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Biomedical subjects

P Ronco

Publications and source records attributed to P Ronco.

142 records · Page 8Linked to original sources
PubMed1981

Lymphocytic choriomeningitis infection in the nude mouse. An immunopathological study.

Immunopathological studies of the kidney, determination of circulating immune complexes and interferon blood levels were obtained in adult congenitally-athymic nude mice ((nu/nu) infected with lymphocyte choriomeningitis (LCM) virus as well as in their phenotypically-normal litter mates (nu/+). As previously reported, intracerebral or intraperitoneal infection in nu/nu mice did not induce any mortality and resulted in a carrier state characterized by persistently high levels of virus in the circulation. Interferon was present in the circulation for approximately 6 days. Circulating immune complexes were not detectable and glomerulonephritis assessed by light microscopy, electron microscopy and immunofluorescence, was either absent or very mild. These observations show that although a carrier state can be induced in adult nude mice, circulating immune complexes and glomerulonephritis do not develop. This situation is markedly different from that induced in normal Swiss mice infected at birth, which is characterized by raised levels of circulating immune complexes and development of glomerulonephritis in all infected mice.

Animals↗
PubMed1980

Severity of lymphocytic choriomeningitis virus disease in different strains of suckling mice correlates with increasing amounts of endogenous interferon.

A marked difference was observed in the severity of disease in lymphocytic choriomeningitis (LCM) virus-infected suckling BALB/c, Swiss, and C3H mice. BALB/c mice had minimal liver lesions and none died, whereas C3H mice had extensive liver lesions and all mice died. An intermediate pattern was oberved for Swiss mice (36% mortality). Although there was no difference in the titers of LCM virus in the plasma or liver between these three strains of mice, there was a marked difference in the amount of interferon produced and the duration of interferonemia. C3H mice produced more interferon than Swiss mice which produced more interferon than BALB/c mice, indicating a direct correlation between the amount of interferon induced by LCM virus and the extent of disease. Inoculation of a potent anti-mouse interferon globulin markedly reduced the incidence of mortality in virus-infected C3H mice. BALB/c mice were as sensitive to the effects of interferon as C3H mice because daily administration of potent interferon preparations did induce disease in this strain. This ensemble of results supports our contention that endogenous interferon is in large part responsible for the manifestaions of acute LCM virus disease in suckling mice.

Animal Population Groups↗
PubMed1980

The effect of exogenous interferon: acceleration of autoimmune and renal diseases in (NZB/W) F1 mice.

To determine the effect of prolonged administration of exogenous interferon on the autoimmune disease of NZB/W female mice, forty-four NZB/W mice received three injections per week of 6.4 x 10(4) interferon units from birth to 33 weeks, forty mice were injected with mock interferon and forty-eight mice were left untreated. In mice injected with interferon growth was delayed, survival was decreased, and the severity of the glomerulonephritis was enhanced. Interferon increased the titre of serum anti-ssDNA and anti-soluble nucleoprotein antibodies, but had no effect on the circulating immune complex load. These results suggest that interferon in some way affects local deposition of immune complexes within the glomerulus.

Animals↗
PubMed1980

[Nephropathy and nodular regenerative hyperplasia of the liver (author's transl)].

A renal biopsy performed on a young woman with proteinuria showed a nephropathy consisting of major interstitial infiltration by lipophages and thickening of the glomerular capillary walls with a large amount of "spikes". Anti-IgG, IgM, C3 and C1q sera bound themselves to the extramembranous deposits and the anti-IgM serum to the endomembranous deposits. This striking finding was associated with a regenerative nodular hyperplasia of the liver, an entity that has been observed in only about 20 cases. An underlying immunological defect was suggested by the continuous presence of a mixed cryoglobulinemia.

Adult↗
PubMedDate not supplied

Plasma cell dyscrasia-related glomerulopathies and Fanconi's syndrome: a molecular approach.

Considerable advances in the understanding of renal complications of dysglobulinemia have occurred in the last 10 years. They mostly result from sequence studies of nephritogenic immunoglobulin chains and comparison with sequence database, and from a careful analysis of clinicopathological features including electron microscopy characteristics of immunoglobulin deposits. These advances should help define subpopulations of patients with plasma cell dyscrasia at risk of developing renal complications and to design novel therapeutic approaches. Although renal complications of plasma cell dyscrasias may be considered as anecdotal diseases, understanding their pathophysiology may help dissect the mechanisms of glomerular and proteinuria-induced interstitial fibrosis.

Amyloidosis↗
PubMedDate not supplied

[Value of the kidney revascularization in renovascular hypertension with kidney failure].

The effects of renal revascularization on blood pressure and renal function were evaluated in 8 hypertensive patients with renal impairment and renal artery stenosis in both kidneys (6 cases) or in a solitary kidney (2 cases). Mean age was 66 +/- 7 years. The mean duration of arterial hypertension was 13 +/- 8 years. In spite of treatment with 3 antihypertensive drugs (or more in 5 cases) blood pressure values ranged from 170-90 to 260-150 mmHg. Adding captopril (in 3 cases) or minoxidil (in 1 case) resulted in control of hypertension in 1 patient and further deterioration of renal function in 2. Two patients underwent surgery after failure of percutaneous transluminal angioplasty. There were 6 revascularizations and 2 nephrectomies with contralateral revascularization. One patient died post-operatively. In the remaining 7 patients, the hypertension was controlled with one or two drugs and the renal function remained stable or improved over a mean follow-up period of 2 years. We consider that these results warrant radiological exploration in all patients, even old, with renal impairment and drug-resistant hypertension. Renal revascularization must be performed as early as possible in view of the rapid degradation of renal function under medical treatment in these patients.

Acute Kidney Injury↗
PubMedDate not supplied

Release of cyclic nucleotides from the apical and basolateral poles of cultured human glomerular epithelial cells.

We have examined the intracellular accumulation and the release of cGMP and cAMP from the apical and basolateral poles of SV40-transformed human glomerular visceral epithelial cells (HGVEC) cultured on filters. After treatment of the cells by atrial natriuretic peptide (ANP), cGMP did not accumulate in the cells and was rapidly released mainly into the apical medium (86% of its total secretion). Its apical secretion was inhibited by 83% in the presence of probenecid, an organic acid transport inhibitor, and by 90% in the presence of nocodazole, a microtubule disrupter. cAMP was released more slowly than cGMP after it had accumulated in the cells. Apical polarization of the secretion still existed but was less marked than for cGMP (70% of its total secretion). Similarly, probenecid and nocodazole inhibited to a lesser degree cAMP egression (66 and 33%, respectively, for the apical secretion). Polarization of HGVEC was confirmed by the vectorialized secretion of lactate dehydrogenase. These results indicate that cGMP release from HGVEC is essentially apical and depends on a probenecid-sensitive organic acid transport and also on an intact microtubular network. cAMP release appears to be less polarized and less sensitive to the two drugs studied. Vectorially secreted cGMP in the urinary space in response to ANP could act downstream in the nephron and thus permit ANP to stimulate cells which do not necessarily possess ANP receptors.

Cell Line, Transformed↗