Mechanical Ventilation and the Kidney

Abstract

Acute lung injury (ALI) and acute kidney injury (AKI) are complications often encountered in the setting of critical illness. Both forms of end-organ injury commonly occur in similar settings of systemic inflammatory response syndrome, shock, and evolving multiple organ dysfunction. Recent elucidation of the pathobiology of critical illness has led to a more basic mechanistic understanding of the complex interplay between injured organs in patients with multiple organ dysfunction syndrome; this has been aptly called ‘the slippery slope of critical illness’ [Kidney Int Suppl 1998;66:S25–S33]. Distant organ effects of apparently isolated injuries to the lungs, gut, and kidneys have all been discovered in recent years. In this article, we will review the harmful bidirectional interaction between ALI and AKI, which appears to be a common clinical syndrome with routine clinical implications. We will review the current understanding of lung-kidney interactions from both perspectives, including the renal effects of ALI and mechanical ventilation, and the pulmonary sequelae of AKI. In this review of the emerging evidence of deleterious bidirectional organ cross talk between lung and kidney, we will focus on the role of ventilator-induced kidney injury in the pathogenesis of AKI in patients with ALI.

Spillover of Cytokines and Reactive Oxygen Species in Ventilator-Induced Lung Injury Associated With Inflammation and Apoptosis in Distal Organs

“…Moreover, previous studies proposed a possible mechanism by which mechanical ventilation may induce acute renal failure mediated by alveolar stretch-induced pulmonary inflammatory reaction with systemic release of mediators. 33,34 Our findings are in agreement with previous results showing that several circulating cytokines, including tumor necrosis factor alpha, IL-1␤, and IL-8 (MIP-2), which can result in acute renal failure, are increased during mechanical ventilation in animal and human studies. 34,35 In addition, renal failure is the most prevalent organ dysfunction associated with VILI in patients with ARDS.…”

Sepsis and cardiorenal syndrome: Etiopathogenesis, diagnosis and treatment

“…Acute lung injury (ALI) (arterial oxygen tension PaO 2 and fractional inspired oxygen FiO 2 ratio below 300), acute respiratory distress syndrome (ARDS) (PaO 2 /FiO 2 ratio below 200) and mechanical ventilation contribute to the development of acute kidney injury (direct interconnectedness between lungs and kidneys) [36][37][38]. Positive pressure ventilation (PPV) (mechanical ventilation) lowers renal perfusion with its haemodynamic and non-haemodynamic effects.…”

“…Positive pressure ventilation increases the pressure in the chest cavity and decreases venous return (preload reduced), resulting in decreased heart rate and cardiac output and, consequently, the activation of neurohormonal systems, such as the renin-angiotensin-aldosterone system, sympathetic nervous system and non-osmotic vasopressin system, release and ANP production. Finally, the activation of neurohormonal systems will reduce renal blood flow, decrease glomerular filtration rate (GFR), and increase sodium and water retention in the patient's body [36][37][38]. Patients in septic shock with acute respiratory failure should undergo protective lung ventilation using low respiratory volume (tidal volume of 6 mL/ kg of ideal body weight), with end-inspiratory pressure plateau below 30 cmH 2 O, while using the smallest positive endexpiratory pressure (positive end-expiratory pressure -PEEP) to achieve satisfactory oxygenation [36][37][38].…”

“…Finally, the activation of neurohormonal systems will reduce renal blood flow, decrease glomerular filtration rate (GFR), and increase sodium and water retention in the patient's body [36][37][38]. Patients in septic shock with acute respiratory failure should undergo protective lung ventilation using low respiratory volume (tidal volume of 6 mL/ kg of ideal body weight), with end-inspiratory pressure plateau below 30 cmH 2 O, while using the smallest positive endexpiratory pressure (positive end-expiratory pressure -PEEP) to achieve satisfactory oxygenation [36][37][38].…”

Success or failure predictive indexes of extubation in renal transplants patients under mechanical ventilation – pilot study

“…The main ones are: whether the causes which led to respiratory failure and mechanical ventilation were resolved, what are the guidelines used to reduce ventilatory support and the criteria for extubation. (7,8) According to Mancintyre, 42% of mechanical ventilation time is for the process of weaning from ventilation, (8) but the extubation success will also depend on the degree of immunosuppression, nutritional status, metabolic balance and stabilization of associated comorbidities. (9) Even after the success of the transplant, the presence of frequent infections, the need for mechanical ventilation and immobility lead these patients to sequels, such as significant loss of muscle fibers and irreversible lung problems that associated with chronic kidney condition, can hamper the weaning and extubation of patients.…”