Preeclampsia is a pregnancy-specific condition generally defined as the new onset of persistent hypertension (diastolic blood pressure ≥90 mmHg) and proteinuria (≥300 mg in a 24-h urine collection) at or after 20 weeks’ gestation [17]. It is hypothesized that a disturbance in the placental function in early pregnancy causes preeclampsia, with a particular role for the impaired remodeling of the spiral artery [18]. Preeclampsia can be asymptomatic, especially in the early stages or with mild disease, but symptoms can include epigastric and right upper quadrant pain (40–90 %), headache, visual changes, nausea, and vomiting [19]. Severe preeclampsia and the HELLP syndrome account for about 40 % of cases of AKI in pregnancy [20]. Although preeclampsia is one of the most important causes of pregnancy-related AKI, the majority of preeclamptic patients do not develop severe AKI. Otherwise, severe preeclampsia, characterized by multiple organ involvement (i.e., pulmonary edema, oliguria [<500 mL/24 h], and thrombocytopenia [platelet count <100,000 μL]) has a higher risk for AKI. The incidence of overt renal failure in severe preeclampsia is estimated at 1.5–2 % based on two case series [21, 22].

Severe preeclampsia is a progressive condition requiring prompt attention of the clinician. Women at term diagnosed with preeclampsia are best managed by induction of labor. After giving birth the symptoms usually resolve, but in some women the symptoms worsen during the first 48 h postpartum. These women are particularly at risk for pulmonary edema, AKI, HELLP syndrome, and stroke [18].

The HELLP syndrome can occur in 4–14 % of cases of preeclampsia. Characteristic laboratory abnormalities of HELLP syndrome include microangiopathic hemolysis (anemia, decreased haptoglobin, increased lactate dehydrogenase [LDH], and a peripheral blood smear with signs of red cell destruction), elevated liver enzymes, and low platelet count. The platelet count is a marker of the severity of the disease and coincides with liver impairment [23].

Thrombotic microangiopathies (TMA) are defined by the occurrence of thrombi of fibrin and/or platelets in the microcirculation of multiple organs. TMA during pregnancy are very uncommon cause for AKI. Pregnancy-related TMA used to be subtyped as thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). Recently TMA has been reclassified into four subtypes, and pregnancy is considered only a precipitating factor [24].

Treatment of TMA should be aimed at treating the underlying pathogenic mechanism in a multidisciplinary approach, which can be either fresh frozen plasma infusions with or without plasma exchange or inhibition of complement activation by eculizumab, as recently advocated by Fakhouri [24].

It can be a diagnostic challenge to differentiate TMA and preeclampsia/HELLP because thrombocytopenia and microangiopathic hemolytic anemia can present in both syndromes. Historical features such as the time of onset (after 20 weeks of gestation), earlier reported proteinuria, elevated liver enzymes, and/or hypertension support a diagnosis of preeclampsia/HELLP.

Acute fatty liver of pregnancy (AFLP) is a rare complication, with reported incidence of between 1 in 7,000 and 1 in 20,000 pregnancies [25, 26]. AFLP is characterized by acute liver failure and coagulopathy with sudden onset during the third trimester. The severity of liver involvement is variable, ranging from moderate isolated hepatic transaminase elevations to fulminant liver failure with encephalopathy [25]. Other features include elevated bilirubin, prolonged partial thromboplastin time, thrombocytopenia, hypoglycemia, and anemia [27]. Acute (typically nonoliguric) kidney dysfunction is common and seen in approximately 60 % of patients. Renal recovery typically follows delivery and dialysis is rarely needed [25, 27]. Early diagnosis, supportive measures, and prompt delivery are critical in the management. Clinical clues help to distinguish AFLP and HELLP syndrome, although the distinction is academic since the appropriate treatment of both conditions is prompt delivery.

Renal cortical necrosis (RCN) is a rare condition in the developed world. In the developing world reported RCN has become more infrequent over the last decades [28]. In a prospective cohort study of over 4,500 late pregnancy-related AKI, Prakash et al. found AKI occurred in 1 in 56 live births (85 cases), of which only two were attributed to RCN [3]. RCN presents characteristically on ultrasound or CT-scan with hypoechoic or hypodense areas in the renal cortex. Calcifications are a late finding, usually occurring after 1–2 months. Treatment is supportive, with a significant chance for persistent loss of kidney function and need for renal replacement therapy.

Pregnant patients are at risk for four specific infectious complications: urinary tract infections, chorioamnionitis (including septic abortion), endometritis (often post Caesarean section), and pneumonia. Progression to sepsis and septic shock is extraordinary, but poses significant mortality for mother and child. Urinary tract infections and sepsis may cause AKI.