Pregnancy rewrites the rules for the kidney, and the first task is to read the creatinine correctly. A value that looks reassuringly normal can signal real injury, because pregnancy lowers the baseline. Beyond that interpretive trap, pregnancy brings a set of conditions found nowhere else — pre-eclampsia, HELLP, acute fatty liver, and a thrombotic-microangiopathy differential that turns on the timing of delivery. The stakes are doubled, the drug list is constrained, and the definitive treatment is often delivery itself.
Reading the kidney through pregnancy's changes
Pregnancy increases renal plasma flow and raises GFR by roughly 40 to 50%, so serum creatinine falls — a normal pregnancy value sits around 0.4 to 0.6 mg/dL. The clinical consequence is a trap: a creatinine of 0.8 or 0.9, unremarkable in a non-pregnant adult, may represent substantial AKI in a pregnant woman, and reading it against the non-pregnant range will miss the injury. The other adaptation to keep in mind is a physiologic hydronephrosis, more marked on the right, produced by progesterone and mechanical compression of the ureters by the gravid uterus; it is normal and should not be mistaken for obstruction. Plasma volume expands, a dilutional anaemia is expected, and a compensated respiratory alkalosis lowers the baseline bicarbonate. Interpret every renal value through these changes.
Causes by trimester
The causes sort usefully by timing. Early in pregnancy, hyperemesis gravidarum causes volume depletion and pre-renal AKI, and septic abortion — now uncommon where care is good — can cause septic ATN. The late and peripartum period holds the serious, pregnancy-specific entities: pre-eclampsia and its HELLP variant, acute fatty liver of pregnancy, obstetric haemorrhage, and the thrombotic microangiopathies. Throughout pregnancy, urinary infection and pyelonephritis are more frequent and more severe, and pre-existing kidney disease or a lupus flare can present or worsen. Knowing the trimester narrows the differential before any test returns.
Pre-eclampsia, HELLP, and acute fatty liver
Pre-eclampsia is fundamentally an endothelial disease driven by an anti-angiogenic imbalance — the placenta releases soluble factors that antagonise the angiogenic signals the maternal endothelium needs, producing the glomerular endotheliosis, hypertension, and proteinuria that define it, with AKI in the more severe cases. Its defining feature for this chapter is that delivery is the definitive treatment: removing the placenta removes the source. HELLP is a severe variant adding haemolysis, elevated liver enzymes, and low platelets, with AKI in a subset, and it too is treated by delivery and support. Acute fatty liver of pregnancy is a distinct late-pregnancy emergency — microvesicular fatty infiltration of the liver causing liver failure, hypoglycaemia, coagulopathy, and AKI — and is likewise managed by prompt delivery and intensive support. In all three, the obstetric and renal teams move together, and the kidney usually recovers once the pregnancy is ended.
The pregnancy TMA differential
The most demanding diagnostic problem in this chapter is the pregnancy-associated thrombotic microangiopathy, because three conditions overlap in presentation — microangiopathic haemolysis, thrombocytopenia, and AKI — yet diverge sharply in treatment. Pre-eclampsia and HELLP are the commonest and resolve within days of delivery. TTP is defined by a severely deficient ADAMTS13 activity, can occur through the second and third trimesters, often carries neurological features, and is treated with plasma exchange. Pregnancy-associated atypical HUS is complement-mediated, characteristically presents or worsens postpartum, is dominated by AKI, and — crucially — does not resolve with delivery; it is treated with complement inhibition. The single most useful discriminator is timing relative to delivery: a microangiopathy that improves within days of delivery was pre-eclampsia or HELLP, whereas one that persists or first appears postpartum and worsens should raise atypical HUS. ADAMTS13 separates TTP, and the response — or non-response — to delivery separates the rest.
Haemorrhage and cortical necrosis
Obstetric haemorrhage — placental abruption, post-partum haemorrhage — causes AKI through hypovolaemic shock and the pre-renal-to-ATN injury of Chapter 2, often compounded by disseminated intravascular coagulation. Its feared, pregnancy-classic complication is bilateral renal cortical necrosis: severe, prolonged ischaemia with microvascular thrombosis destroys the renal cortex, producing an AKI that is often only partially reversible or permanent. Pregnancy is one of the few settings where cortical necrosis is seen with any frequency, and the lesson is the same as elsewhere — control the haemorrhage early and restore perfusion fast, because the cortex does not recover once it is infarcted.
Treatment within pregnancy's constraints
Management is the usual AKI management, bent around pregnancy's constraints. Blood pressure is controlled with agents safe in pregnancy — labetalol, nifedipine, methyldopa, and hydralazine for acute control — while ACE inhibitors, ARBs, and SGLT2 inhibitors are avoided because they are fetotoxic, damaging the developing fetal kidney. Magnesium sulfate is given to prevent eclamptic seizures, but it is renally excreted, so in AKI it accumulates toward toxicity — loss of reflexes, then respiratory depression — which means monitoring levels and reflexes and reducing the dose. The thrombotic microangiopathies get their specific therapy: plasma exchange for TTP, complement inhibition for atypical HUS, with the appropriate meningococcal precautions. Volume is given cautiously, because pre-eclampsia's leaky capillaries make pulmonary oedema easy to provoke. When dialysis is required — whether for AKI or for a woman conceiving on established dialysis — it is delivered intensively, with longer and more frequent sessions and lower urea targets, because intensive dialysis improves fetal outcomes. And renal biopsy is generally deferred to the postpartum period, given its higher bleeding risk in pregnancy, unless the result would genuinely change management before delivery.
Where the diagnosis is hard, and the principles firm
Two things deserve emphasis at the close. The diagnosis is genuinely hard — the overlap between pre-eclampsia, HELLP, TTP, and atypical HUS is real, the conditions can coexist, and the discriminating tests take time to return — so the experienced approach is to treat the most dangerous and treatable possibilities in parallel while the timing relative to delivery and the specific assays clarify the picture. The principles, by contrast, are firm: read the creatinine against the lowered baseline, deliver for pre-eclampsia and its variants, avoid the fetotoxic drugs, dose magnesium for renal function, give the microangiopathies their specific therapy, and manage everything with a multidisciplinary team. Hold the diagnostic humility and the procedural discipline together.
