOLOGY
ARF
is a common condition in the general population, with an annual incidence of
approximately 200 cases per million population per year.2 The incidence rate is
higher in hospitalized patients, 5% of whom may require RRT (Table 42–1).7 The
highest incidence of ARF is in hospitalized patients in the intensive care
unit. Depending on the definition used, ARF develops in 2% to 25% of patients
in intensive care units.8−10
Many patient-specific factors cause a predisposition to the development of ARF.
In nonhospitalized patients, ARF is often druginduced. Common causes of
drug-induced ARF include nonprescription
nonsteroidal
anti-inflammatory drugs (NSAIDs), prompting the FDA to convene an advisory
committee to re-examine labeling
of
these products.11 This drug class alone may be responsible for 500,000 to
2,500,000 cases of nephrotoxicity in the United States per year.
OUTCOMES
The
development of ARF is one of the most serious events that can happen to a
hospitalized patient, regardless of the reason for hospitalization. In patients
admitted for cardiac surgery, the mortality risk is seven- to eightfold higher
if the patient develops ARF.19 Patients who develop ARF following
administration of intravenous radiocontrast dye and requiring dialysis have
twice the mortality rate of similar patients receiving radiocontrast dye who do
not experience an increase in their serum creatinine values.13 The outcome of a
patient with ARF predominantly depends on the cause of the condition. In general,
higher mortality rates are seen in conditions that result in hypoxia to the
kidney causing acute tubular necrosis (ATN; 60%) or cortical necrosis (100%)
compared to the lower mortality associated with autoimmune ARF causes like
glomerulonephritis (9% to 25%), vasculitis (45%), or interstitial nephritis
(13%).2 Similarly, postrenal causes like obstructive ARF tend to have lower
mortality rates (27%), ostensibly because these obstructions can be surgically
repaired before permanent damage can be done to the kidney. Other patient
factors influence ARF outcomes. Understandably, those patients with higher
severity of illness have higher mortality rates than those who do not.18
Critically ill patients with ARF due to sepsis have mortality rates that are
significantly
higher
than those of patients who develop ARF for other reasons (74% vs. 45%).
ETIOLOGY:
Prerenal renal failure
Functional
acute renal failure
Acute intrinsic renal failure
Postrenal
renal failure
(obstruction)
|
Systemic hypoperfusion
Isolated
renal hypoperfusion
Vascular
Glomerular
Acute
tubular necrosis
Acute
interstitial nephritis
Bladder
outlet obstruction
Ureteral
(bilateral or unilateral with
solitary
functioning kidney)
Renal
pelvis or tubules
|
Intravascular volume depletion
Dehydration
Hemorrhage
CHF
Liver
disease
Nephrotic
syndrome
Overdiuresis
Bilateral
renal artery stenosis (unilateral renal
artery
stenosis in solitary kidney)
Emboli
Cholesterol
Thrombotic
Medications:
Cyclosporine
ACEIs
NSAIDs
Hypercalcemia
Hepatorenal syndrome
Vasculitis
Polyarteritis
nodosa
Thrombotic
thrombocytopenic purpura
Hemolytic
uremic syndrome
Emboli
Cholesterol
Thrombotic
Systemic
lupus erythematosus
Poststreptococcal
glomerulonephritis
Antiglomerular basement membrane
disease
Ischemic
Hypotension
Vasoconstriction
Exogenous
toxins
Contrast
dye
Heavy
metals
Drugs
(amphotericin B, aminoglycosides, etc.)
Endogenous
toxins
Myoglobin
Hemoglobin
Drugs
Penicillins
Ciprofloxacin
Sulfonamides
Infection
Streptococcal
Prostatic hypertrophy
Improperly placed bladder catheter
Cervical
cancer
Retroperitoneal fibrosis
Crystal deposition
Oxalate
Indinavir
Sulfonamides
Acyclovir
Tumor lysis syndrome
|
PATHOPHYSIOLOGY
A
basic knowledge of renal function facilitates the understanding of how ARF
manifests itself clinically. The most logical approach to understanding renal
function is to divide the kidney into its four basic component parts: the
vasculature, the glomeruli, the tubules, and the interstitium surrounding the
other three component parts.
1.RENAL
VASCULATURE
The
kidney is a highly vascular organ with blood vessels ranging from the very
large (renal arteries) to the very small capillaries providing blood to each
individual glomerulus. Obstruction of the renal artery will result in an
increase in serum creatinine, hematuria, and proteinuria, but obstruction of
smaller vessels will only cause infarction of the downstream parenchyma. If
this area is small, no change in serum creatinine will occur. Smaller vessels
may be obstructed with cholesterol emboli, vascular
lesions,
or platelet plugs, all of which will present as isolated decreased perfusion of
the glomeruli. The serum creatinine frequently is increased since the lesions
are usually diffuse. However, the urinalysis most commonly will be normal since
the kidney itself is not ischemic and the glomeruli are not involved. The
urinary indices suggest prerenal azotemia (i.e., a low urine sodium
concentration and a low fractional excretion of sodium) in the absence of
systemic hypotension or a decrease in effective blood volume. The urine volume may
or may not be diminished. However, the onset of oliguria secondary to diffuse
arterial lesions within the kidney, such as that which occurs with hemolytic
uremia syndrome, denotes a poor chance for salvage of renal function.
2.GLOMERULI
The
glomerulus consists of an enlargement of the proximal end of the renal tubule
to incorporate a vascular tuft connecting the afferent and efferent arterioles
(Fig. 42–1). The production of glomerular ultrafiltrate is predominantly
dependent on the transcapillary hydrostatic pressure (dictated by the afferent
and efferent arteriolar resistance) and the glomerular surface area. Afferent
arteriolar tone is determined primarily by the local levels of angiotensin II
(which induces vasoconstriction)
and
prostaglandins (which induce vasodilation). Efferent arteriolar tone is
predominantly determined by the local concentration
of
angiotensin II. Pathophysiologic processes and medications that result in
alterations of the afferent and efferent arteriolar tone (i.e., systemic hypotension,
hypercalcemia, or use of ACEIs, angiotensin II receptor blockers, or NSAIDs)
reduce glomerular ultrafiltrate production as a result of a decrease in
glomerular hydrostatic pressure. Under these conditions, the serum creatinine
will rise, the urine sediment will be normal, and the urine indices will
suggest prerenal azotemia. However, the urinary solutes may or may not be
maximally concentrated, depending on the circulating level of antidiuretic
hormone
that
is necessary to maximally concentrate the urine. Damage to the glomerular
capillary tuft (e.g., acute glomerulonephritis) results in a decline in the
production of glomerular ultrafiltrate as a result of a decrease in glomerular
capillary surface area. Under these conditions the serum creatinine rises and
the urinalysis is significant for hematuria and proteinuria because of the
increased permeability of the damaged glomerular capillaries. Proteinuria
exceeding 3 g/day is often referred to as nephrotic range proteinuria.
Prolonged heavy proteinuria secondary to glomerular damage may result in the nephritic
syndrome.
3.RENAL
TUBULE
Under
normal conditions, approximately 180 L of glomerular ultrafiltrate are produced
per day, the vast majority of which must be reabsorbed by the renal tubules to
maintain homeostasis. Clinically, the renal tubule can be divided into three
major sections: the proximal tubule, Henle’s loop, and the distal nephron,
which includes the distal tubule, the cortical collecting tubule, and the
medullary collecting ducts. In the proximal tubule, approximately 60% to 70% of
the filtered load of water and solute is isovolemically reabsorbed, as is the vast
majority of filtered amino acids, glucose, and bicarbonate. In addition to its
other functions, Henle’s loop is responsible for a significant portion of the
total reabsorption of potassium, calcium, and magnesium, as well as for
generating the osmotic gradient within the kidney that is necessary for the
concentration of urinary solutes. Damage
to
this portion of the nephron results in wasting of potassium and magnesium by
the kidney and an inability of the kidney to concentrate the urine. The medullary
portions of Henle’s loop are very sensitive to ischemia secondary to
hypoperfusion. Consequently, in severe prerenal azotemia with renal
hypoperfusion, there may be a loss of urinary concentrating ability despite the
continued presence of a low urinary sodium concentration and a low fractional
excretion of sodium. Major functions of the distal nephron include the
regeneration of bicarbonate, the excretion of acid (hydrogen ion), the
secretion of
potassium,
and the reabsorption of water. Damage to this portion of the nephron may
present as significant acidemia and either hypoor hyperkalemia, depending on
the mechanism of injury.
4.INTERSTITIUM
The
interstitium of the kidney provides the structural support for the kidney and
serves to provide the environment in which concentrating gradients can be
established. In addition, the interstitium of the kidney plays a major role in
urinary ammonia handling. To facilitate the regeneration of bicarbonate and the
excretion of acid by the distal nephron, the kidney utilizes ammonia as a
urinary buffer. When the interstitium of the kidney is damaged (e.g., in acute
allergic interstitial nephritis), the concentrating gradient within the kidney
may be dissipated and ammonia handling disrupted. Consequently, patients presenting
with acute interstitial nephritis frequently are unable to concentrate the
urinary solutes. The urinalysis may show mild proteinuria
and
hematuria. However, the striking finding on microscopic examination of the
sediment is the presence of numerous WBCs and WBC casts.
C L I
N I C A L PRESENTATION OF ACUTE RENAL FA I L U R E
GENERAL
Outpatients
often are not in acute distress; hospitalized patients may develop ARF after a
catastrophic event
SYMPTOMS
Outpatient:
Change in urinary habits, weight gain, or flank pain
Inpatient:
Typically ARF is noticed by clinicians before it is noticed by the patient
SIGNS
Patient
may have edema; urine may be colored or foamy.
Vital
signs may indicate orthostatic hypotension in volumedepleted patients
LABORATORY
TESTS
Urine
and blood chemistries may determine prerenal cause complete blood cell count
(CBC) and differential rules out
infectious
causes Urine microscopy may reveal casts, WBCs, RBCs, and eosinophils
OTHER
DIAGNOSTIC TESTS
Renal
ultrasound or cystoscopy may be needed to rule out obstruction; renal biopsy
reserved for difficult diagnoses
TREATMENT
NONPHARMACOLOGIC
In
situations in which administration of a nephrotoxin cannot be avoided, such as
when radiocontrast dye is to be administered, nonpharmacologic therapies can be
employed to prevent ARF. The key to nonpharmacologic ARF prevention is the
elimination of the patient’s risk factors to the degree that is possible. The
best-studied examples of this are the interventions used to maximize renal
perfusion when radiocontrast dye is administered. Adequate hydration and sodium
loading prior to radiocontrast dye administration have been shown to be
beneficial therapies. A trial comparing infusions of 0.9% NaCl or 5% dextrose
with 0.45% NaCl administered prior to radiocontrast dye infusion conclusively
demonstrated that the normal saline was superior in preventing ARF.26 The
intravenous solution infusion rate used in this study was 1 mL/kg per hour
beginning the morning that
the
radiocontrast dye was going to be given, and all subjects were encouraged to
drink fluids liberally as well. The benefits of 0.9% NaCl infusions have been
found in similar studies,27 suggesting this regimen should be used in all
at-risk patients who can tolerate the sodium and fluid load.
PHARMACOLOGICAL
HYDARTION,
MANNITOL, LOOP DIURETIC, DOPAMINE, CCBs, THEOPHYLLINE, ACETYLCYSTEINE,
FENOLDOPAM, INSULIN.
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