Effects of Pulmonary Hypertension and Right Ventricular Function in Short and Long-Term Kidney Function

Abstract

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.

Risk factors for acute kidney injury after pediatric cardiac surgery: a meta-analysis

“…There is some consensus in the literature that the primary mechanism through which pulmonary hypertension leads to AKI is through venous congestion and an increase in central venous pressure [38]. This in turn decreases effective kidney perfusion, triggering activation of the renin-angiotensin-aldosterone system, the sympathetic nervous system, and pro-inflammatory cascades [39]. Our meta-regression analysis also revealed that this effect was mainly seen in younger patients.…”

Causes and outcomes of ICU hospitalisations in patients with pulmonary arterial hypertension

“…In the present study, renal dysfunction, defined as eGFR <60 mL·min −1 per 1.73 m 2 at the time of ICU admission, was a significant risk factor for ICU mortality (OR 5.3; p=0.04) and highlights the significance of the cardiorenal axis. The primary mechanism through which PH leads to renal dysfunction is due to increased central venous pressure and consequent renovascular congestion, mediated by RV dysfunction [ 34 ]. This results in decreased effective renal perfusion due to reduced trans-glomerular pressure gradients.…”

Decreased Expression of Canstatin in Rat Model of Monocrotaline-Induced Pulmonary Arterial Hypertension: Protective Effect of Canstatin on Right Ventricular Remodeling

“…Chang et al demonstrated that cathepsin S activity was increased in serum and lung in a rat model of monocrotaline-induced PAH [ 18 ]. Acute and chronic kidney diseases are relatively common in PAH patients and the increase in venous pressure by RV dysfunction leads to kidney injury [ 19 ]. Steubl et al demonstrated that the serum level of cathepsin S was increased in mice with a decrease in the glomerular filtration rate [ 20 ].…”