A review of Covid-19 and acute kidney injury: from pathophysiology to clinical results

Abstract

Acute kidney injury (AKI) in hospitalized patients with COVID-19 is associated with higher mortality and a worse prognosis. Nevertheless, most patients with COVID-19 have mild symptoms, and about 5% can develop more severe symptoms and involve hypovolemia and multiple organ dysfunction syndrome. In a pathophysiological perspective, severe SARS-CoV-2 infection is characterized by numerous dependent pathways triggered by hypercytokinemia, especially IL-6 and TNF-alpha, leading to systemic inflammation, hypercoagulability, and multiple organ dysfunction. Systemic endotheliitis and direct viral tropism to proximal renal tubular cells and podocytes are important pathophysiological mechanisms leading to kidney injury in patients with more critical infection, with a clinical presentation ranging from proteinuria and/or glomerular hematuria to fulminant AKI requiring renal replacement therapies. Glomerulonephritis, rhabdomyolysis, and nephrotoxic drugs are also associated with kidney damage in patients with COVID-19. Thus, AKI and proteinuria are independent risk factors for mortality in patients with SARS-CoV-2 infection. We provide a comprehensive review of the literature emphasizing the impact of acute kidney involvement in the evolutive prognosis and mortality of patients with COVID-19.

Cardiorenal syndrome: long road between kidney and heart

“…Despite the described and known benefits of RAAS blockade in the isolated heart or kidney and its cardioprotective and renoprotective effects, the role of this system and its implications in cardiorenal patients requires further examination. Recently, worldwide researchers have focused their attention on the regulatory axis of SARS-CoV-2, which highlights the protective action of ACE2/ Ang 1-7 on the cardiovascular system [39][40][41].…”

Rhabdomyolysis-Induced AKI (RIAKI) Including the Role of COVID-19

“…Although the incidence of AKI in COVID-19 has shown a decreasing trend over time [ 60 ], it remains a common complication of SARS-CoV-2 infection [ 20 , 21 , 22 ]. AKI prolongs the duration of hospitalization and worsens the prognosis and increases the mortality of COVID-19 patients [ 21 , 23 , 61 ]. The factors that are associated with an increased risk of developing AKI have been identified and include older age [ 20 , 23 ], male gender [ 23 , 60 ], black race, and comorbidities such as diabetes mellitus [ 20 , 23 , 60 ], cardiovascular diseases, hypertension [ 20 , 23 ], CKD, or obesity [ 23 , 60 ].…”

“…Ng et al [ 61 ] mention prerenal azotemia, acute tubular injury, glomerular diseases, thrombotic microangiopathy, and treatment-related AKI among the pathological mechanisms of AKI formation in COVID-19. However, Pecly et al [ 23 ] indicate that rhabdomyolysis may also contribute to AKI. The pathomechanism of rhabdomyolysis-induced AKI in the course of COVID-19 is based on the release of significant amounts of myoglobin, which results in myoglobinuria, and this leads to the formation of pigment casts.…”

“…The pathomechanism of rhabdomyolysis-induced AKI in the course of COVID-19 is based on the release of significant amounts of myoglobin, which results in myoglobinuria, and this leads to the formation of pigment casts. This results in intratubular obstruction [ 23 ].…”

“…Acute kidney injury (AKI) is also a common complication of COVID-19 [ 20 , 21 , 22 ]. Many causes of its onset have been cited, one of which is rhabdomyolysis leading to intratubular obstruction [ 23 ].…”