C1q nephropathy, first proposed by Jennette and Hipp [Am J Clin Pathol 83:415-420, 1985; Am J Kidney Dis 6:103-110, 1985], was described as a distinct glomerular disease entity characterized by extensive mesangial deposition of C1q, with associated mesangial immune complexes, and the absence of any clinical and laboratory evidence of systemic lupus erythematosus. Now, 20 years since the first report, the disease entity is gradually attaining recognition, particularly in the field of pediatrics. C1q is the subcomponent of C1 in the classical pathway of complement activation. Generally, C1q deposition is caused by the activation of C1 by immunoglobulin G (IgG) and IgM; therefore, C1q nephropathy is considered as an immune complex glomerulonephritis. However, in C1q nephropathy, it remains unclear whether the deposition of C1q in the glomeruli is in response to the deposition of immunoglobulin or immune complex, or whether deposition is non-specific trapping that accompanies increased glomerular protein trafficking associated with proteinuria. Since not only the pathogenesis of C1q deposition in glomeruli but also its significance are still uncertain, it has not yet been established as an independent disease. From recent publicati...Continue Reading
Audit of the use of calcium carbonate as a phosphate binder in 100 patients treated with continuous ambulatory peritoneal dialysis
Hepatitis B infection and renal disease: clinical, immunopathogenetic and therapeutic considerations
Nonsystemic mesangiopathic glomerulonephritis with "full house" immunofluorescence. Pathological and clinical observation in five patients
Pan-nephritis (glomerulonephritis, arteriolitis, and tubulointerstitial nephritis) associated with predominant mesangial C1q deposition and hypocomplementemia: a variant type of C1q nephropathy?
An adolescent with relapsing nephrotic syndrome: minimal-change disease versus focal-segmental glomerulosclerosis versus C1q nephropathy
Type I membranoproliferative glomerulonephritis in a renal allograft: A recurrence induced by a cytomegalovirus infection?
De novo C1q nephropathy in the renal allograft of a kidney pancreas transplant recipient: BK virus-induced nephropathy?
HIV-associated immune complex glomerulonephritis with "lupus-like" features: a clinicopathologic study of 14 cases
Segmental membranous glomerulonephritis in children: comparison with global membranous glomerulonephritis
IgG4 anti-phospholipase A2 receptor might activate lectin and alternative complement pathway meanwhile in idiopathic membranous nephropathy: an inspiration from a cross-sectional study
Progressive myoclonus epilepsy with nephropathy C1q due to SCARB2/LIMP-2 deficiency: clinical report of two siblings
World Small Animal Veterinary Association Renal Pathology Initiative: Classification of Glomerular Diseases in Dogs
Megalocytic interstitial nephritis following acute pyelonephritis with Escherichia coli bacteremia: a case report
C1q nephropathy in adults is a form of focal segmental glomerulosclerosis in terms of clinical characteristics
Significance of Glomerular Immune Reactivity in Time Zero Biopsies for Allograft Survival Beyond IgA.
Antibodies: Complement Activation
The complement system can be activated by antigen-associated antibody. In the classical pathway of complement activation, C1q, C4b, and C3b are all able to bind to the Fc portion of IgG or IgM. Find the latest research on antibodies and complement activation here.