Purpose of reviewHypertensive disorders of pregnancy remain a highly morbid condition that affects both the mother and fetus, complicate approximately 10% of pregnancies worldwide, and contribute to immediate and longterm cardiovascular outcomes. There is still much to learn regarding pathogenesis and treatment goals. Recent findingsThere is updated information on the pathogenesis of preeclampsia and treatment thresholds for HTN in pregnancy. L-Kynurenine, a metabolite of the essential amino acid L-tryptophan, has been implicated in preeclampsia as decreased levels were found in a uninephrectomized pregnant mouse model of preeclampsia, where replacement of L-kynurenine rescued the preeclamptic state. Further, data from CHIPS (The Control of HTN in Pregnancy Study) and CHAP (Chronic HTN and Pregnancy) trials demonstrate not only the safety of lowering blood pressure to either a diastolic goal of 85 mmHg (CHIPS) or less than 160/ 105 mmHg (CHAP) without detriment to the fetus but the CHAPS trial has also shown a decrease in the rate of preeclampsia in the treatment group.

Cardiovascular disease is a major cause of death worldwide especially in patients with chronic kidney disease (CKD). Troponin T and troponin I are cardiac biomarkers used not only to diagnose acute myocardial infarction (AMI) but also to prognosticate cardiovascular and all-cause mortality. The diagnosis of AMI in the CKD population is challenging because of their elevated troponins at baseline. The development of high-sensitivity cardiac troponins shortens the time needed to rule in and rule out AMI in patients with normal renal function. While the sensitivity of high-sensitivity cardiac troponins is preserved in the CKD population, the specificity of these tests is compromised. Hence, diagnosing AMI in CKD remains problematic even with the introduction of high-sensitivity assays. The prognostic significance of troponins did not differ whether it is detected with standard or high-sensitivity assays. The elevation of both troponin T and troponin I in CKD patients remains strongly correlated with adverse cardiovascular and all-cause mortality, and the prognosis becomes poorer with advanced CKD stages. Interestingly, the degree of troponin elevation appears to be predictive of the rate of renal decline via unclear mechanisms though activation of the reninangiotensin and other hormonal/oxidative stress systems remain suspect. In this review, we present the latest evidence of the use of cardiac troponins in both the diagnosis of AMI and the prognosis of cardiovascular and all-cause mortality. We also suggest strategies to improve on the diagnostic capability of these troponins in the CKD/end-stage kidney disease population.

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