GLOMERULONEPHRITIS ASSOCIATED WITH LIVER CIRRHOSIS

The glomerular changes of 50 autopsy cases of liver cirrhosis of different etiologies, such as alcohol abuse, HB virus infection, and nonA–nonB virus infection, were studied by light, immunofluorescence and electron microscopy. The glomerular changes observed were as follows; membranoproliferative glomerulonephritis (MPGN) type 1 (7 cases), mild form or early stage of MPGN type 1 (7 cases), mesangial proliferative glomerulonephritis with sub–endothelial deposits (13 cases), and mesangial proliferative glomerulonephritis without subendothelial deposits (12 cases). These glomerular changes were frequently accompanied by predominant IgA deposition (78% of the immunofluorescence positive cases). Minimal glomerular changes without electron dense deposits were 11 cases, in which IgA was not present in the glomeruli. Thus, glomerulonephritis associated with liver cirrhosis has revealed a]spectrum'of glomerular changes from MPGN type 1 to mesangial proliferative glomerulonephritis with a common feature of predominant IgA deposition, despite various etiological factors of liver cirrhosis, such as alcohol abuse, hepatitis B virus infection, and nonA–nonB virus infection. A pathophysiological condition of liver cirrhosis, e.g. reduced phagocytic activity of the reticuloendothelial system of the cirrhotic liver, Is thought to be a major factor for development of these glomerular changes. The pathogenesis of IgA predominant glomerulonephritis associated with liver cirrhosis may be concerned in the pathogenesis of IgA nephropathy, which still remains to be clarified. ACTA PATHOL. JPN. 33: 333–346, 1983.     

Morphologic variations of dense deposit disease: Light and electron microscopic,immunohistochemical and clinical findings in 10 patients

Twenty-one renal biopsy specimens obtained from 10 patients with dense deposit disease (DDD) were investigated using light microscopy, electron microscopy and immunohistochemistry. The patients included four females and six males aged 6 to 35 years (mean 16.1 years). A morphological diagnosis of DDD was made following the ultrastructural detection of continuous intramembranous dense deposits (CIMDD) in some capillary loops of at least one of the series of the repeated biopsies from each patient. With light microscopy, six patients showed membranoproliferative glomerulonephritis (MPGN). The other four patients showed diffuse proliferative glomerulonephritis (DPGN) with acute lesions showing intraglomerular neutrophilic infiltration, hump formation and endothelial swelling in three and minor glomerular abnormalities in one. Follow-up biopsies were obtained in six patients. Two patients progressed from DPGN to MPGN within 7 months, whereas three patients with MPGN showed morphologic improvement that featured increased capillary patency and regional disappearance of dense deposits along with the reduction of proteinuria. Dense deposit disease did not always feature typical amorphous and osmiophilic CIMDD spreading across the whole width of the lamina densa. This classical ultrastructural manifestation was mainly found in the patients with histologic non-MPGN and a linear peripheral pattern of complement component (C3) deposition. The MPGN patients with a granular peripheral pattern of C3 deposition also had CIMDD, but also additionally featured less dense subepithelial deposits superimposed on the CIMDD to produce an appearance simulating membranous transformation. Humplike epimembranous massive dense deposits were also identified in connection with the deposition of immunoglobulin G (IgG), suggesting that immune complex deposition at the glomerular basement membrane occurs in some cases of DDD. Immunoglobulin M (IgM) or complement component 1q (C1q) deposition was often associated with intraglomerular neutrophilic infiltration and endothelial swelling as well as with ultrastructural subendothelial edema. Continuous dense deposits were found not only in the lamina densa but also just beneath the subendothelium in four patients. Thus, the present investigation demonstrated the morphologic variety of DDD in a correlative study of light microscopy, electron microscopy and immunohlstochemistry.     

Diffuse proliferative glomerulonephritis—how many types?

Fifty-four biopsies of diffuse proliferative glomerulonephritis were subdivided into two groups, diffuse endocapillary proliferative glomerulonephritis (DEPGN) and mesangial proliferative glomerulonephritis (MPGN) according to current morphological criteria. The two groups were then compared by light microscopy, cell counting techniques, electron microscopy, immunofluorescence or immunoperoxidase techniques, and a clinical survey. The results show that DEPGN differs from MPGN in only three points: (1) the former has a greater degree of mesangial proliferation, (2) the former has a less favourable short-term prognosis and (3) large subepithelial deposits (humps) are much more common in DEPGN than in MGPN (in this series no MPGN cases showed such deposits), while small dark deposits are present in or on the glomerular capillary basement membrane in more cases of MPGN than of DEPGN. It is proposed that biopsies showing diffuse proliferation of mesangial cells should be classified as diffuse proliferative glomerulonephritis of a mild, moderate or severe degree, as the current classification has been interpreted as implying separate aetiologies and suggests that these are two distinct disease entities.     

Experimental proliferative glomerulonephritis in the cat.

A model of chronic serum sickness was used to induce immune-complex glomerulonephritis in seven experimental cats, by daily intravenous inoculation of an increasing dose (5 to 35 mg) of human serum albumin (HSA). At week four, two of the seven animals developed anterior uveitis. At week 23, two different animals developed the subcutaneous oedema characteristic of the nephrotic syndrome (NS), whilst the other five cats appeared clinically normal. The kidneys were examined at necropsy by light microscopy and by transmission electron microscopy. The glomeruli of four animals (three with both proteinuria and uraemia, and one with proteinuria only) showed morphological changes under light microscopy. The abnormalities suggested that a diffuse mesangial proliferative glomerulonephritis (GN) had been induced in three cats and diffuse membranoproliferative GN induced in another. Ultrastructural studies revealed electron-dense deposits (immune-complexes) in six of the seven cats. Two cats without glomerular abnormalities by light microscopy had mesangial deposits and three cats with mesangial proliferative GN had deposits at mesangial, subendothelial and/or subepithelial sites. The single cat with membranoproliferative GN had deposits at mesangial, subendothelial, subepithelial and intramembranous sites. Immunohistological examination (peroxidase-antiperoxidase technique) showed that HSA and immunoglobulin (IgG and IgM) were deposited in the glomeruli of these cats. Deposits were the most dense in cats with more severe renal lesions. Deposits of IgM were most abundant. An extensive cellular infiltrate, comprising macrophages, neutrophils and plasma cells, was observed only in the four animals which showed abnormalities in glomerular ultrastructure. The disease induced in these cats thus appears to differ from the membranous nephropathy previously described in the cat and bears a close resemblance to immune complex (IC) disease in man. In view of the relatively few specific animal models of IC-mediated proliferative GN, this model has potential for application to the study of human IC disease.     

Diagnostic dilemmas in atypical postinfectious glomerulonephritis

This study discusses the differential diagnosis of atypical postinfectious glomerulonephritis (PIGN) which may mimic a great variety of glomerular diseases. These include mild mesangial and/or endocapillary glomerulonephritis (GN) focal segmental glomerulosclerosis (FSGS) with diffuse IgM mesangial deposits, crescentic GN with C3 hump-like deposits, focal mesangiocapillary GN superimposed on endocapillary pattern, membranous GN with diffuse exudative changes, crescentic GN with microabscesses, and postinfectious glomerulonephritis with anti-GBM linear deposits.     

Cellular aspects of rabbit Masugi nephritis. III. Mesangial changes.

Lytic disarrangement of mesangial matrix was noted in acute proliferative glomerulonephritis induced in the rabbit by injection of duck nephrotoxic antibody. The severity of the change was variable depending upon dose of the antibody injected. With severe mesangiolysis, mesangial areas were highly obscured by marked hypertrophy and proliferation of mesangial cells along with massive infiltration of monocytes into the loosened mesangium and subendothelial space. In addition, there was random mobilization of the mesangial cells as shown by peripheral interposition and intraluminal projection with capillary subdivision. Glomerular capillaries were thus narrowed and distorted. The ultrastructural hallmark of the proliferated mesangial cells was prominence of the Golgi complex and endoplasmic reticulum which suggested accelerated protein synthesis, most likely for repair of the damaged matrix. In the affected glomeruli, exclusive of those undergoing rapid obliteration due to basement membrane rupture, resolution of the acute inflammatory process occurred within 2 weeks. At this stage, two types of glomerular changes became manifest, consisting of: (1) prominent mesangial stalk thickening and cellularity with occasional peripheral interposition of mesangial cells, and (2) segmental capillary subdivisions due to mesangial bridges built between the original mesangium and peripheral loop. It is suggested that chronic glomerular disease may develop based upon these persistent alterations of the glomerular structure. When a smaller dose of the duck antibody was employed, the process was much less prominent and complete recovery from acute glomerulonephritis took place.     

Pathomorphological differential diagnosis of glomerular lesions in diabetics

In renal biopsy specimens taken from 165 diabetics 3 cases with amyloidosis and 25 with glomerulonephritis (GN) were found. Among these were 13 cases with membranous and 10 with mesangial proliferative GN. This remarkably high rate may be partly due to selection, but, it can also be explained by the techniques of investigation because most of the GN cases were diagnosed by semithin sections and/or immune histology, respectively. In paraffin sections these alterations may be misinterpreted as diffuse glomerulosclerosis (GS), borderline lesions or normal findings. This is understandable because in mesangial proliferative GN, as well as in diffuse GS, the mesangium is broadened; similarly the spike formation or basement membrane doubling of membranous GN may simulate a thickening of the basement membrane. In addition, the differential diagnosis between GS and other diseases/lesions is discussed. We conclude that the examination of specimens by adequate methods will reveal "nondiabetic" glomerular lesions in diabetics more frequently than previously reported in the literature.     

THE SIGNIFICANCE OF IN VITRO ACTIVATION OF GUINEA PIG COMPLEMENT IN GLOMERULI OF HUMAN RENAL BIOPSY MATERIALS FROM VARIED SUBTYPES OF GLOMERULONEPHRITIS

To measure the potential ability of complement activation by glomerular-bound immune complex or G3 convertase, the in vitro fixation of guinea pig complement (GPC) components to glomeruli was examined by Immunofluorescence on the frozen sections of human renal biopsy materials, from the varied subtypes of glomerulonephritis (GN). Study for the pathway of complement activation in each subtype was also done. The extent of GPG activation fairly well paralleled with those of the autologous immunoreactants depositions and further with the morphological alterations of glomeruli in the cases of proliferative GN, advanced membranoproliferative GN (MPGN), lupus nephritis, purpurs nephritis of non-IgA nephritis type and advanced focal segmental glomerular sclerosis. The ability of GPC activation was present but generally weak in the cases of post-streptococcal acute GN (post-str. AGN) and subsiding MPGN. The rate of positivity was further reduced in the cases of membranous nephropathy (MN), IgA nephritis and related purpura nephritis. The dominant alternative pathway of GPC activation was found in MPGN, post-str. AGN, IgA nephritis, and related purpura nephritis, the only classical pathway was noted in MN.     

A quantitative immunohistochemical study of the expression of mesangial α-smooth muscle actin and the proliferation marker Ki-67 in glomerulonephritis in man

Using a specific marker 1A4 (DAKO), a quantitative evaluation of α-smooth muscle actin (ASMA) in glomeruli has been performed on human renal biopsies from patients suffering from acute, postinfectious, endocapillary glomerulonephritis (GN; 9 biopsies), IgA nephropathy (11 biopsies) and membranoproliferative GN (11 biopsies) and appropriate controls expressing a very weak ASMA reactivity. A significantly increased expression was found in all categories of GN. The glomeruli from IgA nephropathy showed variation of ASMA expression (range 0.1–27.7%) and a pattern of ASMA staining that was mesangial, global and diffuse. This pattern was also seen in cases of IgA nephropathy with focal, segmental, proliferative GN. In all biopsies, the glomerular cell number and proliferation index was determined. All the categories of GN showed significantly increased glomerular cellularity and proliferation index. Among the three types of GN, the glomerular cellularity and proliferation was lowest in IgA nephropathy. The mean number of Ki-67-positive intraglomerular nuclei and the proliferation index were both significantly correlated with the mean number of glomerular cell nuclei. Morphometric estimates demonstrate increased ASMA expression in types of GN with different prognosis. This finding and the lack of correlation with proliferation markers together indicate that the role of ASMA in GN is complex. This method of ASMA estimation may be useful in further studies of its role in disease activity and prognosis.     

Ultrastructure of transplant glomerulopathy

Thirty-one specimens of tissue were obtained from 15 renal allografts 3–96 months after transplantation and studied by light, electron and in some cases also by immunofluorescence microscopy. All patients had a degree of renal insufficiency and almost all had proteinuria and moderate hypertension; nephrotic syndrome was present in one and hematuria in two. On histological examination one patient showed cellular proliferation suggestive of glomerulonephritis (recurrent or de novo ) and another patient had numerous crescents. The most frequent glomerular lesion was widening of the lamina rara interna with subendothelial accumulation of finely granular material, formation of new subendothelial basement membrane and deposition of microfibrils and fine filaments. The mesangial changes were mainly those of mesangiolysis and mesangial sclerosis with deposition of mesangial matrix and microfibrils, but little cellular proliferation. Fragmented red blood cells were seen in nearly half of the patients. In another seven patients the lesion resembled focal segmental glomerulosclerosis. This combination of changes termed transplant glomerulopathy leads to diffuse glomerular sclerosis. Arterial intimal thickening and occasionally also thrombosis produced ischaemic changes in the kidney and in the glomeruli and contributed significantly to the process of transplant rejection.     

Glomerular endothelial endocytosis of subendothelial electron dense deposits

In 16 of 52 cases (32.5 per cent) of glomerulonephritis associated with glomerular subendothelial electron dense deposits, we detected endothelial endocytosis of osmiophilic material. Twelve patients had systemic lupus erythematosus, two had poststreptococcal glomerulonephritis, and two had idiopathic immune complex glomerulonephritis. The endocytosis was not observed in 13 patients suffering from membranoproliferative glomerulonephritis, in seven suffering from focal sclerosing glomerulonephritis, and in one suffering from hereditary nephritis. Therefore, the potential for endocytosis appeared to vary according to the illness.By light microscopy the 16 specimens exhibited features of acute proliferative glomerulonephritis. All the 14 with tissue sufficient for immunofluorescence study displayed deposition of immunoglobulins and complement along capillary loops and within the mesangium. By electron microscopy many of the subendothelial deposits were unassociated with endocytosis of osmiophilic matter, yet when endocytosis occurred, it was prominent. Hypertrophied endothelial cells occurred in zones of endocytosis. In nine of 16 cases small vacuoles within endothelial cells contained material of an electron density comparable to that of intramembranous and subendothelial deposits, but lyosomal degradation of the material was not noticed. There was frequent direct communication between osmiophilic material in capillary lumens, the subendothelial aspect of the glomerular basement membrane, and endothelial cytoplasmic processes. These communications suggested movement of osmiophilic material in some fashion. Neutrophils featuring vacuoles that contained osmiophilic material were only rarely observed, indicating that they may not assume a major role in degradation of deposits. Phagocytic activity of mesangial cells and nonresident monocytes was not studied.On the basis of our findings we propose that endothelial endocytosis of osmiophilic material might constitute a component of a transport mechanism or a digestive mechanism of glomerular immune deposits located in the subendothelial region.     

RENAL GLOMERULAR CHANGES ASSOCIATED WITH LIVER CIRRHOSIS

Renal glomerular changes associated with 79 liver cirrhosis cases were studied by light and electron microscopy, and immunofluorescent methods. The glomerular changes were classified as follows: 1) Mixed membranous and proliferative glomerulonephritis type having subepithelial, subendothelial, mesangial and paramesangial deposits (37 cases), 2) membranous glomerulonephropathy type (6 cases), 3) IgA nephropathy type (3 cases), and 4) glomerulosclerosis type (5 cases). Clinically, the patients with marked renal glomerular changes had proteinuria, hematuria, and retention by the PSP test. It was suggested that the essential renal glomerular changes in liver cirrhosis was immune-complex mediated glomerulonephritis and that glomerular sclerosis was merely a secondary change to glomerulonephritis.     

Membranoproliferative glomerulonephritis. Localization of early components of complement in glomerular deposits.

A body of evidence suggests that in membranoproliferative glomerulonephritis (MPGN), complement is activated by the alternate pathway. Therefore, deposition of early components of complement should not be expected in glomeruli. The renal tissues of 16 patients--13 with classic MPGN and 3 with dense deposit disease, a variant of MPGN--were studied by light and electron microscopy and by means of elution and immunofluorescence for the localization of complement (C1q, C4, and C3), immunoglobulins (1gG, IgM, and 1gA), and other serum proteins. Variable amounts of C3, C4 and/or C1q, and IgM were detected in the glomeruli of all patients, whereas IgG and IgA were present, respectively, in 15 of 16 and 6 of 16 patients. Deposits were localized in mesangium and in peripheral capillary loops in a typical lobular distribution. The specificity of each antiserum was verified by immunodiffusion, immunoelectrophoresis, and blocking experiments utilizing unlabeled antibody. Glomerular-bound IgG was eluted with acid citrate buffer, suggesting that IgG might be complexed with antigen(s) in glomerular deposits. By light microscopy, lesions ranged from focal proliferation and lobulation to more severe involvement with typical splitting of glomerular basement membranes, sclerosis, and less frequently, crescent formation. Ultrastructurally, all patients with classic MPGN exhibited mesangial and subendothelial deposits, and in 5 of these patients, subepithelial deposits were demonstrated. With the exception of ultrastructural lesions, patients with the dense deposit variant lacked distinguishable features when compared with those with classic MPGN. The significance of these findings is discussed in relation to a) activation of complement and the possible role of an immune complex mechanism and b) the variability of the morphologic expression.     

Glomerulonephritis in congenital cytomegalic inclusion disease

Except for renal transplant recipients, glomerulonephritis has only very rarely been associated with renal cytomegalovirus (CMV) infection. The kidneys of five infants with congenital cytomegalic inclusion disease, including renal infection, were examined at autopsy. Two of the infants had glomerulonephritis. The younger, a 4-month-old female, had diffuse proliferative and necrotizing glomerulonephritis; virus was present in nuclei and cytoplasm of glomerular endothelial cells and, possibly, in leukocytes as well. There were no electron-dense deposits. The other infant, a 5-month-old male, had diffuse mesangial and focal segmental proliferative and sclerosing glomerulonephritis; electron-dense mesangial deposits were seen ultrastructurally. Three additional infants (a newborn male, a 2-day-old male, a 6-week-old female), all with CMV in tubules and one with a single glomerular inclusion, had only rare glomerular abnormalities, i.e., mesangial proliferation in less than 10 per cent of glomeruli (one infant) and segmental sclerosis in less than 1 per cent of glomeruli (all three infants). Thus, congenital renal CMV infection was associated with proliferative glomerulonephritis in the two infants who survived the longest. The three with shorter survival times had only minor glomerular alterations.     

The action of cyclophosphane in different morphological variants of glomerulonephritis in mice

Heterologous serum glomerulonephritis (GN) was induced in CBA and C57BL mice. CBA mice developed diffuse proliferative GN. Glomerular changes in C57BL mice corresponded to the mesangial GN with proliferation of glomerular mesangial cells and mesangial infiltration with mononuclear phagocytes. Single administration of cyclophosphamide (CP) at the time of immunization exerted different effect on the development of the two morphological variants of GN. In CBA mice CP treatment resulted in disappearance of the immune complexes deposits with no influence on the cell reactions. In C57BL mice CP completely inhibited the development of the glomerular morphological changes. The lack of morphological similarity is most likely connected with the immunological differences in the histocompatibility complex (H-2).     

IgA nephropathy with subendothelial deposits

Summary IgA nephropathy with subendothelial deposits in the capillary walls of the glomeruli (IgA type 2) was compared histometrically and clinically with IgA nephropathy without subendothelial deposits (IgA type 1) and membranoproliferative glomerulonephritis with subendothelial deposits (MPGN). Study cases consisted of 32 biopsies from 26 patients of IgA type 1, 25 biopsies from 20 patients of IgA type 2 and 31 biopsies from 27 patients of MPGN. Histological changes of the glomeruli consisted of an increase in the mesangial matrix and hypercellularity in the mesangium in both types of IgA nephropathy, and the degree of the changes was a little higher in IgA type 2 than in IgA type 1 (0.02<P<0.05). Mesangial changes of MPGN were marked as compared with IgA type 1 and IgA type 2 (P< 0.001). Histometry of the mesangium on the cases followed up showed that the degree of mesangial thickening increased with lapse of time in IgA type 2 and MPGN, whereas it remained unchanged up to 13 years in IgA type 1. Proteinuria tended to be mild in IgA type 1, moderate in IgA type 2, and marked in MPGN. The impairment of renal function was observed in 21.9% of IgA type 1, in 36.0% of IgA type 2 and in 58.1% of MPGN. IgA type 2 has been shown to be pathologically and clinically intermediate between IgA type 1 and MPGN. These results suggest that there is a clinicopathological overlap between IgA nephropathy and MPGN with IgA deposition.     

AITD合并肾小球肾炎自身抗体检测及临床病理分析

目的：观察自身免疫性甲状腺疾病合并肾小球肾炎的甲状腺自身抗体表达及临床病理特点。方法：自1998年～2007年行肾活检的肾小球肾炎合并AITD患者20例,分析其甲状腺自身抗体表达及临床与病理特点。结果：AITD 20例（男6,女14）,平均年龄（35.7±9.4）岁,Graves’病9例,桥本氏甲状腺炎5例,甲减6例。甲状腺球蛋白抗体（TGA）、甲状腺微粒体抗体（TMA）、甲状腺过氧化物酶抗体（TPO-Ab）三种自身抗体中,TPO-Ab阳性率较高。肾损害表现为隐匿性肾炎3例,慢性肾小球肾炎8例,肾病综合征6例,急进性肾炎3例。病理提示膜性肾病9例,4例为系膜增生性肾小球肾炎,3例为坏死性肾小球肾炎,2例为局灶节段硬化,2例为系膜毛细血管性肾炎。结论：自身免疫性甲状腺疾病合并肾小球肾炎肾损害主要表现为慢性肾炎和肾病综合征,肾脏病理类型多为膜性肾病,TPO-Ab阳性率较高。大多数患者预后较好。     

Morphology of IgA nephritis (Berger disease). Immunohistologic, light- and electron microscopic findings

An IgA nephritis was diagnosed in 109 (24%) out of 445 renal biopsies with glomerular disease in the years from 1977 to 1985. The mean age of the patients in question was 29 years. The male:female sex ratio was 2.6:1. Immunohistologically, the characteristic branching mesangial IgA deposits were uniformly present. In addition 96% showed mesangial C3 and 54% mesangial IgG and/or IgM deposits. Besides, immunoglobulin and/or C3 deposits could be detected at glomerular basement membranes (20%). The histological types of IgA nephritis were minor glomerular abnormalities (10%), focal/segmental glomerulonephritis (29%), diffuse mesangioproliferative (58%), membranoproliferative (1 case), and sclerosing glomerulonephritis (2 cases). Additional tubulointerstitial lesions were found in 55%. Electron microscopically, in 53 cases under study, mesangial electron dense immunodeposits were seen. At the glomerular basement membranes, deposits could be found only in 23 examined cases (43%). The comparison of clinical data with morphological findings showed relationships between the degree of proteinuria and creatinine level increase with the histological type of IgA nephritis and with the degree of glomerular sclerosis, tubulointerstitial lesions, and electron microscopically proved glomerular basement membrane deposits. Hematuria seemed not to correlate with the morphological picture.     

CR1 stump peptide and terminal complement complexes are found in the glomeruli of lupus nephritis patients

The number of CR1 on podocytes is reduced in nephropathies with severe glomerular damage, especially in the diffuse proliferative glomerulonephritis (DPGN) of systemic lupus erythematosus (SLE). Reduction of CR1 number on erythrocytes is due to proteolysis of CR1 by macrophage proteases activated by the reaction of their complement receptors, which leaves a ‘CR1 stump peptide’ on the erythrocyte [1]. In the present study, we demonstrated the presence of the terminal complement complex (TCC) and the CR1 stump in histological sections of biopsies from patients with SLE by the indirect immunoperoxidase technique. Less severe glomerular lesions presented TCC deposits mainly in the mesangium (mesangial pattern). In lupus nephritis, with more severe glomerular damage, TCC deposits were detected both in the mesangium and in the capillary loops with podocyte involvement (mixed pattern). Patients with highly active DPGN presented a marked reduction of intact podocyte CR1 receptors in association with increased reactivity to the anti-CR1 stump antibody and with glomerular TCC deposits of mixed histological pattern. These results suggest that the decrease in the number of podocyte CR1 receptors in severe glomerular lesions of SLE may be due to a local proteolytic activity associated with activation and deposition of TCC.     

Proliferative glomerulonephritis in mice induced by sea snake (Aipysurus laevis) venom.

Aipysurus laevis venom has been shown to have a direct nephrotoxic effect in mice. A single subcutaneous injection (0.075 mg/kg body wt.) of the whole venom caused acute renal tubular degeneration and proliferative glomerulonephritis. The tubular changes appeared within 1 hour and remained for at least 14 days. Mesangial proliferative glomerulonephritis developed within 3-10 days, and is characterised by mild mesangial proliferation, mesangial and glomerular basement membrane deposits. This is followed by a partial resolution and subsequent mesangial sclerosis. The exact pathogenesis of venom-induced glomerulonephritis is not clear although it may have an immunological basis similar to that seen in human poststreptococcal glomerulonephritis. It was not possible to clarify the nature of the deposits by conventional immunohistochemical stains.