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Biomedical subjects

V Pardo

Publications and source records attributed to V Pardo.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effects of in vitro and in vivo anticanine T lymphocyte and anticanine class II-specific monoclonal antibodies in the beagle.

Two murine anticanine lymphocyte monoclonal antibodies, designated T83 and B1F6, were assessed for (1) in vitro antiepitope activity to circulating lymphocyte subsets, their functional effects on lymphoproliferative assays and binding specificities to diverse cell suspensions and tissue sections; (2) in vivo effects after administration on cells expressing the target epitopes, lymphoproliferation, and allograft survival; and (3) the host immune response to the injected murine immunoglobulins. The monoclonal antibody T83 (IgG3) appeared to be specific for a T cell subset with an up-regulating function on lymphoproliferation. It caused a profound depletion of cells with the appropriate epitope after intravenous administration but it bound to lymphocyte membrane epitopes on some cells in peripheral blood that did not become depleted and putatively caused other modulating effects on lymphocyte function. The monoclonal antibody B1F6 (IgG2a, previously described) was immunologically specific in vitro for cells expressing class II major histocompatibility complex antigens. In the dog, this also consisted of 50% of T lymphocytes. After intravenous administration, there were functional effects similar to those of T83. A modest prolongation of survival of renal allografts was observed when both mAbs were used as the sole immunosuppressive agent. These studies also demonstrated the occurrence of natural canine antimurine IgG antibodies. Administration of either monoclonal antibody was followed by a rapid increase in the concentration of the antimouse antibody(s). We postulate that the presence of canine natural antimouse IgG markedly influenced the biologic effects of in vivo administered monoclonals.

Animals↗
PubMed1987

Renal involvement in essential mixed cryoglobulinemia.

Essential mixed cryoglobulinemia (EMC) is infrequently recognized in this country. We report studies performed in six patients with EMC evaluated by us over the last 6 years. Purpura was present in three patients and glomerulonephritis in all. Two patients had chronic hepatitis B infection. Positive cryoglobulins and C1q binding, hypocomplementemia (especially low C4), positive rheumatoid factor titer, and negative anti-DNA antibodies were characteristic laboratory findings. The cryoprecipitate had strongly positive rheumatoid factor activity and contained a monoclonal IgM, kappa type in one of the two patients evaluated. The predominant lesion by renal biopsy was mesangiocapillary glomerulonephritis type I; electron microscopy revealed typical fibrillar structures in four cases. The above-mentioned features help distinguish EMC from other forms of glomerulonephritis.

Adult↗
PubMed1987

AIDS-related glomerulopathy: occurrence in specific risk groups.

The histopathology and incidence of AIDS-related glomerulopathy was evaluated by renal biopsy (N = 24) or at autopsy in 159 patients, including 131 adults and 28 infants and children with AIDS. Thirty-five patients had overt clinical manifestations of renal disease characterized by a nephrotic syndrome with focal and segmental glomerular sclerosis (FSS). Fifteen patients had diffuse glomerular mesangial hyperplasia (MH) without or with minimal clinical renal disease and 109 had intact or minimally involved glomeruli. Whereas 15 of 30 (50%) i.v. drug users with AIDS had evidence of renal disease, only one of 53 (2%) homosexuals had clinical renal disease and only 6 (11%) had histologic evidence of glomerular pathology. The study confirms the important risk of i.v. drug use as a pathogenic factor of renal disease and shows a rarity of renal disease in homosexual or bisexual men with AIDS. On the other hand, 30% of adult Haitians with AIDS had FSS or diffuse MH, although i.v. drug use is not an important risk factor in this population. Moreover, eight of 28 (29%) children with perinatal AIDS had evidence of renal involvement, including four with a nephrotic syndrome and FSS. The data provide strong evidence for the existence of an AIDS-related glomerulopathy independent of i.v. drug use, but suggest that unrecognized co-factors may be important in the development of renal disease.

AIDS-Related Complex↗
PubMed1987

In vivo and in vitro induction of class II molecules on canine renal cells and their effect on the mixed lymphocyte kidney cell culture.

Canine renal cortical cells were obtained by collagenase extraction from allogeneic haploidentical, donor-recipient beagle littermate pairs and from unrelated mongrels. Peripheral blood lymphocytes (PBL) of the mongrels, as well as of one member of the beagle pair that exhibited high mixed lymphocyte culture (MLC) reactivity against the other were also stimulated by renal cortical cells derived from both normal and rejected transplanted kidneys in mixed lymphocyte kidney cell culture (MLKC). A moderate autologous MLKC reactivity occurred in response to normal renal cortical cells. However, rejected kidney cortical cells were markedly more stimulatory than normal renal cortical cells in both allogeneic and autologous MLKC reactions. Lymphocytes from donor animals responded more strongly to autologous cortical cells isolated during rejection of the transplant than to cortical cells from normal allogeneic kidneys. Recipient infiltrating lymphocytes and propagated T cell lines extracted from the rejected kidney also responded more strongly than PBL to cortical cells from this kidney. Gradient purification of the stimulating cortical cells resulted in one virtually pure preparation of distal tubular epithelial cells, as demonstrated by immunohistochemical stains and electron microscopy, which caused enhanced stimulation in MLKC. Class II marker analysis of the canine renal cells from rejected kidneys revealed the presence of these molecules on tubular cells that were absent on normal kidney cells. A 16-hr coculture of normal renal cortical cells not exhibiting class II surface markers in the presence of allogeneic or autologous lymphocytes induced the expression of these molecules, associated with an increased stimulatory capacity. This also occurred to a lesser extent with MLC (and MLKC) cell culture media supernatants. However, the low level of class II expression by all the various gradient-purified fractions in the absence of rejection or coculture, and the increased but equivalent expression on all fractions after coculture did not correlate with the preferential stimulatory capacity of the purified distal tubular cell layer. We conclude that two signals are necessary for the MLKC reaction, one involving tissue (kidney)-associated epitopes (the nominal antigen demonstrated in this study to be present in normal distal tubular cells), the other involving class II molecules as costimulatory (amplification) moieties.

Animals↗
PubMed1987

Glomerular function and morphology after renal mass reduction in dogs.

To determine whether the proteinuria, glomerular sclerosis, and decline in glomerular filtration rate (GFR) described in rodents after renal mass reduction develop in another species, 24-hour proteinuria, glomerular structure, and fasting and postfeeding GFR were examined in dogs subjected to seven-eighths reduction in renal mass. All dogs were fed a diet containing 26% protein. Six dogs with a GFR less than 10 ml/min (8% to 17% of control two-kidney GFR) were killed within 6 months after renal mass reduction. Twenty-four-hour urinary protein excretion was modestly although definitely increased (236 +/- 26 mg/24 hr, P less than 0.01). All remnant kidneys demonstrated structural changes of mesangial hyperplasia or focal glomerular sclerosis. Ten dogs with a remnant kidney and early GFRs 16% to 39% of control values were followed for 18 to 39 months. In seven dogs, GFR showed little tendency to decrease with time. In one of them, proteinuria was 106 mg/24 hr with normal-appearing glomeruli at 14 months. In three dogs, proteinuria was progressive, averaging about 1 gm/24 hr at 18 months and 2 gm/24 hr at 24 to 34 months; glomerular pathologic findings progressed from focal mesangial hyperplasia or focal glomerular sclerosis at 8 to 16 months to focal and segmental sclerosis or diffuse glomerular obsolescence at 25 to 34 months; and fasting GFR progressively declined starting at 21 to 24 months after renal mass reduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The biologic significance of the mixed lymphocyte kidney culture in humans.

The mixed lymphocyte kidney culture (MLKC) in humans has been studied in normal and abnormal clinical conditions. Human renal cortical cells were extracted by collagenase treatment from the kidneys of "normal" heart-beating cadaver organ donors (n = 13), patients with end-stage renal disease (ESRD) at pretransplant bilateral nephrectomy and splenectomy (n = 13), and from irreversibly rejected renal allografts at the time of graft nephrectomy (n = 5). Proliferation of peripheral blood T lymphocytes of 2-DR-mismatched volunteers occurred in response to kidney cortical cells extracted from each of the 3 donor categories in a reaction termed the allogeneic mixed lymphocyte kidney culture. Additionally, splenic T cells from cadavers and patients with ESRD were seen to react to their autologous kidney cells. The renal cortical cells extracted from ESRD kidneys were more stimulatory in the allogeneic and autologous MLKC responses than those extracted from "normal" cadaver kidneys even when the ESRD kidneys were 99% depleted of passenger T and B lymphocytes by treatment with monoclonal antibodies T11 and B1. In order to help define the antigens operative in the MLKC, we pretreated stimulating lymphocytes and renal cortical cells with anti-class II monoclonal antibodies. The allogeneic mixed lymphocyte reaction and MLKC were inhibited ca. 80% and 30%, respectively. The autologous MLKC was unaffected by this treatment. To further support that tissue-specific immune mechanisms were operative in the reaction, experiments were performed with infiltrating lymphocytes isolated from the ESRD kidneys, which were seen to generate a proliferative response when stimulated with autologous cortical cells. However, the response of these same infiltrating lymphocytes when stimulated with allogeneic lymphocytes (MLR), was markedly weaker than the response of the patients' autologous spleen cells. In addition, two kidneys were obtained at rejection from recipients that had received grafts from HLA-MLR-identical sibling donors. A lymphoproliferative reaction of recipient peripheral blood T lymphocytes occurred in response to (donor) renal cortical cells, but not to donor peripheral blood lymphocytes. In contrast, infiltrating (recipient) kidney lymphocytes responded to the kidney cortical cells and to donor peripheral blood lymphocytes. Moreover, peripheral blood T lymphocytes of the HLA-identical donor responded to his own kidney cortical cells, which were isolated from the rejected recipient kidney, and did not respond to recipient peripheral blood lymphocytes. Finally, a "normal" cadaveric kidney was fortuitously available at the same time that a rejected transplant (cadaver)

Graft Rejection↗
PubMed1985

T cell lines and clones preferentially recognizing kidney-associated antigens in end-stage renal disease.

The specificity in the mixed lymphocyte kidney culture (MLKC) of T cell lines and clones derived from human end-stage renal disease (ESRD) kidneys was studied using collagenase dispersed kidney cells compared with lymphocytes as stimulating cells. These experiments were performed because of previous studies in which infiltrating lymphocytes freshly isolated from ESRD kidney tissue at nephrectomy (as well as autologous splenic T cells) were seen to directly generate this lymphoproliferative MLKC response when stimulated with autologous renal cortical cells. In the current studies, histopathologic staining of tissues and suspensions of infiltrating kidney lymphocytes showed predominance of OKT4 labeled phenotypes, and the stimulation indices in MLKC in general showed a direct relationship with the percentage of helper cells seen in the infiltrates. When T cell lines and clones derived from lymphocytes infiltrating the ESRD kidneys were tested in MLKC, there was evidence of kidney-associated, as opposed to lymphocyte-associated (MLC) reactivity using (3H) thymidine uptake as a reflection of a lymphoproliferative response. Several cell lines and clones derived from these T lymphocytes exhibited a dual reactivity. They served as responding cells in the MLKC reaction and completely suppressed a non-specific allogeneic MLC when added as third-party cells. Quantitatively, some clones suppressed when third-party x-irradiated cells were only 5% of the responding cell number in coculture. In addition to the dual reactivity, phenotypic analysis of these same cell lines and clones employing monoclonal antibodies revealed that individual cells expressed both OKT4 and OKT8 determinants. However, approximately 90% of the cells in the MLC enhancing line were labeled with OKT4. These results indicate that there is a complexity in the autologous MLKC response in that cells with both helper/inducer and suppressor/cytotoxic function take part in the reaction. Although delayed-type hypersensitivity to kidney-associated antigens is inferred as a result of these in vitro assays, nonspecific suppression of other Ia-dependent reactions can simultaneously occur.

Antibodies, Monoclonal↗
PubMed1984

The clinical significance of mesangial IgM deposits and mesangial hypercellularity in minimal change nephrotic syndrome.

Some patients with minimal change nephrotic syndrome (MCNS) present on biopsy mesangial IgM deposits, which may be associated with mesangial hyperplasia. These patients have been considered as a possible subset with a different response to therapy as well as prognosis and designated as mesangial IgM nephropathy or mesangial proliferative glomerulonephritis. However, the clinical relevance of these biopsy findings has been questioned by others. We reviewed the clinical, biopsy, and follow-up data in 61 MCNS children, 33 with mesangial IgM and 28 free of immunoglobulins. There were no significant differences in response to therapy or prognosis between these two groups. The lack of IgM elution and heterologous in vitro C3 fixation in the biopsies of some MCNS cases with IgM mesangial deposits does not support the possibility that the deposited IgM plays an immunologic role.

Adolescent↗
PubMed1984

Glomerular lesions in the acquired immunodeficiency syndrome.

Between January 1982 and December 1983, 75 patients with the acquired immunodeficiency syndrome were identified in our hospitals: 35% used intravenous drugs, 50% had proteinuria in excess of 0.5 g/dL, and 10% were nephrotic. Glomerular changes seen at autopsy in 36 patients included frequent mesangial lesions and deposits associated with mild asymptomatic proteinuria. Focal and segmental glomerular sclerosis was found in 5 patients and 4 of these had the nephrotic syndrome. Whereas reversible episodes of acute renal failure were not uncommon, terminal episodes of acute renal insufficiency occurred in 14 patients. The short survival of these patients may prevent the development of chronic renal failure.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Effect of duration of diabetes on the protection observed in the diabetic rat against gentamicin-induced acute renal failure.

We have previously shown that the rat with experimental diabetes (DM) of 4-6 months' duration exhibits complete functional and morphologic protection against gentamicin-induced acute renal failure. To assess the role of the duration of the diabetic state per se on the resistance to gentamicin, female Sprague-Dawley rats with diabetes of short (5 days, n = 7), intermediate (5 weeks, n = 5) and long duration (5 months, n = 7) were studied. Diabetes was induced by streptozotocin, 50-65 mg/kg b.w. i.v. Controls were identically treated sex- and age matched nondiabetic rats. The animals were kept in individual metabolic cages for 2 weeks and all received gentamicin 40 mg/kg/day for 9 days. Sham animals (DM and control) received Ringer's solution in place of gentamicin. Prior to gentamicin, plasma glucose levels and creatinine clearances (Ccr) were higher in the DM long duration group (619 +/- 25 (SE) mg/dl; 2.6 +/- 0.2 ml/min, respectively) than in the DM short (514 +/- 24; 2.0 +/- 0.1) and DM intermediate duration (442 +/- 30; 2.1 +/- 0.1) groups, while urine volume and glycosuria were similar. Following gentamicin the three control groups developed acute renal failure (maximal decrease in Ccr of 60 +/- 7, 72 +/- 9 and 71 +/- 7%, respectively; p less than 0.01 to less than 0.001), lysozymuria and acute tubular necrosis. There were no significant differences in the degree of renal impairment observed among the three control groups. In marked contrast, in the three DM groups these changes were absent and the renal cortical gentamicin content was lower than that of the control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1981

Glomerular disease in two patients with urticaria-cutaneous vasculitis and hypocomplementemia.

We assessed the clinical, serologic, and renal abnormalities of two patients with the syndrome of hypocomplementemia, vasculitis, and urticaria. Both patients presented with recurrent urticaria and were found subsequently to have glomerulonephritis. Both manifested depletion of the early complement (C) components, and their Cl inhibitor levels were normal. Circulating immune complexes were detected by two of three assays in both patients. One patient had a high titer of Sm antibodies. The detectable immune complexes were of high molecular weight, and were more suggestive of classical lupus erythematosus than the low molecular weight (7S) Clq precipitins which characterize some cases of hypocomplementemia-vasculitis-urticaria syndrome. Biopsy of the skin lesions in both patients revealed leukocytoclastic vasculitis with immunoglobulin and C deposits at the dermal-epidermal junction. Renal biopsy specimens showed segmental or diffuse proliferative mesangial glomerulonephritis. The results suggest that patients with this syndrome do not conform to a discrete entity but rather exhibit a spectrum of diseases ranging from systemic lupus erythematosus to the syndrome of urticaria, hypocomplementemia, and low molecular weight Clq precipitins.

Adult↗
PubMed1981

Delayed form of Wegener's granulomatosis.

We have described a patient in whom renal manifestations preceded the pulmonary findings of Wegener's granulomatosis by two years. He presented with rapidly progressive glomerulonephritis requiring chronic hemodialysis despite treatment with prednisone and azathioprine. Wegener's granulomatosis was diagnosed only after other signs of the generalized form of the disease had become manifest. Review of the literature revealed four similar cases. In patients with similar clinical presentations, serious consideration should be given to this delayed form of the syndrome. A course of cytotoxic therapy should be tried while the patient is followed up for further manifestations of generalized Wegener's granulomatosis.

Cyclophosphamide↗
PubMed1978

A mononuclear cell component in experimental immunological glomerulonephritis.

An accelerated form of nephrotoxic serum nephritis in the rat was examined. The experimental model consisted of preimmunization of the rat with rabbit IgG 5 days before injection of subnephrotoxic doses of rabbit anti-rat kidney serum. The immunized rats developed proteinuria during the first 24 h, increasing by 48-96 h. The early 24-h proteinuria correlated with a neutrophilic infiltration of glomeruli and with deposition of rat Ig and C. The 48- to 96-h proteinuria was associated with a glomerular infiltration by mononuclear cells and proliferation of intrinsic glomerular cells. Many of the mononuclear cells were morphologically identical to monocytes and macrophages. [3H]thymidine labeling experiments indicated that the mononuclear cells originated from dividing precursors localized outside the kidney. Preimmunized rats given systemic irradiation (the kidney being protected by a shield) showed loss of the mononuclear cell infiltrate and absence of 48- to 96-h proteinuria. We conclude that mononuclear phagocytes can infiltrate the kidney in immunological glomerular disease and might contribute to the functional abnormalities.

Animals↗