Background: Preeclampsia is a multisystem vascular disorder of pregnancy that remains a leading cause of maternal and fetal morbidity and mortality. Preeclampsia remains an underrecognized risk factor for future cardiovascular and kidney disease in women and represents the confluence of preexisting vascular risk factors with superimposed endothelial injury from placental mediated anti-angiogenic factors. Summary: This review highlights the close relationship between preeclampsia and future cardiovascular and kidney disease. It describes the pathophysiology and current understanding of biomarkers that form the molecular signature for long-term endothelial dysfunction in preeclamptic women. Finally, it describes strategies for early identification and management of women with preeclampsia with elevated risk for cardiovascular and kidney disease. Key Messages: Future rigorous studies on cardiovascular risk modification in this phenotype of disease are essential to reduce the burden of cardiovascular and kidney disease, in women with preeclampsia.

No abstract

BackgroundKidney transplantation is the treatment of choice for end stage kidney disease, but acute rejection remains a limiting factor in optimizing allograft and patient survival. Needle biopsy is the current standard of care for this diagnosis. The potential for complications with repeat biopsies limits the ability to obtain temporal immune surveillance of the allograft. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) have been shown to be strong predictors of inflammation and of worse prognosis in a variety of conditions.Material/MethodsThis is a single center retrospective case control study which included all patients who underwent a “for -cause biopsy” of a transplanted kidney. NLR and PLR were calculated 1 month prior, at the time, and 6 months and 1 year after the biopsy.ResultsA total of 159 biopsies were reviewed; 127 (79.9%) of these satisfied all inclusion and exclusion criteria, and 63.0% of the sample cohort (n=80) demonstrated acute cellular rejection (ACR). Patients without evidence of ACR had an average NLR of 26.8, which was approximately 7-fold greater than those patients with findings of ACR (P<0.01). A similar trend was found for PLR, where patients without ACR had a 5.5-fold greater PLR compared to those with rejection (P<0.01). The ROC showed AUC of 0.715 and 0.716 respectively. The NLR cutoff of 9.5 had a positive predictive value (PPV) of 80% and a negative predictive value (NPV) of 77.8%; the PLR cutoff of 380 had a PPV of 75% and a NPV of 100%.ConclusionsThis study showed that NLR and PLR are easily obtainable and reproducible predictors of ACR in the kidney allograft. Serial monitoring of these ratios will help identify subclinical inflammation before evidence of allograft dysfunction.

Systemic sclerosis-associated pulmonary arterial hypertension (SSc-PAH) is a catastrophic complication of one of the most common and devastating autoimmune diseases. Once diagnosed, it becomes the leading cause of mortality among this patient population. Screening modalities and risk assessments have been designed and validated by various organizations and societies in order to identify patients early in their disease course and promptly refer them to expert centers for a hemodynamic assessment and formal diagnosis. Moreover, several large multicenter clinical trials have now included patients with SSc-PAH to assess their response to therapy. Despite an improved understanding of the condition and significant advances in supportive and targeted therapy, outcomes have remained far from optimal. Therefore, rigorous phenotyping and search for novel therapies are desperately needed for this devastating condition.

No abstract

No abstract

RationalePulmonary arterial hypertension (PAH) is a rare disease characterised by limited survival despite remarkable improvements in therapy. The causes, clinical burden, and outcomes of patients admitted to the intensive care unit (ICU) remain poorly characterised.ObjectivesTo describe patient characteristics, causes of ICU hospitalisation, and risk factors for ICU and 1-year mortality.MethodsData from patients enrolled in the Johns Hopkins Pulmonary Hypertension Registry were analyzed for the period between January 2010 to December 2020. Clinical, functional, hemodynamic, and laboratory data were collected.Measurements and Main Results102 adult patients with 155 consecutive ICU hospitalisations were included. The leading causes for admission were right heart failure (RHF, 53.3%), infection (17.4%), and arrhythmia (11.0%). ICU mortality was 27.1%. Mortality risk factors included Na<136 mEq mL−1 (OR: 3.10, 95% CI: 1.41–6.82), elevated proBNP (OR: 1.75, 95% CI: 1.03–2.98), hyperbilirubinemia (OR: 1.40, 95% CI: 1.09–1.80), hyperlactemia (OR: 1.42, 95% CI: 1.05–1.93), and need for vasopressors/inotropes (OR: 5.29, 95% CI: 2.28–12.28), mechanical ventilation (OR: 3.76, 95% CI: 1.63–8.76), and renal replacement therapy (OR: 5.57, 95% CI: 1.25–24.76). Mortality rates at 3, 6 and 12 months were 17.5%, 27.6%, and 39.0%, respectively. Connective tissue disease-associated PAH has lower 1-year survival compared to idiopathic PAH (51.4% versus 79.8%, log-rank test p=0.019).ConclusionsRHF is the most common cause for ICU admission. In-hospital and 1-year mortality remain exceedingly high despite improved ICU care. Recognising specific risk factors on admission can help identifying patients at risk for poor outcomes.

Background: Pulmonary hypertension is not uncommon in patients with renal disease and vice versa; therefore, it influences treatments and outcomes. There is a large body of literature on pulmonary hypertension in patients with kidney disease, its prognostic implications, economic burden, and management strategies. However, the converse, namely the hemodynamic effects of pulmonary hypertension on kidney function (acute and chronic kidney injury) is less studied and described. There is also increasing interest in the effects of pulmonary hypertension on kidney transplant outcomes. The relationship is a complex phenomenon and multiple body systems and mechanisms are involved in its pathophysiology. Although the definition of pulmonary hypertension has evolved over time with the understanding of multiple interplays between the heart, lungs, kidneys, etc; there is limited evidence to provide a specific treatment strategy when kidneys and lungs are affected at the same time. Nevertheless, available evidence appears to support new therapeutics and highlights the importance of individualized approach. There is sufficient research showing that the morbidity and mortality from PH are driven by the influence of the pulmonary hemodynamic dysfunction on the kidneys. Conclusion: This concise review focuses on the effects of pulmonary hypertension on the kidneys, including, the patho-physiological effects of pulmonary hypertension on acute kidney injury, progression of CKD, effects on kidney transplant outcomes, progression of kidney disease in situations such as post LVAD implantation and novel diagnostic indices. We believe a review of this nature will fill in an important gap in understanding the prognostic implication of pulmonary hypertension on renal disease, and help highlight this important component of the cardio-reno-pulmonary axis.