Page 1349 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

922 PART 8: Renal and Metabolic Disorders

because COX-2 is constitutively expressed and physiologically active in involvement, leukocytoclastic vasculitis, neuropathy, or other stig-
the kidney. The second type of acute renal injury is allergic interstitial mata of autoimmune disease may increase the index of suspicion
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nephritis, as discussed below. Chronic NSAID use is also associated with for this diagnosis, but it must be emphasized that a skilled urinalysis
papillary necrosis and is thought to occur in patients who are taking demonstrating an “active” sediment in a patient with AKI may make
multiple analgesics. this diagnosis alone. In fact, the presence of erythrocyte casts is
pathognomonic of GN; associated with AKI, this is essentially diag-
Acute Tubulointerstitial Nephritis: AKI due to acute interstitial nephritis nostic of RPGN.
(AIN) is most often caused by allergic reaction to various drugs (allergic
AIN), but there are also a variety of infectious (Legionnaire disease, cyto- ■ VASCULAR CAUSES OF ACUTE RENAL FAILURE
megalovirus, and Hantavirus), autoimmune (lupus), alloimmune (renal
transplant rejection), and infiltrative (sarcoidosis, leukemia, and lym- Vascular causes of AKI are categorized into small-vessel diseases and
https://kat.cr/user/tahir99/
phoma) disorders that can cause AIN (see Table 97-2). The most common large-vessel diseases (see Table 97-2). Diseases involving small vessels
drugs that cause allergic AIN are penicillins, cephalosporins, ciprofloxacin, include microscopic polyarteritis (vasculitis in polyarteritis nodosa and
rifampin, sulfonamides (furosemide, thiazide diuretics, and trimethoprim- Kawasaki disease involves medium-sized vessels), granulomatosis with
sulfamethoxazole), proton pump inhibitors (increasingly recognized as a polyangiitis (Wegener), mixed cryoglobulinemia, and conditions that
cause of AIN), H -blockers, allopurinol, and NSAIDs. are categorized as thrombotic microangiopathies, including thrombotic
2
Patients with AIN classically present with AKI temporally related thrombocytopenic purpura, hemolytic uremic syndrome, scleroderma
to drug therapy or infection, associated with a triad of fever, rash, and renal crisis, malignant hypertension, and antiphospholipid antibody
eosinophilia. Urinalysis findings include leukocyturia with eosin- syndrome. Large-vessel renal vascular diseases include thromboembolic
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ophiluria, leukocyte casts, and low-grade proteinuria. Although all these diseases and renal vein thrombosis. Atheroembolic disease should be
signs are present in the majority of patients with AIN, absence of these considered in patients who develop AKI after instrumentation of the
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does not exclude the diagnosis of AIN. In particular, these findings are aorta, particularly in patients with known atherosclerotic disease.
usually absent in NSAID-induced AIN. Proteinuria is mild to moderate Renal vein thrombosis is usually a complication of nephrotic syndrome,
except in NSAID-induced AIN, in which nephrotic syndrome caused and if bilateral can cause AKI. Abdominal compartment syndrome (see
by a minimal change lesion has been described. Tubular dysfunction Chap. 114) is present when the intra-abdominal pressure (IAP) reaches
(eg, Fanconi syndrome, distal renal tubular acidosis, or hyperkalemia) 20 to 25 cm H O, and unless decompressed, irreversible organ failure
2
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occurs in the majority of patients with AIN. may result. The pathogenesis of oliguria and AKI in abdominal com-
AIN is usually suspected from the history and laboratory findings. In partment syndrome involves venous compression (decreased venous
the absence of urinary tract infection, detection of large numbers of uri- return and renal vein compression), ureteral compression with obstruc-
nary eosinophils (>5%) strongly suggests the diagnosis of drug-induced tive uropathy, and possibly changes in renovascular resistance and
tubulointerstitial nephropathy (TIN). Hansel stain of the urine is more intrarenal blood flow distribution. Regardless of the underlying cause, a
sensitive than Wright stain for the detection of urinary eosinophils. reduction in urine output with or without azotemia in the presence of a
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The Hansel method correctly identified 10 of 11 patients with TIN, as measured intra-abdominal pressure over 15 cm H O is cause for concern
2
opposed to only 2 of 11 correctly classified using Wright stain. False- and should prompt intervention.
positive results with the Hansel technique are most commonly caused by
rapidly progressive GN or acute prostatitis. Diagnosis can be confirmed RENAL FUNCTION MONITORING AND DIAGNOSTIC
by renal biopsy if AKI is progressive and treatment of an alternative APPROACH TO ACUTE RENAL FAILURE
diagnosis is considered (eg, rapidly progressive GN), or if there is no
recovery of renal function after discontinuation of the medication sus- ■ MONITORING RENAL FUNCTION IN THE ICU
pected to have caused AIN.
No therapy is recommended in patients with mild renal insufficiency, Attempts to develop strategies to prevent or treat AKI in the ICU have
and in patients who respond after discontinuation of the offending been hampered by the lack of sensitive real-time methods to monitor
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medication. AIN is usually reversible after withdrawal of the offending renal perfusion and function in the clinical setting. There are no direct
agent and treatment of underlying disease. The optimal therapy of AIN measures of renal perfusion in clinical use. Of the available research
is unknown, since there are no randomized controlled trials or large techniques for this purpose, para-aminohippuric acid (PAH) clearance
observational studies. Corticosteroid therapy is unproven, and generally is not a valid method to assess renal plasma flow because renal PAH
recommended only in patients with biopsy-confirmed acute allergic extraction is impaired in critical illness, after cardiac surgery, postrenal
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interstitial nephritis who do not respond to conservative management, transplantation, and in AKI. Clinical indices such as plasma concentra-
and have no contraindication to immunosuppression. tions of urea nitrogen and creatinine, urine output, urine chemistries,
and urinalysis may be assessed in combination to monitor renal per-
Rapidly Progressive Glomerulonephritis: Glomerulonephritis such as fusion and function, but alterations in these markers are insensitive,
postinfectious glomerulonephritis, lupus nephritis, and Goodpasture indirect, and often delayed manifestations of renal hypoperfusion and
syndrome can cause acute or subacute renal failure (see Table 97-2). injury. Although relatively insensitive, it should be recognized that
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Rapidly progressive glomerulonephritis (RPGN) causing AKI is an emer- progressive elevation of serum creatinine is a specific sign of decreased
gency. The combination of AKI with an “active” urine sediment (heavy GFR and diagnostic of AKI. As depicted in Figure 97-3, daily serum
proteinuria, hematuria, leukocyturia, and erythrocyte/leukocyte/ creatinine increments of 0.5 to 1 mg/dL (depending on muscle mass, and
mixed cellular casts) should prompt urgent evaluation with renal in the absence of rhabdomyolysis) signal severe depression of GFR.
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biopsy and serologies. The underlying pathologic lesion is classically In the absence of obstruction or renal hypoperfusion, this is usually
necrotizing crescentic glomerulonephritis, treated with high-dose diagnostic of ATN.
pulse corticosteroid therapy to stabilize renal function, followed by Direct measurement of GFR is probably the most relevant marker of
intensive immunosuppression (with or without plasmapheresis). renal function to monitor in the ICU, and can be used as an index of
Causes include inflammatory disorders with immune complex depo- adequate systemic perfusion, a marker of organ dysfunction, a guide
sition (lupus, postinfectious, or cryoglobulinemia), anti–glomerular to medication dosing, and to determine timing of initiation of renal
basement membrane antibodies (Goodpasture syndrome, when replacement therapy. GFR measurement methods more sensitive than
associated with pulmonary hemorrhage), and pauci-immune glo- monitoring serum creatinine and urea nitrogen have been validated in
merulonephritis (usually with small-vessel vasculitis; see below). this population, but are not yet in widespread clinical use. 72,75 Abbreviated
Associated clinical features such as pulmonary hemorrhage, sinus creatinine clearance measurements (2-4 hours) provide a more accurate

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