Diffuse proliferative glomerulonephritis in a patient with COVID-19 infection.

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.

Successful Treatment of COVID-19-Related Immune- Complex Glomerulonephritis, Case Report.

Acute kidney injury (AKI) , proteinuria in the nephrotic or subnephrotic range and hematuria might be seen in patients with coronavirus disease 2019 (COVID-19) infection. In this case study we present a 59 years old manwho was diagnosed with immune-complex glomerulonephritis after development of rapidly progressive kidney failure accompanied by pulmonary hemorrhage, 2 months after COVID-19 infection. The patient was hospitalised with the diagnosis of acute kidney injury and nephrotic syndrome. Hemodialysis was performed due to uremic symptoms. Cyclophosphamide, methylprednisolone and plasmapheresis were started. Pathologic examination of kidney biopsy revealed features compatible with immune complex-related acute glomerulonephritis. Cyclophosphamide and plasmapheresis were discontinued , and treatment with 1 mg/kg/day methylprednisolone was continued. Immune-complex glomerulonephritis can be seen following COVID-19 infection. It is important to diagnose this disease entity as soon as possible . Steroidtherapy and other supportive modalities might be sufficient in the treatment.  DOI: 10.52547/ijkd.6527.

More difficult still: Treating severe rapidly progressive glomerulonephritis in the context of COVID-19 pneumonia.

We present the case of a male patient with severe SARS-CoV-2 pneumonia, with simultaneous onset of p-ANCA positive rapidly progressive glomerulonephritis. We discuss the different therapeutic possibilities, emphasising the appropriateness of their administration according to the time in the course of the infection.

ANCA associated glomerulonephritis in tuberculosis: a paradoxical reaction.

We present a case of antineutrophil cytoplasmic antibodies (ANCA)-associated rapidly progressive glomerulonephritis in the context of treatment of pulmonary tuberculosis (TB). A 42-year-old woman was treated for drug-susceptible pulmonary TB and represented with paradoxical worsening of symptoms and radiological features. She was HIV negative. A severe acute kidney injury with features of glomerulonephritis was evident on admission. Perinuclear ANCA and antimyeloperoxidase antibodies were present in serum and renal biopsy was consistent with ANCA-associated vasculitis. The patient was successfully treated with both antituberculous therapy and immunosuppression (corticosteroids and mycophenolate mofetil) with subsequent clinical improvement and amelioration of renal function. We propose this is the first case that describes the association between paradoxical reactions during TB treatment and ANCA-associated glomerulonephritis.

Kinin B1 Receptor Is Important in the Pathogenesis of Myeloperoxidase-Specific ANCA GN.

BACKGROUND: Myeloperoxidase-specific ANCA (MPO-ANCA) are implicated in the pathogenesis of vasculitis and GN. Kinins play a major role during acute inflammation by regulating vasodilatation and vascular permeability and by modulating adhesion and migration of leukocytes. Kinin system activation occurs in patients with ANCA vasculitis. Previous studies in animal models of GN and sclerosing kidney diseases have demonstrated protective effects of bradykinin receptor 1 (B1R) blockade via interference with myeloid cell trafficking. METHODS: To investigate the role of B1R in a murine model of MPO-ANCA GN, we evaluated effects of B1R genetic ablation and pharmacologic blockade. We used bone marrow chimeric mice to determine the role of B1R in bone marrow-derived cells (leukocytes) versus nonbone marrow-derived cells. We elucidated mechanisms of B1R effects using in vitro assays for MPO-ANCA-induced neutrophil activation, endothelial adherence, endothelial transmigration, and neutrophil adhesion molecule surface display. RESULTS: B1R deficiency or blockade prevented or markedly reduced ANCA-induced glomerular crescents, necrosis, and leukocyte influx in mice. B1R was not required for in vitro MPO-ANCA-induced neutrophil activation. Leukocyte B1R deficiency, but not endothelial B1R deficiency, decreased glomerular neutrophil infiltration induced by MPO-ANCA in vivo. B1R enhanced ANCA-induced neutrophil endothelial adhesion and transmigration in vitro. ANCA-activated neutrophils exhibited changes in Mac-1 and LFA-1, important regulators of neutrophil endothelial adhesion and transmigration: ANCA-activated neutrophils increased surface expression of Mac-1 and increased shedding of LFA-1, whereas B1R blockade reduced these effects. CONCLUSIONS: The leukocyte B1R plays a critical role in the pathogenesis of MPO-ANCA-induced GN in a mouse model by modulating neutrophil-endothelial interaction. B1R blockade may have potential as a therapy for ANCA GN and vasculitis.

Results from the IRoc-GN international registry of patients with COVID-19 and glomerular disease suggest close monitoring.

The effects of SARS-CoV-2 infection on individuals with immune-mediated glomerulonephritis, who are often undergoing immunosuppressive treatments, are unknown. Therefore, we created the International Registry of COVID infection in glomerulonephritis (IRoc-GN) and identified 40 patients with glomerulonephritis and COVID-19 followed in centers in North America and Europe. Detailed information on glomerulonephritis diagnosis, kidney parameters, and baseline immunosuppression prior to infection were recorded, as well as clinical presentation, laboratory values, treatment, complications, and outcomes of COVID-19. This cohort was compared to 80 COVID-positive control cases from the general population without glomerulonephritis matched for the time of infection. The majority (70%) of the patients with glomerulonephritis and all the controls were hospitalized. Patients with glomerulonephritis had significantly higher mortality (15% vs. 5%, respectively) and acute kidney injury (39% vs. 14%) than controls, while the need for kidney replacement therapy was not statistically different between the two groups. Receiving immunosuppression or renin-angiotensin-aldosterone system inhibitors at presentation did not increase the risk of death or acute kidney injury in the glomerulonephritis cohort. In the cohort with glomerulonephritis, lower serum albumin at presentation and shorter duration of glomerular disease were associated with greater risk of acute kidney injury and need for kidney replacement therapy. No differences in outcomes occurred between patients with primary glomerulonephritis versus glomerulonephritis associated with a systemic autoimmune disease (lupus or vasculitis). Thus, due to the higher mortality and risk of acute kidney injury than in the general population without glomerulonephritis, patients with glomerulonephritis and COVID-19 should be carefully monitored, especially when they present with low serum albumin levels.

Newly Diagnosed Glomerulonephritis During COVID-19 Infection Undergoing Immunosuppression Therapy, a Case Report.

During the COVID-19 pandemic, we had a 25 years old male case without any underlying disease or history of autoimmune disease in COVID-19 Clinic, Isfahan, Iran. He presented with arthralgia and weakness so we started COVID-19 therapeutic regimen. In his hospitalization, creatinine increases and abnormalities in random urine sediment was seen. Methylprednisolone and cyclophosphamide were prescribed due to suspected glomerulonephritis. After renal biopsy the diagnose was confirmed as crescentic proliferative glomerulonephritis. The patient also, underwent plasmapheresis and intravenous immunoglobulin injection. He was discharged healthy without development of new pulmonary symptoms despite immunosuppressive treatment.