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Biomedical subjects

J C Jennette

Publications and source records attributed to J C Jennette.

At least 127 records · Page 7Linked to original sources
PubMed1988

Analysis of a murine B cell lymphoma, CH44, with an associated non-neoplastic T cell population. I. Proliferation of normal T lymphocytes is induced by a secreted product of the malignant B cells.

A non-neoplastic T cell population associated with a murine monoclonal B cell malignancy, CH44, was analyzed. Immunofluorescence on cell suspensions and immunoperoxidase staining on tissue sections using monoclonal antibodies to the antigens Thy1.2, Ly-1, L3T4, and Lyt-2 confirmed the presence of both TH (Ly-1/L3T4+, Lyt-2-) and Tc/s (Ly-1/L3T4-, Lyt-2+) T cell subpopulations. The non-neoplastic T cells were present in both a 0.6 and 2.1 g CH44-bearing spleen. T cells, not normally in liver in significant numbers, were found in liver tissue when the CH44 tumor cells were present. These data implied an active proliferation of the T cell populations within tissues containing the malignant B cells. Supernatant from an in-vitro-adapted cell line of CH44 (CH44.LX) was tested for its ability to induce proliferation of normal murine splenocytes and thymocytes. As assayed by tritiated thymidine incorporation, both spleen and thymus cells proliferated in the presence of CH44.LX supernatant. Although supernatant from two of nine other B cell lines was able to stimulate the proliferation of spleen cells, only CH44.LX could induce proliferation of thymus cells. Supernatant from the seven other B cell lines and three hybridomas had no measurable effect on either splenocytes or thymocytes in this assay. It is hypothesized that the presence of a non-neoplastic proliferating T cell population associated with a neoplastic B cell lymphoma during in vivo passaging of the tumor is the result of effects derived from a secreted product of the malignant B cells. Whether the T cells have any effect on the growth of the malignant B cells is not known.

Animals↗
PubMed1987

Overlapping IgA and membranous nephropathy.

Four patients with overlapping IgA nephropathy and membranous nephropathy recently have been reported from two different medical centers in Japan. The authors describe two patients from the United States with the concurrence of IgA and membranous nephropathy and a third patient who may have the same overlapping glomerular lesions. All three patients had hematuria and nephrotic range proteinuria. Renal biopsy specimens from two of the patients revealed focal proliferative glomerular lesions, large mesangial and numerous subepithelial electron-dense deposits, exclusively mesangial intense immunostaining for IgA, and extensive granular capillary wall immunostaining for IgG. The third patient is a sibling of one of the other patients and was shown to have focal proliferative glomerular lesions, mesangial immunostaining for IgA, and numerous subepithelial electron-dense deposits. Pathogenic possibilities are discussed.

Adolescent↗
PubMed1987

Localization of S protein and its relationship to the membrane attack complex of complement in renal tissue.

The S protein (S) binds to the attack complex of complement (C5b-9) in plasma preventing cytolysis. Using immunofluorescence microscopy, the authors determined the distribution of S in human renal tissue and its relationship to C5b-9, immunoglobulins, C3, albumin, and fibronectin. They examined normal and diseased human kidney tissue from patients with several forms of glomerulonephritis, diabetic nephropathy, and arterionephrosclerosis. S and C5b-9 were found in all diseased tissues; their amounts and distribution directly correlated with severity and location of injury. S and C5b-9 were colocalized in all immune deposits and in all injured glomeruli, tubular basement membranes, and vessel walls. Other than within immune deposits, S and C5b-9 were usually not colocalized with C3. This study demonstrates that S is deposited in areas of tissue injury and thus may participate in the pathogenesis of renal damage. Because in tissue S and C5b-9 are always associated, the attack complex in tissue must either be derived from the circulation as SC5b-9 or it must be capable of binding S after the formation in situ of C5b-9.

Anions↗
PubMed1987

Amelioration of immune complex-mediated glomerulonephritis by synthetic protease inhibitors.

Proteases are involved in the pathogenesis of inflammatory diseases by participating in the activation of mediator systems and by producing proteolytic tissue injury. Homeostatic control of inflammation is accomplished in part by physiologic protease inhibitors. The authors investigated the effectiveness of a number of synthetic protease inhibitors in ameliorating the glomerular injury induced by immune complex-mediated glomerulonephritis in mice. Two amidine-type protease inhibitors, bis (5-amidino-2-benzimidazolyl)methane and 1,2-bis (5-amidino-2-benzimidazolyl)ethane, had the greatest effects. They caused a marked reduction in glomerular necrosis (P less than 0.001) but did not affect the amount or site of immune complex localization or leukocyte influx. The inhibition constants of the protease inhibitors against nine purified physiologic proteases were determined. These results were discussed in relation to the effectiveness of the protease inhibitors in reducing glomerular injury. This investigation indicates that the administration of synthetic protease inhibitors can have a beneficial effect on immune-mediated inflammatory injury.

Amidines↗
PubMed1986

Immune complex induced glomerular lesions in C5 sufficient and deficient mice.

The role in the pathogenesis of immune complex-mediated glomerulonephritis of C5 or some terminal complement component dependent upon C5 for activation was explored in a congenic strain of C5 sufficient (NSN) and C5 deficient (OSN) mice. When these mice were given daily injections of heterologous protein, horse apoferritin (HAF), there were profound differences between the strains in the development of glomerulonephritis and renal dysfunction. When NSN and OSN mice produced low levels of anti-HAF, NSN mice developed extensive glomerular deposits of HAF and immune reactants and a mild proliferative glomerulonephritis. In contrast, comparable OSN mice developed only trace mesangial localization of HAF and no glomerular lesions by light microscopy. When NSN and OSN mice produced high levels of anti-HAF, both strains had equivalent glomerular immune deposits; however, NSN mice developed a severe necrotizing and crescentic glomerulonephritis, while OSN mice had much less glomerular injury. Compared to OSN mice, these NSN mice also had much more severe tubulointerstitial injury, and significantly higher serum creatinine levels. Thus, in this experimental model, the absence of C5 resulted in reduced glomerular immune complex localization when there were small amounts of circulating immune reactants; and in markedly reduced glomerular leukocyte influx, necrosis and crescent formation, when large amounts of immune reactants have localized in glomeruli. These effects could be mediated by C5 (such as C5a) or by some terminal complement component(s) dependent upon C5 for activation.

Age Factors↗
PubMed1986

The epithelial antigen phenotype of glomerular crescent cells.

There is controversy over the origin of cells in glomerular crescents. Although crescent cells were once considered to be of epithelial lineage, recent data have suggested that they are derived from the mononuclear phagocyte system. To further define the histogenesis of crescents, the authors evaluated 26 renal biopsy specimens having cellular crescents, using immunoenzyme and immunofluorescence microscopy, and a battery of 11 antibodies reactive with renal epithelial cells and 5 antibodies reactive with leukocytes. Although minor populations of macrophages were present in most crescents, in only 1 of 23 specimens evaluated with anti-macrophage antibodies were these the major cell type. Of 23 specimens evaluated with anti-epithelial antibodies, all but one had crescents with most of the cells expressing one or more epithelial antigens. Crescent cells shared antigens with glomerular and tubular epithelial cells, but the antigen phenotype of crescents often differed from that of normal tubular or glomerular epithelial cells.

Antibody Specificity↗
PubMed1985

A genetically determined murine model of infantile polycystic kidney disease.

We have evaluated a congenic strain of mice with congenital polycystic kidney disease in which the disease process appears to closely resemble human infantile polycystic kidney disease. Cysts formed first in the proximal tubules of the nephron and appeared, by light microscopy, to be preceded by vacuolization of the cells. These spaces, as seen by electron microscopy, occurred between adjacent cells. The pancreas was severely involved with reduction of both exocrine and endocrine elements. Cyst formation in the liver was minimal. Serum samples evaluated for urea nitrogen and creatinine were significantly elevated in affected mice. Serum glucose was within normal limits.

Animals↗
PubMed1985

C1q nephropathy: a distinct pathologic entity usually causing nephrotic syndrome.

The presence, distribution, and intensity of glomerular C1q localization were evaluated by direct immunofluorescence microscopy in 800 renal biopsy specimens which were also studied by light and electron microscopy. Identified were 15 patients with extensive (mean: 3.6 + out of 4 +), predominantly mesangial, C1q localization along with C3 and immunoglobulins, but no evidence for systemic lupus erythematosus. Pathologically, this lesion most closely resembled lupus nephritis. Clinical and pathologic data from these 15 C1q nephropathy patients were compared to data from 30 lupus nephritis and 223 other proliferative glomerulonephritis patients, and the C1q nephropathy patients were found to be dissimilar to both groups. The 15 C1q nephropathy patients had an average age of 17.8 years, 8 males, 7 females, 9 Black, 100% had proteinuria (mean 7.5 g/d), 40% hematuria, 0% hypocomplementemia, and 0% antinuclear antibodies. By electron microscopy, 100% had mesangial dense deposits, 20% capillary wall dense deposits, and 0% endothelial tubuloreticular inclusions. Nine patients treated with steroids had no definite resolution of proteinuria. We proposed that C1q nephropathy is a distinct clinicopathologic entity, usually causing steroid-resistant nephrotic syndrome in older children and young adults.

Adolescent↗
PubMed1985

Low incidence of IgA nephropathy in blacks.

The clinical and pathologic features were evaluated in 106 IgA nephropathy patients identified in 1,753 consecutive patients undergoing renal biopsy in the southeastern United States. Special attention was paid to the proportion of Blacks among the IgA nephropathy patients compared with non-IgA nephropathy patients, and any differences in clinical or pathologic findings between Whites and Blacks with IgA nephropathy. The incidence of IgA nephropathy was approximately six times lower in Blacks (6 out of 461) than in Whites (100 out of 1,292) undergoing renal biopsy (P less than 0.001). There were no morphologic or immunohistopathologic differences between Whites and Blacks with IgA nephropathy. The only clinical difference was a marked shift in the male to female sex ratio from 3.5:1 in Whites to 1:5 in Blacks (P less than 0.004). The low incidence and reversed sex ratio of IgA nephropathy in Blacks were also supported by a review of previously published data.

Adult↗
PubMed1985

Immunohistopathologic evaluation of C1q in 800 renal biopsy specimens.

The frequency, distribution, and intensity of C1q localization were evaluated in 800 renal biopsy specimens, and these observations were correlated with light, immunofluorescence, and electron microscopy findings. Intense C1q immunostaining was most frequent in proliferative and membranous lupus glomerulonephritis and in a recently described form of proliferative glomerulonephritis designated "C1q nephropathy." Moderate intensity C1q immunostaining was observed in most cases of type I but not type II, membranoproliferative glomerulonephritis. Unlike lupus membranous glomerulopathy, non-lupus membranous glomerulopathy usually did not have extensive C1q localization. C1q was scanty or absent in IgA nephropathy and antiglomerular basement membrane antibody mediated glomerulonephritis. C1q, along with IgM and C3, was often present at sites of glomerular sclerosis, especially in focal segmental glomerulosclerosis. Extraglomerular C1q was most frequent and most intense in cases of lupus nephritis having extraglomerular immune deposits. The presence or absence and intensity of C1q immunostaining were shown to be useful in the differential diagnosis of some glomerulopathies.

Autoantibodies↗
PubMed1985

Squamous metaplasia of the breast. An ultrastructural and immunologic evaluation.

Squamous metaplasia in the breast is rare. This case of an intracystic papilloma of the breast with prominent squamous change was found by electron microscopy and immunohistochemistry to contain evidence of squamous differentiation within myoepithelial cells. The findings suggest that squamous metaplasia of the breast may result from myoepithelial cell differentiation in a manner analogous to the development of squamous lesions in the cervix and salivary gland. The possible relationship of this finding to the development of squamous lesions of the breast is discussed.

Adult↗
PubMed1985

Reversal of Bartter's syndrome by renal transplantation in a child with focal, segmental glomerular sclerosis.

A four-year-old girl with growth failure and clinical and laboratory evidence of Bartter's syndrome responded to indomethacin treatment with decreased urinary prostaglandin excretion, symptomatic and chemical improvement, and accelerated growth. Large doses of aspirin produced a comparable decrease in prostaglandin excretion but no improvement in any other metabolic abnormality thus suggesting that abnormalities in prostaglandins were the result rather than the cause of the electrolyte abnormalities. Progressive renal insufficiency while on indomethacin prompted a renal biopsy, which revealed morphological changes of focal, segmental glomerular sclerosis. Subsequently, the child underwent renal transplantation with complete resolution of symptoms and abnormal metabolic findings. This observation suggests that extrarenal factors were not responsible for the development of Bartter's syndrome in this child.

Alkalosis↗
PubMed1985

Primary cerebral lymphoma with glomerular renal involvement.

We report a case of primary cerebral lymphoma metastasizing to the kidney with exclusive involvement of the glomeruli. We discuss the possible explanations of this unusual phenomenon, and present some of the unusual clinical features of the case. Nephropathologists interpreting glomerular hypercellularity should always consider metastatic neoplasms as a possible, though rare, cause.

Biopsy↗
PubMed1985

Renal medullary lymphatics: microradiographic, light, and electron microscopic studies in pigs.

Although renal cortical lymphatics have been extensively studied, the existence of renal medullary lymphatics has not been well documented. We studied renal microlymphatics in pig kidneys by retrograde ureteral injection of barium-sulfate-gelatin-saline mixture. Lymphatics filled as a result of forniceal rupture and interstitial extravasation. Microradiographs were correlated with histology and electron microscopy. We traced renal microlymphatic vessels from the arcuate level not only into the cortex but also into the pyramidal region, and therefore concluded that medullary lymphatics existed.

Animals↗
PubMed1985

Familial thrombotic microangiopathy.

A family in which there were two certain and three possible cases of thrombotic microangiopathy in two generations is presented. All afflicted members studied presented with acute renal failure, and accelerated hypertension. No abnormal platelet-aggregating activity could be identified in the plasma of asymptomatic family members or in the surviving patient in remission. Although an increase in the Factor VIII: von Willebrand's factor level was found in the sole surviving patient, the multimer pattern was normal. Platelet-associated IgG level was also normal in this individual. Thus, individuals predisposed to this familial form of thrombotic microangiopathy do not have a demonstrable marker which can be implicated in the development of the disorder. Long-term study of this kindred is required to determine the factors which are important in the pathogenesis of thrombotic microangiopathy in the affected individuals.

Acute Kidney Injury↗
PubMed1984

Kimura's disease: report of a pediatric case in the United States.

A 14-year-old male adolescent is described with a 6-year history of active lymphadenopathy, skin rash, peripheral blood eosinophilia, and markedly elevated serum-IgE level. Complete histopathologic and immunologic evaluations established the diagnosis of Kimura's disease as first described in Japan. Because of its relative infrequency and varied features, this disorder can be difficult to diagnose when it is encountered in the United States.

Adolescent↗
PubMed1983

Radiation nephritis causing nephrotic syndrome.

Clinical symptoms of acute radiation nephritis with nephrotic syndrome developed in a fifty-six-year-old woman after abdominal radiation therapy for an astrocytoma of the spinal cord. The diagnosis of radiation nephritis was confirmed by renal biopsy. To our knowledge, this is the first documented case of radiation nephritis associated with nephrotic syndrome.

Acute Disease↗