The diagnostic criteria for urinary tract infection is the presence of white blood cells, epithelial cells, red blood cells (hematuria), or all on urine biochemistry. A group of nephrologists at North well studied the association of acute kidney injury with SARS-CoV-2. They found out that 40% of the population presented with either WBCs or RBCs (hematuria) on urine analysis [5]. There is ample literature reporting adult SARS-CoV-2 infections, including the atypical ones compared to children, probably because pediatric patients are less commonly diagnosed due to lesser severity and mortality [4, 6]. We report here a similar case of COVID-19 with urinary tract infection in a pediatric patient. The patient took prior medication from a local clinic for urinary tract infection but failed to respond. On the contrary, the fever showed an increasing pattern. He presented to the emergency department in sick condition and was cyanosed with SpO2 91%. The patient had to be resuscitated. According to the World Health Organization (WHO), a patient presenting with fever, cough, and shortness of breath can be labeled as a case of suspected SARS-CoV-2 [3]. The patient having diarrhea is also not an uncommon presentation [1]. But there are no studies on SARS-CoV-2 and its association with the urinary tract [7].

Marand et al. reported the presence of WBCs and RBCs on urine analysis in SARS-CoV-2-positive patients which was associated with an increased mortality [8]. Almeida et al. reports the case of a 10-year-old female patient with hematuria, who was diagnosed with SARS-CoV-2 infection but with milder symptoms [9]. Our patient had leukocytosis (20 PHF), with predominant neutrophils. This might indicate the SARS-CoV-2-induced superimposed infection [10]. Hematuria and renal injury have been commonly described in viral respiratory tract infections including influenza A and B, adenovirus, and other pathogens. Kidney injury in adults hospitalized with COVID-19 infection appears to be a frequent finding, with a wide range of manifestations, from mild hematuria to severe renal failure. The pathogenesis of the renal injury is probably multi-factorial, as SARS-CoV-2 carries the spike protein (s protein) on its surface, binds to ACE2 receptor on the cell surface, and gets internalized. ACE2 is present in the alveolar epithelial cells, lining of the intestine, endothelial cells of both arteries and veins, and also arterial smooth muscle cells of various organs, including the direct cytopathic effects of the virus [11]. It also causes immune-complex mediated damage, as well as indirect effects on renal tissue, such as hypoxia, shock, and rhabdomyolysis and damage to urothelial cells hence resulting in hematuria and urinary tract infection (Fig. 3) [12].

Mechanism of SARS-CoV-2 associated bladder injury

The prevalence of renal manifestations is found to be 13.9%. Data from the adult population showed the prevalence of acute kidney injury in about half of the hospitalized patients with laboratory-confirmed COVID-19 infection, of whom 25% required ICU admission and 1/5 required dialysis with mortality as high as 50% [13]. The emergence of new variants like B.1.1.7, the 501Y.V2 has played a vital role in the spread of the disease with atypical symptoms as they are mutated to a newer and deadly form [3]. Therefore, it is paramount to identify such new variants and identify their pathophysiology as soon as possible in order to control the spread of infection further. It is also necessary to have a well-organized diagnostic criterion for atypical presentation of SARS-CoV-2; as false-negative tests might lead the patients to relax their adherence to health protocols. Improved RT-PCR tests for urine can isolate the pathogen from the urinary tract. But serological tests should be mandatory in order to overcome the false negatives. It is also a timely requirement to arrange a particular program including risk-stratified protocols for patients suspected of having COVID-19 who present with atypical symptoms [14].