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G Colasanti

Publications and source records attributed to G Colasanti.

At least 37 records · Page 2Linked to original sources
PubMed1985

Idiopathic IgA mesangial nephropathy. Clinical and histological study of 374 patients.

Histological features and data on the natural history after 1 to 45 years (mean 6.56 +/- 8.55) of total apparent duration and 1 to 13 years (mean 3.48 +/- 5.04) of post-biopsy follow-up, are reported in 374 patients (mean age, 33.9 +/- 11.9 yrs) with idiopathic mesangial IgA nephropathy, who presented with a history of macroscopic hematuria (56%), recurrent in two-thirds of the patients, or with persistent microscopic hematuria and no previous episodes of gross hematuria (44%). Mesangial cell proliferation ranged from minimal to diffuse. Associated varying degrees of extracapillary proliferation, segmental and global glomerular sclerosis, tubulo-interstitial damage and arteriolar hyalinosis usually correlated with each other and with the extent of mesangial proliferation (P less than 0.05). The actuarial curve of progression to renal death showed a 75% survival after 20 years from apparent onset. Progression to renal failure was more rapid in patients with: an older age at onset (P = 0.0582); male sex (P = 0.0730); no history of recurrent gross hematuria (P = 0.0406); high blood pressure (P = 0.0011); more marked global (P = 0.0007) and segmental (P = 0.0026) glomerular sclerosis; more severe interstitial sclerosis (P = 0.0147); more diffuse and global mesangial proliferation (P = 0.0820); mesangio-parietal pattern at immunofluorescence (P = 0.0778). However, all these parameters showed a poor predictive value if applied to any single patient.

Adolescent↗
PubMed1983

T-lymphocyte subsets in primary and secondary glomerulonephritis.

T-lymphocyte subsets, using the monoclonal antibodies OKT3 (peripheral T-cells), OKT4 (helper/inducer T-cells) and OKT8 (suppressor/cytotoxic T-cells) were measured in peripheral blood from 110 patients with various forms of primary and secondary glomerulonephritis (GN) (Berger's disease, membranous GN, focal glomerulosclerosis, membranoproliferative GN, lupus nephritis and mixed essential cryoglobulinaemia with GN). We have found a significantly higher OKT4+/OKT8+ ratio in patients with Berger's disease and membranous GN and a rather low OKT4+/OKT8+ ratio in patients with lupus nephritis and mixed essential cryoglobulinaemia, due to a significant decrease in OKT4+ cells. Our results suggest an imbalance in immunoregulatory mechanisms in some forms of GN.

Adolescent↗
PubMed1983

Effect of intensive plasma exchange (PE) in rapidly progressive crescentic glomerulonephritis (RPCGN).

Ten adult patients with RPCGN (crescents in greater than 70% of glomeruli), primary in 6 and associated with systemic diseases in 4, were treated with PE, associated with oral steroids (P) and cyclophosphamide (C) in all cases and with intravenous methylprednisolone pulses (MP) in 7 cases. Four out of ten patients were anuric and needed dialysis treatment at the start of treatment. Therapeutic benefit, i.e. reversal of the trend to further deterioration and substantial improvement of GFR, was achieved in 8 out of 10 patients (80%), including 2 of 4 anuric patients, and in 7 of those (8) who had still active cellular crescents (87.5%). Similar therapeutic benefit had been achieved only in 10% of a comparable population of 10 patients with RPCGN treated before 1980 with P and C, without PE or MP pulses. It is difficult to establish whether the better therapeutic results in the more recently treated group were due to PE or to MP pulses of to both the new approaches, even though the clinical improvement obtained in all the 3 patients treated with PE without concomitant MP suggest a specific beneficial role for PE. RPCGN is a catastrophic illness characterized by progressive deterioration of kidney function, resulting in oliguria and uremia, usually within weeks or months. The most consistent histopathologic finding is the presence of extensive glomerular crescents resulting from proliferation of the extracapillary epithelial cell lining of Bowman's capsule. It is apparent that RPCGN is not a homogeneous entity, clinically, histologically or immunohistologically, but rather a clinicopathologic syndrome, the features of which may be seen in a variety of systemic disorders, including SLE, polyarteritis nodosa, Wegener's granulomatosis, Henoch-Schönlein purpura, cryoglobulinemia, and subacute bacterial endocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1982

Glomerular localization of circulating antiglobulin activity in essential mixed cryoglobulinemia with glomerulonephritis.

Kidney biopsy samples from 27 patients with essential mixed cryoglobulinemia of the IgG-IgM(k) type and glomerulonephritis were studied to assess whether glomerular immunodeposits display antiglobulin (AG) activity similar to that of serum cryo-IgM. A preparation of heat-aggregated human IgG (FAIgG) was used to search for tissue AG activity, and blocking tests and reactivity tests were carried out to define the nature of this activity. Glomerular localization of FAIgG was observed in 17 out of 27 kidney specimens, the positive findings being always associated with IgM deposits. Prior exposure of tissue sections to anti-IgM serum blocked the FAIgG reaction, but no such effect was produced by the pretreatment with other antisera. The positive FAIgG tissue specimens yielded a similar fluorescence pattern with aggregated alkylated-reduced IgG, but did not react at all with the aggregated F(ab')2 or aggregated albumin. The IgM recovered in the eluate of a kidney biopsy specimen displayed AG activity. Patients with AG deposits showed more severe histologic changes and a greater renal functional impairment than did those without. The data support the notion that circulating cryo-IgM anti-IgG participates in the formation of glomerular immunodeposits and in the genesis of renal damage.

Adult↗
PubMed1981

IgA-mesangial nephropathy (Berger's disease) with rapid decline in renal function.

End-stage renal failure requiring dialysis treatment developed within 5 years in 11 patients with IgA mesangial glomerulonephritis (out of 94 affected by this nephropathy) whose serum creatinine levels were less than 2 mg/100 ml at the time of biopsy. We compared these patients (Group 1) with 10 patients (Group 2) whose serum creatinine was comparable at the time of biopsy (1.2 +/- 0.3 vs 1.4 +/- 0.3 mg/100 ml) but remained unchanged (1.1 +/- 0.4 mg/100 ml) at the end of a minimum post-biopsy follow-up of 5 years. The analysis of clinical findings, at the time of biopsy, showed that the mean duration of disease, from apparent onset, was shorter in Group 1. Recurrent macroscopic hematuria, never reported in this group, was present in 40% of patients of Group 2, whereas minimal urinary abnormalities, discovered by chance, were the only findings in 73% of patients of Group 1 and in 30% of Group 2. No difference was present between the patients in the two groups in the amount of proteinuria and in the incidence of high IgA serum levels, whereas hypertension was more frequent (45% vs 20%) in Group 1. The analysis of histological lesions demonstrated that in Group 1 there was a greater incidence of diffuse mesangial proliferation (82% vs 30%), of extensive glomerular obsolescence (64% vs 0) and of severe interstitial fibrosis (54% vs 0). Immunofluorescence findings were similar in the two groups. Although no single clinical or morphological parameter was characteristic of the patients with subsequent rapid decline of renal function, some features were more commonly observed, or more severe, in these patients, and therefore should be considered reliable predictors of an unfavourable outcome.

Adult↗
PubMed1981

Renal lesions in essential mixed IgG-IgM cryoglobulinemia. Study of 48 cases.

56 renal biopsies in 48 patients affected by essential mixed IgG-IgM cryoglobulinemia have been examined by light microscopy and immunofluorescence. Patients were classified in four groups: 1) minimal lesions (4 patients); 2) pure proliferative mesangial lesions (9 patients); 3) membranoproliferative glomerulonephritis (23 patients); 4)proliferative glomerulonephritis with prominent intraluminal thrombi (12 patients). In this last group large intraluminal thrombi intensely fixing anti-IgG and IgM antisera were present; unlike the preceding groups, few deposits on capillary walls were seen. These four groups differed in renal clinical syndrome at presentation: in particular, proteinuria or nephrotic syndrome was the predominant manifestation in group 3, acute nephritic syndrome in group 4. In the latter, reversal of renal failure and regression of lesions could be observed. Various morphological aspects tend to show that in this disease more than one mechanism is operating in producing renal damage, including local trapping of abnormal circulating proteins.

Cryoglobulinemia↗
PubMed1980

Significance of glomerular C3b receptors in human renal diseases.

In order to elucidate their role in mediating renal immune injury in man, the glomerular C3b receptors have been analyzed in frozen sections of 205 kidneys biopsied from 199 patients affected by various well-defined renal diseases. Using fluoresceinated C3b-coated bacteria as the indicator system, the receptor activity has been compared with that found in 10 normal human kidneys. In 76 out of 98 cases (77%) of glomerulonephritis (GN) with capillary wall abnormalities, a significant loss of receptor activity has been observed. No difference was present between the 89 patients affected by GN presumably due to immune complexes (ICX) parietal deposition (membranoproliferative, membranous, acute poststreptococcal GN and proliferative GN of SLE and cryoglobulinemia) and the 9 patients affected by GN presumably due to anti-GBM antibodies (Goodpasture's syndrome and extracapillary GN). In the group of ICX-GN, no correlation could be demonstrated between inhibition of C3b receptors and the presence of parietal C3 deposits. A significant loss of receptors activity has been also demonstrated in 12 out of 13 patients with amyloidosis or diabetic glomerulosclerosis. On the contrary, inhibition of C3b receptors has been observed in only 3 out of 20 patients with nonglomerular renal diseases (interstitial and vascular nephropathies) and in only 11 out of 57 patients (19%) affected by mesangial GN with no capillary wall abnormalities (Berger's disease, Henoch-Schonlein purpura and mesangial GN of SLE). C3b receptors were normal in 13 out of 17 patients affected by lipoid nephrosis (minimal change GN or focal glomerulosclerosis). In conclusion, the analysis of C3b receptors in renal diseases do not support the hypothesis of their involvement in parietal localization of C3b-bearing ICX: these results rather suggest that the receptors become undetectable in many glomerular diseases (immune-mediated or not) with lesions of capillary walls, because of the loss of integrity of C3b receptor-bearing visceral epithelial cells.

Antigen-Antibody Complex↗
PubMed1977

The prognostic value of some clinical and histological parameters in membranoproliferative glomerulonephritis (MPGN): report of 112 cases.

112 cases of MPGN, whose diagnosis was made on light microscopy, were reviewed. Histological examination showed 66 cases of 'classical' MPGN, 33 of MPGN with a lobular pattern and 13 of MPGN with epithelial crescents. In 11 patients dense intramembranous deposits were observed. On immunofluorescence (95 cases) 62 patients showed deposits of C3 together with immunoglobulins, 20 had a predominant deposition of C3 and in 13 C3 alone was present. At the moment of biopsy 57 patients had nephrotic syndrome, 43 hypertension, 43 impaired renal function and 65 hypocomplementaemia. In 23 cases, one or more episodes of macroscopic haematuria occurred. The actuarial survival was 70% after 10 years and 50% after 20 years from onset. At last observation 25 patients were dead or on haemodialysis, 22 had impaired renal function, 62 had normal renal function and 2 were in complete remission. The histological variety with epithelial crescents had a significantly worse outcome. The presence of dense deposits or of any specific immunofluorescence pattern had no prognostic significance. Nephrotic syndrome, renal function impairment and hypertension indicated a poor prognosis: however, macroscopic hamaturia or hypocomplementaemia did not influence the outcome.

Adolescent↗
PubMed1977

C3b receptors in glomerular disease.

Using two indicator systems--sheep erythrocytes or fluoresceinated S. typhi coated with C3b the presence of a receptor for C3b (but not C3d) in the normal human glomerulus is confirmed. No receptor could be detected in other species tested (mouse, rat, guinea-pig, rabbit and rhesus monkey). Binding of indicator particles was reduced or lost in diseases associated with glomerular capillary deposition of C3, but not in those with mesangial deposition alone. However in some cases the receptor was lost in the absence of detectable C3 deposition. No receptors were detected in proliferating cells in glomerular crescents.

Animals↗
PubMed1977

Long term follow up of IgA mesangial deposits glomerulonephritis.

The clinical course of IgA Mesangial Deposits Glomerulonephritis (MDGN) has been investigated in 178 patients for 1 to 32 years (mean 6 years) from the onset of symptoms. Impairment of renal function occurred in 28 patients, 13 of whom required RDT or died in uraemia. Hypertension was observed in 67 patients. The actuarial survival rate at ten years was 91%. A significant correlation was observed between the occurrence of renal failure and the following features: absence of episodes of gross haematuria, early appearance of hypertension, marked proteinuria and sclerosing glomerular lesions. These data suggest that IgA MDGN has generally a very prolonged course, but in a few cases may evolve, sometimes early, to chronic renal failure.

Adolescent↗
PubMed1976

Immunofluorescence patterns in chronic membranoproliferative glomerulonephritis (MPGN).

90 patients, whose renal biopsies showed on light microscopy a pattern of MPGN, have been studied by immunofluorescence. 10 cases showed dense intramembranous deposits. Fluoresceinated antisera against IgG, IgA, IgM, C3, fibrinogen, IgD, IgE, C4, C1q, properdin and C3A were employed. Granular depostis of C3 were observed in all cases; IgG, IgM, properdin, C1q and C4 were found in 2/3 cases; IgA, IgE and C3A were rarely found. The localization of these deposits was parietal and often also mesangial. On the basis of glomerular deposition of C3 with or without immunoglobulins (Ig), we separated the cases into three groups: 1) C3 + Ig (59 cases), 2) predominant C3 (19 cases), 3) isolated C3 (12 cases). Most patients with dense deposits disease were classified in the third group. Deposits of C1q and C4 were found only in the first two groups. The localization of C3 deposits showed a more frequent mesangial extension in the second and third groups. Patients in these 3 groups also had different serum complement profiles. No significant differences in the major clinical features could be found in the 3 groups. Variable immunofluorescence patterns, in agreement with other serological parameters, confirm the heterogeneity of pathogenetic mechanisms in patients with MPGN.

Complement C1↗