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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
• Medications
Nonsteroidal anti-inflammatory drugs (NSAIDS) inhibit cyclo-
oxygenase, thereby decreasing prostaglandin synthesis. The subsequent renal vasoconstriction decreases the GFR.
ACE inhibitors and angiotensin receptor blockers allow a greater
magnitude of vasodilation in the efferent arteriole as compared
with the afferent arteriole, leading to decreased GFR.
Tacrolimus and cyclosporine cause afferent arteriolar vasocon-
striction.
Diagnosis
The diagnosis of prerenal AKI is best made by employing concepts in pathophysiology.
2
Table 1 lists laboratory tests that help delineate the diagnosis.
Treatment
• Fluid by mouth or intravenously. Isotonic solution is most effective in
achieving intravascular repletion. Normal saline and intravenous fluid
with sodium bicarbonate are appropriate choices. It is important to
ensure that the fluid is isotonic (not hypertonic) (Table 2).
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T.K. Kim
Fig. 1. Pathophysiology of prerenal AKI.
Decreased Absolute or Relative
Effect Intravascular Volume
Stimulation of Angiotensin II & Norepinephrine
Renal Vasoconstiction
(preferential blood flow to vital organs)
Decreased Renal Blood Flow &
Glomerular Hydrostatic Pressure
Decreased GFR
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Acute Kidney Injury
Table 1. Diagnosis of Prerenal AKI
Test Prerenal AKI Mechanism
Serum BUN: Cr >20:1 Increase in proximal tubule sodium and water
reabsorption. Water reabsorption increases
the tubular fluid concentration of urea,
leading to an increase in proximal tubular
urea reabsorption down a favorable
concentration gradient. Creatinine is not
reabsorbed.
Urine sodium <20 mEq/L Decreased renal blood flow in the
prerenal state is associated with an
appropriate increase in proximal tubular
sodium and water reabsorption. Since more
sodium is reabsorbed, the urine sodium
excreted is decreased.
Fractional <1% Since there is reabsorption of both sodium
excretion of and water in prerenal states, sometimes
sodium (FeNa) the urine sodium will not be <20 mEq/L
because the urine is so concentrated.
Calculating the fractional excretion of
sodium allows sodium handling to be
assessed directly without the confounding
effect of water reabsorption.
Urine osmolarity >500 mOsm/kg or Antidiuretic hormone (ADH) is stimulated
> serum Osm by volume depletion, resulting in
reabsorption of water (independent of
sodium) at the collecting ducts.
Fractional <35% Loop diuretics (NaK2Cl transporter inhibitor
excretion of at the loop of Henle) and thiazide diuretics
urea (FeUrea) (sodium chloride transporter inhibitor at the
distal tubule) render the evaluation of urine
sodium or FeNa less accurate. Urea is
predominantly handled in the proximal
nephron, thereby allowing the evaluation of
the true volume status of the patient despite
loop diuretics or thiazides.
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Cr
100
P
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U
Cr
U
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• Reverse the underlying cause of hypoperfusion. Prerenal AKI with
absolute decrease in effective arterial volume reverses relatively
quickly with fluids. Optimizing cardiac output in CHF and hepatic
function in cirrhosis can improve renal function. Prolonged prerenal
AKI can lead to tubular damage, which can become irreversible.
Intrarenal (Intrinsic) AKI
Definition
Intrarenal AKI is AKI in which there is direct injury to kidney parenchyma.
There are certain aspects in the history or lab findings which will
heighten suspicion that the AKI is intrarenal. The clinical settings in
which intrarenal AKI is commonly seen are listed in Table 3.
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T.K. Kim
Table 2. Isotonic Intravenous Fluids
Important Elements to Monitor
IVF Sodium Content Before and During Infusion
Normal saline 154 mEq • Excessive hydration with NS can be
associated with a dilutional
acidosis.
½ NS with 75 mEq 152 mEq • Avoid bicarbonate in lactic acidosis
sodium bicarbonate (unless pH < 7.1 or 7.2), because it
can worsen lactic acidosis.
• Alkalization can decrease ionized
calcium. Ensure ionized calcium is
normal or near-normal prior to
infusion and monitor ionized
calcium during infusion.
• Alkalization can cause hypokalemia.
Monitor potassium.
D5W with 150 mEq 150 mEq • Ensure lactic acidosis is not present.
sodium bicarbonate • Monitor ionized calcium as above.
• Monitor glucose due to the D5W.
Plasmalyte or lactated 140 mEq • May want to avoid in AKI, given the
ringers potassium content (5 mEq/L).
Diagnosis
The urinalysis, urine electrolytes, and urinary sediment are key factors in
making this distinction (Table 4).
Treatment
Removal of the inciting cause and supportive therapy are the core components of treatment of intrarenal AKI. Hyperkalemia is often encountered in AKI. The details of management of hyperkalemia are covered in
a separate chapter. Obtaining an EKG is a critical step in the management.
Hyperkalemic EKG changes warrant initiation of telemetry monitoring.
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Acute Kidney Injury
Table 3. Clinical Settings for Intrarenal (Intrinsic) AKI
Part of Nephron
Involved Diseases Features
Glomerular disease Nephritic or nephrotic • Proteinuria ≥3 or 3.5 g
syndromes (nephritic diseases per day in nephrotic
are more commonly associated diseases; less in nephritic.
with AKI than nephrotic) • Presence of hematuria
in nephritic diseases;
not predominant
feature in nephrotic.
• Consider renal biopsy.
Interstitial disease Acute interstitial • Associated with certain
nephritis (AIN) antibiotics (penicillins
and cephalsporins).
Tubular disease Acute tubular • Ischemic: hypotension
necrosis (ATN) • Toxic: IV contrast for CT
scan and cardiac
catheterization,
aminoglycoside, other
medications, myoglobin
in rhabdomyolysis,
hemoglobin in hemolysis.
Potassium should be frequently checked throughout the treatment, as
repeat rounds of therapy to further decrease the potassium may be necessary. Hyperkalemia refractory to medical treatment is an important indication for dialysis.
Prevention of Contrast-Induced Nephropathy
The pathology of contrast-induced nephropathy (CIN) is ATN. The specific pathogenesis remains unclear. Toxic and ischemic injury mediated in
part by reactive oxygen species is seen in animal and in vitro studies.
3
The risk factors for developing CIN include:
• Chronic kidney disease (elevated baseline creatinine and/or proteinuria)
• Diabetes
• Age >75 years
• Volume depletion around the time of the contrast administration
• CHF
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T.K. Kim
Table 4. Diagnosis of Intrarenal (Intrinsic) AKI vs. Prerenal AKI
Test Prerenal AKI Intrarenal AKI
Serum BUN: Cr > 20:1 < 20:1
Urine Na (mEq/L) < 20 > 20
Fractional excretion of < 1% >1%
sodium (FeNa)
Urine osmolarity >500 mOsm/kg or ~ 300 mOsm/Kg (very similar
> serum Osm to plasma Osm)
Fractional excretion of <35% >35%
urea (FeUrea)
Urine sediment Normal Glomerular: RBCs or RBC
casts in nephritic diseases.
Interstitial: WBCs or WBC
casts in AIN.
Tubular: muddy-brown
granular casts in ATN.
• Cirrhosis
• Hypertension
• NSAID use
• Hypotension
• Volume of contrast
Prognosis of CIN
Most cases of CIN occur within 24–72 hr of contrast administration.
Creatinine can return to the baseline within 3–10 days. However, there are
cases in which the creatinine remains above the baseline. Thirteen to 50%
of patients with CIN who require dialysis after contrast exposure become
dialysis-dependent.
4,5
Prevention of CIN
• Low osmolar contrast medium at the lowest possible dose.
• Intravenous fluid with either normal saline or ½ NS. A dose com-
monly used is 1 mL/kg/hr 12 hr before contrast administration and 12
hr after administration.
• Intravenous fluid with bicarbonate
Some studies cite intravenous fluid with sodium bicarbonate (at
3 mL/kg/hr 1 hr bolus before contrast administration, then
1 mL/kg/hr for 6 hr after administration) as being superior to
other forms of hydration.
6,7
Can order ½ NS with 75 mEq of sodium bicarbonate. Can opt to
lower the bolus dose, especially in elderly patients or any patient
easily susceptible to volume overload.
• N-acetylcysteine — results of studies have been inconsistent, but
report few adverse effects.
8
The most commonly used dose is 600 mg
orally every 12 hr on the day before contrast, and every 12 hr on the
day of contrast (for a total of four doses).
419
Acute Kidney Injury
Postrenal AKI
Postrenal AKI is defined as AKI from the obstruction of urinary outflow
tracts.
The clinical settings in which postrenal AKI is commonly seen are:
• Benign prostatic hypertrophy (BPH)
• Prostate cancer
• Cervical cancer
• Bladder or urological tumor
• Large bilateral kidney stones (rare) or obstructing kidney stones in the
setting of a solitary kidney
The pathophysiology of postrenal AKI is based on Starling’s forces.
The driving force for the GFR depends on the glomerular hydrostatic
pressure being greater than the capsular (Bowman’s capsule) hydrostatic
pressure. In postrenal AKI, the obstruction causes an increase in the capsular hydrostatic pressure, thereby decreasing the net outward pressure.
This effect decreases the GFR.
Diagnosis
Placement of a Foley catheter or imaging with ultrasound can diagnose
postrenal AKI.
Treatment
Foley catheter placement can treat postrenal AKI if the obstructing lesion
is at or below the bladder neck. If the obstruction is above this level, percutaneous nephrostomies or surgical stent placement is required. Prompt
relief of obstruction is critical, because the longer the obstruction is present, the lower the likelihood of returning to baseline creatinine will be.
Obstruction leads to tubular dysfunction and inability to reabsorb
sodium and urea. After the obstruction is relieved, postobstructive diuresis
(an osmotic diuresis) can occur from this additional solute. Therefore, it is
very important to closely monitor urine output after relief of obstruction.
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T.K. Kim
Intravenous Fluids for Postobstructive Diuresis
The kidney’s ability to concentrate and dilute the urine is impaired in
obstruction. In postobstructive diuresis, the most appropriate fluid is ½
NS. The rate of ½ NS can be 2/3 mL for every 1 mL of urine output.
Frequent re-evaluation of urine output (at least every 8 hr) must be done
to assess changes needed in the intravenous fluid rate. More frequent reevaluation is required in large volumes of polyuria.
Parameters to Monitor in Postobstructive Diuresis
• Vitals: hypotension and tachycardia can result from falling behind in
fluid repletion. Strict “ins and outs,” daily weights, and lung exams
are essential.
• Electrolyte and acid/base disturbances in postobstructive diuresis are
outlined in Table 5.
9
Checking a chemistry panel at least every 8 hr is
necessary. More frequent testing may be needed if the projected 24 hr
urine output is excessive.
Medications and Procedures in AKI
It is prudent to avoid certain common medications and procedures in AKI
(see Table 6). Since creatinine clearance is assumed to be < 10 mL/min in
a patient whose creatinine is rising daily, medication dose adjustment is
important in order to prevent possible untoward effects due to overdosage
(such as antibiotics, digoxin, famotadine, allopurinol, or colchicine).
Renal Consult for AKI
Involving nephrologists earlier in the course of management may be beneficial if the initial tests show renal AKI, or if there are significant electrolyte or acid/base disturbances in any form of AKI. If there is significant
proteinuria or hematuria in a patient with resolving or resolved prerenal
AKI, a renal consult can determine if there is any underlying renal
parenchymal disease. Nephrologists can also help determine if a renal
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Acute Kidney Injury
422
T.K. Kim
Table 5. Electrolyte and Acid/Base Disturbances in Postobstructive Diuresis
Changes Observed in
Blood Chemistry Postobstructive Diuresis Mechanism
Sodium Increased Water and salt excretion are
increased after obstruction is
relieved. If urine output is not
adequately matched in the setting of
postobstructive diuresis,
hypernatremia may ensue.
However, if there is excessive
repletion of urine output with
hypotonic solution, hyponatremia
results.
Potassium Decreased Polyuria is associated with
increase in potassium excretion.
Magnesium Decreased Polyuria is associated with increase
in magnesium excretion.
Bicarbonate Decreased Defective urinary acidification.
Table 6. Medications and Procedures to Avoid in AKI
Low-molecular-weight heparin Patients with AKI or creatinine clearance
< 30 mL/min have elevated anti-Xa, placing
them at higher risk for major bleeding events.
10
Phosphate-containing laxatives Calcium phosphate deposits have been
or enemas associated with acute phosphate nephropathy in
certain patients (AKI and deaths are reported).
11
Meperidine The accumulation of a metabolite
(normeperidine) in renal impairment lowers the
seizure threshold in patients with AKI.
12
Hydromorphone is the preferred narcotic in
AKI or CKD.
13
NSAIDS Renal vasoconstriction induced by NSAIDS
reduces GFR
Metformin Discontinue in patients with AKI or creatinine
clearance < 60–70 mL/min, men with serum
creatinine > 1.5 mg/dL, or women with
serum creatinine > 1.4 mg/dL.
14
(Continued )
biopsy is warranted, and assess the indications for and the timing of dialysis initiation if there is no recovery.
References
1. Thadhani R, Pascual M, Bonventre J. (1996) Acute renal failure. New
Engl J Med 334: 1448–1460.
2. Carvounis C, Nisar S, Guro-Razuman S. (2002) Significance of the
fractional excretion of urea in the differential diagnosis of acute renal
failure. Kidney Int 62: 2223–2229.
3. Katholi R, Woods W Jr, Taylor G, et al. (1998) Oxygen free radicals
and contrast nephropathy. Am J Kidney Dis 32: 64–71.
4. Tepel M, Van der Geit M, Schwartzfeld C, et al. (2000) Prevention of
radiographic-contrast-agent–induced reductions in renal function by
acetylcysteine. New Engl J Med 343: 180–184.
5. Rudnick M, Berns J, Cohen R, Goldfarb S. (1994) Nephrotoxic risks
of renal angiography: Contrast-media associated nephrotoxicity
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Acute Kidney Injury
Table 6. (Continued )
Peripherally inserted central PICCs will sclerose the entire length of the vein
venous catheters (PICCs) in which it is inserted. Since there is a chance
that a patient with AKI can progress to CKD,
preserving the integrity of veins is important
for possible future arteriovenous access for
dialysis. Hickman catheters (inserted in the
internal jugular vein) are preferred if long term
intravenous access is required.
Subclavian vein Subclavian lines can cause central venous
central lines stenosis, rendering all veins distal to this
site inadequate for future AV fistula use.
Internal jugular lines are preferred.
CT with intravenous contrast See section on CIN.
MRI with gadolinium Gadolinium in patients with AKI or creatinine
clearance <30 mL/min is contraindicated,
owing to the possibility of nephrogenic
systemic fibrosis, which has been
associated with reported fatalities.
15