A Case Report on COVID-19-Related Illnesses from the Alveoli to the Glomeruli - carehealth

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Tuesday, June 7, 2022

A Case Report on COVID-19-Related Illnesses from the Alveoli to the Glomeruli

A Case Report on COVID-19-Related Illnesses from the Alveoli to the Glomeruli
A Case Report on COVID-19-Related Illnesses from the Alveoli to the Glomeruli


Abstract

The most common consequence of severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) infection is hypoxemic respiratory failure. COVID-19 (coronavirus disease-19) is no longer regarded as a separate respiratory infection. It can directly or indirectly affect other organs, such as the kidneys, through immunological activation, cytokine storm, microthrombi, and hemodynamic instability. COVID-19 has a worse prognosis when multiple organs are involved.

The most common renal pathology is tubulopathy, which is followed by glomerulopathies. Immunoglobulin A (IgA) nephropathy is the least common of the glomerulopathies. From a therapeutic and prognosis standpoint, distinguishing tubulopathy from glomerulopathy is critical. The presence of glomerulopathy as a cause of renal involvement cannot be predicted by laboratory tests, including urine microscopy. As a result, it is critical to do a kidney biopsy as soon as possible in order to get a definitive diagnosis.

We discuss the case of a 33-year-old man who had proteinuric acute renal damage three weeks after recovering from COVID-19. IgA nephropathy was discovered during a kidney biopsy.

Introduction

The most prevalent symptom of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is involvement of the respiratory system, resulting in hypoxemic respiratory failure [1]. Coronavirus disease-19 (COVID-19) affects the kidneys in up to 36.6 percent of cases [2]. When there is renal involvement, the mortality rate of COVID-19 pneumonia is greater. Acute kidney injury (AKI) is known to occur more commonly in ventilated patients, with one-third of them dying [3].

Older age, diabetes, cardiovascular disease, previous chronic renal disease, black ethnicity, hypertension, and the need for ventilation and vasopressor medicines are all risk factors for AKI [4]. Renal involvement has been linked to a variety of mechanisms, including direct cytotoxicity caused by viral infection of the renal parenchyma via angiotensin-converting enzyme receptors, hemodynamic instability, microthrombi, drug toxicity, and cytokine-induced injury leading to renal tubular damage [5]. Renal biopsies from China and the United States of America (USA) typically reveal tubulopathies, with immune-mediated glomerulopathies as collapsing focal segmental glomerulonephritis (FSGS), membranous nephropathy, and anti-glomerular basement membrane disease (anti- GBM illness) being rare [6,7].

Only one of 12 COVID-19 patients' postmortem kidney biopsies was found to have IgA nephropathy [8]. Nicolas et al. [7] described a case of Henoch Schönlein Purpura (HSP) with IgA nephropathy in a young guy who had no prior medical history other than COVID-19. In a 78-year-old man with COVID-19, Suso found HSP and IgA nephropathy [9].

We present the case of a 33-year-old man who developed proteinuria and AKI after recovering from COVID-19 infection, and whose kidney biopsy revealed IgA nephropathy.

Presentation of a Case

A 33-year-old male with a seven-day history of fever, cough, and shortness of breath presented to the hospital. Based on his clinical symptoms and a positive reverse transcriptase-polymerase chain reaction (RT-PCR) on a nasopharyngeal swab, he was diagnosed with COVID-19. He had a mild SARS-CoV-2 infection, according to the World Health Organization's (WHO) COVID-19 classification, and was treated appropriately. The results of his complete blood count, C-reactive protein, urinalysis, liver, and renal function tests were all normal.

After two weeks, his symptoms had greatly improved. He developed weakness, headaches, and moderate edoema in his feet a week later. He returned to the hospital for a second opinion. On room air, his pulse was 84 beats per minute, his blood pressure was 160/100 mmHg, his temperature was 97 degrees Fahrenheit, and his oxygen saturation was 96 percent. He had pitting pedal edoema on both sides. There was no rash on the skin. The systemic investigation revealed nothing unusual. He was brought to the hospital for additional examination. A complete blood count, liver function tests, renal function tests, C-reactive protein, urinalysis, chest X-ray, EKG, and echocardiogram were all performed on him. Table 1 summarises the most important findings from the investigations.

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