Prof Mark Brown
Professor of Renal Medicine & Obstetric Medicine Physician, St George Hospital & University of New South Wales, Sydney, Australia
Mark Brown is Professor of Renal Medicine and an Obstetric Medicine Physician at St George Hospital and the University of New South Wales, Sydney, Australia. He is the current President of the International Society for the Study of Hypertension in Pregnancy.

Prof. Brown has a busy clinical practice that includes all aspects of nephrology with specific interests in the fields of hypertension in pregnancy and, addressing the other end of life, Renal Supportive (Palliative) care.

He has been involved in teaching at all levels and in program development of postgraduate medical education for many years.

Research activities have centred on scientific and clinical studies of hypertension and renal disease in pregnancy, with about 230 peer reviewed publications. The focus of his research has been on blood pressure measurement, renal function and the renin-angiotensin system, and studies that change clinic practice in hypertensive pregnancies. Current research is focused on the long-term outcomes of women who have had hypertensive pregnancies.


Chronic Hypertension in Pregnancy
Mark A Brown
Dept. Renal Medicine. St. George Hospital & University of NSW. Sydney. Australia.

Chronic hypertension (CH) is present in about 1 of every 50 pregnancies; it refers to essential hypertension (EH), hypertension associated with renal disease (CKD), or less commonly with another secondary cause for hypertension. EH is by far the most prominent cause of CH in pregnancy, nowadays associated with obesity and sedentary lifestyle.
CH is recognised by a known pre-pregnancy history or the new hypertension before 20 weeks; once renal disease is excluded the diagnosis should be confirmed by home or 24hr. BP monitoring as about one-quarter will have ‘white-coat’ hypertension (WCH), a disorder with a better pregnancy outcome than true EH but not as safe as normal pregnancy.
CH carries high pregnancy risks including about 25% risk for superimposed pre-eclampsia (PE) – which may be worse than de novo PE, 40% likelihood of Caesarean section, 28% pre-term delivery, 17% low birth weight and 4% perinatal death. Factors at about 20 weeks associated with subsequent progression to PE include elevated sFlt1/PlGF ratio, low plasma renin activity, high plasma uric acid and systolic BP >140mmHg.

Benefits of treating CH with antihypertensives were first shown in 1968; more recently the CHIPS trial has shown benefit without harm of targeting a diastolic BP <85mmHg in women with CH, using primarily labetalol or methyldopa. Several antihypertensives are recommended by SOMANZ as suitable for use in pregnancy; there is recent recognition that CH per se may be associated with congenital abnormalities, confounding any potential adverse effects of antihypertensives. Whilst ACEI are contraindicated in pregnancy there are some women in whom they should be used up until conception. The optimum time for delivery in CH is debatable, some suggesting 38-39 weeks.

Despite pregnancy being a peak opportunity to recognise CH in young women, post-partum follow up is often lacking, undoubtedly leading to worse long-term outcomes in these women.

Controversies in Pre-eclampsia
Mark A Brown.
Dept. Renal Medicine. St. George Hospital & University of NSW. Sydney. Australia.

Pre-eclampsia (PE) is a major contributor to world-wide maternal and baby mortality and morbidity; this disorder probably kills up to 40% as many people per year as does HIV. Hence, one of the first controversies in pre-eclampsia medicine is being able to diagnose this disorder. Is it really a single disorder or are there multiple disorders? e.g. is ‘early onset’ PE a different and worse disorder than ‘late onset’ PE?

Current research addresses the role of angiogenic factors not just in the pathogenesis of PE but also as diagnostic tools to predict the development or clinical course of the disorder and, this year, to ‘rule out’ PE (at least for one week) in women who have signs that may suggest imminent PE. While this research is paramount to improving our understanding of PE we should not be using this in routine clinical practice yet.

We remain at a point where it is still best to seek a good clinical diagnosis of pre-eclampsia based upon accurate blood pressure measurement, clinical features, evidence of abnormal liver function, renal function, haemolysis (rare in Australia & New Zealand) or thrombocytopenia, and/or proteinuria. The latter is now accepted internationally as not being mandatory for a diagnosis of PE, with the exception of the NICE (UK) group. Similarly, prediction of PE remains best done by good clinical assessment at the start of or even pre-pregnancy. Undoubtedly both diagnosis and prediction will be possible through one or more tests at some stage in the near future.

We now recognise the long term cardiovascular and other consequences of PE but some now suggest these risks are confined to those with post-partum hypertension. Ongoing research continues to address these issues.