IgA Nephropathy: Acute Renal Failure, Acute Tubular Necrosis, and Features of Postinfectious Acute Glomerulonephritis

Abstract

From 1976 to 1987 on our Nephrological Unit, 57 patients with IgA nephropathy (IgAN) proven by renal biopsies were found. Three of those presented with acute tubular necrosis (ATN) and glomerulitis, without extrarenal predisposing cause in two; and showed, as prominent manifestation, a severe acute renal failure syndrome (ARFS), needing dialytic treatment. All three had hematuria, which was macroscopic in two and microscopic in one. Thus the prevalence of the association of glomerulitis and ATN was about 5.2%. There was complete recovery of renal functions in all three patients, but the usual symptomatology of IgAN. Two patients presented polymorphonuclear neutrophils infiltration of glomerular capillaries and in one of them, electron-dense deposits on the epithelial side of glomerular basement membrane ("humps") were observed, as well as those identified in the mesangial area. The glomerular polymorphonuclear neutrophils infiltration and endothelial cells proliferation (cases 1 and 3), the presence of "humps" (case 1), high antistreptolysin O (ASO) titers (cases 1 and 2), and low serum complement levels (case 1), suggest the possibility that antigens able to cause postinfectious glomerulonephritis (streptococcal or not) could induce in some individuals, by another immunopathogenetic route, mixed histopathological and clinical features of IgAN and postinfectious glomerulonephritis.

Protection of Renal Ischemia Injury using Combination Gene Silencing of Complement 3 and Caspase 3 Genes

“…It has been documented that I/R injury is associated with complement activation (1) and renal cell apoptosis (2). Both anaphylatoxin (C3a, C5a)-dependent and membrane attack complex-dependent mechanisms have been proposed as means by which the complement cascade induces tissue injury in animal models of renal I/R injury (3)(4)(5)(6)(7).…”

Preventing Renal IschemiaReperfusion Injury Using Small Interfering RNA by Targeting Complement 3 Gene

“…In addition, ischemic acute renal failure, conventionally referred to as acute tubular necrosis (ATN) (2), has a high mortality rate, approaching an average of 50% in some series (3). Although the pathogenesis of human ATN is complex and incompletely understood, recent studies in animals have demonstrated a pivotal role for the complement system in mediating renal IRI (4)(5)(6). There appear to be two primary complement pathways in the development of IRI, the classical pathway and the alternative pathway, both dependent on complement activation (7)(8)(9)(10)(11).…”

“…The kidney is unique in organ IRI and complement, since activation subsequent to IRI occurs only via the alternative pathway (12). Both anaphylatoxin (C3a, C5a)-dependent and membrane attack complex (MAC)-dependent mechanisms have been proposed as a means by which the complement cascade induces tissue injury in animal models of renal IRI (4)(5)(6)13,14). The kidney represents a major extra-hepatic site for the synthesis of the third complement component (C3), and therefore, has an important pro-inflammatory role in renal transplantation.…”

Pattern of double glomerulopathy in children

“…PSGN or PIGN is one of the common glomerulopathies superimposed on various types of original glomerular diseases, including IgA nephropathy [3][4][5][6][7][8][9], membranous nephropathy [27], and focal segmental glomerulosclerosis [31]. In the present study, five patients (56%) had PSGN or PIGN as a superimposed glomerulopathy.…”

“…Several reports have concerned IgA nephropathy superimposed by PSGN or PIGN [3][4][5][6][7][8][9]. The incidences of IgA nephropathy and PSGN/PIGN are relatively high, but no relationship between their pathogenesis is known.…”