Cardio-Pulmonary-Renal Interaction (CPRI) - A Syndrome of Death

Abstract

Two deaths due to renal failure in the last 2 month led me to a review the current, state-of-the-art understanding of cardio-pulmonary-renal interactions and their related pathophysiology, perpetuating nature, and cycles of increased susceptibility and reciprocal progression. It indicates that Organ injury is the consequence of maladaptive neurohormonal activation, oxidative stress, abnormal immune cell signalling, and a host of other mechanisms that precipitate adverse functional and structural changes. This syndrome has many complex physiologic, biochemical, and hormonal abnormalities and its pathophysiology is not fully understood. The possible mechanisms include reduced kidney perfusion due to decreased forward flow, increased right ventricular and venous pressure, and neurohormonal adaptations. Assessment of biomarkers are valuable clinical strategies to screen and detect disease, assist in diagnosis, assess prognosis, and predict recovery or progression to chronic disease or even death. Reduced kidney function is associated with increased mortality in such patients.

Treatment options include inotropic medications; diuretics; ultrafiltration; and medications, such as β-blockers, inhibitors of the renin-angiotensinaldosterone system, and more novel treatments. Recent observational studies suggest that treatments that result in a decrease in venous pressure and lead to haemoconcentration may be associated with improved outcomes.

I report here a male and female case who succumbed to Cardiac failure following renal failure in the last 2 months.