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Biomedical subjects

A J Valdes

Publications and source records attributed to A J Valdes.

10 recordsLinked to original sources
PubMed1994

Free fragments of gamma chain in the urine. A possible source of confusion with gamma heavy-chain disease.

With currently used microconcentrators, high-resolution electrophoresis, and immunofixation electrophoresis, relatively homogeneous free fragments of gamma chain (FFGC) unaccompanied by light chains, which cannot be found in the serum, may be discovered in the alpha-2 region during routine examination of the urine. The urinary alpha-migrating FFGC is of no apparent clinical significance and should not be confused with the antigenically related FFGCs of gamma heavy-chain disease. In gamma heavy-chain disease, the FFGCs are often demonstrable in the urine, but are always present in the serum and migrate in the beta-gamma region.

Diagnosis, Differential↗
PubMed1987

Intraglomerular tubular epithelial cells. A marker of glomerular hematuria.

The occurrence of intraglomerular tubular epithelial cells (ITEC) was investigated in 202 consecutive renal biopsy specimens and were present in 111 (55%). Minimal, focal, or diffuse glomerular diseases were all represented. Of the patients with ITEC 110 (99%) had gross or microscopic hematuria, either alone or associated with proteinuria; however, ITEC were found only in one of 79 proteinuric patients with no documented hematuria. Intraglomerular tubular epithelial cells did not occur in four patients with drug-induced interstitial nephritis and microscopic hematuria, or in 11 normal controls. The pathogenesis of ITEC is not known, but our data indicate that the phenomenon is almost constantly found in association with glomerular hematuria. Identification of ITEC, therefore, should help to confirm the glomerular origin of hematuria when histologic alterations are minimal.

Biopsy↗
PubMed1978

Effect of cortisone upon vascular permeability to antibody.

In rabbits actively sensitized to bovine serum albumin, intracorneal injection of 1 mg. of fluorescein-labeled bovine serum albumin evokes a circular band of fluorescence secondary to precipitation of the diffusing antigen with antibody migrating from the limbal blood vessels. Cortisone treatment prevented or markedly decreased this phenomenon indicating that cortisone exerts a definite inhibitory effect upon vascular permeability to antibody molecules.

Animals↗
PubMed1977

Congenital hepatic fibrosis, liver cell carcinoma and adult polycystic kidneys.

In reviewing the literature, we found no liver cell carcinoma (LCC) or well-documented adult polycystic kidneys (APK) associated with congenital hepatic fibrosis (CHF). We report a 69-year-old man with CHF, LCC, APK, duplication cyst of distal portion of stomach, two calcified splenic artery aneurysms, myocardial fibrosis and muscular hypertrophy of esophagus. The LCC was grossly predunculated and microscopically showed prominent fibrosis and hyaline intracytoplasmic inclusions in the tumor cells.

Aged↗
PubMed1977

On the origin of urinary fibrin-fibrinogen-related antigen in glomerulonephritis.

A model of antiglomerular basement membrane nephritis in the rat was used to elucidate the origin of urinary fibrin-fibrinogen-related antigen (FRA). The intrarenal distribution and excretion of 125I-rat fibrinogen was examined to determine whether there was increased filtration of bibrinogen or fibrin degradation products (FDP) or lysis of intraglomerular fibrin. 125I-protein appeared in the urine immediately after injection of 125I-fibrinogen and fell in parallel with the fall in plasma 125I-fibrinogen. Renal retention of 125I-fibrin averaged less than 0.2 percent of the administered dose of 125I-fibrinogen. The infusion of epsilon aminocaproic acid (EACA) had no significant effect on either FRA excretion or 125I-protein excretion. Plasma FDP levels and the elution patteren of 125I-protein from the urine were not significantly changed by EACA infusion. These observations support the view that ruinary FRA excretion in glomerulonephritis is derived predominantly from increased filtration of plasma fibrinogen rather than from breakdown of intraglomerular fibrin.

Aminocaproates↗
PubMed1976

Angioimmunoblastic lymphadenopathy with dysproteinemia. Immunohistologic and ultrastructural studies.

Immunoblasts of the B-cell line and immunoblasts of the T-cell line have very similar light-microscopic appearances but different immunologic compositions. The immunoblasts of a patient with angioimmunoblastic lymphadenopathy with dysproteinemia were found to bear surface immunoglobulin and complement receptor. They lacked receptor for cytophilic antibody. Surface villous projections were demonstrated by scanning electron microscopy. These features strongly indicate their B-cell origin.

Aged↗
PubMed1975

Heparin therapy in anti-basement membrane nephritis.

The effect of heparin on the development and progression of a form of antiglomerular basement membrane nephritis was examined in the rat. Animals which received heparin before and throughout the period of immunological insult developed lesions which were as severe, and perhaps more severe, than rats which did not receive heparin. Inulin clearances were lower in heparin-treated animals than in untreated rats. Animals in both groups exhibited renal fibrin-fibrinogen deposition and had increased rates of urinary fibrin-fibrinogen related antigen excretion. These results indicate that heparin per se has no beneficial effect on the development of this form of glomerulonephritis in this species.

Animals↗
PubMed1975

Fatal immune complex glomerulonephritis without deposits.

Repeated intravenous injections of egg albumin in rabbits produced small antigen-excess complexes and severe glomerulonephritis. Immunoglobulins and complement in the glomeruli were not clearly demonstrated by immunofluorescence; deposits were found to be sparse by electron microscopy. This study demonstrates that soluble immune complexes are responsible for the glomerular reaction. The apparent absence of deposits is thus not sufficient to exclude an immune complex pathogenesis.

Animals↗