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S Colon

Publications and source records attributed to S Colon.

At least 55 records · Page 3Linked to original sources

[An infrequent cause of acute renal failure].

The clinical history of this patient was characterized by an acute localized then diffused pneumopathy, artificial respiratory assistance being necessary. At the same time, acute renal failure appeared with oligoanuria, the evolution of which being favorable after 15 days. The etiology of the pneumopathy was proved by the strongly positive ornithosis serodiagnosis: 1/512. The occupation of the patient, a country worker, correlated well with this diagnosis. The type and mechanism of the acute renal failure should be discussed. Renal biopsy disclosed a tubulo-interstitial nephritis. There was no shock during the whole clinical story. Very high CPK level in the blood was found early in the course of the disease. So, it seems probable that myolysis of viral origin, might be responsible of the renal defect.

Acute Kidney Injury↗

Antigen recognition by H-2-restricted T cells. II. A tryptic ovalbumin peptide that substitutes for processed antigen.

A 17-amino acid tryptic peptide of chicken ovalbumin, designated P323-339, that substituted for processed antigen when presented by glutaraldehyde prefixed accessory cells to specific I-restricted T hybridomas was characterized. The peptide antigen could not be demonstrated to have any specific or stable interactions with accessory cell Ia antigens by either direct binding or functional assays for inhibition of specific T cell activation. In addition, the T cell receptor for I-restricted antigen had no affinity for free antigen alone. A rabbit antibody specific for the antigenic peptide inhibited presentation when introduced before but not after binding of the peptide to accessory cells. These results extend our earlier finding that accessory cell-mediated processing of chicken ovalbumin can be completely explained by the fragmentation of the native molecule into smaller m.w. peptides, and suggests that if an antigen/Ia complex is important in T cell activation, it forms significantly only in the presence of the T cell receptor for I-restricted antigen.

Amino Acid Sequence↗

The nephrotic syndrome in adults aged over 60: etiology, evolution and treatment of 76 cases.

A study of the clinical, etiological and histological features of the nephrotic syndrome occurring in 76 adults aged over 60 was performed. Membranous nephropathy was the most frequent type (40%). 32% of the cases of membranous nephropathy were associated with another disease which was a malignant one in 22% of the cases. In 2 cases a renal vein thrombosis was associated with the malignant disease. Amyloidosis appeared to be the most frequent cause of the secondary nephrotic syndrome (13%), and was often associated with plasma cell dyscrasia. The study also showed the importance of lipoid nephrosis among elderly patients with the nephrotic syndrome (20%). Amongst these cases it is necessary to consider the association of minimal changes with a systemic disease, and the histological diagnosis of focal hyalinosis. Indeed the presence in elderly patients of arteriolar, interstitial and glomerular lesions of hyalinosclerosis makes interpretation difficult. With corticosteroid therapy complete remission was frequent in patients with lipoid nephrosis.

Age Factors↗

Distant evolution of kidney arteriolar lesions and hypertension after pregnancy toxemia.

60 patients were studied 3 months to 4 years after pregnancy. All had high pressure, gross proteinuria, and edema. In many cases, typical glomerular lesions and proteinuria disappeared rapidly. When arteriolar lesions are of grade I or II, they progressively disappear or remain unchanged and blood pressure returns to normal values. When arteriolar lesions are of grade III (endotheliitis, hyperplasia and edema of the media and subendothelial deposits), blood pressure remains at a high level or increases, without changes during the time of observation of the arteriolar lesion or of renal function.

Adult↗

Mesangial IgA glomerulonephritis in HLA-identical brothers.

Two HLA identical brothers with mesangial IgA glomerulonephritis are reported. Patient 1 developed gross hematuria at age 12 and required chronic hemodialysis at age 20. Patient 2 presented at age 21 with gross hematuria and normal renal function, the follow up period is only 9 months. Neither of these patients had nerve deafness, ocular defects or complement abnormalities. The family history did not support a diagnosis of classical hereditary nephritis, but a genetic linkage is strongly suggested by the identical HLA phenotypes of these brothers (A10 - A32 - B13 - B35). The B35 antigen has previously been suspected to be linked to this disease. These observations strongly support the hypothesis of an aberrant, genetically controlled, immune response, in patients with mesangial IgA glomerulonephritis.

Adolescent↗

Nephrotic syndrome in procainamide induced lupus nephritis.

We report a case of the nephrotic syndrome occurring in a patient with procainamide induced LE. It was associated with bilateral pleural effusions, pericarditis, fever, positive LE cell preparation and a high titer of antinuclear antibodies. No anti-DNA antibodies were found. Renal biopsy showed mesangial proliferation with few IgM and C3 deposits and interstitial infiltrates; electron microscopy revealed subendothelial deposits. Clinical improvement occured after steroid therapy and there was no recurrence 24 months after withdrawal of prednisone.

Aged↗

[Late diagnosis of cystinosis in 2 brothers: histological and ultrastructural renal study].

Cystinosis was discovered by chance in two adolescent boys who had proteinuria with minor tubular abnormalities. Renal biopsies were examined by light microscopy, electron microscopy and immunofluorescence. There were few histological changes but crystals were present in the epithelial cells of the glomerulus and occasionally in the tubules. A further unusual feature was the detection of IgA deposits in the mesangium.

Adolescent↗

[Association of nephrotic syndrome and Hodgkin's disease. Role of the Epstein-Barr virus].

The clinical association between glomerulonephrtis (GN) and malignant hematological disease is very rare. We report, in a 24 years old male, the occurrence of an apparently idiopathic nephrotic syndrome with minimal change glomerular lesions. This GN was in fact closely related to the progression of a stage 2A of Hodgkin's disease, following an infectious mononucleosis contracted one year ago. The nephrotic syndrome responded well to the therapy by Prednisone and Chlorambucil, and the complete remission persisted after eradication of Hodgkin's disease and despite early treatment discontinuation. Renal vein thrombosis, renal amyloidosis and renal interstitial infiltration with malignant cells were ruled out. Immunofluorescent and electron microscopy examination of the renal biopsies were consistent with, but not demonstrative of, an immune complex nephritis. Because of the chronological succession of infectious mononucleosis, Hodgkin's disease, and GN, we are stressing the possible oncogenic and immunogenic role of the Epstein-Barr virus.

Adult↗

Thrombocytopenia, macrothrombocytopathia, nephritis and deafness.

The association of thrombocytopenia, macrothrombocytopathia, nephritis and deafness is rare. Reported here is a new case of this triple association. The clinical course, the nephropathologic findings and the bilateral neurologic hearing loss were similar to those already reported, with a slowly progressive impairment of renal function accompanied by a persistent proteinuria. The platelet diameters were increased. These macroplatelets contained granules of normal structure but with an irregular distribution in the cytoplasm. In other areas the cytoplasm was rich in surface connected system. The survival of these platelets and their contraction were normal. Their aggregation and excretion in response to collagen, adenosine diphosphate and thrombin, and the values of platelet factor 3 activity were all decreased. The degranulation defect, also present, was observed in the absence of a decrease in intracellular cyclic adenosine 5'-monophosphate (AMP) suggesting a relationship between these two findings.

Adenosine Diphosphate↗

[Renal venous thrombosis in the adult].

Eleven cases of renal vein thrombosis (RVT) are reported, 9 of which presented with nephrotic syndrome (NS) and 2 with acute renal failure (ARF). Hematuria, enlarged kidneys, assymetric peripheral edema and collateral vein dilatations were the classic symptoms. Phlebography was employed in 101 suspected cases and permitted definitive diagnosis in 11 percent. Phlebography was performed in 13 percent of the NS cases and 11 percent of the ARF cases, but in none of the other cases. Fifteen kidney biopsies (KB) were performed in 8 patients, 6 with NS and 2 with ARF. In the 6 cases of NS, 4 presented a pattern of membranous glomerulonephritis and 2 had mild thickening of the basement membrane. This was confirmed by electromicroscopy in 5. In the 2 with ARF capillary dilatations, polynuclear infiltrates and interstitial edema was found. Repetitive KB, performed in 3 cases, revealed the same histological pattern in 2, while in the other case granular membranous deposits were found on the second biopsy that were not apparent in the first. This last patient was free from clinical manifestations at the time of this last biopsy. Immunofluorescent studies (iF) were performed on 7 KB of 5 patients, 4 with NS and 1 with ARF. Three of the 4 with NS presented a pattern of membranous deposits. On i.F one patient was found to have IgG and C3 deposits, one IgG and fibrinogen and one no detectable IgG, IgA, IgM, IgE, C3 or fibrinogen. The fourth with minimal histological changes was also negative for i.F, as was the case of ARF. Sequential treatment by heparin and antivitamin K was administered in 8 patients. Recovery occurred in 3 and stabilization in 4, while in 1 case this treatment was without effect.

Acute Kidney Injury↗

Immunodeficiency diseases. I. T-lymphocyte precursors and T-lymphocyte differentiation in partial Di George syndrome.

Immunological and pathological studies in a case of partial Di George syndrome revealed an absence of parathyroids, a major hypoplasia of thymus but a relatively moderate decrease in peripheral T-lymphocyte numbers and functions. After in vitro incubation with normal thymus extracts, a normal proportion of bone marrow cells was induced to differentiate into cells with characteristics of T lymphocytes, thus establishing the presence of T-cell precursors in the patient's bone marrow.

Antigen-Antibody Reactions↗