Diffuse proliferative glomerulonephritis in a patient with COVID-19 infection

Abstract

COVID-19 primarily presents with respiratory involvement. Extrapulmonary manifestations as the sole manifestation also occur although rare. The kidney, being one of the organs with the greatest number of ACE receptors, is usually reported as part of multiorgan involvement. We report an early adolescent boy who presented with nephrotic–nephritic syndrome with severe kidney dysfunction from COVID-19 infection. He had low C3 and undetected antineutrophil cytoplasmic antibodies, antinuclear antibody and antistreptolysin O. Kidney biopsy revealed findings consistent with diffuse proliferative glomerulonephritis with a focal glomerular crescent formation and thin basement nephropathy. Due to the rapidly progressive deterioration of kidney function, he was given pulse methylprednisolone therapy followed by oral prednisone. Complete recovery was documented 12 weeks after the onset of post-infectious glomerulonephritis. The possible pathogenesis of glomerulonephritis in a patient with COVID-19, its differential diagnosis and treatment are discussed.

From Emergence to Endemicity: A Comprehensive Review of COVID-19

“…Mechanism of injury noted from autopsy studies revealed evidence of viral infection in innate monocytes, macrophages, NK (natural killer) cells, evidence of viral replication in renal parenchymal cells, which was thought to cause tissue damage in the form of ATN, and glomerulosclerosis [ 111 ]. Other suggested mechanisms include hypoxia, hypoperfusion of kidneys causing ATN, immune complex deposition of viral particles in the kidneys [ 109 ], and induction of a proinflammatory state [ 98 ].…”

“…Diverse renal manifestations reported worldwide include acute tubular necrosis (ATN), collapsing focal segmental glomerulosclerosis, albuminuria, hematuria, electrolyte derangements [98], minimal change disease, crescentic glomerulonephritis, thrombotic thrombocytopenic purpura (TTP), atypical hemolytic uremic syndrome (aHUS), IgA nephropathy, renal vein thrombosis, diffuse proliferative glomerulonephritis, acute kidney injury [106][107][108][109][110].…”

COVID-19: From Emergence to Endemicity - A Comprehensive Review

“…Renal manifestations: Diverse renal manifestations reported worldwide include acute tubular necrosis (ATN), collapsing focal segmental glomerulosclerosis, albuminuria, hematuria, electrolyte derangements (98), minimal change disease, crescentic glomerulonephritis, thrombotic thrombocytopenic purpura (TTP), atypical hemolytic uremic syndrome (aHUS), IgA nephropathy, renal vein thrombosis, diffuse proliferative glomerulonephritis, acute kidney injury (106)(107)(108)(109)(110).…”

“…Mechanism of injury noted from autopsy studies revealed evidence of viral infection in innate monocytes, macrophages, NK (natural killer) cells, evidence of viral replication in renal parenchymal cells which was thought to cause tissue damage in the form of ATN (acute tubular necrosis), and glomerulosclerosis (111). Other suggested mechanisms include hypoxia, hypoperfusion of kidneys causing ATN, immune complex deposition of viral particles in the kidneys (109), and induction of a proinflammatory state (98).…”

COVID-19 and Kidney: The Importance of Follow-Up and Long-Term Screening

“…The most common pathogenesis involved in COVID-19-induced AKI is the activation of the complement cascade, acute and chronic inflammation with immune cell infiltration in the kidney, hypercoagulopathy, formation of microvascular thrombi, endothelial dysfunction (due to vascular endotheliitis), pigment nephropathy, and mitochondrial dysfunction. AKI is also caused by the direct invasion of the SARS-CoV-2 virus into podocytes and proximal convoluted tubule involving angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2) [1,[11][12][13][14][15][16] (Figure 1).…”