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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Renal and autoimmune disease

Obstetrics and gynaecology · UK scope · Sources checked 7 Sept 2026 · Clinical review pending

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Rising creatinine with systemic deterioration

Oliguria, pulmonary oedema, severe hypertension, hyperkalaemia or rapidly evolving neurological symptoms in a pregnant patient with kidney or autoimmune disease require urgent hospital assessment. A known diagnosis of lupus does not explain every deterioration.

Action: Arrange immediate obstetric and renal review, with rheumatology and critical care when indicated. Assess circulation, oxygenation, fluid balance and urine output; obtain urgent renal, hepatic, haematological and urine studies while investigating pre-eclampsia, infection, thrombotic microangiopathy and inflammatory relapse in parallel.

Overview

Interpret renal changes during pregnancy, distinguish inflammatory relapse from placental disease, and maintain effective treatment while protecting maternal and fetal health.

Pregnancy increases renal plasma flow and filtration, so serum creatinine usually falls. A value acceptable outside pregnancy may therefore represent impaired function during gestation. The clinical task is to identify the patient's baseline, explain the cause of kidney disease and follow change over time. Renal impairment, hypertension, proteinuria and inflammatory activity contribute separately to risk; a diagnostic label alone does not predict the course. Someone with preserved kidney function and controlled disease may have a successful pregnancy with surveillance, whereas active nephritis or advanced impairment can threaten both maternal renal reserve and placental function.

Autoimmune disease introduces further questions: is an abnormal result evidence of active inflammation, established organ damage, treatment toxicity, infection or a pregnancy-specific complication? These processes can coexist. Preconception care should bring nephrology or rheumatology together with obstetric medicine, allowing treatment conversion and assessment of disease stability before pregnancy. During pregnancy, continue routine antenatal care alongside specialist surveillance. Discuss likely birth setting, analgesia, medicines, breastfeeding and postpartum review early enough to make the plan useful if preterm birth becomes necessary.

Practice

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Obstetrics and gynaecologyOriginal SBA

Renal measurement in pregnancy

A woman with previous glomerulonephritis attends at 24 weeks. Her creatinine has risen from 64 to 89 micromol/L, although the laboratory automatically reports an eGFR above 60. Which approach best assesses her renal function?

Choose one answer, then submit
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Sources and review status6 sources · checked 7 Sept 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 7 Sept 2026; clinical approval remains outstanding.

  • UK Kidney Association pregnancy and renal disease guideline
  • Clinical practice guideline on pregnancy and renal disease full publication
  • BSR prescribing antirheumatic medicines in pregnancy and breastfeeding
  • BSR systemic lupus erythematosus guideline 2026
  • NICE NG121 intrapartum care with existing medical conditions
  • NICE NG133 hypertension in pregnancy recommendations

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Key points

  • Assess renal function in pregnancy using serum creatinine and its trajectory; laboratory eGFR equations are not validated for pregnancy.
  • Record early pregnancy blood pressure and quantified urine protein so that later changes have an interpretable baseline.
  • Aim for conception during sustained disease control on medicines suitable for pregnancy; active lupus nephritis particularly increases adverse outcomes.
  • Continue effective pregnancy-compatible treatment such as hydroxychloroquine; abrupt withdrawal may provoke a damaging autoimmune flare.
  • New hypertension or organ dysfunction after 20 weeks warrants assessment for superimposed pre-eclampsia, including in patients already proteinuric.
  • Anti-Ro/SSA and anti-La/SSB antibodies require counselling and a fetal and neonatal assessment plan, even if maternal symptoms are mild.
  • Nephrotic-range proteinuria warrants assessment for antenatal and postpartum thromboprophylaxis, alongside bleeding and delivery considerations.

Aetiology

01

Pre-existing kidney disorders

Diabetic nephropathy, glomerulonephritis, congenital abnormalities and inherited diseases can reduce renal reserve before conception. Baseline hypertension and proteinuria influence pregnancy risk independently of the underlying diagnostic label.

02

Systemic autoimmune inflammation

Lupus and vasculitis may cause active renal injury or leave chronic damage after inflammation settles. Antiphospholipid antibodies and anti-Ro/La antibodies introduce additional pregnancy risks through different mechanisms.

03

Superimposed pregnancy illness

Pre-eclampsia, infection, haemorrhage and obstructive uropathy may injure kidneys already affected by chronic disease. Several mechanisms can operate together and require simultaneous assessment.

Pathophysiology

  1. 1
    Gestational hyperfiltration

    Renal blood flow and filtration increase in normal pregnancy, lowering serum creatinine. Reduced renal reserve may limit this adaptation, while conventional eGFR equations fail to account appropriately for pregnancy physiology.

  2. 2
    Glomerular inflammatory injury

    Immune-mediated injury disrupts the glomerular barrier, producing proteinuria, haematuria and sometimes casts. Active inflammation can reduce filtration, whereas residual proteinuria can persist after immunological activity has subsided.

  3. 3
    Placental vascular dysfunction

    Maternal vascular disease and inflammation can impair placental function, contributing to fetal growth restriction and hypertensive complications. Placental disease may then worsen maternal renal function through endothelial injury.

  4. 4
    Antibody-mediated fetal effects

    Maternal anti-Ro/SSA and anti-La/SSB antibodies can cross the placenta and affect fetal tissues. Cardiac conduction injury is distinct from maternal lupus activity and warrants dedicated fetal assessment planning.

Clinical features and red flags

Kidney disease before pregnancy

Establish the underlying diagnosis, previous creatinine and protein measurements, blood pressure, transplant or dialysis history, and previous pregnancy outcomes. Proteinuria identified before 20 weeks usually suggests pre-existing renal pathology. Ask about inherited conditions, recurrent urinary infection, diabetes and prior nephrotoxic exposure rather than assuming all renal disease is autoimmune.

Active lupus or vasculitis

New inflammatory arthritis, photosensitive rash, mouth ulcers, serositis or systemic symptoms may accompany renal relapse. Haematuria and urinary casts support glomerular inflammation. However, fatigue and oedema are nonspecific, and infection can mimic flare. Assess the entire pattern before increasing immunosuppression.

Superimposed placental disease

A new maternal organ abnormality after 20 weeks can indicate pre-eclampsia even when proteinuria and hypertension preceded pregnancy. Escalating antihypertensive requirements or a substantial rise in proteinuria should trigger reassessment. Neither finding alone reliably distinguishes placental disease from renal progression or active nephritis.

Antiphospholipid and antibody risks

Previous thrombosis, recurrent pregnancy loss or severe placental complications may indicate antiphospholipid syndrome. A positive antibody test alone is not synonymous with the clinical syndrome. Anti-Ro/SSA and anti-La/SSB antibodies create a different risk involving neonatal lupus and congenital heart block, requiring a separate surveillance discussion.

Acute kidney injury around birth

Consider haemorrhage, sepsis, obstruction, medicines and hypertensive disease when urine output falls. Disproportionate haemolysis or thrombocytopenia raises concern for thrombotic microangiopathy. Persistent deterioration following delivery needs renewed renal and haematology assessment rather than an assumption that every case will resolve as pre-eclampsia.

Investigations

  1. 01
    Serum creatinine and electrolytesFirst step
    Why
    Define renal reserve and detect evolving kidney injury.
    Interpretation and limitations
    Compare creatinine with preconception and earlier pregnancy results, together with potassium, bicarbonate and urine output. Do not stage a new pregnancy deterioration using the automatically reported eGFR. A rising value may be important before conventional nonpregnant reference limits are crossed.
  2. 02
    Urine protein ratio and microscopy
    Why
    Quantify protein loss and investigate glomerular inflammation.
    Interpretation and limitations
    Use urine protein:creatinine ratio or albumin:creatinine ratio; a routine 24-hour collection is unnecessary. Interpret change against baseline. Request microscopy for suspected nephritis and culture when infection is possible, because blood or infection can complicate interpretation of a dipstick.
  3. 03
    Full blood count, liver tests and haemolysis studies
    Why
    Identify systemic disease and competing pregnancy complications.
    Interpretation and limitations
    Anaemia and thrombocytopenia have several causes, including immunological disease, treatment toxicity and pre-eclampsia. Blood film, lactate dehydrogenase and haemolysis assessment help when thrombotic microangiopathy is suspected. Trends and the clinical context matter more than isolated abnormalities.
  4. 04
    Complement, anti-dsDNA and relevant autoantibodies

Differential diagnosis

01

Pre-eclampsia with renal involvement

New hypertension, systemic organ abnormalities or placental dysfunction after mid-pregnancy may indicate pre-eclampsia. Pre-existing proteinuria complicates recognition, and inflammatory nephritis may coexist rather than provide an alternative explanation.

02

Pyelonephritis or systemic infection

Fever, urinary symptoms and inflammatory abnormalities suggest infection, although immunosuppression can blunt typical signs. Urine culture and assessment for systemic compromise are necessary before attributing deterioration to autoimmune activity.

03

Thrombotic microangiopathy

Kidney injury accompanied by haemolysis and thrombocytopenia requires consideration of HELLP syndrome and other microangiopathies. Persistence after delivery can change the likely diagnosis and need for disease-specific treatment.

04

Drug or obstructive injury

Nephrotoxic exposure, calcineurin inhibitor toxicity and urinary obstruction can worsen renal function. Medication review and targeted imaging may identify a reversible contributor that intensified immunosuppression would not correct.

Management

01Before conceptionStabilise disease and revise medicinesFirst stepA patient with CKD or systemic autoimmune disease is considering pregnancy.+
  1. 1Review renal function, blood pressure, proteinuria, previous organ involvement and obstetric history in a joint specialist consultation.
  2. 2For lupus nephritis or vasculitis, aim for disease quiescence for at least six months before conception, explaining that individual risk also depends on residual organ damage.
  3. 3AlternativeReplace teratogenic immunosuppression before attempting pregnancy and demonstrate stability on an effective alternative. Mycophenolate requires at least six weeks off treatment before conception; renal guidance advises a three-month interval to support conversion and stability.
  4. 4Agree how ACE inhibitors or angiotensin receptor blockers will be withdrawn or replaced, taking account of the renal indication and pregnancy detection plan. Arrange pregnancy-compatible blood pressure control and contraceptive cover during treatment changes.

Complications

01

Loss of renal reserve

Pregnancy-associated kidney injury may leave persistent impairment, particularly when baseline function is reduced. Postpartum reassessment distinguishes recovery from continuing disease and supports decisions about long-term renal protection.

02

Placental and birth complications

Pre-eclampsia, fetal growth restriction and medically indicated preterm birth occur more often with renal impairment, proteinuria or active disease. Surveillance aims to recognise deterioration while balancing maternal and neonatal consequences.

03

Thrombosis and fluid overload

Nephrotic protein loss increases thrombotic risk, while impaired salt and water handling predisposes to pulmonary oedema. Labour, intercurrent illness and postpartum fluid shifts can expose these vulnerabilities.

04

Treatment and neonatal consequences

Immunosuppression may increase maternal infection or metabolic complications, whereas undertreatment permits inflammatory relapse. Antibody exposure and specific medicines can also create neonatal monitoring needs that should be communicated before birth.

Monitoring and follow-up

  • Set the renal review interval according to baseline impairment, proteinuria, blood pressure and current trajectory; increase frequency promptly when any component deteriorates.
  • Track autoimmune activity clinically as well as biochemically, including infection symptoms and adverse effects of immunosuppressive treatment.
  • Document maternal fluid balance and avoid both dehydration and excessive fluid administration, particularly during labour, acute illness and the postpartum fluid shift.
  • Arrange a postpartum renal review with a named team and timeframe; persistent proteinuria or kidney impairment requires investigation and a continuing management plan.
  • Reconcile medicines after birth, including renal dose changes, breastfeeding compatibility, contraception and any planned return to previously withheld treatment.

Special situations

Complement requires a pregnancy baseline

A normal printed complement result cannot exclude lupus activity. Compare with earlier results because gestational changes may conceal a clinically relevant fall; integrate this with urine sediment, anti-dsDNA and extrarenal symptoms.

Nephrotic protein loss changes thrombosis risk

Heavy urinary protein loss, immobility and pregnancy can combine to increase venous thrombosis risk. Anticoagulation decisions must account for renal clearance, bleeding, anticipated procedures and the planned interval around neuraxial analgesia.

Transplant pregnancy needs drug continuity

A stable transplant can support pregnancy, but rejection and treatment toxicity remain possible. Preconception conversion away from mycophenolate should preserve immunosuppressive efficacy, and pregnancy-related changes in tacrolimus concentrations need specialist interpretation.

Dialysis becomes a pregnancy-specific prescription

Established dialysis patients require early specialist review of frequency, duration, ultrafiltration and nutrition. Maternal biochemistry and fetal growth influence the prescription; a standard nonpregnant dialysis schedule cannot simply be assumed adequate.

Antibody exposure crosses specialty boundaries

An anti-Ro/La surveillance plan should reach fetal medicine and the neonatal team. A mother with little current disease activity may still have relevant antibodies, while an affected previous pregnancy can materially change counselling.

Common pitfalls

  1. 01

    Using a reassuring calculated eGFR to dismiss a rising serum creatinine during pregnancy.

  2. 02

    Labelling every increase in proteinuria as lupus nephritis without assessing pre-eclampsia and infection.

  3. 03

    Stopping hydroxychloroquine or all immunosuppression immediately after a positive pregnancy test.

  4. 04

    Equating isolated antiphospholipid antibody positivity with established obstetric or thrombotic antiphospholipid syndrome.

  5. 05

    Prescribing routine postpartum NSAIDs without considering renal impairment, volume status and concurrent nephrotoxic medicines.

Red flags requiring action

  • New breathlessness or hypoxaemia accompanied by reduced urine output or rapidly increasing oedema.
  • Sustained systolic blood pressure of 160 mmHg or above or diastolic pressure of 110 mmHg or above, severe headache, visual disturbance or epigastric pain.
  • A creatinine concentration rising substantially from the patient's pregnancy baseline, even if the laboratory flags it as normal.
  • Fever or rigors during immunosuppression, especially with hypotension, confusion or flank pain.
  • Haemolysis, falling platelets and kidney injury that persist or worsen after birth.
Why
Support disease activity assessment and pregnancy risk planning.
Interpretation and limitations
In lupus, falling complement and rising anti-dsDNA may support relapse but cannot establish it alone. Complement normally tends to rise in pregnancy, so a meaningful fall can occur within the laboratory reference interval. Establish anti-Ro/La and antiphospholipid status where relevant before pregnancy or promptly afterwards.
  • 05
    Renal and fetal imaging
    Why
    Investigate reversible obstruction and assess placental consequences.
    Interpretation and limitations
    Renal ultrasound can assess obstruction and structural pathology without ionising radiation. Third-trimester fetal growth assessment is recommended in CKD, with frequency adjusted to maternal disease and findings. Suspected congenital heart block needs fetal medicine and cardiology assessment rather than routine growth scanning alone.
  • 5Discuss anti-Ro/La or antiphospholipid findings, inherited disease counselling where appropriate, aspirin eligibility and the anticipated antenatal team.
    • 02During pregnancyProtect renal and placental functionPregnancy is confirmed with established renal or autoimmune disease.+
    1. 1Establish an early serum creatinine, quantified protein measurement and blood pressure record, then individualise review frequency to renal reserve and disease activity.
    2. 2Continue necessary pregnancy-compatible medicines and arrange renal, obstetric and rheumatology input as appropriate; do not wait for a clinical flare to organise shared care.
    3. 3Offer low-dose aspirin for pre-eclampsia prevention when indicated, including CKD, and manage blood pressure towards the documented pregnancy target, generally 135/85 mmHg or less.
    4. 4For nephrotic-range proteinuria, defined in renal pregnancy guidance as uPCR above 300 mg/mmol or uACR above 250 mg/mmol, offer low-molecular-weight heparin unless contraindicated, with delivery and bleeding planning.
    5. 5Arrange fetal growth surveillance and an antibody-specific fetal assessment plan. Explain which symptoms should prompt contact between scheduled appointments.
    03New deteriorationSeparate flare from pregnancy complicationsProteinuria, creatinine, blood pressure or systemic symptoms worsen during pregnancy.+
    1. 1Assess maternal stability first and refer urgently for severe hypertension, respiratory compromise, oliguria, major electrolyte disturbance or suspected sepsis.
    2. 2Compare current findings with baseline and investigate nephritis, pre-eclampsia, infection, obstruction and treatment toxicity together; use urine sediment, complement trends and systemic features to refine the differential.
    3. 3Discuss uncertain severe presentations jointly. Placental growth factor based testing may assist suspected preterm pre-eclampsia in the appropriate NICE pathway, but cannot replace clinical assessment or independently exclude inflammatory disease.
    4. 4Treat the identified process using pregnancy-compatible therapy where possible, while discussing any life-threatening exception with specialists and the patient. Renal biopsy is a specialist decision when histology would change pregnancy management.
    5. 5Determine birth timing from maternal and fetal condition. Stable early-stage CKD alone does not require caesarean birth or an automatic early delivery.
    Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
    Maintains lupus control and reduces the likelihood of relapse during pregnancy.

    Hydroxychloroquine

    Continue the established oral regimen, usually 200–400 mg daily; BSR pregnancy guidance supports doses up to 400 mg daily. Individualise the dose for disease control, body size, renal function and toxicity risk.

    Do not discontinue solely because pregnancy is confirmed. Check relevant ocular monitoring, interactions and renal impairment; breastfeeding is compatible under BSR guidance, with individual review of the complete regimen.

    Treats inflammatory flares when ongoing disease threatens maternal or fetal health.

    Prednisolone

    Use the lowest oral dose that controls the specific inflammatory manifestation. BSR advises keeping the dose below 20 mg daily where possible and tapering with effective pregnancy-compatible steroid-sparing treatment; severe organ disease may require specialist higher-dose or intravenous treatment.

    Dose and duration depend on the affected organ and response. Monitor blood pressure, glucose, infection and adrenal suppression; avoid abrupt withdrawal after prolonged treatment and plan intrapartum steroid cover when indicated.

    Provide pregnancy-compatible steroid-sparing disease control or maintain transplant immunosuppression.

    Azathioprine and calcineurin inhibitors

    Continue or initiate only through the relevant renal or rheumatology regimen. Azathioprine dosing depends on body weight, blood counts, liver function and thiopurine metabolism; tacrolimus dosing additionally depends on measured drug concentrations and interacting medicines.

    Pregnancy compatibility does not remove toxicity monitoring. Review blood count and liver tests for azathioprine, and renal function, blood pressure, glucose and drug levels for calcineurin inhibitors; coordinate postpartum dose reassessment.

    Reduces the risk of placental hypertensive disease in high-risk pregnancies.

    Aspirin for pre-eclampsia prevention

    Give 75–150 mg orally once daily from 12 weeks until birth under the NICE prevention pathway for eligible patients, including those with CKD.

    Check aspirin hypersensitivity, active bleeding and the complete antithrombotic plan. In obstetric antiphospholipid syndrome, aspirin may be combined with heparin; previous thrombosis changes anticoagulant intensity and requires specialist planning.