Acute cardio-renal and Reno-Cardiac syndromes in critical care

Cardiorenal syndrome (CRS) encompasses a spectrum of disorders in which acute or chronic dysfunction of the heart or kidneys are the key drivers of injury. CRS types 1 and 3 are the subtypes most frequently encountered in the intensive care unit (ICU) and carry a mortality exceeding 50% when renal replacement therapy is required.

We performed a narrative review of the literature published between January 2000 and October 2025, searching PubMed, OVID, and Embase using the terms "cardiorenal syndrome", "renocardiac syndrome", and "intensive care unit". Studies involving human and animal models, published in English, were included to provide the theoretical basis for the narrative review.

CRS pathophysiology extends well beyond reduced cardiac output to encompass venous congestion, neurohormonal activation, oxidative stress, inflammatory cytokine cascades, and mitochondrial dysfunction. Early tubular injury biomarkers detect AKI 12-24 h earlier than serum creatinine. Natriuretic peptides and high-sensitivity troponins provide prognostic stratification but require careful interpretation given impaired renal clearance. Whole body Point-of-care ultrasound enables real-time hemodynamic phenotyping and guides treatment. Goal-directed hemodynamic optimization targeting mean arterial pressure, cardiac output, and venous decongestion are the cornerstone of CRS management. Diuretic strategies should be guided by dynamic congestion assessment. Continuous renal replacement therapy is preferred in haemodynamically unstable patients, while emerging therapies - including sodium-glucose cotransporter-2 (SGLT2) inhibitors and mechanical circulatory support - offer additional organ-protective potential in selected patients.

A structured multimodal approach, combining novel biomarkers, point-of-care ultrasound, goal-directed hemodynamic optimization, and individualized renal replacement therapy, is essential to improve outcomes in critically ill patients with acute CRS.