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MD, DNB, FISN, FRCP (London), FAMS
Professor & Head, Department of Nephrology
Osmania Medical College, Hyderabad, Telangana
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Dr. Manisha Sahay is one of India’s most respected nephrology leaders, with 290+ publications, extensive national and international teaching experience, and pioneering contributions to CAPD, deceased donor transplantation, vascular access programs, and tele-nephrology.
She has served as Vice President, Indian Society of Nephrology, Chair, CME Committee, International Society of Nephrology, and Emeritus Editor-in-Chief, Indian Journal of Transplantation. Her academic work uniquely bridges classical nephrology with real-world critical care — particularly in complex pregnancy-related kidney disease.
A 28-year-old primigravida at 32 weeks of gestation is admitted to the ICU with severe hypertension, thrombocytopenia, rising transaminases, and oliguria.Â
Over 24 hours, serum creatinine rises from 0.6 mg/dL (baseline unknown) to 1.4 mg/dL.Â
Urine output declines despite adequate fluid resuscitation.Â
Lactate is mildly elevated, LDH is high, and haemolysis is suspected.Â
Fetal monitoring shows intermittent decelerations.
(Click / Tap on Questions to Reveal Content)
Answer:
Yes — this is true Pregnancy associated AKI.
Serum creatinine (S Cr) is lower in normal pregnancy because of increased GFR (~40–50% higher). Dilution may further lower the creatinine and muscle changes can also distort the number. Thus, normal serum creatinine in pregnancy is 0.40-0.8 mg/dl depending on the period of gestation. AKI in pregnancy is defined by KDIGO criteria as there are no pregnancy specific criteria at present. 1 A rise from 0.6 to 1.4 mg/dL represents more than a doubling of baseline and meets KDIGO stage 2 AKI.
The patient has presented with features of haemolytic anemia and thrombocytopenia with Pr-AKI in the 3rd trimester of pregnancy. The common differentials in this setting include preeclampsia/HELLP and pregnancy-associated TMA (aHUS/TTP). Other differentials include acute fatty liver of pregnancy.
Majority of PE-HELLP occur in 3rd trimester. About 20% can occur post-partum. Thrombocytopenia, haemolysis ( low haptoglobin, raised LDH), elevated liver enzymes are seen in HELLP. The elevated lactate reflects microangiopathic circulatory dysfunction and impaired organ perfusion. Most cases start resolving within 72 hours of delivery. This is the most common cause of Pr-AKI and may be considered in this patient. The definitive treatment is delivery of foetus and placenta. 2,3
 TTP occurs in 3rd trimester. Unlike HELLP-AKI and aHUS, renal involvement is mild in TTP while thrombocytopenia is severe (platelets < 30,000/mm3). Fever and neurological symptoms are often seen. Coagulation parameters are normal. Testing for ADAMTS-13 is confirmatory. Plasmapheresis is the treatment of choice and should be initiated after drawing the sample for ADAMTS-13. This patient has a significant dysfunction and hence TTP seems unlikely
aHUS occurs most commonly in the post-partum and the AKI persists beyond 72 hours of delivery. Haemolysis with >2% schistocytes on peripheral smear, thrombocytopenia and severe hypertension are important features. There is no coagulopathy. Confirmation rests on testing for Complement factors and Eculizumab is the treatment of choice. In this patient aHUS is unlikely unless the Pr-AKI fails to resolve even after 72 hours of delivery.
 Acute fatty liver of pregnancy is another important cause or Pr-AKI in the 3rd trimester and can manifest in a similar manner. However, it is characterised by hyperbilirubinemia, hypoglycaemia, hypofibrinogenemia and marked coagulopathy. It is a rare cause of Pr-AKI and the treatment is termination of pregnancy.
Sepsis can present with Pr-AKI and haemolysis however hypertension is unusual and leucocytosis and elevated CRP may be seen.
DIC can present with thrombocytopenia and coagulopathy but hypertension is uncommon.
Assessing true intravascular volume in a hypotensive or vasopressor-dependent pregnant patient is challenging because there is an increase in blood volume (up ~40–50%) and cardiac output in pregnancy and vasodilatation of the vascular bud. With super added critical illness  there maybe capillary leak, vasoplegia and cardiac dysfunction. The patient may have massive oedema with a depleted intravascular volume. In preeclampsia, the patient is often “wet in the tissues but dry in the circulation.” Pulse rate may be elevated due to pregnant state, high BP may be noted despite volume depletion due to pre-eclampsia. Hence relying on a single measure of fluid assessment may be misleading.  A combination of clinical examination and imaging is recommended for fluid assessment. Clinical examination should include urine output, oedema, tachycardia, postural dizziness, cool extremities and pulse pressure. Measurement of lactate levels and Point of care Ultrasound (POCUS) assessment: IVC, lung B-lines, VeXUS (Venous excess ultrasound) and focussed cardiac echocardiogram (FOCUS) is the best bedside assessment of volume status in pregnancy-associated AKI. Frequent assessment of clinical and lab parameters is essential to monitor trends.
FeNa / Urine sodium:
A FeNa (<1%), low urine Na <20 meq/l, l Fe Urea <35% and a high urine osmolality are commonly used to diagnose volume depletion and pre-renal AKI in non-pregnant state. However, they are not reliable measures of volume depletion in pregnancy due to altered renal hemodynamics. In pregnancy the kidneys are in a salt-avid, hyperfiltering state, which affects urine electrolytes even without AKI.
In Preeclampsia / HELLP kidneys are vasoconstricted and leaky and FENa is often low (<1%) despite endothelial injury. Urine indices may falsely suggest “prerenal” though there is an intrinsic renal injury.In  Sepsis urine indices fluctuate and are hard to interpret. Haemorrhage, on the other hand is a true prerenal state. In Acute Fatty Liver of Pregnancy there is intrinsic renal dysfunction but urine sodium may still be low due to systemic vasoconstriction. Thus these indices may be supportive, not diagnostic. Administration of fluids based on low FeNa is especially dangerous in preeclampsia, where overhydration can cause pulmonary edema.
Urine examination is more useful. The presence of muddy brown casts suggests ATN and heavy proteinuria and hypertension may point towards PE.
Serum creatinine is low in pregnancy, rises late and may  look “normal” despite significant injury. Hence the use of biomarkers is being tested to detect kidney damage earlier.
The biomarkers are used in research for risk prediction, early AKI detection and when creatinine values are equivocal but these cannot replace history, clinical examination, urine output, BP, trends in routine lab tests and imaging.4
The indications to initiate RRT in PrAKI are similar to non-pregnant AKI and include intractable hyperkalaemia, refractory acidosis, fluid overload with cardiopulmonary compromise and uremic pericarditis or encephalopathy. There’s no pregnancy-specific RRT timing guideline and decision should be individualized. Early RRT may be considered if metabolic derangements cannot be managed medically and/or if maternal status is deteriorating.
Choice is based on hemodynamic status: CRRT / SLEDD is preferred in hemodynamically unstable patients (less fluctuation in BP, gentler fluid removal). Intermittent haemodialysis is  indicated if patient is stable hemodynamically and needs rapid solute removal. In any case, rapid ultrafiltration should be avoided. Frequent or continuous therapies may better maintain steady hemodynamics, potentially protecting uteroplacental blood flow but evidence is lacking.
Multidisciplinary discussions (obstetrics, nephrology, neonatology, critical care) are crucial. Fetal lung maturity is achieved by 34 weeks and if required pregnancy can be terminated beyond 34 weeks. In pregnancies <34 weeks careful decision making is required as prolonging pregnancy to ensure fetal maturity may be risky for the mother while early termination may result in fetal lung immaturity. In this patient fetal heart irregularity indicates utero placental insufficiency and termination of pregnancy is indicated. Antenatal corticosteroids are given for lung maturity if maternal and fetal conditions allow a delay in delivery (ideally 24 hours), but urgent delivery  should not be postponed in unstable HELLP syndrome solely to complete steroid dosing. Even one dose before delivery provides some neonatal benefit. BP should be controlled using Labetalol and anti-seizure prophylaxis is given using Magnesium sulphate. If there is worsening of renal function renal replacement therapy may be indicated.
Some women remain dialysis-dependent after PrAKI. In many others even with apparent recovery, renal function may remain impaired and risk of hypertension and CKD is higher. Women with prior preeclampsia have a 2–4-fold increased long-term risk of CKD and ESRD. AKI may recur in subsequent pregnancies. Hence a structured nephrology follow-up after discharge at  3-6 months is recommended to monitor for persistent renal dysfunction and manage long-term risk.2,5
