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F Mampaso

Publications and source records attributed to F Mampaso.

At least 73 records · Page 4Linked to original sources
PubMed1991

Acute interstitial nephritis superimposed on glomerulonephritis: report of a case.

A 7-year-old boy with a history of recurrent acute renal failure and macroscopic haematuria is reported. A renal biopsy performed during the first episode of renal function deterioration showed mesangial glomerulonephritis with C3 mesangial deposits. Macroscopic haematuria associated with respiratory infections recurred four times over the next 14 months, each time in association with acute derangement of renal function. A second biopsy showed acute interstitial nephritis and similar glomerular abnormalities. Retrospectively, a causal relationship between the ingestion of paracetamol and the appearance of the symptoms was observed. No derangement of renal function was present in subsequent episodes of macroscopic haematuria following removal of the offending drug. This is a case of drug-induced acute interstitial nephritis superimposed on a glomerular disease, and suggests the importance of recognizing this association.

Acetaminophen↗
PubMed1991

Evidence that addition of azathioprine improves renal function in cyclosporine-treated patients with allograft dysfunction.

Several approaches have been attempted to manage renal allograft dysfunction in cyclosporine-prednisone (CsA-Pred)-treated patients. Conversion to conventional therapy and perioperative triple drug have been associated with high rates of acute rejection episodes, infections, or neoplasms. We report our experience in delayed addition of azathioprine (1-2 mg/kg/day) to CsA/Pred protocol in three groups of patients. Group I (n = 9) had chronic renal function deterioration due to chronic rejection; group II (n = 10) had repeated or severe acute rejection episodes despite adequate CsA levels; and group III (n = 8) had CsA toxicity despite drug tapering. In group I, serum creatinine (SCr) had risen from 2.2 +/- 0.9 to 2.9 +/- 0.7 mg/dl over the 6 months prior to Aza addition (P less than 0.05), renal function declining at a rate of -0.14 +/- 0.12 Cr-1/year. In the 6-month post-Aza, renal function improved at a rate of 0.06 +/- 0.06 Cr-1/year and during the entire follow-up at a rate of 0.04 +/- 0.12 Cr-1/year (P less than 0.05) with stable CsA levels (288 +/- 167 vs. 251 +/- 172 ng/dl, NS). In group II response was worse, though the rate of declining renal function prior to Aza (-0.10 +/- 0.10 Cr-1/year) was almost stopped after Aza. In group III there was very good response to Aza addition, as 7 out of 8 patients improved graft function (baseline SCr 2.5 +/- 0.7 mg/dl vs. 1.9 +/- 0.6 mg/dl at last follow-up, P less than 0.05), with significantly decreased CsA levels (480 +/- 97 vs. 268 +/- 120, P less than 0.05). One patient from group II died from pneumonia, and 6 patients (1 from group I and 5 from group II) lost their grafts. Fifteen patients improved graft function, and 9 worsened after addition of Aza. The bad-responders had significantly higher SCr at baseline compared with the good-responders (3.8 +/- 1.8 vs. 2.7 +/- 0.6 mg/dl, P less than 0.01). Amelioration of chronic graft dysfunction can be achieved by delayed addition of Aza to CsA-Pred in patients with chronic rejection or CsA toxicity. This is accompanied by low rate of acute rejection, good patient and graft survival, and low rate of infections. A worse outcome can be seen in patients with high-baseline SCr levels, suggesting the need for addition of Aza in the initial chronic graft dysfunction.

Azathioprine↗
PubMed1991

Natural killer function in the rat with interstitial nephritis.

Brown Norway (BN) rats with tubulointerstitial nephritis (TIN) have an augmented NK activity. Immunological manifestations of the disease indicate the existence of a highly activated B-cell system, as reflected in the high levels of circulating antibodies and in the predominant spontaneous IgG-producing B-cells in cultures. In addition, NK cells appear to induce positive signals for antibody production either when co-cultured with B-cells alone or after treatment with poly I:C. Our results suggest that NK cells might play a role in the immunoregulation of the humoral response in this disease.

Animals↗
PubMed1991

Recurrence of IgA nephropathy with nephrotic syndrome after kidney transplantation.

Two patients on maintenance hemodialysis after terminal renal failure due to mesangial glomerulonephritis with IgA deposits and the nephrotic syndrome, received cadaver renal allografts. After several years of functioning transplants, both patients developed slowly progressive proteinuria and finally the nephrotic syndrome, 1 of them with renal function deterioration. Renal biopsies revealed findings indicating recurrence of the original disease.

Adult↗
PubMed1991

Thrombotic microangiopathic nephropathy in scleroderma and lupus anticoagulant.

A 47-year-old woman with overlap scleroderma-polymyositis syndrome and positive circulating lupus anticoagulant developed scleroderma nephropathy, characterized by rapidly progressive renal failure caused by thrombotic microangiopathy with widespread thrombi in small arteries and glomeruli. The possible relationship between lupus anticoagulant and the development of thrombosis at the small renal vessels level with the triggering of the scleroderma crisis is discussed.

Female↗
PubMed1990

Immunotactoid glomerulopathy associated with mycosis fungoides.

A patient with mycosis fungoides developed a nephrotic syndrome. Renal biopsy revealed deposits of a highly organized fibrillar material which did not stain with the typical amyloid stains; this picture was consistent with the diagnosis of non-amyloidotic fibrillary glomerulopathy or immunotactoid glomerulopathy. We believe this is the first case reported of immunotactoid glomerulopathy associated with mycosis fungoides. Possible pathogenetic implications are discussed with reference to previous publications.

Female↗
PubMed1990

Evidence suggesting a role for platelet-activating factor (PAF) in experimental nephrotic syndrome.

Sprague-Dawley rats injected with a single dose of adriamycin at 7.5 mg/kg/day developed an important and persistent proteinuria from day 14. Animals treated from day 0 to 3 weeks with PAF-receptor antagonists (BN 52021 or alprazolam) did not present (p less than 0.0005) the adriamycin-induced proteinuria or only to a very low extent. Furthermore, epithelial glomerular cells presented in these animals a normal aspect, while in rats injected with adriamycin, but not treated, the epithelial cells showed effacement of foot processes and intensive degenerative changes. By contrast, rats treated with steroids or cyclosporin did not present a significant reduction in proteinuria or improvements in epithelial cell lesions. Rats injected with adriamycin also presented an increase in the number of inflammatory infiltrating cells, chiefly la(+)-reactive cells (OX6+ cells), macrophages (ED1+ cells) and T-cytotoxic/suppressor cells (OX8+ cells). Concomitant administration of PAF-receptor antagonists induced a significant reduction in the number of these cells. Glomerular cells from normal control rats incubated with adriamycin incorporated 3H-acetate into a polar lipid with biological and migratory characteristics on thin-layer chromatography similar to synthetic PAF. On the whole, our data suggest a role for PAF in the pathogenesis of experimental nephrotic syndrome induced by adriamycin.

Acetates↗
PubMed1990

Membranous nephropathy, antitubular basement membrane antibodies and alveolar hemorrhage in a diabetic child.

We describe an 8-year-old boy who was diagnosed as having diabetes mellitus at the age of 3 months. During the follow-up the diabetes was uncontrolled, and he presented nephrotic syndrome with renal function impairment, a renal biopsy showing a membranous nephropathy. Subsequently he had episodes of anemia and dyspnea, due to alveolar hemorrhage, and he also developed Fanconi's syndrome. A later renal biopsy showed membranous glomerulonephritis and interstitial nephritis. The presence of antitubular basement membrane antibodies was noted but antialveolar basement membrane antibodies were not detected. We do not believe that this unusual clinical picture was a coincidence, and we speculate about a possible explanation.

Antibodies↗
PubMed1989

Characterization of circulating idiotypes containing immune complexes and their presence in the glomerular mesangium in patients with IgA nephropathy.

The possible pathogenic role for idiotype-anti-idiotype interactions in kidney diseases has recently been suggested. Since patients with IgA nephropathy often present antibodies against alimentary antigens, like bovine serum albumin (BSA), we isolated an idiotypic antibody with BSA specificity from one of these patients. By means of a specific anti-idiotypic antibody raised in rabbits, we have studied the participation of these idiotypes in circulating and renal deposited immune complexes (IC) in patients with IgA nephropathy. On indirect immunofluorescence, the presence of cross-reactive idiotypes was detected in the glomeruli of 12 out of 42 (28%) patients with IgA nephropathy, but in none of 15 membranous or mesangiocapillary nephritis examined. The staining was located within mesangial and paramesangial areas, with a similar, but less intensive, pattern distribution than IgA. Previous adsorption of rabbit anti-idiotype antibodies on an idiotype-Sepharose column completely abolished that staining. A close relationship was found between the presence of cross-reactive idiotypes on mesangial immunoglobulins and the existence of increased levels of serum idiotypes and idiotype-containing IC. Serum analytical ultracentrifugation showed that circulating IC containing idiotypes have chiefly a large (greater than 19 S) and intermediate (13 S-19 S) size, while those containing anti-BSA antibodies were only between 7 S-13 S fractions, or absent. Our results suggest that in patients with IgA nephropathy, shared idiotypes participate in the formation of circulating and renal deposited IC. It is possible that the apposition of free anti-idiotype to idiotype already bound to glomeruli, and vice versa, could contribute to increasing the amount and size of mesangial immune deposits, and, therefore, facilitate or perpetuate tissue injury.

Adult↗
PubMed1988

Allograft membranous glomerulonephritis and renal-vein thrombosis in a patient with a lupus anticoagulant factor.

A circulating lupus anticoagulant factor was detected in a 38-year-old man with end-stage renal disease and a 'lupus-like' syndrome with a diffuse proliferative glomerulonephritis. When treated with steroids, the 'lupus' complications were controlled and the anticoagulant factor disappeared; however, renal function did not recover and the patient commenced regular haemodialysis. Four months later the patient received a cadaver kidney transplant. At transplantation and during follow-up there was neither clinical nor laboratory evidence of lupus activity, but 19 months after transplantation, when steroids were tapered to a low dose, the lupus anticoagulant factor was detected, and renal-vein thrombosis complicated by sepsis led to the patient's death. A membranous glomerulonephritis was found on autopsy. This is the first time in which a (probably 'de novo') membranous glomerulonephritis has been detected in the allograft of a patient with circulating lupus anticoagulant factor.

Adult↗
PubMed1987

Role of platelet-activating factor in adriamycin-induced nephropathy in rats.

The effect of steroids, heparin and specific PAF-acether antagonists (BN 52021 and triazolobenzodiazepines) on proteinuria and renal histological changes induced in rats by adriamycin was studied. Adriamycin evoked a marked proteinuria that was unaffected by methylprednisolone and slightly reduced by heparin. In contrast, adriamycin-injected rats treated with PAF-acether antagonists had a low proteinuria, if any, and no ultrastructural glomerular alterations. These data suggest that PAF-acether could play a major role in the occurrence of proteinuria and that PAF-acether antagonists might provide a new therapeutic approach in certain human nephropathies.

Animals↗