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ABSTRACT: In a previous investigation into corneal autoimmunity, it was demonstrated that a putative autoantigen, a protein of 66 kDa, present in bovine corneal epithelium, binds circulating autoantibodies in approximately 60% of patients with Wegener's granulomatosis (WG). The aim of the present study was to characterize and identify the 66-kDa protein.
A purification protocol was established for the 66-kDa protein using standard chromatography techniques. During the purification procedure it became clear that the 66-kDa protein detected in patients' sera was in fact two proteins, both running at 66 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, that eluted in different fractions on DE-52 chromatography columns. These two proteins have been labeled bovine corneal epithelial antigen-A and -B (BCEA-A and BCEA-B). Further investigations of antibody binding have demonstrated that patients' sera bind to either one or the other of these proteins with no cross-reactivity between them. Separated BCEA-A and BCEA-B protein extracts were immunoblotted with 27 WG patients' sera, 10 Churg-Strauss syndrome (CSS) patients' sera, 31 rheumatoid arthritis (RA) patients' sera, and 40 healthy control subjects' sera from the blood bank.
Forty-six percent of WG patients' sera had antibodies to one of the 66-kDa antigens, whereas none of the healthy control subjects' sera had 66-kDa antibodies (P < 10(-5)). In the WG group, 31% were positive to BCEA-A (versus controls, P = 0.0023), and 15% were positive to BCEA-B. WG patients with peripheral ulcerative keratitis (PUK) had a significant association with anti-BCEA-A antibodies when compared with healthy control subjects (50%, P < 10(-6)). However, in the RA group with no eye disease there was an association with BCEA-A (25%, P = 0.011) but not in the RA group with PUK. The frequency of anti-BCEA-B antibodies was significantly increased in patients with CSS (60%, P < 10(-7)).
In summary, it has been shown that vasculitis patients have antibodies to two 66-kDa corneal antigens and that autoantibodies to these antigens are mutually exclusive. It has also been shown that antibodies to BCEA-B are associated with CSS, whereas BCEA-A antibodies are associated with WG and RA.
Investigative Ophthalmology & Visual Science 01/1999; 39(13):2594-601. · 3.60 Impact Factor
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ABSTRACT: The benefits of using cyclosporin in organ transplantation to prevent graft rejection outweigh its potential disadvantages, but with the use of low-dose cyclosporin in relatively healthy individuals, such as those with psoriasis, the risk:benefit ratio is altered. The effects of low-dose cyclosporin (< 5 mg/kg body weight) on liver function and serum lipids and lipoproteins were examined in 40 normolipidaemic, normotensive psoriasis patients with normal renal function. After 3 months of treatment, serum cholesterol and bilirubin concentrations and alkaline phosphatase activity increased significantly (p = 0.001), and glomerular filtration rate (GFR) declined from 107 to 96 ml/min/1.73 m2 (p = 0.05). All these values returned to pretreatment levels 3 months after cessation of cyclosporin. In 15 patients in whom lipoproteins were isolated by ultracentrifugation, there was an increase in plasma low-density lipoprotein (LDL) cholesterol (p = 0.05), but very-low-density lipoprotein cholesterol, high-density lipoprotein (HDL) and HDL2 and HDL3 cholesterol concentrations did not change. The increases in serum bilirubin, alkaline phosphatase activity and LDL cholesterol, seen in individuals with normal baseline liver and renal function, which reverted to baseline following cessation of cyclosporin, suggest that cyclosporin-induced hypercholesterolaemia may be due to either decreased biliary excretion of cholesterol or impaired catabolism of LDL.
QJM: monthly journal of the Association of Physicians 03/1995; 88(2):109-13. · 2.33 Impact Factor
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ABSTRACT: Abnormalities of the renin-angiotensin system after low-dose cyclosporin (5 mg/kg/day or less) have not been adequately defined in patients with normal kidneys. 27 patients with psoriasis were assessed before starting cyclosporin, after three months of cyclosporin (5 mg/kg/day or less) and then finally three months after finishing cyclosporin. On each occasion plasma renin activity (PRA), aldosterone, angiotensin II and atrial natriuretic peptide (ANP) were measured together with total renal blood flow (RBF), GFR and filtration fraction (FF) following an i.v. bolus injection of Tc-99m DTPA. Significant renal hemodynamic toxicity was defined as > 25% fall in RBF or > 20% fall in GFR. Using these criteria we identified 12 patients with hemodynamic toxicity (Group A) and 15 patients whose GFR and RBF did not fall significantly (Group B). In Group A a significant fall in GFR (p < 0.001) and reduction in renal blood flow (p < 0.04) were associated with significant rises in both ambulant and recumbent angiotensin II (p < 0.0005). PRA, aldosterone and ANP did not significantly alter. GFR partially recovered after withdrawal of cyclosporin although RBF remained significantly lower compared to initial values. In Group B there was no significant change in GFR or RBF although there was a reversible fall in FF (p < 0.02). There were no significant differences in angiotensin II, PRA, aldosterone or ANP. Circulating angiotensin II rises in patients who develop cyclosporin nephrotoxicity and may be responsible for mediating the hemodynamic effects.
Clinical nephrology 07/1994; 41(6):350-6. · 1.17 Impact Factor
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ABSTRACT: 1. Cyclosporin A, an immunosuppressive drug used to treat psoriasis, stimulates renal synthesis of 1,25-dihydroxyvitamin D in rats. 1,25-Dihydroxyvitamin D can also reduce the activity of psoriasis, and in the present study we have examined the possibility that cyclosporin A mediates some of its actions in psoriasis by renal or extra-renal production of 1,25-dihydroxyvitamin D. 2. Treatment of 12 psoriatic patients with cyclosporin A (5 mg day-1 kg-1) for 3 months significantly improved the psoriasis activity and severity index and reduced glomerular filtration rate, but serum 1,25-dihydroxyvitamin D levels were not changed. However, 1-3 months after stopping cyclosporin A treatment, an increase in the psoriasis activity and severity index score was accompanied by a small, but significant, increase in serum 1,25-dihydroxyvitamin D concentration. Plasma 1,25-dihydroxyvitamin D levels in rats gavaged with cyclosporin A (15 mg day-1 kg-1 for 2 weeks) were significantly increased compared with controls, but a lower dose of cyclosporin A (2.4 mg day-1 kg-1) had no effect. Renal 25-hydroxyvitamin D-24-hydroxylase activity in rat kidney homogenates was not different between control and cyclosporin A-treated rats. Renal 25-hydroxyvitamin D-1 alpha-hydroxylase activity was not detectable in these homogenates. Extra-renal production of 1,25-dihydroxyvitamin D by activated macrophages isolated from the synovial fluid of patients with inflammatory arthritis was reduced after incubation with cyclosporin A (0.1-10 mumol/l) for 30 h or 5 days.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical Science 06/1994; 86(5):627-32. · 4.61 Impact Factor
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ABSTRACT: To improve the monitoring of patients on low doses of cyclosporine there is a need for new tests of tubular function. N-1 methylnicotinamide (NMM) is an endogenous organic cation that is secreted by the proximal tubule and its clearance can be measured. In 27 patients with psoriasis, serial measurements of NMN clearance, plasma aldosterone, plasma chloride, bicarbonate, and magnesium were compared with changes in the radionuclide measurement of glomerular filtration rate and renal blood flow before, during, and after a 3-month course of low-dose cyclosporine (< 5 mg/kg/d). N-1 methylnicotinamide clearance decreased significantly with cyclosporine only (2.5 mg/kg/d, n = 10, P < 0.01). Recovery of NMN clearance lagged behind that of glomerular filtration rate and renal blood flow. Serum magnesium decreased significantly on cyclosporine (2.5 mg/kg, n = 10, P < 0.01; 5 mg/kg, n = 9, P < 0.0001). In the whole group, plasma potassium increased significantly (n = 27, P < 0.02) and plasma aldosterone was inappropriately low. Low doses of cyclosporine in psoriasis cause a reduced clearance of NMN, hypomagnesemia, and a variable hyperchloremic acidosis. Nifedipine may alter these biochemical variables without necessarily improving renal hemodynamics. The delayed recovery of NMN clearance in comparison with renal haemodynamic measurements following cyclosporine therapy suggests that this noninvasive test of tubular function may be a marker of persisting cyclosporine nephrotoxicity and that it should be evaluated further.
American Journal of Kidney Diseases 02/1994; 23(1):23-30. · 5.43 Impact Factor
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ABSTRACT: Two insulin-dependent diabetic women with severe retinopathy who were referred for the management of nephrotic syndrome are presented. On the basis of clinical risk factors, such as retinopathy and severe hypertension, both patients were expected to develop progressive end-stage renal failure. One woman has shown a gradual decline in creatinine clearance over 7 years while the plasma creatinine of the other has remained normal for 11 years. The unexpectedly good outcome of both these patients may be related to maintaining a normal blood pressure despite neither patient receiving a prolonged course of an angiotensin-converting enzyme inhibitor. Because of the efficacy of current antihypertensive therapy, the outcome of diabetic nephropathy cannot be so easily predicted and needs to be formally reassessed.
American Journal of Nephrology 02/1994; 14(3):233-5. · 2.54 Impact Factor
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ABSTRACT: It is unclear whether cyclosporin A (CsA) alters the synthesis of 1,25-dihydroxyvitamin D3 [1,25(OH)2D] by the normal human kidney. Serial changes in 1,25(OH)2D, parathyroid hormone (PTH), GFR and renal blood flow were compared in 14 patients with psoriasis who were being treated with less than 5 mg/kg/day of cyclosporin for 3 months. GFR fell significantly although there were no significant changes in serum 1,25(OH)2D, 25-hydroxyvitamin D or PTH. Absolute values for GFR and PTH were negatively correlated (rP = -0.54; p < 0.001) as were the changes in GFR and PTH observed during CsA therapy (rP = -0.73; p < 0.05). The significant fall in serum magnesium was not significantly correlated with changes in PTH. The close relationship between changes in GFR and PTH suggests that a reduction of GFR within the normal range is enough to stimulate production of PTH. CsA does not appear to stimulate the synthesis of 1,25(OH)2D3 in man.
Mineral and Electrolyte Metabolism 01/1994; 20(5):250-4.
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Biochemical Society Transactions 12/1993; 21(4):422S. · 3.71 Impact Factor
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ABSTRACT: Dysregulated cytokine expression has been implicated in the pathogenesis of IgA nephropathy, but the mechanisms and selectivity of this response are poorly understood. In this study we have examined the expression of a range of immunoregulatory cytokine mRNAs by peripheral blood mononuclear cells (PBMNCs) from 45 patients with IgA nephropathy stratified empirically according to urinary red cell excretion: 10 in remission, and 35 with active disease (21 mild, 14 moderate), and 17 normal, and 15 disease, controls. We used a semi-quantitative polymerase chain reaction (PCR) technique. None of the patients had experienced recent episodes of macroscopic hematuria. Simultaneous analysis of monocyte class II antigen (DR) expression was also performed by two-color immunoflow cytometry. TGF-beta 1 mRNA was detected in 68% (24 of 35) of patients with active, and 70% (7 of 10) inactive IgA nephropathy, but in only 18% (3 of 17) normal (P < 0.005), and 27% (4 of 15) disease controls. IL-6 transcripts were identified in 37% (13 of 35) of patients with active IgA nephropathy, compared with 6% (1 of 17) normal controls (P = 0.015), with no significant increase in IgA remission, or disease control groups. TNF-alpha mRNA was detected in 29% (5 of 17) of normal and 53% (8 of 15) disease controls, but in only 7% (3 of 35) of patients with IgA nephropathy (P = 0.015). There was no significant change in TGF-beta 2, gamma-IFN, IL-2, IL-4, IL-1 alpha or IL-1 beta detection between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Kidney International 12/1993; 44(6):1298-308. · 6.61 Impact Factor
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Biochemical Society Transactions 12/1993; 21(4):423S. · 3.71 Impact Factor
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British Journal of Dermatology 09/1993; 129(2):222. · 3.67 Impact Factor
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ABSTRACT: To determine the effects of a three month course of low dose cyclosporin on the expression of epidermal cell adhesion molecules.
Eighteen patients with psoriasis were treated for 12 weeks with either 2.5 or 5 mg/kg/day of oral cyclosporin. Biopsy specimens taken from skin before, during, and after cyclosporin treatment were stained immunohistochemically for CD 54 (ICAM-1), CD 29 (beta-1 integrins), and CD18 (beta-2 integrins).
There was a highly significant (p < 0.01) clinical response after 12 weeks of cyclosporin as assessed by the Psoriasis Area and Severity Index (PASI) score. The staining of CD 29 on keratinocytes of affected and unaffected psoriatic skin was not affected by cyclosporin. Epidermal CD54 was variably expressed in active psoriatic plaques and changed unpredictably after cyclosporin (p = NS). Staining for CD18 on large epidermal dendritic cells was reduced after cyclosporin (p < 0.02). The expression of CD18 by large epidermal dendritic cells during treatment correlated strongly with the PASI score at that time and one month after stopping cyclosporin (p < 0.02).
Persistence of epidermal staining for CD 54 in psoriasis is compatible with a good clinical response to cyclosporin. Residual staining for CD 18 on large epidermal dendritic cells may be a useful marker for early clinical relapse.
Journal of Clinical Pathology 08/1993; 46(8):713-7. · 2.31 Impact Factor
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ABSTRACT: Ten patients with psoriasis received a 3-month course of cyclosporin (2.5 mg/kg/day) followed by a 3-month washout period, before commencing a 3-month course of cyclosporin and nifedipine SR 20 mg b.d. Serial haemodynamic and biochemical measurements were performed before, during, and after treatment. Total renal blood flow (RBF) was measured following an intravenous injection of [99mTc]-DTPA based on a renographic analysis of the first-pass effect in the kidneys, and GFR was estimated from the subsequent clearance of this radiotracer. A significant individual change in RBF or GFR was taken as 25% and 20% respectively. Simultaneous assays of the circulating vasoactive mediators renin, aldosterone, angiotensin II, and atrial natriuretic peptide were performed. Two patients withdrew from the study because they could not tolerate nifedipine, leaving eight for complete analysis. The significant reductions in RBF and GFR which occurred on cyclosporin alone (P < 0.05; ANOVA) did not occur with added nifedipine. Four months after this second course, RBF and GFR had recovered. The response to nifedipine was, however, variable and unpredictable. Of the four patients to show a significant decline in GFR on cyclosporin alone, only two showed a significant improvement on the combined therapy. Of the six patients who showed a significant decline in RBF on cyclosporin alone, only four showed benefit from the added nifedipine. Nifedipine suppresses the increase in blood pressure which occurred on cyclosporin alone. The circulating concentration of angiotensin II was significantly less on cyclosporin and nifedipine than on cyclosporin alone (P < 0.05; Student's t test).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrology Dialysis Transplantation 01/1993; 8(10):1071-8. · 3.40 Impact Factor
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ABSTRACT: Two colour flow cytometry was used to analyse in situ cytokine expression by human monocytes. Whole blood was cultured in siliconised glass bottles, with or without E. coli lipopolysaccharide (LPS), for various times, and the mononuclear cells (MNCs) then exposed to a variety of permeabilisation procedures prior to flow cytometric analysis. Paraformaldehyde (PF)/saponin fixation preserved cellular morphology, and caused a reproducible degree of permeabilisation (estimated by propidium iodide inclusion: mean 94%, range 86-99% (n = 33)). After fixation with 4% PF and permeabilisation with 1% saponin at 0 degrees C in PBS containing 20% human serum, MNCs were incubated with phycoerythrin(PE)-conjugated mouse anti-CD14 (monocyte phenotype) and polyclonal rabbit anti-human interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumour necrosis factor alpha (TNF-alpha), or control rabbit IgG. Binding of rabbit antibodies was detected using goat anti-rabbit IgG fluorescein isothiocyanate (FITC). FITC fluorescence was increased in CD14 PE positive cells with the three anti-cytokine antibodies following LPS stimulation, compared with controls. There was a reproducible dose related response in monocyte IL-1 beta and TNF-alpha expression following LPS stimulation, with early peaks in TNF-alpha (2 h), compared with IL-1 beta (4 h), and IL-1 alpha (12 h). Specificity of this cytokine detection system was confirmed by inhibition studies using the corresponding recombinant human cytokines, by an absence of staining in CD14 negative or unpermeabilised MNCs, and by the characteristic cytoplasmic localisation of the different cytokines visualised with UV immunochemistry. Hence, the methods described here provide a reproducible, semiquantitative and specific assay for the detection of cell associated monokines. The technique may be applicable to the analysis of a variety of different cytokines in other phenotypically defined cell populations.
Journal of Immunological Methods 10/1992; 154(1):11-20. · 2.20 Impact Factor
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ABSTRACT: 1. Henoch-Schoenlein nephritis and IgA nephropathy share clinical and immunological features, but the pathogenesis of neither condition is established. We have recently described IgG autoantibodies to glomerular components in active IgA nephropathy and have now sought evidence for a similar autoimmune component in Henoch-Schoenlein purpura. 2. Sera from 26 patients with Henoch-Schoenlein nephritis and six patients with Henoch-Schoenlein purpura without accompanying nephritis were studied and compared with sera from 20 patients with other forms of glomerulonephritis and 40 normal subjects. E.l.i.s.a.s were developed to detect IgA and IgG binding to the ligand from whole human glomeruli previously described, laminin, DNA, cardiolipin (diphosphatidylglycerol) and a panel of dietary constituents (BSA, alpha-caesin, beta-lactoglobulin, ovalbumin and wheat gliadin). 3. Sera from 16 of the 26 patients with Henoch-Schoenlein nephritis displayed increased IgG binding to the human glomerular extract compared with the normal control group (P < 0.001), whereas IgG binding was not significantly raised in the patients with Henoch-Schoenlein purpura without evidence of renal involvement. IgA binding was not raised compared with control subjects. Serum IgA and IgG binding to other potential autoantigens or antigens present on dietary constituents was not significantly different in patients with Henoch-Schoenlein nephritis or patients with Henoch-Schoenlein purpura without nephritis compared with control subjects. 4. Western blotting of the denatured and reduced glomerular extract revealed binding of IgG, from the sera of patients with active Henoch-Schoenlein nephritis, to glomerular components of M(r) 48,000 and 58,000, similar to the M(r) of the glomerular antigens identified in IgA nephropathy.(ABSTRACT TRUNCATED AT 250 WORDS)
Clinical Science 10/1992; 83(3):281-7. · 4.61 Impact Factor
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ABSTRACT: We have measured complement activation markers, C3dg and C5b-9 in plasma and urine from patients with idiopathic membranous nephropathy and IgA nephropathy. There was no significant difference in levels of plasma C5b-9 between the patient groups. However, high plasma concentrations of C3dg were associated significantly with IgA nephropathy with 45% of patients having levels over 25 U/ml (P less than 0.001). High concentrations of urinary C3dg and C5b-9 were associated significantly with membranous nephropathy (43% and 43% of the patient group, respectively) compared to patients with IgA nephropathy (10% and 0%, respectively, P less than 0.001). In a retrospective analysis of 31 patients with membranous nephropathy, 66% of patients with high initial urinary C5b-9 showed an unstable clinical course compared to 18% of patients with initially absent or low C5b-9 (P less than 0.001). We suggest that high urinary C5b-9 identifies those patients with a membranous lesion which retains an active immunological component contributing to the pathology of progressive glomerular damage.
Kidney International 05/1992; 41(4):933-7. · 6.61 Impact Factor
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ABSTRACT: We have been investigating the possibility of using the renal clearance of endogenous N-1-methylnicotinamide (NMN) as a marker of renal tubular function. Sixty-three subjects (11 healthy volunteers and 52 patients with renal impairment) were used for this study. The subjects were divided into three groups according to their creatinine clearance: group 1, over 80 ml/min; group 2, between 30 and 80 ml/min, and group 3, less than 30 ml/min. The correlation between NMN and creatinine clearance was compared for each group. A good correlation (r = 0.84) was found for groups 1 and 3 (r = 0.76), whereas for group 2, a poor correlation was found (r = 0.43). For subjects with mild renal impairment (group 2), there was clear evidence of glomerulo-tubular imbalance manifest by a larger variability in NMN clearance than creatinine clearance and an essentially non-parallel decline in these two parameters for this group. When all subjects were grouped together, the relationship between the clearance of NMN and of creatinine was best described by a 3-term polynomial equation (r = 0.93). NMN clearance is a potentially useful non-invasive marker of renal tubular function in man and provides additional information to that provided by the measurement of creatinine clearance alone. This substance should be more fully evaluated as a potential diagnostic aid.
Nephron 02/1992; 60(1):12-6. · 13.26 Impact Factor
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ABSTRACT: The vascular disturbance associated with ciclosporin (CS) nephrotoxicity is poorly defined in both the normal and transplanted human kidney. Six bone marrow transplant recipients were studied before, during and after administration of CS. By analysis of time activity curves and clearance of Tc-99m DTPA, renal blood flow (RBF), filtration fraction (FF) and GFR were shown to fall on CS (GFR: p less than 0.001; RBF, FF: p less than 0.01). These haemodynamic variables did not fully recover with dose reduction or after discontinuation of therapy. Plasma renin activity (PRA) aldosterone and atrial natriuretic peptide did not change although there appeared a tendency for PRA to fall on CS. There was a reversible normokalemic metabolic acidosis. CS levels stayed within the therapeutic range. The partial reversibility of GFR, RBF and FF is consistent with CS-induced functional disturbance and reflects sensitivity to microvascular and tubular injury of the normal human kidney.
Nephron 02/1992; 60(1):17-24. · 13.26 Impact Factor
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ABSTRACT: Volumetric analysis of urinary red blood cells (RBCs) was performed in two groups of patients: (a) 91 with glomerulonephritis (GN), 158 with non-glomerular diseases (non-GN) and 53 controls without haematuria; (b) 97 with GN and 41 with non-GN diagnoses and greater than or equal to 2+ haematuria, analysed after modified sample preparation (isotonic dilution and haemolysis to eliminate non-RBC debris). In group A, diagnostic ranges were established for modal, mean and differential (urinary-peripheral blood modal) RBC volumes to differentiate GN from non-GN sources of blood loss according to RBC size. 54% (135/249) of modal volumes and 68% (124/183) with greater than or equal to 2+ haematuria were within a diagnostic range of values, i.e. 40-180 fl (sensitivity), and the source of haematuria was correctly identified in 85% (115/135) and 87% (108/124) of these, respectively (specificity). Of the remainder, with modal volumes less than 40 or greater than 180 fl, 45% (51/114) were from GN and 55% (63/114) from non-GN specimens, along with 94% (48/53) controls without haematuria (non-diagnostic analyses). In contrast, whilst 90% (74/82) of mean volumes greater than or equal to 110 fl and 94% (62/66) of differential volumes greater than or equal to 0 fl were from non-GN specimens, values below these were common to both diagnostic groups so that diagnostic sensitivities were reduced to 38% (82/219) and 34% (66/193), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
American Journal of Nephrology 02/1992; 12(1-2):41-8. · 2.54 Impact Factor
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ABSTRACT: The autoantigen(s) that we have previously described in human glomeruli, recognized in IgA nephropathy, has (have) been identified as mesangial cell in origin. Cultured mesangial cells expressed 48- and 55-kD components binding IgG isotype autoantibodies (IgG-MESCA) present in sera of patients with both IgA nephropathy and Henoch-Schönlein purpura (HSP). IgG-MESCA were not detected in sera of normals, or patients with other autoimmune-mediated glomerulonephritides: anti-glomerular basement membrane disease, Wegener's granulomatosis, or in IgM-mesangial proliferative disease. Binding specificity was proven by F(ab')2 studies in enzyme-linked immunosorbent assay (ELISA) and Western blotting, and there was no significant affinity of IgA or IgM immunoglobulins. Fluorescein isothiocyanate-conjugated IgG from ELISA-positive sera localized to the mesangium and peripheral capillary loops of glomeruli, supporting the belief that the antigen is expressed in normal human renal tissue. However, only about one third of mesangial cells in culture showed affinity for IgG from ELISA-positive sera, suggesting variable expression of the antigen(s) in vitro. The only autoantigen(s) present in glomeruli, and extractable from whole normal glomeruli by the techniques employed, localized on the mesangial cell. In both IgA nephropathy and HSP, autoimmunity was intermittently present, with fluctuating levels of IgG-MESCA detectable in sera. There were positive correlations with the degree of glomerular injury assessed by erythrocyturia and proteinuria in IgA nephropathy, but significance was reached with only the degree of hematuria in HSP. These findings suggest a contributing role in the pathogenesis of the mesangial proliferative lesions and demonstrate autoimmunity common to both IgA nephropathy and HSP.
Journal of Clinical Investigation 12/1991; 88(5):1522-30. · 15.39 Impact Factor
