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• W3105517818 abstract "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. 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. Since the emergence of the novel coronavirus disease 2019 (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in December 2019, our understanding of the clinical consequences of COVID-19 on the kidney and the implications of infection in patients with kidney disease have grown. Urinary abnormalities and acute kidney injury are common in patients with COVID-19 from the general population.1Chen T. Wu D. Chen H. et al.Clinical characteristics of 113 deceased patients with coronavirus disease 2019: Retrospective study.BMJ. 2020; 368: m1091Crossref PubMed Scopus (2577) Google Scholar, 2Cheng Y. Luo R. Wang K. et al.Kidney disease is associated with in-hospital death of patients with COVID-19.Kidney Int. 2020; 97: 829-838Abstract Full Text Full Text PDF PubMed Scopus (1724) Google Scholar, 3Benedetti C. Waldman M. Zaza G. et al.COVID-19 and the kidneys: an update.Front Med (Lausanne). 2020; 7: 423Crossref PubMed Scopus (68) Google Scholar The susceptibility of individuals with kidney disease to SARS-CoV-2 is unclear, but available evidence suggests that patients with chronic kidney disease,4Yamada T. Mikami T. Chopra N. et al.Patients with chronic kidney disease have a poorer prognosis of coronavirus disease 2019 (COVID-19): an experience in New York City.Int Urol Nephrol. 2020; 52: 1405-1406Crossref PubMed Scopus (32) Google Scholar renal transplantation,5Banerjee D. Popoola J. Shah S. et al.COVID-19 infection in kidney transplant recipients.Kidney Int. 2020; 97: 1076-1082Abstract Full Text Full Text PDF PubMed Scopus (280) Google Scholar, 6Alberici F. Delbarba E. Manenti C. et al.A single center observational study of the clinical characteristics and short-term outcome of 20 kidney transplant patients admitted for SARS-CoV2 pneumonia.Kidney Int. 2020; 97: 1083-1088Abstract Full Text Full Text PDF PubMed Scopus (270) Google Scholar, 7Hartzell S. Bin S. Benedetti C. et al.Evidence of potent humoral immune activity in COVID-19-infected kidney transplant recipients.Am J Transplant. 2020; 20: 3149-3161Crossref PubMed Scopus (51) Google Scholar, 8Cravedi P. Mothi S.S. Azzi Y. et al.COVID-19 and kidney transplantation: results from the TANGO International Transplant Consortium.Am J Transplant. 2020; 20: 3140-3148Crossref PubMed Scopus (268) Google Scholar or on dialysis9Valeri A.M. Robbins-Juarez S.Y. Stevens J.S. et al.Presentation and outcomes of patients with ESKD and COVID-19.J Am Soc Nephrol. 2020; 31: 1409-1415Crossref PubMed Scopus (226) Google Scholar have higher mortality from COVID-19 than the general population. Nonetheless, there are no published data regarding the outcomes of COVID-19 in adult patients with underlying glomerular diseases.10Kronbichler A. Gauckler P. Windpessl M. et al.COVID-19: implications for immunosuppression in kidney disease and transplantation.Nat Rev Nephrol. 2020; 16: 365-367Crossref PubMed Scopus (71) Google Scholar,11Angeletti A. Drovandi S. Sanguineri F. et al.COVID-19 in children with nephrotic syndrome on anti-CD20 chronic immunosuppression.Clin J Am Soc Nephrol. 2020; 15: 1494-1495Crossref PubMed Scopus (22) Google Scholar Although this is a heterogeneous group of patients spanning a wide age range and encompassing diverse disease mechanisms, it is reasonable to believe that these patients may represent a particularly vulnerable group with a heightened risk of severe disease manifestations due to an interplay of factors related to the immunosuppressive medications, underlying immune dysfunction, and comorbidities. Given the relative rarity of glomerular diseases, we created an International Registry of COVID infection in glomerulonephritis (IRoc-GN) to characterize the clinical course of COVID-19, identify risk factors associated with severe complications, and evaluate nonrenal and renal outcomes in glomerulonephritis (GN) patients. We compared outcomes of GN patients with those of a control cohort of COVID-19–positive individuals from the general population without GN. Among more than 5000 patients with GN actively followed at the participating centers in 5 countries (Supplementary Table S1), 48 cases with biopsy-proven GN and COVID-19 and 80 hospitalized controls without GN were entered into the registry from 20 April 2020 to 20 August 2020. Eight GN cases (2 on hemodialysis before COVID-19, 3 renal transplant recipients, 1 with thrombotic microangiopathy, 2 duplicates) were excluded from the analysis. Therefore, this study included 120 patients: 40 patients with GN and 80 controls. Age and sex were similar between GN patients and controls (Table 1). GN patients had lower Hispanic/Latino representation than controls (48% vs. 79%, P < 0.001). Hypertension and diabetes were the most common comorbidities and were present with similar frequency in both groups. There was a higher prevalence of obesity in the GN group, but BMI was not statistically different from controls.Table 1Baseline characteristics of GN patients and controls with COVID-19CharacteristicsGN (n = 40)DeathControls (n = 80)DeathP valueYes (n = 6)No (n = 34)Yes (n = 4)No (n = 76)Age (yr)60.3 ± 17.770.2 ± 10.558.5 ± 18.262.5 ± 15.672.0 ± 13.662.0 ± 15.60.21Sex, n (%) Female23 (57.5)3 (50.0)20 (58.8)30 (37.5)1 (25.0)29 (38.2)0.051 Male17 (42.5)3 (50.0)14 (41.2)50 (62.5)3 (75.0)47 (61.8)Race33 (82.5)6 (100.0)27 (79.4)72 (90.0)4 (100.0)68 (89.5)0.38 White3 (7.5)03 (8.8)5 (6.3)05 (6.6) Black/AAm3 (7.5)03 (8.8)3 (3.8)03 (4.0) Other1 (2.5)01 (2.9)000Ethnicity<0.001 Hispanic/Latino19 (47.5)4 (66.7)15 (44.1)63 (78.8)4 (100.0)56 (73.7)BMI27.7 ± 6.3 (n = 26)32.0 ± 7.2 (n = 5)26.7 ± 5.8 (n = 21)32.0 ± 16.9 (n = 67)42.1 ± 6.3bP < 0.01 versus number of deaths in the same cohort.29.4 ± 6.3 (n = 63)0.16Glomerular disease Lupus nephritis10 (25.0)2 (33.3)8 (23.5) Vasculitis6 (15.0)2 (33.3)4 (11.8) FSGS5 (12.5)05 (14.7) IgA nephropathy5 (12.5)05 (14.7) Membranous nephropathy4 (10.0)04 (11.8)NANANANA Minimal change3 (7.5)03 (8.8) Postinfectious3 (7.5)1 (16.7)2 (5.9) AA amyloidosis2 (5.0)1(16.7)1 (2.9) Membranoproliferative2 (5.0)02 (5.9)Kidney parameters (pre-COVID-19) sCr (mg/dl)1.41 (0.89–1.91)1.72 (1.40–1.87)1.29 (0.87–1.93)0.90 (0.79–1.01)(n = 70)0.90 (0.76–1.14)0.90 (0.79–1.01)(n = 66)0.006 eGFR (ml/min/1.73 m2)47.9 (30.6–80.2)32.6 (29.3–39.1)49.1 (34.5–87.8)83.4 (72.1–92.3)(n = 70)79.2 (62.7–86.8)83.4 (72.1–97.0)(n = 66)<0.001 Serum albumin (g/dl)3.54 ± 0.62 (n = 38)3.47 ± 0.433.56 ± 0.66 (n = 32)3.92 ± 0.55 (n = 35)3.23aCannot be computed due to n = 1 in 1 of the comparison groups (died n = 1). (n = 1)3.94 ± 0.54 (n = 34)0.018 HematuriaNo/negative18 (47.4) (n = 38)2 (33.3)16 (50.0) (n = 32)1+5 (13.2)05 (15.6)2+4 (10.5)2 (33.3)2 (6.3)3+3 (7.9)1 (16.7)2 (6.3)Comorbidities Hypertension22 (55.0)4 (66.7)18 (52.9)42 (52.5)4 (100.0)38 (50.0)0.78 Diabetes8 (20.0)2 (33.3)6 (17.7)21 (26.3)1 (25.0)20 (26.3)0.51 Obesity7 (17.5)2 (33.3)5 (14.7)4 (5.0)1 (25.0)3 (4.0)0.015 Cardiovascular disease6 (15.0)2 (33.3)4 (11.8)17 (21.3)2 (50.0)15 (19.7)0.56 COPD6 (15.0)4 (66.7)cP < 0.05 versus number of deaths in the same cohort.2 (5.9)3 (3.8)03 (4.0)0.081 Asthma3 (7.5)1 (16.7)2 (5.9)5 (6.3)05 (6.6)0.87 Other chronic lung disease2 (5.0)1 (16.7)1 (2.9)2 (2.5)02 (2.6)0.41 Liver disease3 (7.5)2 (33.3)1 (2.9)3 (3.8)03 (4.0)0.38 Stroke3 (7.5)03 (8.8)0000.032 Cancer2 (5.0)1 (16.7)1 (2.9)1 (1.3)01 (1.3)0.41 HIV/AIDS1 (2.5)01 (2.9)0000.086 Current smoker1 (2.5)1 (16.7)04 (5.0)04 (5.3)0.12 Ex-smoker7 (17.5)1 (16.7)6 (17.7)000<0.001Clinical presentation Fever31 (77.5)6 (100.0)25 (73.5)61 (76.3)3 (75.0)58 (76.3)0.46 Cough25 (62.5)4 (66.7)21 (61.8)21 (26.3)1 (25.0)20 (26.3)<0.001 Dyspnea16 (40.0)5 (83.3)cP < 0.05 versus number of deaths in the same cohort.11 (32.4)53 (66.3)3 (75.0)50 (65.8)0.016 Fatigue14 (35.0)3 (50.0)11 (32.4)4 (5.0)04 (5.3)<0.001 Myalgia13 (32.5)3 (50.0)10 (29.4)6 (7.5)06 (7.9)<0.001 GI symptoms11 (27.5)1 (16.7)10 (29.4)24 (30.0)024 (31.6)0.92 Anorexia8 (20.0)1 (16.7)7 (20.6)2 (2.5)002 (2.6)0.006 Chills4 (10.0)1 (16.7)3 (8.8)4 (5.0)04 (5.3)0.14 Nasal congestion3 (7.5)1 (16.7)2 (5.9)01 (25.0)00.010 Sore throat3 (7.5)03 (8.8)3 (3.8)02 (2.6)0.38 Anosmia2 (5.0)01 (2.9)13 (16.3)013 (17.1)0.18 Neurologic symptoms1 (2.5)02 (5.9)000.086Use of RAASi at diagnosis18 (45.0)1 (16.7)17 (50.0)4 (5.0)1 (25.0)3 (4.0)<0.001Laboratory values at presentation sCR, mg/dl1.93 (1.09–4.36)(n = 27)3.67 (2.30–5.04)(n = 2)1.93 (1.09–3.81)(n = 25)0.83 (0.75–1.06)(n = 77)1.03 (0.89–1.73)0.83 (0.75–1.05)(n = 73)0.022 Serum albumin, g/dl2.83 ± 0.88 (n = 22)2.75 ± 0.78 (n = 2)2.83 ± 0.90 (n = 20)3.60 ± 0.86 (n = 62)2.67 (n = 1)3.61 ± 0.86 (n = 61)0.019 Lymphocytes (×1000/ul)0.9 ± 0.6 (n = 30)0.8 ± 0.4 (n = 5)0.9 ± 0.6 (n = 25)1.2 ± 0.8 (n = 78)0.7 ± 0.2cP < 0.05 versus number of deaths in the same cohort.1.3 ± 0.8 (n = 74)0.041 Neutrophils (×1000/ul)6.4 ± 3.6 (n = 30)7.4 ± 3.1 (n = 5)6.2 ± 379 (n = 25)6.2 ± 2.5 (n = 28)4.44 (n = 1)6.3 ± 2.5 (n = 27)0.86 Hemoglobin (g/dl)11.1 ± 2.0 (n = 30)11.0 ± 1.7 (n = 5)11.2 ± 2.1 (n = 25)12.9 ± 2.7 (n = 30)14.6 (n = 1)12.9 ± 2.8 (n = 29)0.009 Platelets (×109/l)242.6 ± 108.1 (n = 30)230.2 ± 107.5 (n = 5)245.1 ± 110.3 (n = 25)246.2 ± 130.5 (n = 31)140.0 (n = 1)249.7 ± 131.2 (n = 30)0.96 Ferritin (ng/ml)694 (455–1637)(n = 19)694 (506–1708)(n = 3)720 (338–1564)(n = 16)544.5 (220.5–1015.5)(n = 60)364.7 (n = 1)555.0 (201.0–1042.0)(n = 59)0.88 CRP (mg/L)23.1 (6.1–72.6)(n = 27)19.8 (2.7–40.5)(n = 4)23.1 (6.3–94.0)(n = 23)82.5 (24.9–141.1)(n = 76)320.0 (170.7–396.0)77.5 (24.9–136.5)(n = 72)0.014 D-dimer (ng/ml)1170.0 (440.0–2916.5)(n = 20)2200.0 (1460.0–2733.0)(n = 3)649.0 (409.0–3080.0)(n = 17)751.0 (377.0–1207.0) (n = 70)1294.0 (592.0–1445.0)(n = 3)739.0 (375.0–1109.0)(n = 67)0.91AA, amyloid A protein; AAm, African American; BMI, body mass index; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; COVID-19, coronavirus disease 2019; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; FSGS, focal segmental glomerulosclerosis; GI, gastrointestinal; GN, glomerulonephritis; NA, not applicable; RA, rheumatoid arthritis; RAASi: renin–angiotensin–aldosterone system inhibitors; sCR, serum creatinine; SLE, systemic lupus erythematosus.Data are mean ± SD, or median (interquartile range); frequencies are n (%). Full age range is 18–90 vs. 32–90 for GN patients versus controls, respectively. Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Percentages may not add to 100 due to rounding or missing or not applicable responses. Pre-COVID refers to the latest values before infection. P values are for GN versus control subjects; comparisons between GN and controls were adjusted for ethnicity. We did not report variables with <40% values available.a Cannot be computed due to n = 1 in 1 of the comparison groups (died n = 1).b P < 0.01 versus number of deaths in the same cohort.c P < 0.05 versus number of deaths in the same cohort. Open table in a new tab AA, amyloid A protein; AAm, African American; BMI, body mass index; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; COVID-19, coronavirus disease 2019; CRP, C-reactive protein; eGFR, estimated glomerular filtration rate; FSGS, focal segmental glomerulosclerosis; GI, gastrointestinal; GN, glomerulonephritis; NA, not applicable; RA, rheumatoid arthritis; RAASi: renin–angiotensin–aldosterone system inhibitors; sCR, serum creatinine; SLE, systemic lupus erythematosus. Data are mean ± SD, or median (interquartile range); frequencies are n (%). Full age range is 18–90 vs. 32–90 for GN patients versus controls, respectively. Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Percentages may not add to 100 due to rounding or missing or not applicable responses. Pre-COVID refers to the latest values before infection. P values are for GN versus control subjects; comparisons between GN and controls were adjusted for ethnicity. We did not report variables with <40% values available. The most common GN diagnoses were lupus nephritis (25%) and vasculitis (15%), followed by focal segmental glomerulosclerosis, IgA nephropathy, and membranous nephropathy (Table 1). More than one-third of patients suffered from GN for more than 5 years. Before COVID-19, median proteinuria was in the subnephrotic range (1.0 [0.33–3.20] g/d), and hematuria was present in 43% of patients. Half of GN patients were taking immunosuppressants at the time of COVID-19 diagnosis (Table 2); the majority (65%) of patients on immunosuppression had a diagnosis of lupus nephritis or vasculitis (Supplementary Table S2). One-third of GN patients were on oral corticosteroids (85% of whom were on 5–10 mg/d), 18% were on mycophenolate mofetil, 5% on calcineurin inhibitor, 5% on azathioprine, and 18% were on hydroxychloroquine. Four (10%) patients had received rituximab before COVID-19 diagnosis, and 3 of them received it within 1 month of diagnosis.Table 2Immunosuppression and use of RAAS inhibitors at time of COVID-19 diagnosis in all GN patients versus hospitalized GN patientsAll GN (n = 40)DeathP valueHospitalized (n = 28)DeathP valueYes (n = 6)No (n = 34)Yes (n = 5)No (n = 23)ImmunosuppressionaAt time of infection.20 (50.0)5 (83.3)15 (44.1)0.1815 (53.6)5 (100.0)10 (43.5)0.044Steroids13 (32.5)4 (66.7)9 (26.5)0.07511 (39.3)4 (80.0)7 (30.4)0.062Mycophenolate mofetil/mycophenolic acid7 (17.5)1 (16.7)6 (17.7)1.07 (25.0)1 (20.0)6 (26.1)1.0Hydroxychloroquine7 (17.5)1 (16.7)6 (17.7)1.05 (17.9)1 (20.0)4 (17.4)1.0Rituximab4 (10.0)2 (33.3)2 (5.9)0.104 (14.3)2 (40.0)2 (8.7)0.14Calcineurin inhibitor2 (5.0)02 (5.9)1.01 (3.6)01 (4.4)1.0Azathioprine2 (5.0)1 (16.7)1 (2.9)0.281 (3.6)1 (20.0)00.18Methotrexate2 (5.0)02 (5.9)1.01 (3.6)01 (4.4)1.0Sulfasalazine1 (2.5)01 (2.9)1.01 (3.6)01 (4.4)1.0Use of RAASi at diagnosisARB11 (27.5)1 (16.7)10 (29.4)1.08 (28.6)1 (20.0)7 (30.4)1.0ACE inhibitors (n = 39)7 (18.0)07 (21.2)0.574 (14.8)(n = 27)04 (18.2)(n = 22)0.56ACEI, angiotensin converting enzyme inhibitors; ARB, Angiotensin receptor blockers; COVID-19, coronavirus disease 2019; GN, glomerulonephritis; RAAS, renin–angiotensin–aldosterone system; RAASi, renin–angiotensin–aldosterone system inhibitors.Data are n (%).a At time of infection. Open table in a new tab ACEI, angiotensin converting enzyme inhibitors; ARB, Angiotensin receptor blockers; COVID-19, coronavirus disease 2019; GN, glomerulonephritis; RAAS, renin–angiotensin–aldosterone system; RAASi, renin–angiotensin–aldosterone system inhibitors. Data are n (%). Before COVID-19, GN patients had higher serum creatinine (1.41 [0.89–1.91] vs. 0.90 [0.79–1.01] mg/dl, respectively, P = 0.006), lower glomerular filtration rate (47.9 [30.6–80.2] vs. 83.4 [72.1–92.3] ml/min/1.73 m2, P < 0.001), and lower serum albumin (3.54 ± 0.62 vs. 3.92 ± 0.55 g/dl, P = 0.018) than controls (Table 1). At the time of COVID-19 diagnosis, almost half of the GN patients compared with only 5% of controls were on renin–angiotensin–aldosterone inhibitors (RAASi) (P < 0.001). The most common presenting symptom of COVID-19 in both cohorts was fever (Table 1). Fatigue, cough, myalgia, anorexia, and nasal congestion were more common in GN patients, whereas dyspnea was more common in controls. The majority of GN patients (70%) and all controls were hospitalized. At COVID-19 presentation, serum creatinine in GN patients was higher [1.93 (1.09–4.36) vs. 0.83 (0.75–1.05) mg/dl, P = 0.022], whereas serum albumin (2.83 ± 0.88 vs. 3.60 ± 0.86 g/dl, P = 0.019), hemoglobin (11.1 ± 2.0 vs. 12.9 ± 2.7 g/dl, respectively, P = 0.009), and lymphocyte counts (0.9 ± 0.6 vs. 1.2 ± 0.8 × 1000/ul, P = 0.041) were significantly lower than in controls (Table 1). C-reactive protein values were higher in the control group. There were no differences in other inflammatory markers, but the interpretation is limited by missing values. The most frequently used therapies for COVID-19 were hydroxychloroquine, antivirals, and azithromycin (Table 3). There was more frequent use of hydroxychloroquine and azithromycin in controls but similar use of corticosteroids, interleukin-6 receptor antagonist (tocilizumab), and antibiotics in both groups. Almost half of GN and control patients received prophylactic anticoagulation.Table 3COVID-19–related therapies among GN and control patientsGN patients (n = 40)Controls (n = 80)P valueAntivirals Hydroxychloroquine15 (37.5)60 (75.0)<0.001 Azithromycin10 (25.0)37 (46.3)0.008 Lopinavir5 (12.5)12 (15.0)0.72 Ritonavir3 (7.5)10 (12.5)0.27 Other antivirals2 (5.0)1 (1.3)0.21 Darunavir1 (2.5)2 (2.5)0.35Antiinflammatory Oral steroids7 (17.5)9 (11.3)0.47 IV methylprednisoloneaRange for total IV methylprednisolone dosage was 200 to 750 mg for GN patients and 300 to 1000 mg for controls.5 (12.5)25 (31.3)0.052 Tocilizumab2 (5.0)11 (13.8)0.095Antibiotics2 (5.0)10 (12.5)0.23Anticoagulants19 (48.7)(n = 39)39 (48.8)0.58COVID-19, coronavirus disease 2019; GN, glomerulonephritis.Data are n (%) and may not add up to 100 due to rounding or missing/not available responses. Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Comparisons between GN and controls were adjusted for ethnicity.a Range for total IV methylprednisolone dosage was 200 to 750 mg for GN patients and 300 to 1000 mg for controls. Open table in a new tab COVID-19, coronavirus disease 2019; GN, glomerulonephritis. Data are n (%) and may not add up to 100 due to rounding or missing/not available responses. Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Comparisons between GN and controls were adjusted for ethnicity. Among 20 GN patients on immunosuppression at the time of COVID-19 presentation, antimetabolites (azathioprine or mycophenolate) were discontinued in most (89%), and calcineurin inhibitors were discontinued in 1 patient. Steroids were maintained with the same dosage in 61%, increased in 31% (predominantly due to concerns of adrenal insufficiency or flare of underlying GN), and discontinued in 8%. Patients on hydroxychloroquine before infection were maintained on this treatment. RAASi were discontinued in 7 GN patients (39%) due to the presence of acute kidney injury (57%), hypotension (29%), hyperkalemia (14%), and theoretical concerns about enhancing SARS-CoV-2 viral entry (14%). More deaths occurred in GN patients compared with controls (15 % vs. 5%, P = 0.026) (Table 4). On the basis of multivariable analyses, the odds ratio (OR) of death in GN patients was 6.33 times higher than in controls (95% confidence interval [CI]: 1.38–29.04, P = 0.018) and older age associated with death in the study cohort overall (OR = 1.05. 95% CI: 1.002–1.102 P = 0.042). Among GN patients, nonsurvivors were more likely to have chronic obstructive pulmonary disease (67% vs. 6%, P = 0.002) and dyspnea at COVID-19 presentation (83% vs. 32%, P = 0.029) (Table 1). Among controls, nonsurvivors had higher BMI (42.1 ± 6.3 vs. 29.4 ± 6.3, P = 0.004) and lower lymphocytes (0.7 ± 0.2 vs. 1.3 ± 0.8 × 1000/ul, P = 0.023) than survivors. The use of RAASi was not associated with a significant difference in mortality in GN cases (P = 0.20) or in controls (P = 0.19).Table 4Nonrenal and renal complications and outcomes of GN and control patients during COVID-19 infectionGN patients (n = 40)Controls (n = 80)P valueHospitalized28 (70.0)80 (100.0)<0.001Description of illness Pneumonia21 (52.5)41 (51.3)0.66 ARDS, noninvasive ventilation3 (7.5)22 (27.5)0.12 ARDS, intubated3 (7.5)8 (10.0)0.27 Days of intubation9.0 (4.0–14.0) (n = 2)16.0 (10.0–37.0)0.99 Septic shock2 (5.0)3 (3.8)0.86Inotropes or other vasopressors2 (7.1) (n = 28)6 (8.1)0.55Developed AKI15 (38.5) (n = 39)11 (13.9)0.047 Stage 13 (25.0)2 (18.2)0.82 Stage 23 (25.0)2 (18.2) Stage 36 (50.0) (n = 12)7 (63.6)(n = 11)RRT new onset7 (17.5)5 (6.3)0.40 Days of RRT25.0 (15.0–33.0) (n = 6)aOne patient died while on RRT.30.0 (26.0–30.0)0.40 Discharged on RRT4 (80.0) (n = 5)1 (20.0)0.13Nonrenal complications CardiacMI2 (5.6)00.12Arrhythmia1 (2.8)6 (7.9)0.034 GI3 (8.1) (n = 36)5 (6.6) (n = 76)0.76 CNS1 (2.7) (n = 36)2 (2.6) (n = 76)0.44 HematologicPE2 (5.0)00.16DVT2 (5.0)3 (5.0)0.60 Superimposed bacterial infection6 (15.8) (n = 38)8 (10.7)0.91Length of hospital stay15.0 (8.0–21.0) (n = 27)7.0 (5.0–12.0) (n = 77)0.29Death6 (15.0)4 (5.0)0.026AKI, acute kidney injury; ARDS, acute respiratory distress syndrome; CNS, central nervous system; COVID-19, coronavirus disease 2019; DVT, deep vein thrombosis; GI, gastrointestinal; GN, glomerulonephritis; MI, myocardial infarction; PE, pulmonary embolism; RRT, renal replacement therapy.Data are n (%), or median (interquartile range). Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Percentages may not add to 100 due to rounding or missing/not available responses. Comparisons of GN versus controls adjust for ethnicity. All comparisons are adjusted for ethnicity.a One patient died while on RRT. Open table in a new tab AKI, acute kidney injury; ARDS, acute respiratory distress syndrome; CNS, central nervous system; COVID-19, coronavirus disease 2019; DVT, deep vein thrombosis; GI, gastrointestinal; GN, glomerulonephritis; MI, myocardial infarction; PE, pulmonary embolism; RRT, renal replacement therapy. Data are n (%), or median (interquartile range). Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Percentages may not add to 100 due to rounding or missing/not available responses. Comparisons of GN versus controls adjust for ethnicity. All comparisons are adjusted for ethnicity. In GN patients, GN diagnosis, estimated glomerular filtration rate, proteinuria, or serum albumin before COVID-19 or at presentation did not significantly differ between survivors and nonsurvivors (Table 1). There was no difference in death between those on immunosuppression (including use of steroids) at the time of COVID-19 versus those not on immunosuppression (P = 0.18) (Tables 2 and 5); however, among 15 hospitalized GN patients, all 5 who died were on immunosuppression (100% of 5 vs. 44% of 10, P = 0.044) (Table 2).Table 5Duration of disease and immunosuppression in GN patients stratified by outcomeGN (n = 40)AKI any stage (n = 39)aOne patient died at home; therefore, no information for development of AKI was available.RRT requirementDeathYes (n = 15)No (n = 24)Yes (n = 7)No (n = 33)Yes (n = 6)No (n = 34)Duration of GN disease <6 mo11 (27.5)7 (46.7)bObserved differences in subsets: duration of GN disease was associated with AKI yes versus no (P = 0.043) and RRT yes versus no (P = 0.023).4 (16.7)5 (71.4)bObserved differences in subsets: duration of GN disease was associated with AKI yes versus no (P = 0.043) and RRT yes versus no (P = 0.023).6 (18.2)3 (50.0)8 (23.5) 6–12 mo2 (5.0)1 (6.7)1 (4.2)02 (6.1)02 (5.9) 12–24 mo6 (15.0)2 (13.3)4 (16.7)06 (18.2)2 (33.3)4 (11.8) 2–5 yr6 (15.0)1 (6.7)4 (16.7)1 (14.3)5 (15.2)06 (17.7) >5 yr15 (37.5)4 (26.7)11 (45.8)1 (14.3)14 (42.4)1 (16.7)14 (41.2)Immunosuppression at presentation20 (50.0)6 (40.0)13 (54.2)4 (57.1)16 (48.5)5 (83.3)15 (44.1) Steroids13 (32.5)5 (33.3)8 (33.3)2 (28.6)11 (33.3)4 (66.7)9 (26.5) Mycophenolate mofetil7 (17.5)4 (26.7)3 (12.5)1 (14.3)6 (18.2)1 (16.7)6 (17.7) Hydroxychloroquine7 (17.5)2 (13.3)5 (20.8)2 (28.6)5 (15.2)1 (16.7)6 (17.7) Rituximab4 (10.0)2 (13.3)2 (8.3)1 (14.3)3 (9.1)2 (33.3)2 (5.9) Calcineurin inhibitor2 (5.0)01 (4.2)1 (14.3)1 (3.0)02 (5.9) Azathioprine2 (5.0)02 (8.3)02 (6.1)1 (16.7)1 (2.9) Methotrexate2 (5.0)02 (8.3)02 (6.1)02 (5.9) Sulfasalazine1 (2.5)01 (4.2)01 (3.1)01 (2.9)On immunosuppressionYes20 (50.0)6 (40.0)13 (54.2)4 (57.1)16 (48.5)5 (83.3)15 (44.1)No20 (50.0)9 (60.0)11 (45.8)3 (42.8)17 (51.)1 (16.7)19 (55.9)AKI, acute kidney injury; GN, glomerulonephritis; RRT, renal replacement therapy.Data are n (%). Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Percentages may not add to 100 due to rounding or missing/not available responses.a One patient died at home; therefore, no information for development of AKI was available.b Observed differences in subsets: duration of GN disease was associated with AKI yes versus no (P = 0.043) and RRT yes versus no (P = 0.023). Open table in a new tab AKI, acute kidney injury; GN, glomerulonephritis; RRT, renal replacement therapy. Data are n (%). Sample sizes are listed if they are fewer than the respective denominators shown in the header row. Percentages may not add to 100 due to rounding or missing/not available responses. Thirteen percent of GN patients and 10% of controls required admission to the intensive care unit. Acute respiratory distress syndrome developed in 15% of GN patients and in 38% of controls (Table 4). There were no differences in percentages of patients intubated, requirement for vasopressors, length of hospital stay, and nonrenal complications in GN versus controls, except for arrhythmias, which were more frequent in controls (3% vs. 8%, P = 0.034). Five of six (83%) controls who developed arrhythmias were receiving treatment with hydroxychloroquine; arrhythmia in the GN patient was not associated with antimalarial treatment. Four (10%) GN patients had venous thromboembolic events, despite prophylactic anticoagulation in 3. Serum albumin levels during infection were lower in GN patients who experienced venous thromboembolic events (1.67 ± 0.38 vs. 2.94 ± 0.83 g/dl, P = 0.048). There were no significant difference in death between patients with kidney-limited GN versus GN associated with systemic diseases (lupus or vasculitis) (8% vs. 25%, respectively, P = 0.20), or in other non-renal complications (Supplementary Table S3) despite the greater overall density of immunosuppressive agents (81% vs. 29%, P = 0.00" @default.
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• W3105517818 date "2021-01-01" @default.
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• W3105517818 title "Results from the IRoc-GN international registry of patients with COVID-19 and glomerular disease suggest close monitoring" @default.
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• W3105517818 doi "https://doi.org/10.1016/j.kint.2020.10.032" @default.
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