COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), spreads worldwide, there is increasing awareness of potential renal dysfunction in patients infected with SARS-CoV-2. It has been suggested that the mechanisms of kidney injury may have a direct effect on hemodynamic instability, coagulopathy, cytokine storm, and the renin-angiotensin-aldosterone system [6].
Thromboembolic events occurring in COVID-19 patients affect both the arterial and venous systems [7]. The reason for this is that the virus causes diffuse intravascular coagulation and endotheliopathy by direct or indirect mechanisms. Coagulation occurs when the production of thrombin, fibrin, and other coagulation factors is increased, while endotheliopathy occurs when SARS-CoV-2 binds to blood vessel endothelial cells using angiotensin-converting enzyme 2 receptors. Bound viruses reproduce here and induce apoptosis of endothelial cells [8]. As a result of these conditions, renal infarction may develop. In the report of the autopsy series performed in 26 patients, when kidney tissue was examined, it was found that COVID-19 infection directly caused infection in the kidney parenchyma and endothelial damage [9].
Acute renal infarction is a rare renal vascular pathology that can cause parenchymal loss by disrupting renal blood supply [10]. It occurs as a result of occlusion in the main renal artery or its branches. Its incidence was found to be 0.007%.[11] Its diagnosis can be missed due to not presenting a specific symptom [12].
The patients are generally admitted to the hospital with acute onset abdominal or flank pain, nausea and vomiting. Especially it can be confused with urinary tract stone diseases [12, 13].
In this study, patients were admitted to the hospital with abdominal and flank pain, diarrhea and dyspnea complaints.
In the diagnosis, contrast-enhanced CT and increased Lactate dehydrogenase (LDH) levels are important tools. Leucocytosis and increased C-reactive protein (CRP), Alanine transaminase (ALT), Aspartate transaminase (AST) levels can be seen. Hematuria may accompany the symptoms in some of the cases [14].
There are many predisposing reasons for the development of renal infarction. Fibromuscular dysplasia, antineutrophil cytoplasmic antibody proteinase 3 positive vasculitis, connective tissue diseases, cardiogenic causes (atrial fibrillation, infarction, dilated cardiomyopathy), thrombophilias and idiopathic causes can be counted among these [15, 16]. The main risk factors for renal infarction are smoking, atrial fibrillation, obesity, peripheral vascular disease and estrogen use [17, 18].
In this study, patients with a history of malignancy, atrial fibrillation, post-traumatic renal infarction, deep vein thrombosis or pulmonary thromboembolism were excluded as risk factors and predisposing factors. Bourgault et al. [19] divide the causes of renal infarction into 4 main groups. Cardiac causes, kidney damage, hypercoagulation and idiopathic causes. The most common source of renal infarction is cardiac origin. Especially atrial fibrillation is one of the leading cardiogenic causes [19]. The etiology could not be determined in 132 patients performed by Oh et al.[18] The size of the infarct greater than 50% has been associated with progression to chronic kidney disease [18].
Positive results have been obtained with long-term anticoagulant therapy in the treatment of renal infarction [20]. Thrombolytic treatment can be started within 6 hours of the onset of pain. Selective intra-arterial streptokinase or urokinase infusion is used as new treatment methods, and balloon catheter angioplasty can be applied together [21]. The size of the infarct greater than 50% has been associated with progression to chronic kidney disease [18]. Cases requiring autotransplantation and nephrectomy have been reported in the absence of timely intervention with thrombolytic and anticoagulant therapy [22].
We followed our patients with low molecular weight heparin (LMWH), acetylsalicylic acid (ASA) and other new anticoagulant drugs.
Renal infarction, which developed in a 46-year-old kidney and pancreas transplant recipient, can be interpreted as a finding suggesting that hypercoagulability may continue even if the COVID-19 infection is not active, since he had COVID-19 infection 26 days ago and has no additional risk factors [4].