scholarly journals SIGNIFICANCE OF COMPLEMENT PROFILE AND COMPLEMENT RECEPTOR 1 EXPRESSION IN RBC AND KIDNEY TISSUE IN IMMUNE COMPLEX MEDIATED DISEASE

2003 ◽  
Vol 41 (144) ◽  
pp. 481-484 ◽  
Author(s):  
Nirmal Baral ◽  
M Lamsal ◽  
L M Shrivastava

A study was conducted to evaluate role of complement proteins and complementreceptor 1 (CR1) in pathogenesis of Systemic lupus erythematosus (SLE) and Immunecomplex (IC) mediated glomerulonephritis. C3, C4, C3d and CH100 in serum, CR1 inrenal biopsies and RBC showed these parameters to be of great diagnostic andprognostic values in Immune complex mediated diseases. Our study revealed an overalldecrease in levels of CR1, C3, C4 in IC mediated as compared to non - IC mediateddisease. Whereas C3d in case of SLE 247 ± 39 AU/L including IC mediatedGlomerulonephritis (ICGN) 208 ± 51 AU/L was found to be significantly increased(P < 0.05) than normal control 46 ± 6 AU/L. There was no appreciable increase incase of non - 1C mediated GN (61 ± 12 AU/L) CRI among SLE patients (261 ± 141/E)and IC mediated group (270 ± 107/E) was found to be significantly lower (P < 0.05)than normal control (627 ± 132/E) and non - IC GN (550 ± 86/E). C4 values amongSLE, patients were found to be 191 ± 104 mg/L as compared to control (286 ±110 mg/L). The kidney biopsy of type III and type IV lupus nephritis revealed a completeabsence of CR1 in contrast to minimal change diseases. Thus this study revealed thatabove parameters could be a valuable tool for distinguishing IC versus non-IC mediatedkidney diseases.Key Words: Complement receptor 1 (CR1) Glomerulonephritis, SLE.

2019 ◽  
Vol 9 (02) ◽  
Author(s):  
Haider S Al-Hadad ◽  
Aqeel Abbas Matrood ◽  
Maha Abdalrasool Almukhtar ◽  
Haider Jabur Kehiosh ◽  
Riyadh Muhi Al-Saegh

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease. Few biomarkers for SLE have been validated and widely accepted for the laboratory follow-up of inflammatory activity. In SLE patients, with lupus nephritis (LN), complement activation leads to fluctuation of serum C3 and C4 that are frequently used as clinicalm biomarker of disease activity in SLE. Patients and Methods: In this study the number of patients were 37, seven patients were excluded for incomplete data collection, 28 were females ,2 were males. The duration of the study is two years from 2015 to 2017. Patients were considered to have SLE and LN according to American College of Rheumatology (ACR) criteria, and International Society of Nephrology/ Renal Pathology Society (ISN/RPS). All patients were evaluated withm clinical presentation, laboratory investigations. Our patients underwent kidney biopsy according to standard procedure by Kerstin Amann, and their tissue specimens were studied in the laboratory with light microscope (LM) and immunofluorescence microscope reagents. The relationship between the serological markers and immunofluorescence deposits in kidney biopsy of all patients were studied using the statistical analysis of Pearson correlation and single table student's T test. A P value 0.05 was considered statistically significant. Results: The granular pattern of IF deposits was present in all LN patients, and in more than two third of patients these IF deposits presented in glomerular, tubular, and mesangium sites. While less than one third of patients had IF deposits in the mesangium only. There was no statistically significant correlation between serum ANA, anti-dsDNA, and IF deposits of different types. There was significant correlation between serum C3 and C4 hypocomplementemia and IgG immune deposits in kidney biopsy, and there was significant relationship between serum C3 hypocomplementemia and full house immunofluorescence (FHIF) deposits inm kidney biopsy.Conclusions:Immunofluorescence deposits is mainly granular pattern in LN patients. There was no significant association between serum ANA, anti-dsDNA, and immune deposits in kidney tissue. Immunofluorescence deposits of IgG type correlates significantly with serum C3 and C4 hypocomplemetemia, and these immune deposits in association with low complement levels correlates with LN flare. There was significant correlation between C3 hypocomplementemia and FHIF.


2020 ◽  
Vol 8 ◽  
pp. 2050313X2091002 ◽  
Author(s):  
Umut Selamet ◽  
Ramy M Hanna ◽  
Anthony Sisk ◽  
Lama Abdelnour ◽  
Lena Ghobry ◽  
...  

Drug-induced lupus erythematosus has features distinct from primary systemic lupus erythematosus. It can occur with a wide variety of agents that result in the generation of anti-histone or other types of antibodies. Systemic manifestations of drug-induced systemic lupus erythematosus may include renal dysfunction due to circulating immune complexes or due to other immune reactions to the culprit medication(s). Acute interstitial nephritis occurs due to DNA–drug or protein–drug complexes that trigger an allergic immune response. We report a patient who developed acute kidney injury, rash, and drug-induced systemic lupus diagnosed by serologies after starting chlorthalidone and amiodarone. A renal biopsy showed acute interstitial nephritis and not lupus-induced glomerulonephritis. It is important to note that systemic lupus erythematosus and acute interstitial nephritis can occur together, and this report highlights the role of the kidney biopsy in ascertaining the pathological diagnosis and outlining therapy in drug-induced lupus erythematosus.


2015 ◽  
Vol 67 (2) ◽  
pp. 584-595 ◽  
Author(s):  
Anuja Java ◽  
M. Kathryn Liszewski ◽  
Dennis E. Hourcade ◽  
Fan Zhang ◽  
John P. Atkinson

2004 ◽  
Vol 50 (11) ◽  
pp. 3596-3604 ◽  
Author(s):  
Susan Manzi ◽  
Jeannine S. Navratil ◽  
Margie J. Ruffing ◽  
Chau-Ching Liu ◽  
Natalya Danchenko ◽  
...  

2010 ◽  
Vol 78 (7) ◽  
pp. 3129-3135 ◽  
Author(s):  
Jie Li ◽  
Jennifer P. Wang ◽  
Ionita Ghiran ◽  
Anna Cerny ◽  
Alexander J. Szalai ◽  
...  

ABSTRACT Complement-containing immune complexes can be presented to phagocytes by human erythrocytes bearing complement receptor 1 (CR1). Although this has long been assumed to be a mechanism by which humans are able to protect themselves from “extracellular” bacteria such as pneumococci, there is little direct evidence. In these studies we have investigated this question by comparing results for erythrocytes from transgenic mice expressing human CR1 on their erythrocytes to the results for wild-type mouse erythrocytes that do not express CR1. We demonstrate that human CR1 expression on murine erythrocytes allows immune adherence to beads opsonized with either mouse or human serum as a source of complement. The role of CR1 in immune adherence was supported by studies showing that it was blocked by the addition of antibody to human CR1. Furthermore, human CR1 expression enhances the immune adherence of opsonized pneumococci to erythrocytes in vitro, and the pneumococci attached to erythrocytes via CR1 can be transferred in vitro to live macrophages. Even more importantly, we observed that if complement-opsonized pneumococci are injected intravenously with CR1+ mouse erythrocytes into wild-type mice (after a short in vitro incubation), they are cleared faster than opsonized pneumococci similarly injected with wild-type mouse erythrocytes. Finally, we have shown that the intravenous (i.v.) injection of pneumococci into CR1+ mice also results in more rapid blood clearance than in wild-type mice. These data support that immune adherence via CR1 on erythrocytes likely plays an important role in the clearance of opsonized bacteria from human blood.


2008 ◽  
Vol 84 (1) ◽  
pp. 9-15 ◽  
Author(s):  
N. MADI ◽  
J.-P. PACCAUD ◽  
G. STEIGER ◽  
J. A. SCHIFFERLI

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