Pregnancy in a woman with chronic kidney disease is a two-way risk: her kidney disease threatens the pregnancy, and the pregnancy can threaten her kidney. Much of the harm is preventable, but the prevention happens before conception — in counselling, in optimising blood pressure and proteinuria, and above all in switching the fetotoxic drugs that so much of CKD care relies on. This chapter is the pre-existing-CKD counterpart to the acute-kidney-injury-in-pregnancy chapter of the previous volume, which it cross-references for the shared interpretive traps and the thrombotic microangiopathies.
The bidirectional risk
Two risks run in parallel. First, CKD worsens pregnancy outcomes: pre-eclampsia, preterm birth, fetal growth restriction, low birth weight, caesarean delivery, and stillbirth are all more common, and the excess rises with CKD stage, with hypertension, and with proteinuria — the same three variables that predict renal outcomes also predict obstetric ones. Second, pregnancy can accelerate the CKD itself. In advanced CKD, particularly with hypertension and significant proteinuria, the demands of pregnancy can cause a step-down in function that does not fully recover, a permanent loss of GFR. The reassuring counterpart is that a woman with early CKD, normal blood pressure, and minimal proteinuria usually does well, for herself and her baby. Stratifying this risk — by stage, blood pressure, and proteinuria — is the first task, and it is the basis of honest counselling.
Reading the numbers in pregnancy
The interpretive traps of the acute chapter apply here too. Pregnancy raises GFR by around half and lowers serum creatinine, so a 'normal' non-pregnant creatinine can be abnormal for pregnancy — and in a woman with CKD, the expected gestational fall may be blunted or absent, so a creatinine that merely fails to drop, or that rises, is concerning and signals trouble. Proteinuria, meanwhile, increases physiologically in normal pregnancy, which confounds both the assessment of her baseline CKD proteinuria and the diagnosis of pre-eclampsia, since rising protein can be physiologic, CKD progression, or pre-eclampsia. And the physiologic right-sided hydronephrosis of pregnancy should not be mistaken for obstruction. Every renal number in a pregnant CKD patient must be read against these shifts, not against the non-pregnant range.
Pre-conception counselling: where the work is done
The single most valuable intervention in CKD and pregnancy happens before the pregnancy. Pre-conception counselling lays out the stage-specific risks honestly, optimises the modifiable factors, and times the pregnancy for when the disease is most stable. The aim is to enter pregnancy with the CKD stable, the blood pressure controlled on safe agents, and the proteinuria as low as possible. For the woman with a kidney transplant, this means advising her to wait until the graft is stable — typically one to two years post-transplant — before conceiving. Counselling also covers folic acid, the plan for aspirin prophylaxis, and nephrotoxin avoidance. Done well, it converts a high-risk pregnancy into a planned, optimised one; done not at all — a woman presenting already pregnant on fetotoxic drugs — it forecloses the chance to prevent harm that has, by then, already begun.
The medication switch
CKD care leans heavily on drugs that are fetotoxic, so the medication switch is the practical heart of pre-conception care. The renin-angiotensin blockers — ACE inhibitors and ARBs — cause fetal renal dysgenesis, oligohydramnios, and skull defects and must be stopped before or at conception. SGLT2 inhibitors are stopped for want of pregnancy safety data. In the patient with lupus or a transplant, mycophenolate is teratogenic and is switched to azathioprine, and cyclophosphamide and methotrexate are likewise avoided. The substitutions are well established: azathioprine, tacrolimus or ciclosporin, and hydroxychloroquine (which is continued in lupus for its benefit) are the pregnancy-safe immunosuppressants, and labetalol, nifedipine, and methyldopa are the pregnancy-safe antihypertensives. The discipline is to make these switches deliberately and early — not to discover a pregnant woman still taking an ACE inhibitor.
Managing the pregnancy
Once pregnant, the CKD patient is managed as high-risk by a multidisciplinary team — nephrology, maternal-fetal medicine, and neonatology together. Blood pressure is controlled with the safe agents, low-dose aspirin is given from early in pregnancy because CKD is a high pre-eclampsia-risk state, and GFR, proteinuria, and blood pressure are monitored closely. The recurring diagnostic challenge is distinguishing CKD progression — or, in lupus, a disease flare — from superimposed pre-eclampsia, because all can present with worsening hypertension, proteinuria, and renal function against an already abnormal baseline. The overlap is genuine and hard, and it leans on timing, on new severe features, and on angiogenic markers such as the sFlt-1 to PlGF ratio, with the acute chapter's framework for the thrombotic microangiopathies in reserve. In lupus, remission should be secured before conception, hydroxychloroquine continued, and a flare distinguished from pre-eclampsia so that immunosuppression rather than delivery is escalated when appropriate.
Dialysis in pregnancy
Fertility is reduced in advanced CKD and dialysis, but conception does occur, and a woman may also need dialysis initiated during pregnancy. The key principle, shared with the acute chapter, is intensity: pregnancy in a dialysis patient is managed with intensive, more frequent dialysis — longer hours and more sessions, with lower urea targets — because the cleaner uraemic environment markedly improves fetal outcomes compared with conventional schedules. This is one of the clearest examples in nephrology where doing more dialysis genuinely helps, and it reverses the usual 'standard dose is enough' message precisely because the goal is a healthy fetus in a low-urea milieu rather than adequacy for the mother alone.
After delivery, and the team
The post-partum period is not an afterthought. CKD must be reassessed, because pregnancy may have advanced it, and the medications that were stopped or switched are restarted appropriately — RAAS blockade and SGLT2 inhibition resumed once the patient is no longer pregnant and, where relevant, with attention to breastfeeding compatibility. Contraception is discussed, both to space pregnancies and to allow the kidney to recover and stabilise. Throughout, from pre-conception to post-partum, the care is genuinely multidisciplinary, and the nephrologist's distinctive contributions are the risk stratification, the medication switch, the interpretation of the renal numbers against pregnancy's physiology, and the disentangling of progression, flare, and pre-eclampsia.
Where the evidence is firm, and where it is observational
The firm parts are the drug-safety ones — the fetotoxicity of RAAS blockers, mycophenolate, and the others is well established — and the benefit of intensive dialysis, supported by consistent observational data, along with aspirin prophylaxis for pre-eclampsia. The softer parts are the precise stage-specific risk figures and the management of the progression-versus-pre-eclampsia overlap, which rest on cohort data and judgement rather than trials, since randomising pregnant women is rarely feasible. The honest position is to counsel from the consistent observational risk gradient, to make the well-established drug switches without exception, to deliver intensive dialysis and aspirin prophylaxis, and to manage the diagnostic overlaps with a multidisciplinary team and the interpretive discipline this and the acute chapter share.
