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CHAPTER 97: Acute Kidney Injury 927
■ PREGNANCY AND ACUTE RENAL FAILURE TABLE 97-8 Coexisting Renal and Liver Failure
The incidence of AKI complicating pregnancy has been decreasing for Simultaneous liver and renal injury
the past 25 years. This is attributable to improvements in prenatal care
and obstetric science and fewer complications related to septic abor- Cardiovascular collapse with shock
tions. The timing of AKI in pregnancy has a bimodal distribution. The Drugs and toxins
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early peak, which occurs during the first 20 weeks of gestation, is due Chlorinated solvents
to septic abortions, while the later peak (at 36-40 weeks) is secondary to
preeclampsia and bleeding complications. Heavy metals (arsenic, chromium, and copper)
Preeclampsia and eclampsia are accompanied by decreases in GFR Antibiotics
of 20% to 25% that are seldom clinically significant (see Chap. 127). Isoniazid
However, in a small proportion of pregnant women, the renal dys- Rifampin
function progresses to severe AKI. Women with preeclampsia are at
increased risk for the development of cortical necrosis. Cortical necrosis Tetracyclines
also can occur as a complication of placental abruption (often with Sulfonamides
concealed blood loss) or prolonged intrauterine death. Although severe, Acetaminophen
irreversible renal failure may be seen, partial recovery of renal func-
tion due to patchy cortical necrosis is more common. The diagnosis Mushroom poisoning (Amanita phalloides)
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of complete cortical necrosis should be established by renal biopsy or Infections
arteriography to exclude patchy cortical necrosis and ATN, from either Viral hepatitis
of which a degree of functional recovery is to be expected.
Coexisting AKI and fulminant hepatic failure have been described Bacterial sepsis
in gravid subjects. In women with acute fatty liver of pregnancy, AKI is Miscellaneous
present in over half. Although the mortality rate for both mother and Reye syndrome
fetus in this condition has been reported to be at least 70%, the prognosis
may be improving because of increased recognition of less severe cases. Acute fatty liver
The syndrome known by the acronym HELLP (hemolysis, elevated liver Systemic lupus erythematosus
enzymes, and low platelets) is a variant of unusually severe preeclampsia. Polyarteritis nodosa
The great majority of these patients have evidence of hepatic dysfunc- Sequential liver and renal injury
tion and sinusoidal congestion that may culminate in liver rupture. The
mean creatinine clearance in these women is about 55 mL/min (less than Prerenal azotemia
half normal), while 10% have severe AKI with a creatinine clearance of Ascites
<20 mL/min. Alcoholic cardiomyopathy
The rare but well-defined clinical entity of idiopathic postpartum AKI
is characterized by the onset of AKI in the peripartum period following Emesis
a previously normal pregnancy and childbirth. The serum creatinine Excessive diuresis
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level rises rapidly within a few days to several weeks following parturi- Intrinsic acute renal failure
tion. There is often an associated consumptive coagulopathy. Other
common clinical features include malignant hypertension, lethargy, Cirrhotic glomerulosclerosis
seizures, and a dilated cardiomyopathy. The pathophysiology of this Acute tubular necrosis
disorder is unknown. The outcome is poor; most patients have severe Hepatorenal syndrome
chronic renal failure, require dialysis, or die. Obstructive nephropathy
■ LIVER DISEASE AND ACUTE RENAL FAILURE Blood clots in the collecting system
AKI frequently occurs in the setting of severe liver disease. Prerenal Papillary necrosis
azotemia can be a consequence of ascitic redistribution of the ECF (or
its excessive treatment with diuretics), GI fluid losses (eg, vomiting, renin angiotensin system, sympathetic nervous system, as well as cardio-
diarrhea, or hemorrhage), or cardiac dysfunction (eg, alcoholic cardio- vascular abnormalities. HRS is difficult to distinguish from prerenal
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myopathy). If a coagulopathy is present, blood clots in the collecting AKI in the setting of advanced liver failure. The principal functional
system can cause obstructive uropathy. Cirrhosis may predispose to the abnormalities that have been described are renal vasospasm in the set-
occurrence of papillary necrosis. Intrinsic AKI in subjects with liver ting of peripheral vascular resistance that is abnormally low ; there is no
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disease is classified into disorders that simultaneously injure liver and “typical” structural lesion of HRS. Oliguria and a low FE are frequent,
Na
kidney and those in which the renal disease is a consequence of the if not universal, findings; the diagnosis of HRS should be considered
hepatic process (Table 97-8). The kidney is generally much more sensi- untenable in their absence. There are two types of HRS. Type I HRS is
tive to the effects of potential nephrotoxic agents if jaundice is present. characterized by rapid progressive renal failure defined by doubling of the
A relatively specific glomerular lesion called cirrhotic glomerulosclerosis initial serum creatinine concentrations to a level greater than 2.5 mg/dL
has been identified and is usually asymptomatic; however, it probably (226 µmol/L) in less than 2 weeks. It is associated with a poor prognosis.
predisposes to AKI of other causes. More commonly, patients with hepa- Type II HRS is less severe renal insufficiency than that observed with type
titis B or C with proteinuria have membranous nephropathy or mem- I disease; serum creatinine typically is between 1.5 and 2.5 mg/dL (133
branoproliferative (cryoglobulinemic) glomerulonephritis. Hepatitis B is and 226 µmol/L). It is principally characterized by ascites that is resistant
also associated with polyarteritis nodosa. The most serious of coexisting to diuretics and has a steady or slowly progressive course. 114
hepatic and renal diseases is the hepatorenal syndrome (HRS). Diseases First line therapy for type 1 HRS is albumin replacement and vasocon-
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that may simultaneously involve both liver and kidney are summarized in strictor use. Terlipressin, a long-acting vasopressin analogue, is the most
Table 97-8. HRS is a potentially reversible syndrome that occurs in widely used agent. The mechanism of action of this therapy is not well
patients with acute or chronic liver failure and alcoholic hepatitis. It is understood. It is thought that albumin expands the circulatory volume
characterized by impaired renal function, excessive activation of the improving cardiac output and thereby corrects the circulatory dysfunction.
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