AKI IN PREGNANCY

1. AKI IN PREGNANCY
• PRESENTER – DR PREM MOHAN JHA
• SENIOR REGISTRAR-1
• DNB NEPHROLOGY
• MAX SUPER SPECIALITY HOSPITAL, VAISHALI, GHAZIABAD.

2. • Introduction
• Defition
• Epidemiology
• Physiologic changes during pregnancy
• Etiologies
• Diagnostic approach
• Differential diagnosis
• Treatment

3. INTRODUCTION
• During pregnancy, AKI can be due to any of the same disorders that affect
the general population, such as PRE-RENAL, INTRINSIC And POST-RENAL
Causes.
• AKI may occur as a NEW CONDITION, a PRE-EXISTING, albeit
unrecognized condition, or as a pre-existing condition in patients with
normal or impaired renal function.

4. DEFINITION
• AKI is defined by the abrupt loss of kidney function.
• Several consensus definitions of AKI have been developed for use in the general
population.
• These include the
1. RIFLE
2. Acute Kidney Injury Network (AKIN) definitions
3. Kidney Disease: Improving Global Outcomes (KDIGO) modifications of the
AKIN definition

5. • However, it is not clear that the consensus criteria for AKI are useful in pregnancy.
This is because, during pregnancy, glomerular filtration rate (GFR) increases
significantly (by approximately 50 percent), resulting in a lower baseline serum
creatinine compared with similarly healthy, nonpregnant individuals.
• Most obstetricians do not routinely check the serum creatinine either prior to or
early in pregnancy.
• Thus, seemingly "normal" serum creatinine levels (eg, 0.7 to 0.9 mg/dL) may
represent significant increases from baseline, which may not be appreciated at
the time of presentation.

6. EPIDEMIOLOGY
• AKI during pregnancy is uncommon in the developed world.
• The true incidence is difficult to estimate because of varying diagnostic criteria.
• Most reviews estimate that, in countries with adequate antenatal care, only
approximately 1 in 20,000 pregnancies are affected by AKI severe enough to require
renal replacement therapy (RRT).
• The incidence may be considerably higher in countries where antenatal care is less
available and where illegal abortions are performed.
• Although some single-center series from India and Africa report an incidence as high
as 10 to 20 percent, a series from Egypt reported an incidence of AKI requiring
dialysis of only 0.6 percent of 5600 deliveries.

7. PHYSIOLOGIC CHANGES IN PREGNANCY
• Most organ systems in a pregnant female undergo changes in order to
accommodate the growing fetoplacental unit.
• There are considerable changes that occur in the urinary tract system: both
kidneys and ureters increase in size by 1 to 1.5 cm, accompanied by dilation
of the renal pelvis and calyx.

8. • This dilation of the urinary system is due to the hormonal effects of
progesterone, external compression by the gravid uterus and morphologic
changes in the ureteral wall.
• Progesterone also reduces ureteral peristalsis, contraction and tone.
• Decreased bladder tone, bladder hyperemia and edema potentiate
asymptomatic bacteruria, while bladder flaccidity may affect the
vesicoureteral valve, leading to vesicoureteral reflux.

9. • The result of these physiological changes are
• Increased risks for urinary stasis,
• Urinary tract infection, and,
• Ultimately, pyelonephritis.
• The systemic vasodilatory state, typical of pregnancy, increases renal
perfusion and glomerular filtration rate (GFR).

10. • Due to the rise in GFR, hypouricemia and increased urine protein excretion
occur.
• Systemic vasodilation leads to the stimulation of anti-diuretic hormone
(ADH) release and increased thirst, resulting in a decrease in plasma
osmolality and plasma sodium concentration by 4 to 5 mEq/L .
• Minute ventilation increases due to progesterone-induced stimulation of the
central respiratory center in the brain.
• This results in a decrease in pCO2 and a mild chronic respiratory alkalosis,
which is compensated for by renal excretion of bicarbonate.

11. ETIOLOGIES
• The most common causes of AKI during pregnancy depend on the trimester.
• AKI early in pregnancy (<20 weeks) is most often due to:
• Prerenal disease due to hyperemesis gravidarum.
• Acute tubular necrosis (ATN) resulting from a septic abortion.
• AKI associated with either viral (eg, influenza) or bacterial infection and/or sepsis.

12. • Several disorders can lead to AKI later in pregnancy. These include:
• Severe preeclampsia
• Severe preeclampsia with HELLP syndrome
• Thrombotic thrombocytopenic purpura (TTP, acquired or hereditary) or complement-
mediated hemolytic uremic syndrome (HUS)
• (AFLP)
• ATN or acute cortical necrosis associated with hemorrhage (placenta previa, placenta
abruption, prolonged intrauterine fetal death, or amniotic fluid embolism).

13. • In addition to these conditions, acute pyelonephritis and, less commonly, urinary tract
obstruction have been associated with AKI in pregnant women.
• AKI that is related to pregnancy may also occur in the postpartum period.
• This may be due to causes listed above that were present prior to delivery that have
not resolved (eg, preeclampsia, HELLP syndrome, atypical HUS).
• AKI secondary to ATN may develop due to hemodynamic stress associated with
either hemorrhage or sepsis.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) are used routinely for postpartum
analgesia.
• We have seen AKI associated with NSAID use after delivery, particularly when there
are additional risk factors such as volume depletion or preeclampsia.

14. PREECLAMPSIA WITH OR WITHOUT HELLP
• Preeclampsia is the most common cause of AKI during pregnancy.
• Preeclampsia refers to the new onset of hypertension and either proteinuria or
other signs of systemic disease (including thrombocytopenia, elevated liver
enzymes, AKI, pulmonary edema, cerebral and/or visual disturbances), usually
after 20 weeks of gestation in a previously normotensive woman.
• Preeclampsia complicates 3 to 5 percent of all pregnancies; the risk is increased
among women with hypertension, diabetes, or chronic kidney disease (CKD) from
any cause.

15. • In most women with preeclampsia, the glomerular filtration rate (GFR) decreases on
average by only 30 to 40 percent, which results in only minor increases in the serum
creatinine.
• AKI requiring renal replacement therapy (RRT) is uncommon except in patients with
very severe preeclampsia (eg, characterized by severe hypertension,
thrombocytopenia, elevated liver enzymes, pulmonary edema, cerebral and visual
symptoms) and when there is accompanying hemorrhage and ischemic ATN.
• Preeclampsia may occur with or without features of the HELLP syndrome.
• The HELLP syndrome refers to a variant in which hemolysis, low platelet count, and
elevated liver enzymes are present.

16. • AKI is more common when preeclampsia is accompanied by features of the HELLP syndrome.
• Some studies suggest that AKI occurs in 3 to 15 percent of cases of preeclampsia associated with the
HELLP syndrome.
• AKI is often multifactorial in such cases since, in addition to the renal changes characteristic of
preeclampsia such as endothelial cell swelling and injury, there is associated coagulopathy, which may
result in bleeding, placental abruption, and ATN.
• By contrast, based on clinical observation, AKI is much less common in patients with severe
preeclampsia without features of HELLP syndrome, although there are few published studies that
have examined incidence.
• In some cases, preeclampsia is first diagnosed in the postpartum period, without documentation of
antepartum hypertension and proteinuria.
• Preeclampsia that is first observed in the postpartum period is particularly difficult to distinguish from
microangiopathic disorders such as TTP or HUS. This issue is discussed below.

17. • Severe preeclampsia is an indication for urgent delivery.
• The renal and extrarenal abnormalities typically begin to resolve spontaneously
within two to three days postpartum, and complete recovery of GFR occurs within
eight weeks postpartum.
• Moderately increased albuminuria (ie, between 30 and 300 mg/day [20 to
200 mcg/min], formerly called "microalbuminuria") may persist.
• Women who develop preeclampsia may be at increased risk of developing end-
stage renal disease (ESRD) later in life, but the absolute risk is small.

18. THROMBOTIC THROMBOCYTOPENIC
PURPURA OR HEMOLYTIC UREMIC SYNDROME
• TTP and HUS are both characterized by the presence of microthrombi of
fibrin and/or platelets in multiple organ systems, particularly the kidney and the
brain.
• Presenting features include thrombocytopenia and microangiopathic hemolytic
anemia without another apparent cause and, in many patients,
neurologic and/or renal abnormalities.
• Pregnancy may trigger either TTP or HUS

19. • TTP is caused by an acquired or constitutional deficiency of activity of ADAMTS13, a Von Willebrand
factor-processing protein.
• Pregnancy has been shown to induce the onset or relapse of ADAMTS13 deficiency-related TTP
• Atypical or complement-mediated HUS is caused by mutations in genes that encode complement-
regulatory proteins, which result in uncontrolled complement activation.
• Pregnancy is a well-recognized trigger for episodes of HUS in patients with these mutations.
• A study from France reported 21 patients with pregnancy-associated HUS (defined by the presence of
hemolytic anemia, thrombocytopenia, and AKI).
• Multiple different mutations of genes encoding complement-regulating proteins were identified in 18 of
21 patients (86 percent).
• Serum C3 levels were low at the time of the first complement assessment in 12 of 21 patients (57
percent).

20. • TTP and HUS differ in the timing of onset. TTP associated with ADAMTS13 deficiency occurs
predominantly in the second and third trimesters
• ADAMTS13 levels tend to fall during the last two trimesters of pregnancy, which could
contribute to the time course of development of TTP
• Pregnancy-associated HUS more commonly occurs in the postpartum period; in a report from
France, of 21 patients with pregnancy-associated HUS, 15 occurred after delivery
• AKI may occur in either pregnancy-associated TTP or HUS, though it is more common among
patients with HUS.
• In the French series of 21 patients, 17 (81 percent) required hemodialysis at least transiently,
and 16 (76 percent) had ESRD at last follow-up
• Postpartum HUS may follow a normal pregnancy or be preceded by findings indistinguishable
from preeclampsia

21. • TTP or HUS that initially occurs in nonpregnant women may relapse during a
subsequent pregnancy, and recurrent TTP or HUS may develop during successive
pregnancies
• However, most subsequent pregnancies are uncomplicated, and most children
survive
• The diagnosis is generally made by clinical features. Renal biopsy is usually not
performed, at least initially, due to the increased risk for bleeding associated with
thrombocytopenia.
• However, if the thrombocytopenia and hemolysis resolve but AKI persists, a kidney
biopsy may help to define the etiology and prognosis for recovery of renal function. A
diagnostic approach to pregnant women with AKI is discussed below.

22. • Plasma exchange is an important component of treatment of AKI due to either
pregnancy-associated TTP or HUS.
• In cases of pregnancy-associated HUS, if AKI fails to improve after three to five
treatments with plasma exchanges, treatment with eculizumab, a monoclonal,
humanized immunoglobulin G (IgG) that inhibits complement activation, may be
effective.
• Since HUS usually presents in the postpartum period, issues related to fetal
toxicity due to eculizumab are not a concern.

23. • Treatment of AKI is supportive.
• In addition to plasma exchange and supportive care, delivery may be indicated if
the patient is still pregnant, especially if the diagnosis is not certain.
• This is because the main differential diagnosis is usually preeclampsia with
HELLP syndrome, which will improve after delivery.
• Most patients requiring dialysis, however, are postpartum, and considerations for
RRT are similar to nonpregnant adults with AKI
• Blood pressure control is important and may enhance endothelial cell recovery.

24. ACUTE FATTY LIVER OF PREGNANCY
• Acute fatty liver (fatty infiltration of hepatocytes without inflammation or necrosis) is a rare
complication of pregnancy that is associated with AKI in up to 60 percent of cases
• Patients present in the third trimester with clinical signs consistent with preeclampsia
(hypertension, thrombocytopenia) but also have hypoglycemia, hypofibrinogenemia, liver
function test abnormalities with hyperbilirubinemia, and a prolonged partial thromboplastin time
(PTT) in the absence of abruptio placentae
• The diagnosis should be suspected based on clinical feature
• Therapy consists of treatment of disseminated intravascular coagulation (DIC) and immediate
delivery of the
• The laboratory abnormalities frequently begin to improve within one to two days after delivery

25. RENAL CORTICAL NECROSIS
• Important cause of AKI associated with catastrophic obstetric emergencies such
as placental abruption with massive hemorrhage or amniotic fluid embolism.
• Renal cortical necrosis is now generally considered quite rare in developed
countries, however, and is responsible for only 1 to 2 percent of all cases of AKI
[7].
• Renal cortical necrosis may still be an important clinical problem in parts of the
world where obstetric hemorrhage occurs remote from a hospital setting and is
thus difficult to manage [2,34-37].

26. RENAL CORTICAL NECROSIS
• In addition, a report of 18 cases that occurred in France between 2009 and 2013
suggests that renal cortical necrosis remains a significant potential complication
of postpartum hemorrhage even in developed countries [38].
• The authors of this case series postulated that the use of the
procoagulant, tranexamic acid (which was prescribed to control obstetric
hemorrhage), may have been related to the development of renal cortical
necrosis in some patients.
• However, a randomized, controlled trial including over 20,000 participants showed
no difference in AKI between participants assigned to tranexamic acid versus

27. • Both primary DIC and severe renal ischemia (leading to endothelial damage and secondary
fibrin deposition) likely cause renal cortical necrosis.
• When endothelial injury does occur, the local release of nitric oxide (endothelium-derived
relaxing factor) normally minimizes the degree of thrombus formation by diminishing platelet
aggregation.
• If, however, the endothelial dysfunction is so great that nitric oxide release is impaired, then the
tendency to thrombosis will be accelerated [40].
• Patients with cortical necrosis present with the abrupt onset of oliguria or anuria following an
obstetric catastrophe.
• Oliguria or anuria is frequently accompanied by gross hematuria, flank pain, and hypotension
[34,35]. The triad of oliguria/anuria, gross hematuria, and flank pain is unusual in the other
causes of renal failure in pregnancy

28. • The diagnosis can usually be established by ultrasonography or computed
tomography (CT) scanning, which demonstrates hypoechoic or hypodense areas
in the renal cortex [34].
• No specific therapy has been shown to be effective in this disorder. Many patients
require dialysis, but 20 to 40 percent have partial recovery with a creatinine
clearance that stabilizes between 15 and 50 mL/min [35]

29. ACUTE PYELONEPHRITIS
• Although kidney function is generally well maintained during episodes of acute pyelonephritis (in the
absence of septicemia or hypotension), pregnant women are at increased risk for AKI [2,41].
• Acute pyelonephritis may develop at any time during pregnancy but is more likely to occur after 20
weeks. A retrospective series of 94 cases from Nepal reported that most cases of pyelonephritis
occurred during the second trimester [42].
• The diagnosis is generally made by clinical features, urinalysis, and urine culture
• Kidney biopsy is generally not performed for diagnosis in patients who have AKI and characteristic
features of pyelonephritis.
• The treatment of pregnancy-associated pyelonephritis is discussed elsewhere.
• Renal function generally improves after treatment with antibiotics, although recovery after appropriate
antimicrobial therapy may be incomplete due to irreversible injury.

30. URINARY TRACT OBSTRUCTION
• Relaxation of ureteral smooth muscle and pressure on the ureters by the gravid
uterus result in mild to moderate dilatation of the collecting systems
• This functional hydronephrosis, which tends to be more prominent on the right, is
detectable by ultrasonography but is not usually associated with renal dysfunction.
• Occasionally, obstruction of the ureters by the uterus is sufficient to cause renal
failure [43]. The diagnosis can be established in some cases by the normalization of
renal function in the lateral recumbent position (which relieves pressure on the ureters
by the uterus) and its recurrence when supine.
• AKI resolves with relief of obstruction. This may be achieved by insertion of a ureteric
stent or delivery of the fetus [44].

31. POSTPARTUM AKI ASSOCIATED WITH
NONSTEROIDAL ANTI-INFLAMMATORY DRUGS
• Nonsteroidal anti-inflammatory drugs (NSAIDs) are routinely used for postpartum
analgesia, particularly after cesarean section. Although uncommon, among such
patients who receive NSAIDs, AKI may develop if there are predisposing
conditions such as volume depletion or preeclampsia

32. DIAGNOSTIC APPROACH AND DIFFERENTIAL
DIAGNOSIS
• Identification of the cause of AKI is important in order to administer appropriate
therapy. The initial diagnostic approach to patients with AKI during pregnancy is
similar during all stages of pregnancy.
• First, it is important to exclude causes of AKI that are unrelated to pregnancy,
including glomerulonephritis, interstitial nephritis, or acute tubular necrosis (ATN)
due to toxins, drugs, or hemodynamic stress. The evaluation of AKI due to causes
unrelated to pregnancy is discussed elsewhere.

33. • Careful review of the medical history and prior laboratory values is important. A
history of systemic lupus erythematosus or laboratory evidence of proteinuria or a
reduced estimated glomerular filtration rate (eGFR) prior to pregnancy may suggest
worsening of an underlying glomerular disease that is unrelated to pregnancy
• The history may also suggest causes of prerenal AKI (such as hyperemesis
gravidarum) or ATN/acute cortical necrosis (such as sepsis or hemorrhage related to
obstetrical complications including placenta previa, prolonged intrauterine fetal death,
or amniotic fluid embolism).
• All medications should be carefully reviewed.

34. • In addition to a careful history, physical examination, and medication review, we obtain the following tests:
• ●Dipstick urinalysis and microscopic analysis of sediment
• ●Quantitation of protein excretion by either 24-hour urine collection or by protein-to-creatinine ratio
• ●Urine culture
• ●Hemoglobin level and platelet count with peripheral blood smear to evaluate for microangiopathic hemolysis and
thrombocytopenia
• ●Total, direct, and indirect bilirubin concentration; haptoglobin; and lactate dehydrogenase (LDH) to evaluate for
hemolysis
• ●Serum aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT)
• ●Renal ultrasound

35. • In addition to these tests, in patients with urinary findings consistent with
glomerulonephritis, laboratory tests that suggest other, non-pregnancy-related
causes of AKI may also be obtained (such as complement proteins C3, C4,
antinuclear antibody [ANA], antineutrophil cytoplasmic antibody [ANCA], etc).
• Among patients who are determined to have hemolysis and thrombocytopenia,
other tests are indicated to evaluate for thrombotic thrombocytopenic purpura
(TTP) or hemolytic uremic syndrome (HUS; such as measurement of complement
proteins and ADAMTS13 levels).

36. • ATN and acute cortical necrosis are suggested by the history (sepsis or hemorrhage)
and by microscopic analysis of urinary sediment, which often shows pigmented
granular casts and renal tubular epithelial cells. The diagnosis of cortical necrosis can
usually be established by ultrasonography or computed tomography (CT) scanning,
which demonstrate hypoechoic or hypodense areas in the renal cortex [34].
• Renal calcifications on plain film of the abdomen also suggest renal cortical necrosis,
but this is a late consequence of healing and is not visible for one to two months.
Renal biopsy or arteriography also can be performed to diagnose cortical necrosis,
but these invasive procedures are not required in most cases.

37. • Acute pyelonephritis is suggested by flank
pain, nausea/vomiting, fever, and/or costovertebral angle tenderness and may
occur in the presence or absence of cystitis symptoms

38. • AKI in late pregnancy suggests a possible diagnosis of preeclampsia with or without HELLP
syndrome, TTP or HUS, or acute fatty liver of pregnancy (AFLP). There is considerable overlap
in symptoms and laboratory abnormalities among these disorders. However, an accurate
diagnosis is usually made by careful consideration of the clinical presentation in association with
the pattern of laboratory abnormalities. Renal biopsy is rarely, if ever, required to distinguish
between preeclampsia with or without HELLP syndrome, AFLP, and TTP or HUS and is usually
not performed, at least initially, because of thrombocytopenia. A renal biopsy may be indicated
for confirmation of diagnosis and for prognosis if AKI persists after resolution of the
thrombocytopenia and hemolysis. A renal biopsy can be performed safely by experienced
operators in women with well-controlled blood pressure and normal coagulation indices [45].
Biopsy after week 32 is not recommended; among such patients, we defer biopsy until after
delivery.

39. SOME USEFUL DISTINGUISHING CRITERIA ARE
SUMMARIZED BELOW
• Timing of onset and rate of recovery – Preeclampsia with or without HELLP
syndrome typically develops in the late third trimester, including the intrapartum
period. Only a few percent of cases develop in the postpartum period, usually in
the first 24 to 48 hours. Preeclampsia does not occur before 20 weeks gestation
in nonmolar pregnancies, except occasionally in the presence of thrombophilias,
such as the antiphospholipid antibody syndrome.
• TTP is most common in the second and third trimesters, while HUS most
commonly presents immediately postpartum

40. • AFLP develops in the third trimester and resolves within one to two weeks
postpartum.
• In patients with preeclampsia with or without HELLP syndrome, spontaneous
recovery or improvement within the first two or three days following delivery is
typical, while progression of thrombocytopenia, hemolytic anemia, and renal
failure suggest pregnancy-associated atypical HUS.

41. • Clinical and laboratory features – Both the HELLP variant of severe preeclampsia,
TTP, and HUS are characterized by microangiopathic hemolysis and low platelet
count. The presence of elevated liver enzymes and right upper-quadrant pain is
strongly suggestive of HELLP syndrome or AFLP and is an uncommon feature of TTP
or HUS. In contrast to patients with TTP, who have severe deficiencies of ADAMTS13,
plasma levels of ADAMTS13 are only mildly or moderately reduced in patients with
HELLP syndrome [46]. (See "HELLP syndrome", section on 'Patient presentation'.)
• The thrombotic state in some patients with antiphospholipid antibodies may be
indistinguishable from TTP or HUS.

42. • AFLP has many features of both TTP or HUS and HELLP syndrome and can be
particularly difficult to identify. (See 'Acute fatty liver of pregnancy' above.)
• Women with AFLP often complain of loss of appetite and nausea. They have
elevated liver enzymes, similar to those with HELLP syndrome; however, they
frequently develop more severe jaundice, azotemia, and consumptive
coagulopathy. Hypoglycemia is also a feature of AFLP and has been attributed to
liver dysfunction.

43. TREATMENT
• Treatment is targeted to the specific cause of AKI and is discussed above. The
treatment of AKI is supportive. Dialysis should be initiated based on the usual
criteria for patients in the nonobstetric setting and particularly if oliguria is present.

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• ●Basics topics (see "Patient education: Acute kidney injury (The Basics)")

45. SUMMARY AND RECOMMENDATIONS
• Pregnancy-related acute kidney injury (AKI) is uncommon in developed countries.
The incidence may be considerably higher in countries where antenatal care is
less available and where illegal abortions are performed.
(See 'Introduction' above and 'Epidemiology' above.)
• ●Causes of AKI early in pregnancy (before 20 weeks) include prerenal disease
due to hyperemesis gravidarum and acute tubular necrosis (ATN) resulting from a
septic abortion or other bacterial or viral infection.

46. • Causes of AKI in late pregnancy (after 20 weeks) include preeclampsia,
thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS),
acute fatty liver of pregnancy (AFLP), ATN or acute cortical necrosis, acute
pyelonephritis, and, rarely, urinary tract obstruction. Nonsteroidal anti-
inflammatory drugs (NSAIDs) may cause AKI in the postpartum period.

47. • The evaluation of pregnancy-associated AKI includes urinalysis and microscopic
analysis of sediment; quantitation of protein excretion by either 24-hour urine
collection or by protein-to-creatinine ration; urine culture; hemoglobin level and
platelet count with peripheral blood smear; total, direct, and indirect bilirubin
concentration; serum haptoglobin; serum lactate dehydrogenase (LDH); serum
aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT); and a
renal ultrasound. (See 'Diagnostic approach and differential diagnosis' above.)

48. • Many causes of pregnancy-associated AKI are distinguished by history and
physical examination, urinalysis, and occasionally ultrasound. It is often difficult to
distinguish among preeclampsia with or without HELLP syndrome, TTP, HUS,
and AFLP because of the overlap in symptoms and laboratory abnormalities.
However, an accurate diagnosis is usually made based upon clinical features. A
renal biopsy is rarely performed in this setting. (See 'Diagnostic approach and
differential diagnosis' above.)

49. • The specific treatment for pregnancy-associated AKI depends on the underlying etiology:
• •Preeclampsia-associated AKI is an indication for delivery. Delivery generally results in
completely recovery of renal function, although moderately increased albuminuria (formerly
called "microalbuminuria") may persist. (See 'Preeclampsia with or without HELLP' above.)
• •TTP- or HUS-associated AKI is primarily treated with plasma exchange. (See "Acquired TTP:
Initial treatment".)
• •AFLP-associated AKI includes the treatment of disseminated intravascular coagulation (DIC)
and delivery of the fetus. (See 'Acute fatty liver of pregnancy' above.)
• •In addition to targeted therapies of specific underlying disorders, the treatment of AKI is
supportive. Dialysis should be initiated based on the usual criteria for patients in the
nonobstetric setting.