Histologically confirmed superimposition of post-streptococcal acute glomerulonephritis during IgA nephropathy

We describe a 39-year-old Japanese man with post-streptococcal acute glomerulonephritis (PSAGN) super-imposed on long-term immunoglobulin A nephropathy (IgA-N). The histological findings of the first renal biopsy, done at 21 years of age, revealed mild mesangial proliferative glomerulonephritis with mesangial IgA deposition. Nineteen years later, acute nephritic syndrome with hypocomplementemia and an increasing anti-streptolysin O (ASO) titer developed 2 weeks after the onset of an upper respiratory infection. A second renal biopsy revealed severe segmental endocapillary proliferative and exudative glomerulonephritis, with fibrocellular crescents in about 40% of the glomeruli. Immunofluorescence showed that more C3 than IgA was deposited in the mesangium and that the IgA deposits had decreased. Electron microscopy revealed hump electron-dense deposits on the epithelial side of the glomerular basement membrane. These features were consistent with PSAGN superimposed on IgA-N. After 2 weeks of observation, blood pressure, C3 level, and ASO titer had returned to normal, although the persisting nephritic syndrome necessitated steroid therapy. Six months after the onset of the acute nephritic syndrome, the patient remained asymptomatic, except for microhematuria.     

Primary antiphospholipid antibody syndrome and mesangial IgA glomerulonephritis

The antiphospholipid antibody syndrome (APS) is characterized by recurrent thrombosis, fetal loss, multiorgan involvement, and the presence of lupus anticoagulant and/or anticardiolipin antibody. When not associated with systemic lupus erythematosus, other collagen diseases, or ingestion of medications, the condition is called primary APS. The kidney may be involved in the APS syndrome with acute nephritis and renal failure. The cases with renal biopsy studies have shown variable glomerular morphology, ranging from mild mesangial changes to a diffuse endocapillary proliferative glomerulonephritis. The most frequent lesion is thrombotic microangiopathy or features seen in the hemolytic uremic syndrome. Apart from fibrin thrombus deposition, only a few cases have shown focal and segmental deposits of IgG and/or IgM and/or C3. We describe a patient with primary APS who had thrombosis with lower limb amputation and acute renal failure. The renal biopsy specimen showed a focal proliferative glomerulonephritis with endothelial proliferation and damage, with diffuse heavy mesangial deposits of IgA and fibrinogen. This case with diabetes mellitus, but without diabetic nephropathy, represents the occurrence of primary APS and mesangial IgA nephropathy which potentiated the renal injury, leading to acute renal failure. The relationship to the Henoch-Sch?nlein syndrome is discussed.     

Superimposition of poststreptococcal acute glomerulonephritis on the course of IgA nephropathy

A 17-year-old male with poststreptococcal acute glomerulonephritis (PSAGN) superimposed on the course of IgA nephropathy is presented. The histological findings of the first renal biopsy showed mild IgA nephropathy with a mesangial deposition of IgA and C3. Eighteen months later, acute nephritic syndrome with hypocomplementemia and rising antihyaluronidase titer occurred 10 days following the onset of an upper respiratory infection. The second renal biopsy revealed severe diffuse endocapillary proliferative and exudative glomerulonephritis with cellular crescents in 70% of the glomeruli. Immunofluorescence showed granular staining of C3 alone along the capillary walls. The pre-existing IgA deposits had disappeared. Typical 'humps' were observed by electron microscopy. The symptoms were gradually resolved by intensive steroid and anticoagulant therapy. Five months after the episode of acute nephritic syndrome, the patient was clear of symptoms except for mild proteinuria and hematuria. The third renal biopsy at that time showed morphologic changes similar to those of the first renal biopsy with mild mesangial IgA deposits.     

IgA-associated glomerulonephritis with membranoproliferative glomerulonephritis-like pattern in two children

In this article, we report two patients with IgA-associated glomerulonephritis with a membranoproliferative glomerulonephritis (MPGN) -like pattern. Both patients had nephrotic syndrome at onset. One patient was treated with high-dose alternate-day prednisolone (PSL), and the other with indomethacin and low-dose PSL. One lost the urinary abnormalities 3 years after starting treatment. The other lost the nephrotic state and hematuria over a 5-year period, but proteinuria persisted until the last follow-up. Both patients had diffuse proliferative changes with mesangial interposition and subendothelial deposits, associated with strongly positive deposits of C3 and IgA along the capillary walls of the glomeruli. These two patients showed histological changes compatible with type-I MPGN, but the pattern of IgA deposits was not typical of idiopathic MPGN or IgA nephropathy. We assume this is a rare form of MPGN, not associated with liver disease or other systemic diseases.     

Patient with diffuse mesangial and endocapillary proliferative glomerulonephritis with hypocomplementemia and elevated anti-streptolysin O treated with prednisolone, angiotensin-converting enzyme inhibitor, and angiotensin II receptor antagonist

A 24-year-old woman was admitted to Toyosaka Hospital with proteinuria, hematuria, lymphopenia, hypocomplementemia, positive anti-nuclear antibody (ANA), and elevation of anti-streptolysin O (ASO). Renal biopsy specimen revealed diffuse mesangial and endocapillary glomerulonephritis with crescent formation and duplication of the capillary loop on light microscopic examination. Mild to moderate proliferation of mesangial matrix and cells were observed. On immunofluorescence (IF) examination, deposition of IgG, IgA, IgM, C1q, C3, and C4 to the mesangium and capillary wall were observed. By electron microscopy (EM), mesangial, subendothelial, and subepithelial deposits were recognized. However, microtubular structure in glomerular endothelial cells, fingerprint structures, and circumferential mesangial interposition were not observed by EM. The patient was referred to our hospital, but there was no change in her proteinuria 3 weeks after admission. The elevation of ASO, hypocomplementemia, and endocapillary proliferation suggested acute glomerulonephritis, while lymphocytopenia, positive ANA, the persistent hypocomplementemia, and various deposits detected by IF and EM suggested lupus nephritis; however, she did not fulfill the classification criteria of systemic lupus erythematosus. We started prednisolone (40mg/day) with the diagnosis of chronic glomerulonephritis revealing diffuse mesangial and endocapillary proliferative glomerulonephritis, but it was not effective for the proteinuria. Quinapril (10mg/day) and losartan (25 to 50mg/day) were administered and the proteinuria decreased. It is possible that this use of an angiotensin converting-enzyme inhibitor and an angiotensin II receptor antagonist was effective in reducing the proteinuria in this patient.     

Dense intramembranous deposit disease: new pathologic features

The pathologic and clinical features of 16 patients with dense intramembranous deposit disease are described. By light microscopy nine patients had membranoproliferative glomerulonephritis, five had focal segmental necrotizing glomerulonephritis with segmental epithelial crescents, four of whom also had a prominent tubulointerstitial nephritis, and two had focal segmental mesangial proliferative glomerulonephritis. The patients with membranoproliferative glomerulonephritis and one with focal segmental mesangial proliferative glomerulonephritis had easily recognizable dense intramembranous deposits by optical microscopy. The patients with focal segmental necrotizing glomerulonephritis and one with focal segmental mesangial proliferative glomerulonephritis did not have recognizable peripheral loop dense intramembranous deposits even under oil immersion. In patients with membranoproliferative glomerulonephritis ultrastructural examination revealed extensive capillary wall dense intramembranous deposits. Immunofluorescence revealed diffuse double linear staining along the capillary walls and "mesangial rings" of C3. In the patients with focal segmental necrotizing glomerulonephritis and one with focal segmental mesangial proliferative glomerulonephritis the immunofluorescence study suggested a diagnosis of dense intramembranous deposit disease because of the segmental double linear staining of the capillary walls and "mesangial rings" of C3, but the diagnosis was only established by fine structural analysis where occasional peripheral loop and prominent paramesangial basement membrane dense intramembranous deposits and mesangial nodular deposits were identified. Clinical features prior to biopsy included nephrotic syndrome in eight patients, an acute nephritic syndrome in six patients, and asymptomatic proteinuria and hematuria in two patients. Five of six patients with an acute nephritic presentation had focal segmental necrotizing glomerulonephritis. The acute renal insufficiency in these patients was transitory and appeared to be related to a prominent acute tubulointerstitial nephritis present in four of the biopsy specimens. Depressed serum C3 levels were present in patients with membranoproliferative glomerulonephritis; patients with focal segmental lesions were normocomplementemic. Because of the "atypical" light microscopic features in six of our patients, we support the suggestion that membranoproliferative glomerulonephritis, type II be replaced by the term 'dense intramembranous deposit disease' for this glomerulopathy with variable clinical and histologic features.     

Acute poststreptococcal glomerulonephritis superimposed on IgA nephropathy

Superimposition of poststreptococcal glomerulonephritis (PSGN) on the course of IgA nephropathy (IgAN) is uncommon. A case of PSGN during IgA nephropathy is presented. A 30-year-old man who had alternating gross and microscopic hematuria for 7 months underwent a renal biopsy. The first renal biopsy revealed IgAN with mesangial deposits of IgA and C3. Two months later, the patient suffered generalized edema, proteinuria, hematuria, an increased ASO titer and a decreased C3 level. A second renal biopsy revealed diffuse endocapillary proliferative glomerulonephritis with epimembranous hump-like electron-dense deposits of C3, but the original mesangial IgA deposits had disappeared. A diagnosis of acute PSGN was indicated. Two months after the onset of acute nephritic syndrome, the patient remained asymptomatic, except for microscopic hematuria and proteinuria. Some cases with persistent proteinuria or hematuria after PSGN are probably related to preexisting IgAN.     

Immunopathological findings in idiopathic nephrosis: Clinical significance of glomerular “immune deposits”

Idiopathic nephrosis (IN), which includes minimal change (MCD), diffuse mesangial proliferation (DMP) and focal segmental glomerular sclerosis (FSGS), is classically characterized by the absence of significant deposits by immunofluorescence microcopy (IF), except for the focal lesions of segmental sclerosis and/or hyalinosis of FSGS, which fix IgM and C3 antiserums. Since IF is available in most centres, an increasing number of unexpected findings has been reported. In order to evaluate the clinical significance of the glomerular deposits revealed by IF in some instances, we reviewed the renal biopsy findings of 222 consecutive children presenting with IN and in whom IF microscopy was available. By light microscopy, 122 patients showed MCD, 10 DMP, and 90 FSGS with DMP (11 cases) or without (79 cases). By IF, 125 specimens were negative and served as controls; 54 showed mesangial IgM deposits, 24 mesangial IgG deposits (associated with Clq deposits in 16), 15 scattered granules of C3 and 4 predominant deposits of mesangial IgA. We correlated these findings with initial response to steroid therapy and outcome and could find no significant difference between the various categories defined by IF and the control group. Repeat biopsies, performed in 21 cases, showed the persistence of deposits in 11 and their transformation in 10. The particular problem raised by the patients who present with IN and mesangial IgA deposits is discussed. Our results demonstrate that patients presenting with IN and positive IF, whether showing IgM, IgG and Clq, C3 or IgA, do not represent distinct clinicopathological entities.     

IgA deficiency with membranous glomerulonephritis: a case report and review

Selective immunoglobulin A (IgA) deficiency may result in a predisposition to recurrent sinopulmonary infection and allergic diseases. IgA deficiency may also play a role in the development of autoimmune disorders. Selective IgA deficiency associated with glomerulonephritis was rare, while the clinical presentation in IgA deficiency-associated glomerulonephritis was variable. We report an 83 year-old male with selective IgA deficiency associated with membranous glomerulonephritis. He presented with nephrotic syndrome. Percutaneous renal needle biopsy showed diffuse global thickening and rigidity of glomerular capillary walls, mildly diffuse segmental expansion of mesangial matrix, focal and cortical scar with segmental obsolescence of glomeruli. Heavy IgG and moderate C3 deposits were found on immunofluorescence. We also review the previous cases of IgA deficiency with glomerulonephritis. Several clues were rendered to establish the association between IgA deficiency and membranous glomerulonephritis.     

IgA nephropathy: lessons from an animal model, the ddY mouse

IgA nephropathy is the most common primary chronic glomerulonephritis, and was first described by J. Berger (Transplant Proc. 1969;1:939-944). Histopathologically, IgA nephropathy is characterized by expansion of glomerular mesangial matrix, with mesangial cell proliferation. Glomeruli typically contain generalized-diffuse granular mesangial deposits of IgA, IgG and C3. Since pathogenesis of IgA nephropathy is still obscure, it is important to try to determine the initiation and progression of this disease using a suitable animal model. Several investigators, including Rifai's group (Rhode Island, USA) and Emancipator's group (Cleveland, Ohio, USA), reported various experimental animal models for this disease. In 1985, Imai et al first reported that the ddY strain of mouse can serve as a spontaneous animal model for IgA nephropathy. These mice show mild proteinuria without hematuria, and mesangioproliferative glomerulonephritis with severe glomerular IgA deposits in association with an increase of serum IgA level (Imai et al. Kidney Int. 1985;27:756-761). Electron-dense deposits are observed in the glomerular mesangial areas by electron microscopy. Furthermore, Muso's group succeeded in generating a mouse model of IgA nephropathy with a high incidence and early onset of glomerular IgA deposition (Miyawaki et al. Nephron. 1997;76:201-207). The selection procedure was successful in increasing the serum IgA level of the selected line. The selected ddY line (HIGA mice) showed only mild proteinuria (100-300 mg/dL) and did not show hematuria. These immunohistopathological findings in ddY mice resemble those in IgA nephropathy patients. The objectives of this review are to introduce the genetic background, Th1/Th2 polarization, expansion of extracellular matrices (ECMs) and treatment of IgA nephropathy of the ddY mouse. These findings from the ddY mouse appear to be useful in determining the pathogenesis and treatment of patients with IgA nephropathy.     

Pathogenetic and therapeutic approaches to IgA nephropathy using a spontaneous animal model,the ddY mouse

IgA nephropathy is the most common primary chronic glomerulonephritis in the world and was first described by Berger et al. (J Urol Nephrol 74:694–695;1968). Histopathologically, IgA nephropathy is characterized by expansion of the glomerular mesangial matrix with mesangial cell proliferation. Glomeruli typically contain generalized diffuse granular mesangial deposits of IgA (mainly IgA1), IgG and C3. In advanced patients, global glomerular sclerosis, crescent formation and tubulo-interstitial fibrosis are marked in light microscopy. IgA nephropathy is generally considered to be an immune-complex mediated glomerulonephritis. Although more than 40 years have passed since this disease was firstly described, the pathogenesis/initiation factors of IgA nephropathy are still obscure. The objective of this review is to explain the pathogenesis and treatment based on our previous data of ddY mouse, a spontaneous animal model for IgA nephropathy.     

IgA nephropathy in patients with familial Mediterranean fever

Two patients with a long-standing history of familial Mediterranean fever were found to have both microscopic hematuria and proteinuria during the acute attacks. Kidney biopsies from both patients revealed diffuse mesangial proliferative glomerulonephritis with intense mesangial IgA and C3 deposits and no evidence of amyloidosis. To our knowledge these are the first 2 cases documenting the presence of mesangial IgA nephropathy in patients with familial Mediterranean fever.     

IgM nephropathy: clinical picture and pathological findings in 36 patients

Immunoglobulin M nephropathy (IgMN) is an idiopathic glomerulonephritis characterized by a variable degree of mesangial hyper- cellularity and diffuse IgM deposits. This study describes the clinical presentation and the morphological findings in 36 patients, five adults and 31 children, with IgMN. The initial manifestations of the disease were the nephrotic syndrome in 32 patients, proteinuria in two, hematuria associated with proteinuria in 16 and isolated recurrent gross hematuria in two patients. The nephrotic syndrome was steroid responsive in 9% of the cases, steroid dependent in 25% and steroid resistant in 66%. Five patients were hypertensive at the onset of the disease. The mean follow- up period was 3.4 years (range, 1-7 years). One patient developed end- stage kidney disease five years after the diagnosis. On light microscopy, 24 specimens showed mild focal and segmental mesangial hyper- cellularity, 10 cases were normal in cellularity and two cases showed diffuse global mesangial hyper- cellularity. Four cases showed focal and segmental glomerulosclerosis. Mild interstitial inflammation and fibrosis were observed in 11 cases and focal tubular atrophy and hypertensive hyaline arteriosclerosis were noted in three cases. In addition to IgM, the immunofluorescence study showed C3 deposits in 12 cases, IgG in nine cases and IgA in one case. Electron dense- deposits in the mesangium and para- mesangial areas were demonstrated on electron microscopy in 22 cases. In view of its different clinical presentations and the constant findings of diffuse mesangial IgM deposition in all the cases, it is concluded that this form of nephropathy constitutes a distinct entity separate from minimal change disease or focal and segmental glomerulosclerosis. Patients with IgMN had a higher prevalence of steroid resistance and dependence in the proteinuric group.     

Histology and immunohistology of IgA nephropathy

IgA nephropathy is a histologically diverse glomerular disease characterized by mesangial or mesangial plus peripheral glomerular capillary immune complex deposits that contain IgA as the dominant or co-dominant immunoglobulin type. The most common histologic manifestation of IgA nephropathy is mesangial proliferative glomerulonephritis (GN), most often focal but not infrequently diffuse. However, the light microscopic appearance of IgA nephropathy spans the entire range from histologically normal to diffuse proliferative and crescentic glomerulonephritis, much as is the case with lupus nephritis. This review examines the histologic diversity as well as the immunohistologic features of IgA nephropathy.     

Fibrillary glomerulonephritis associated with monoclonal gammopathy of undetermined significance showing lambda-type Bence Jones protein

A 79-year-old woman was admitted to our hospital because of leg edema due to a nephrotic syndrome. Urinary and serum immunoelectrophoresis showed positive for the lambda type of Bence Jones protein. A bone marrow aspiration test revealed mild plasmacytosis (6.4% of the total cells). These findings confirmed her diagnosis of monoclonal gammopathy of undetermined significance (MGUS). Her renal biopsy specimen revealed mild mesangial cell proliferation and an increase in the mesangial matrix. Immunofluorescence studies showed positive staining for IgG, IgA, C3, and kappa and lambda light chains in the capillary wall and mesangium area. Electron microscopy showed that the electron deposits in the thickened basement membrane were formed by randomly arranged 16- to 18-nm nonbranching fibrils. A Congo red stain for amyloid was negative. These findings corresponded with the diagnosis of fibrillary glomerulonephritis. Therefore, this case showed a rare combination of fibrillary glomerulonephritis and MGUS.     

Clinicopathological study of patients with mesangial isolated C3d deposition in various glomerular diseases

The clinicopathological findings of isolated mesangial C3d deposition in the absence of other complement components or immunoglobulins are summarized. 55 out of 242 individual human renal biopsies examined by immunoperoxidase microscopy had isolated C3d deposition. This group consisted of 12 patients with chronic glomerulonephritis, 8 with minimal-change nephrotic syndrome, 32 with benign recurrent hematuria, 2 with Bartter's syndrome and 1 with Raynaud's syndrome. None of these patients had a disorder of the renal function and in all the patients the disease took a benign clinical course. Light-microscopic findings indicated injuries ranging from minor glomerular abnormality to mild diffuse mesangial proliferative glomerulonephritis, and there were no other remarkable findings such as cellular crescents, global sclerosis or interstitial infiltration. By immunoperoxidase microscopy, fine granular deposits of C3d were identified only in the mesangium, and arteriolar C3 staining was seen in 31 of the 55 patients. In 38 of the 42 patients examined by electron microscopy, electron-dense deposits were identified in the mesangial matrix. These findings suggest that isolated C3d deposition is a new entity with benign features both clinically and pathologically.     

How frequent is glomerulonephritis in diabetes mellitus type II?

A high frequency of glomerulonephritis (GN) in diabetics, or coexistence of GN with diabetic glomerulosclerosis, has been reported by previous authors, but the true prevalence of GN in diabetics remains to be established. In the Department of Pathology, Heidelberg, from 1.1.1987 to 31.12.1989 we examined all consecutive patients (89 male, 121 female, median age 74 years; 47-98) who came to autopsy with the diagnosis of "diabetes mellitus" to assess this issue in an unbiased sample. Five patients had known type I diabetes, the others type II diabetes or diabetes of unknown classification. In 61/159 patients, proteinuria had been present (no information in 51 patients) and in 99/169 patients renal failure, i.e. serum creatinine above 1.4 mg/dl (no information in 41 patients). Paraffin-embedded kidney specimens from the upper pole of the left kidney were examined by immunohistochemistry (PAP technique; rabbit antihuman IgG; IgM; IgAab). 166/210 of the patients had glomerulosclerosis by light microscopy (129 diffuse, 37 nodular GS). Concomitant glomerulonephritis, i.e. typical mesangial IgA (and IgG) deposits, with mesangial enlargement by light microscopy were detected in only one case. Membranous GN was not found. These findings must be interpreted against the observation of mesangial immune deposits in 6 of 250 consecutive non-diabetic patients who had come to autopsy [Waldherr et al. 1989]. The findings show that an excessive prevalence of undiagnosed glomerulonephritis in our cohort of elderly type II diabetics was not to be found.     

强直性脊柱炎肾损害的临床病理特点

目的探讨强直性脊柱炎（AS）合并肾损害的临床及病理特点。方法回顾性分析18例经肾脏活体组织检查的AS患者的临床及肾脏病理表现。结果18例患者中,9例呈隐匿性肾小球肾炎表现,5例呈慢性肾小球肾炎表现,1例呈肾病综合征表现,3例为慢性肾功能不全;4例血压增高,14例血压正常。24h尿蛋白定量平均为（1．17±1．39）g。15例肾功能正常,3例肾功能异常患者血肌酐平均为（153．2±36．8）umol／L。8例患者血清IgA水平升高,10例c反应蛋白升高,13例红细胞沉降率（EsR）增快,且血清IgA水平和C反应蛋白呈正相关（r=0．707,P=0．001）,血清IgA水平和ESR呈正相关（r=0．858,P〈0．001）。病理检查结果发现15例为IgA肾病（其中10例为轻度系膜增生性肾炎,1例为轻度系膜增生性肾炎并慢性肾小管间质肾病,2例为局灶增生性肾炎,1例为局灶增生坏死性肾炎,1例为局灶节段性肾小球硬化症）,1例为膜性肾病,1例为局灶增生性肾炎伴慢性肾小管间质肾病,1例为慢性。肾小管间质肾病。有慢性肾小管间质肾病者均有服中药史。结论AS相关性肾损伤的病理改变多样,但主要为IgA肾病,也可表现为膜性肾病、局灶增生性肾炎和慢性肾小管间质。肾病,其肾损伤可能与AS疾病本身和（或）治疗用药相关。     

Enhanced expression of the CD71 mesangial IgA1 receptor in Berger disease and Henoch-Schönlein nephritis: association between CD71 expression and IgA deposits

ABSTRACT. IgA nephropathy (IgA-N) that comprises Berger disease and Henoch-Sch?nlein Purpura (HSP) nephritis is defined by mesangial IgA deposits. Recently, this group has characterized a new receptor for IgA, the transferrin receptor (CD71), expressed on mesangial cells. To assess whether CD71 was involved in the pathogenesis of IgA-N, its expression was analyzed together with IgA deposits on 16 kidney biopsies from 16 patients with Berger disease (n = 4) or HSP (n = 12). These biopsies were compared with 17 kidney biopsies of a group of 15 patients (control group) with other glomerulonephritis, including systemic lupus erythematosus, poststreptococcal acute glomerulonephritis, membranoproliferative glomerulonephritis, steroid-sensitive minimal change nephrotic syndrome, steroid-resistant idiopathic nephrotic syndrome with focal and segmental glomerulosclerosis, and persistent and isolated proteinuria with minimal change on kidney biopsy. In this control group, IgA deposits could be observed in eight kidney biopsies of seven patients. These biopsies were also compared with normal kidney specimens (normal group). In normal kidney, it was found that CD71 was linearly expressed on tubular epithelium but was either not expressed or very dimly in glomeruli. In contrast, CD71 was strongly expressed in 105 of the 107 glomeruli of the kidney biopsies from the IgA-N group. For the control group, it was found that expression of CD71 in glomeruli was correlated to the presence of IgA deposits. Indeed, among the 87 glomeruli of nine kidney biopsies (eight patients) without IgA fixation, 78 exhibited no CD71 expression and nine exhibited a very dim one. On the other hand, all 49 glomeruli of the eight kidney biopsies (seven patients) in which IgA deposits were detected exhibited CD71 expression (P < 10(-4)). Performance of dual-labeling studies with confocal microscopy on kidney biopsies of IgA-N patients demonstrated that most of the IgA deposits co-localized with CD71. It was also demonstrated that the intensity of the expression of CD71 was not linked to the intensity of clinical or biologic findings but to the intensity of cellular proliferation in both IgA-N and control groups. These results show that mesangial CD71 expression is not specific to IgA-N. However, the association between IgA deposits and CD71 expression and their co-localization in the mesangium provide strong evidence that CD71 is a major IgA receptor on mesangial cells.     

Histological features of IgA glomerulonephritis as predictors of pregnancy outcome

116 pregnancies undertaken by 70 women with IgA glomerulonephritis and their diagnostic renal biopsies have been reviewed. An IgA diffuse mesangial proliferative lesion with superimposed focal and segmental proliferative lesions (IgA FSP) on diagnostic renal biopsy was associated with a greater incidence of maternal complications than IgA diffuse mesangial proliferative glomerulonephritis with no superimposed lesions (IgA DMP) and IgA diffuse mesangial proliferative glomerulonephritis with superimposed focal and segmental hyalinosis and sclerosis (IgA FSHS) (p less than 0.025). Patients with severe vessel lesions had a significantly greater incidence of fetal loss than those with only mild to moderate lesions (p less than 0.025).