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Management of pregnant women with renal disease involves awareness of, and allowance for,
physiological changes including decreased serum creatinine and increased proteinuria. For women
with systemic lupus erythematosus (SLE), pregnancy increases likelihood of flare. These can occur
at any stage, and are more difficult to diagnose, as symptoms overlap those of normal pregnancy.
Renal involvement is no more common in pregnancy. Worsening proteinuria may be lupus flare but
differential includes pre-eclampsia. In women with chronic renal disease, pregnancy may accelerate
decline in renal function and worsen hypertension and proteinuria, with increased risk of maternal (eg,
pre-eclampsia) and fetal (eg, IUGR, IUD) complications, strongly correlating with degree of renal
impairment peri-conception. Pregnancy success rate varies from 20% to 95% depending on base-line
creatinine. Best outcome is obtained if disease was quiescent for 6 months pre-conception. Women
on dialysis or with renal transplants can achieve successful pregnancy but have higher maternal and
fetal complication rates. Acute on chronic renal failure can develop secondary to complications such
as HELLP and AFLP. Management needs to be by a multidisciplinary team involving physicians and
obstetricians, ideally beginning with pre-pregnancy counselling. Treatment of flares includes
corticosteroids, hydroxychloroquine, azothioprine, NSAIDs and MMF. Blood pressure is controlled
with methyldopa, nifedipine or hydralazine. Lupus (2006) 15, 148155.
Key words: nephritis; pregnancy; renal
149
Mild
Moderate
Creatinine (mol/L)
Loss of function
Postpartum deterioration
End-stage renal failure
125
2%
125170
40%
20%
2%
Severe
170220
65%
50%
33%
220
75%
60%
40%
Mild
Moderate
Severe
Creatinine (mol/L)
Maternal complications
eg, pre-eclampsia
IUGR
Preterm delivery
Pregnancy success
125
25%
125250
50%
250
85%
8595%
30%
55%
6090%
60%
70%
2030%
150
151
152
Table 3
Yes
No/caution
Cyclosporin
Tacrolimus
Azathioprine
Prednisolone
Penicillins
Gentamicin
Alpha-blockers
Calcium antagonists
MMF
Cyclophosphamide
Rapamycin
ACE inhibitors and A2RB (OK in first trimester)
Beta-blockers (OK in later pregnancy)
Diuretics
Statins
General management
Pregnancy care is best undertaken by a multidisciplinary team in combined clinics, involving both physicians and obstetricians with expertise in the care of
renal disease in pregnancy.
It is important to establish baseline values in early
pregnancy for Fbc, U and E, serum creatinine, uric
acid, liver function, anti -dsDNA and complement
titres and to quantify any proteinuria. The woman
should have regular assessment of renal function by
serum creatinine and urea, as well as creatinine
clearance and 24-hour protein excretion or protein
creatinine ratio. It may be useful to give the woman
urine testing strips so she can monitor the presence and
severity of any proteinuria or haematuria. The woman
should be assessed regularly for evidence of disease
activity, and other markers, such as dsDNA and
complement titres, repeated as indicated.
Anaemia is common and haematinics should be
prescribed. Maternal hypocalcaemia and hypercalcaemia are both potential problems, and calcium status
should be carefully monitored. Doses of calcium and
vitamin D may need to be altered in pregnancy.
The fetus should be monitored with regular
ultrasound scans for growth and liqor volume. Doppler
assessment of uterine artery blood flow at 2024
weeks is useful in predicting pre-eclampsia and IUGR,
and assesment of the umbilical flow is helpful in the
presence of IUGR.
As already discussed, the indications for renal
biopsy during pregnancy are mostly limited to situations where a delay before delivery is desirable (ie,
before 32 weeks gestation) and a diagnosis of a steroid
or chemotherapy-responsive lesion is suspected.
See Table 3 for a summary of the safety of the
various immunosuppressant, anti-hypertensive, and
other drugs in pregnancy. They are discussed in more
details in the following sections.
Management of lupus flares and medication
Hydroxychloroquine is often used to prevent flares.
It should not be stopped in early pregnancy, as this
Lupus
153
154
Management
This obviously depends on the underlying cause, and
is generally the same as for the management of ARF in
non-pregnant individuals, although there are a few
points specific to pregnancy and pregnancy-related
conditions. Fluid overload must be prevented, especially in pre-eclampsia, because of the susceptibility of
these women to pulmonary oedema. Plasmapheresis is
not needed for HELLP syndrome, which usually
improves with conservative therapy.
Conclusion
Diagnosis
The causes of ARF in pregnancy are listed in Table 4.
Many are associated with a coagulopathy. The commonest cause of ARF in the context of pre-eclampsia
is HELLP (Haemolysis, Elevated Liver enzymes, and
Low Platelets) syndrome (about 50%).
The underlying cause of ARF may be obvious, for
example in the case of abruption and postpartum
haemorrhage, although abruption occurs in 16% of
women with HELLP syndrome and this may be the true
underlying cause. Blood loss may not be recognized or
may be underestimated, and hypotension may be absent
or masked by co-existent pre-eclampsia. If ARF develops, especially post-partum, in a woman with features
of pre-eclampsia, combined with a microangiopathic
haemolytic anaemia and thrombocytopenia, it may be
difficult to differentiate between thrombotic thrombocytopenic purpura (TTP)/haemolytic uraemic syndrome
(HUS), HELLP syndrome and acute fatty liver of
pregnancy (AFLP). Indeed the conditions are closely
related and HUS or AFLP may evolve from HELLP.
HELLP syndrome is far more common, and is characterized by abnormal liver function, a coaguloapthy (not
seen in HUS) and a lower grade haemolysis. Pointers
to HUS are profound thrombocytopenia, and florid
microangiopathic haemolytic anaemia. Features of
AFLP are abormal liver function, hypoglycaemia, high
uric acid, and profound coagulopathy.
References
Table 4 Causes of acute renal failure in pregnancy
Infection
Blood loss
Volume contraction
Post-renal failure
Drugs
Other
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155
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8 Moroni G, Ventura D, Riva P et al. Antiphospholipid antibodies
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Lupus
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