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A study of immunofluorescence of unfractionated Type IV collagen, non-collagenous (NC-1) domain of Type IV collagen, basement membrane (GBM) component detected by Goodpasture's syndrome patient's serum and laminin (LN) in the glomeruli from 10 patients with IgA nephropathy was described. Type IV collagen, non-collagenous (NC-1) domain of Type IV collagen, GBM component or LN was observed linearly in the glomerular capillary walls in all patients with IgA nephropathy examined. The deposition of IgA, IgM or C3 was marked in the glomerular capillary walls in patients in the moderate or advanced stage of IgA nephropathy. However, the staining of Type IV collagen, GBM component or LN in such walls was not altered by the depositions of IgA, IgM and C3. In particular, a wrinkled pattern of NC-1 domain of Type IV or GBM component was detected in the glomerular capillary walls of totally sclerotic glomeruli in some patients with IgA nephropathy. It appears that the deposits of IgA and/or C3 did not influence the major components of glomerular capillary walls in patients with IgA nephropathy. It is concluded that the initiating factors of the collapse and/or sclerosis of glomerular capillary walls might be due to various factors other than the deposition of glomerular IgA-dominant immune-complexes in patients with IgA nephropathy.
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PMID:Immunofluorescent studies on IgA nephropathy: type IV collagen and glomerular basement membrane component detected by Goodpasture's syndrome serum and laminin. 307 23

In this analysis of 43 patients with IgA nephropathy, renal morphology was correlated with clinical data. Gross hematuria and mild proteinuria were typical among younger patients. Among older individuals the clinical spectrum was wider. A comparison with data previously obtained from the normal population indicated that disease-related glomerular sclerosis was present in 1/3 of initial biopsy specimens. The prevalent pattern of glomerular sclerosis was that of global tuft collapse, the type of sclerosis known to result from ischemia. Intrarenal vascular sclerosis was present in 1/3 of initial biopsies. Follow-up specimens from 6 patients showed progression of glomerular sclerosis, vascular sclerosis or both. Hypertension occurred in over 1/4 of patients. It is proposed that progressive renal damage in IgA nephropathy may not be solely immunologically mediated. Glomerular sclerosis may also be mediated by vascular sclerosis, or alterations in intrarenal hemodynamics in glomerulonephritis may have a direct damaging effect on both the glomerulus and the intrarenal vasculature.
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PMID:Intrarenal vascular sclerosis in IgA nephropathy. 714 32

IgA nephropathy (IgAN) may present with several histologic patterns, including lesions resembling primary focal-segmental glomerulosclerosis (FSGS). To examine the clinical significance of these lesions, slides from all cases of IgAN diagnosed in our renal biopsy service between 1980 and 1994 for which diagnostic materials were available were reviewed. Eighteen of the 244 cases (7.4%) reviewed showed focal and segmental glomerular sclerosis with capillary collapse, sometimes associated with an overlying "cap" of visceral epithelial cells, and no more than very mild glomerular hypercellularity limited to mesangial areas. All showed mesangial IgA as the major immunoglobulin present by immunofluorescence, and all showed mesangial electron-dense deposits ultrastructurally. The mean age (34.8 +/- 11.0 years [+/- SD]), gender distribution (72% male), and racial distribution (67% white, 17% Hispanic, 11% black, 6% Asian) among the 18 patients with FSGS-like IgAN were similar to those of patients in our population with other histologic lesions of IgAN. Notably, the racial distribution of these patients was different from that of our patients with primary FSGS (> 35% black). Seventy-one percent of patients with FSGS-like IgAN had hematuria, but only one patient had gross hematuria. Eighty-two percent had nephrotic-range proteinuria. The mean serum creatinine (1.6 +/- 1.2 mg/dL; n = 17) and urine protein (5.5 +/- 2.8 g/24 hr; n = 17) levels in these patients at the time of biopsy were not significantly different from mean levels in 42 previously studied patients with primary FSGS (Haas et al, Am J Kidney Dis 26:740-750, 1995). Follow-up data obtained for 11 patients with FSGS-like IgAN (mean follow-up, 70 +/- 25 months; range, 37 to 120 months) showed only one who progressed to end-stage renal failure, with dialysis initiated 74 months postbiopsy. However, renal survival in these 11 patients was not significantly greater than that in the previously studied cohort of primary FSGS patients.
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PMID:IgA nephropathy histologically resembling focal-segmental glomerulosclerosis: a clinicopathologic study of 18 cases. 880 34

Periglomerular fibrosis (PF) is an interstitial injury observed in various renal diseases. It is speculated that this lesion, by occluding the glomerulo-tubular junction (GTJ) and causing atubular glomeruli, may result functionally in a reduction of the glomerular filtration rate (GFR) and may be a factor contributing to the progression of renal disease. In the present study, 340 renal biopsy specimens were analysed to determine whether or not there was nephron injury derived from such a mechanism, as well as direct glomerular injury, in IgA nephropathy (IgAN). The patients were divided into five groups according to the degree of glomerular sclerosis. The average age was lower in groups with milder sclerosis and serum creatinine (Cr) was elevated in groups with more severe sclerosis. Because the GTJ was assumed to disappear when an atubular glomerulus was formed, the ratio of the number of glomeruli with discernible GTJ to the total number of glomeruli was evaluated. As glomerular sclerosis progressed, discernible GTJ reduced significantly (p <0.001) and the degree of PF increased significantly (p <0.05). By serial section study in cases with pronounced PF, transitions between the stages of stenosis of the GTJ and atubular glomeruli were observed. It is speculated that the occlusion of the GTJ eventually hyalinizes the glomerulus; in such cases, glomerular obsolescence of the collapse type might be formed. On the other hand, obsolescence of the mesangial proliferative type might be formed in the hyalinization derived from direct glomerular injury. In this context, glomerular obsolescence of the collapse type was observed more frequently and was accompanied by more increased PF than obsolescence of the mesangial proliferative type (p <0.001). These results suggest that in addition to direct glomerular injury, nephron injury derived from interstitial damage of this type plays an important contributory role in the progression of IgAN.
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PMID:Glomerulo-tubular junction stenosis as a factor contributing to glomerular obsolescence in IgA nephropathy. 1208 Nov 94

Post-infectious glomerulonephrites (GNs) include a wide spectrum of nephropathies, with known etiological agent, bacterial, parasitic, viral. Among GNs secondary to bacterial infections, post-streptococcal GN is the most frequent; nevertheless, its incidence in developed countries has decreased during the last 20 years, while some of the characteristics such as types of infection, exposed subjects, clinical and evolutionary patterns have changed. Prognosis has worsened and is correlated with some clinical and histological parameters. The viral infection-related GNs include those associated with HBV, HCV, HIV plus other rarer forms. Membranous GN (MGN), membranoproliferative GN (MPGN) and IgA nephropathy may occur in the course of HBV infection, while different GNs can be detected in relation to HCV, the most frequent being mixed cryoglobulinemic GN, a MPGN with peculiar morphological features. Multiple glomerular involvements are seen from HIV infection, the more characteristic form being the so-called HIV associated nephropathy (HIVAN), a focal segmental glomerulosclerosis with tuft collapse affecting African subjects, which starts with a nephrotic syndrome and rapidly develops into uraemia. Other GNs derive from HIV-related immunecomplexes, some with diffuse proliferative characteristics, or lupus like, with less severe clinical manifestations compared with HIVAN. Among the rare viral infections, we ultimately, mention the association between Parvovirus B19 and "collapsing" focal segmental glomerulosclerosis.
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PMID:[Post-infectious glomerulonephritis]. 1274 5

Human immunodeficiency virus (HIV) involves glomerular, tubulointerstitial, and vascular compartments of the kidney. The most common glomerular lesion is HIV-associated focal segmental glomerulosclerosis (FSGS) and related mesangiopathies collectively termed HIV-associated nephropathy (HIVAN). A variety of immune-complex mediated glomerular diseases such as membranoproliferative glomerulonephritis (MPGN), IgA nephropathy, and lupus-like glomerulonephritis also occur. HIVAN is restricted to patients presenting with proteinuria and progressive reduction of renal function and with distinctive but not pathognomonic pathology (FSGS often coexisting with glomerular collapse and tubular microcystic dilatations). The worldwide incidence of collapsing glomerulopathy (CG) in HIV-positive patients is high in Americans. But in India and other Asian countries, other forms of kidney diseases are more commonly seen. We report the first case of CG in the state of Jammu and Kashmir which also happens to be a very low incidence belt for HIV.
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PMID:Collapsing glomerulopathy in an HIV-positive patient in a low-incidence belt. 2120 85

Collapsing glomerulopathy (CG) is a pathological entity characterized by collapse and wrinkling of glomerular tuft, podocyte dedifferentiation and hyperplasia. CG may be idiopathic or secondary to other diseases. CG has been described with IgA nephropathy, membranous glomerulopathy, diabetic nephropathy, and lupus nephritis. However, till date there is no report of CG in association with the anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV). Here, we present a case of CG that developed during follow-up in a case of AAV with biopsy proven pauci-immune glomerulonephritis.
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PMID:Collapsing glomerulopathy in a case of anti-neutrophil cytoplasmic antibody associated vasculitis. 2705 Nov 40