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Biomedical subjects

J Mattana

Publications and source records attributed to J Mattana.

At least 37 records · Page 2Linked to original sources
PubMed1997

Pressure modulates monocyte migration.

Migration of monocytes into the subendothelial space of the aorta has been considered to be an important event in the development of atherosclerosis. Because hypertension is commonly associated with atherosclerosis, we studied the effect of applied pressure on the migration of monocytes. Direct applied pressure increased the migration (P < .001) of monocytes across a filter when compared with normal atmospheric pressure. The migration of monocytes was found to be directly related to the amount of the applied pressure. Amlodipine, a calcium channel blocker, attenuated the migration of monocytes under normal as well as increased pressure conditions in a dose-dependent manner. These studies provide a basis to speculate on the role of direct pressure in the migration of monocytes into the subendothelial space and the possibility that vasoactive agents may modulate the migration of monocytes independent of their pressure-lowering effect.

Amlodipine↗
PubMed1997

Leukocyte-polytetrafluoroethylene interaction enhances proliferation of vascular smooth muscle cells via tumor necrosis factor-alpha secretion.

Intimal hyperplasia of vascular smooth muscle cells (VSMC) at the venous anastomosis of arteriovenous grafts represents the most common cause of vascular access failure in hemodialysis patients. Upstream release of growth factors from leukocytes activated by adhesion to the graft material may play a role in this lesion. We evaluated the effect of interaction of peripheral blood mononuclear cells (PBMC) with polytetrafluoroethylene (PTFE) on proliferation of VSMC. Vascular smooth muscle cell proliferation was significantly increased by conditioned media from human PBMC incubated with PTFE. Peripheral blood mononuclear cell adhesion to PTFE could not be antagonized by the beta 1 integrin ligand-containing peptide GRGDSP, but was attenuated by EDTA consistent with beta 2 integrin-mediated adhesion. Soluble scavenger receptor ligands at high concentrations had no effect on adhesion to PTFE excluding any contributory role of scavenger receptors in this interaction. Neutralizing antibodies to TNF-alpha significantly attenuated the mitogenic effect of PBMC/PTFE conditioned media and a marked increase in TNF-alpha secretion by PBMC on PTFE was detected by ELISA. These studies demonstrate that PBMC interaction with PTFE can promote proliferation of VSMC via increased production of TNF-alpha and perhaps other cytokines. Leukocyte interaction with PTFE causing enhanced secretion of TNF-alpha and consequent VSMC proliferation may account for the development of venous intimal hyperplasia in hemodialysis patients with arteriovenous grafts.

Antibodies↗
PubMed1997

Near-fatal but reversible acute renal failure after massive ibuprofen ingestion.

Adverse effects of nonsteroidal antiinflammatory drugs are frequently seen because of the extremely widespread use of these agents. Nephrotoxicity is relatively uncommon with the drug ibuprofen and, when present, is usually rapidly reversible. Fatal acute renal failure from ibuprofen has never been reported. This is the case of a patient with multiple medical problems who had near-fatal acute renal failure after the ingestion of 36 g ibuprofen, and who required dialysis for several months, at which point renal function improved. He did not admit to ibuprofen ingestion at the time of admission, and some of the clinical manifestations, including anion gap metabolic acidosis, respiratory alkalosis, and mental status abnormalities, could be accounted for by renal failure. Hence, this diagnosis was not considered during admission. However, the patient admitted to ibuprofen ingestion after his mental status improved with hemodialysis. A number of other variables were present that probably contributed to the development of acute renal failure, such as the presence of long-term renal insufficiency, hypotension, and possibly other drug ingestion. Acute renal failure with massive ibuprofen ingestion may be fatal or may show delayed reversibility even after necessitating dialysis for several months.

Acute Kidney Injury↗
PubMed1997

Atypical presentation of stroke in a diabetic hemodialysis patient.

Cerebrovascular disease is a major cause of death in patients with end-stage renal disease, particularly in those with diabetes mellitus. Cardiac disease frequently presents itself atypically in diabetic patients. This awareness has led to earlier detection and treatment of cardiac disease in diabetic patients. Whether cerebrovascular disease may also present itself in a highly atypical fashion in the diabetic patient with end-stage renal disease has never been addressed. We report the case of a diabetic hemodialysis patient who had an extremely unusual manifestation of stroke. A 67-year-old diabetic hemodialysis patient had marked distress secondary to the sudden onset of a foreign body sensation in the oropharynx. Results of a laryngoscopy were negative; x-rays of the neck and computerized tomography of the head and neck showed no abnormalities. Neurologic evaluation revealed an inability to detect oropharyngeal stimuli and an absent gag reflex but no other deficits. Magnetic resonance imaging of the brain revealed an infarction in the left corona radiata that extended to the thalamocapsular region and external capsule, and a lacunar infarct in the right pons. Cerebrovascular disease in the diabetic patient with end-stage renal disease may present itself atypically, and we suggest that cerebrovascular disease in these patients merits the same level of suspicion as cardiac disease.

Aged↗
PubMed1997

Reversible hemiplegia as a consequence of severe hyperkalemia and cocaine abuse in a hemodialysis patient.

Severe hyperkalemia may cause weakness that typically is ascending and symmetric. In an isolated case report, hemiplegia occurred after the development of hyperkalemia in a patient with a known central nervous system lesion. We describe a patient requiring long-term hemodialysis who had near-fatal hyperkalemia, hemiplegia, and rhabdomyolysis after abuse of crack cocaine. The hemiplegia resolved after normalization of serum potassium using emergency dialysis. No brain lesion could be identified during computed tomography or by electroencephalography, and the patient had no residual neurologic deficits. We conclude that this patient had hemiplegia secondary to cocaine-induced cerebral vasoconstriction because no structural lesion could be found and that the neurologic deficit was worsened by severe hyperkalemia, which probably resulted from cocaine-induced rhabdomyolysis. Hence, despite the absence of a structural lesion of the brain, severe hyperkalemia, typically associated with symmetric, ascending muscle weakness, may contribute to causing focal weakness in the condition of cocaine-induced vasoconstriction.

Adult↗
PubMed1997

Laboratory abnormalities in patients with bacterial pneumonia.

STUDY OBJECTIVES: This study was undertaken to evaluate the laboratory abnormalities observed in patients with bacterial pneumonia as predictors of the severity of illness. DESIGN: Retrospective analysis. SETTING: Tertiary care hospital. PATIENTS AND PARTICIPANTS: We studied 302 consecutive patients who were admitted to the Long Island Jewish Medical Center from January through December 1993 and treated for bacterial pneumonia. The patients were subdivided into two groups based on their serum phosphorus level either on hospital admission or 4 days before the onset of pneumonia, if this was acquired in-hospital. Hypophosphatemia (group 1) was defined as serum phosphorus level of < or = 2.4 mg/dL and normophosphatemia > 2.4 mg/dL (group 2). Three hundred randomly selected hospitalized patients treated for conditions other than pneumonia comprised the control group (group 3). MEASUREMENTS: Groups 1 and 2 were compared with respect to laboratory data, mortality rate, and duration of hospitalization. The laboratory data of patients in group 3 were compared with those treated for bacterial pneumonia (groups 1 and 2). Stepwise multivariate logistic regression analysis was employed to identify the variables that best predicted the onset of pneumonia. RESULTS: In groups 1 and 2, a greater (p < 0.0001) number of patients (135 of 302 patients with pneumonia, 44.7%) developed hypophosphatemia compared with patients in group 3 (31 of 300 control subjects, 10.3%). Patients with pneumonia (groups 1 and 2) had higher levels (p < 0.01) of bicarbonate compared with control subjects. Moreover, patients with pneumonia demonstrated lower levels (p < 0.01) of calcium, phosphorus, albumin, cholesterol, and alanine aminotransferase compared with control patients (group 3). Among patients with pneumonia, those with hypophosphatemia (group 1) had significantly lower levels (p < 0.05) of potassium, calcium, and albumin compared to those subjects with normophosphatemia (group 2). Furthermore, hypophosphatemic subjects manifested higher levels of glucose (p < 0.01) and creatine phosphokinase (p < 0.05) compared to their normophosphatemic counterparts. In addition, hypophosphatemic patients experienced a longer duration of hospital stay (hypophosphatemia, 24.6 +/- 2.0 days, vs normophosphatemia, 14.1 +/- 1.0, p < 0.001) and higher (p < 0.001) mortality compared to normophosphatemic subjects. The incidence of nosocomial pneumonia was higher (p < 0.0001) in hypophosphatemic patients compared to those with normophosphatemia. CONCLUSION: We conclude that hypophosphatemia, hypocalcemia, hypokalemia, and hypoalbuminemia may be predictors of the severity of illness in patients admitted to the hospital with bacterial pneumonia.

Aged↗
PubMed1997

Risk of fatal cerebrovascular accident in patients on peritoneal dialysis versus hemodialysis.

Several reports have suggested that the incidence of hemorrhagic stroke may be greater on hemodialysis as compared with that among the general population and that patients with intracranial hemorrhage should be treated with peritoneal dialysis rather than hemodialysis. However, whether the risk of fatal stroke is greater on hemodialysis versus peritoneal dialysis has not been systematically examined. In this study, the case of a diabetic patient with extensive peripheral vascular disease who, after 7 years on hemodialysis, was changed to peritoneal dialysis and subsequently suffered two strokes over a 5-month period, is reported. Recent data from the United States Renal Data System, which allow a comparison of death rates from stroke in large numbers of hemodialysis versus peritoneal dialysis patients, are reviewed. These data suggest that the risk of death from stroke may actually be greater for patients on peritoneal dialysis versus hemodialysis in spite of their having a lesser prevalence of preexisting cerebrovascular disease. This risk was greatest for elderly diabetic black patients and women, who experienced a nearly twofold-greater odds favoring death from stroke on peritoneal dialysis versus hemodialysis. Selection of a dialysis modality for a patient beginning renal replacement therapy may require the consideration of such data, particularly in those patients with extensive preexisting vascular disease.

Cerebrovascular Disorders↗
PubMed1997

Age and sex modulate renal expression of SGP-2 and transglutaminase and apoptosis of splenocytes, thymocytes, and macrophages.

BACKGROUND: Aging in humans has been associated with the progressive loss of renal mass. This has been considered to account for a significant reduction of glomerular filtration rate in the aging population. In addition, aging is associated with a compromised immune system. Macrophages, thymocytes, and splenocytes play an important role in the maintenance of the immune system. We studied the effect of sex and aging on apoptosis of peritoneal macrophages, thymocytes, and splenocytes. In addition, we also studied the effect of sex and aging on mRNA expression of active cell death genes on the renal cortex. METHODS: Rats in groups of 4 to 12 were killed at ages 2, 14, 30, 50, 75, and 100 weeks. Renal cortices, peritoneal macrophages, thymocytes, and splenocytes were isolated. DNA was isolated and run on agarose gel electrophoresis. Apoptosis of renal cells was evaluated by the TUNEL method and transmission electron microscopy. RNA was isolated from renal cortices and probed with specific cDNA probes for genes associated with active cell death, such as SGP-2, cathepsin-B, and tissue transglutaminase. Mesangial cells (MC) derived from younger and older rats were examined for the occurrence of apoptosis. The effect of estradiol and testosterone was studied on mesangial cell apoptosis. RESULTS: At 2 weeks, peritoneal macrophages, thymocytes, and splenocytes showed no DNA fragmentation. Apoptosis of macrophages, splenocytes, and thymocytes increased with age in the males as well as females. Mesangial cells derived from aged rats showed a greater percentage of apoptosis when compared to MC derived from younger rats. Estradiol and testosterone directly affect mesangial cell apoptosis. Renal cortices of male rats showed enhanced mRNA expression of SGP-2 and tissue transglutaminase with aging; whereas expression of cathepsin-B peaked at 30 weeks in both male and female rats. CONCLUSION: Age and sex modulate renal cortical mRNA expression of genes associated with active cell death. Age and sex also modulate apoptosis of macrophages, splenocytes, and thymocytes.

Aging↗
PubMed1996

Absence of edema in HIV-infected patients with end-stage renal disease.

In attempting to identify variables that might account for the frequent absence of edema in HIV-infected patients with end-stage renal disease, we evaluated 24 consecutive patients at our institution who had HIV infection and developed end-stage renal disease. Clinical and laboratory data prior to the initiation of hemodialysis were recorded and compared between patients with and without edema. Only 11 of the 24 study patients had edema while the remainder did not. The prevalence of diarrhea was significantly less in patients with edema (one of 11 patients compared to eight of 13 with no edema, p < 0.02, odds ratio 0.063). Prior weight loss was significantly less in the patients with edema (9.1 +/- 1.3 kg vs 15.5 +/- 2.2 kg, p < 0.05). Use of antiretroviral therapy was significantly greater in patients with edema (p < 0.05, odds ratio 10.1). None of the patients were receiving diuretics. Blood pressure was significantly higher (p < 0.001) in patients with edema, and serum albumin was low in both groups but did not differ (edema, 24 +/- 2 g/L; no edema, 21 +/- 3 g/L). Four patients had albumin levels as low as 2, 8, 9, and 10 g/L, yet they had no edema. CD4 counts were lower in patients without edema (62 +/- 16 x 10(6) cells/L vs 283 +/- 38 x 10(6) cells/L, p < 0.001). Absence of diarrhea was predictive of the presence of edema with a sensitivity of 91% and specificity of 62% while mean arterial blood pressure > 95 mm Hg was predictive of the presence of edema with a sensitivity of 82% and specificity of 77%. CD4 of > 100 x 10(6) cells/L was predictive of the presence of edema with a sensitivity of 91% and specificity of 77%. These data support the hypothesis that hemodynamic factors may play a role in the frequent absence of edema in patients with HIV infection and renal failure, and variables including diarrhea, low blood pressure, weight loss, and more advanced stage of HIV infection may account for this observation. Hence, the absence of edema should not dissuade the clinician from considering the possibility of advanced renal failure in HIV-infected patients.

Adult↗
PubMed1996

Wegener's granulomatosis followed by development of sarcoidosis.

Although both Wegener's granulomatosis and sarcoidosis are considered granulomatous disorders, their clinical courses differ markedly, and typically patients with these two diseases are readily distinguishable. We report an unusual case in which the patient presented with a systemic vasculitis consistent with Wegener's granulomatosis that remitted with therapy and then, months later, developed sarcoidosis. This is the first case report of the sequential development of the two diseases. We review the relationship of vasculitis to sarcoidosis and speculate on the etiopathogenesis that might link the two.

Adult↗
PubMed1996

Morphine-induced macrophage activity modulates mesangial cell proliferation and matrix synthesis.

Glomerular mesangial injury is the predominant renal lesion in patients with heroin addition. We studied the effect of morphine (an active metabolite of heroin)activated macrophages on mesangial cell (MC) proliferation and matrix synthesis. We prepared conditioned media containing either vehicle along (CSP), macrophage secretory products (MSP) and secretory products of morphine treated macrophages (M-MSP), M-MSP increased (P < 0.01) the proliferation of MC when compared with MSP alone. M-MSP increased synthesis of laminin by MC at concentrations of 10 to 50% when compared with cells treated with MSP alone (at 50% concentration, MSP, 126 +/- 19 vs. M-MSP, 312 +/- 14 ng/mg protein, P < 0.001). M-MSP also increased the synthesis of collagen type IV by MC. This effect of M-MSP was attenuated (P < 0.05) by anti-TGF-beta antibodies. Since M-MSP also increased mRNA expression for TGF-beta by MC, it appears that the effected of M-MSP on MC may be mediated through the generation of TGF-beta.

Animals↗
PubMed1996

Native and oxidized low density lipoproteins modulate mesangial cell apoptosis.

Hyperlipidemia has been demonstrated to contribute to hypercellularity of the mesangium in experimental animal models of glomerulosclerosis. We studied whether it also has the potential to convert a hypercellular mesangium into a hypocellular one by inducing mesangial cell (MC) apoptosis. Low density lipoprotein (LDL) enhanced (P < 0.001) mouse mesangial cell (MMC) proliferation at lower concentrations (control, 10.3 +/- 0.3 vs. LDL 100 micrograms/ml, 24.2 +/- 0.3 x 10(4) cells/ml) but augmented (P < 0.001) apoptosis at higher concentrations (control, 5.6 +/- 0.5% vs. LDL, 500 micrograms/ml 26.2 +/- 3.4% apoptotic cells/field). Oxidized (OX) LDL enhanced MMC apoptosis in concentrations of 50 to 200 micrograms/dl. There was a direct relationship between MMC apoptosis and oxidation of LDL as judged by measuring thiobarbituric acid reactive species (TBARS). Since superoxide dismutase (SOD) attenuated (P < 0.001) LDL-induced MMC apoptosis, it seems to be mediated through the generation of free radicals by mesangial cells (control, 4.3 +/- 1.5%; LDL, 200 micrograms/ml, 19.4 +/- 0.5%; LDL + SOD, 8.1 +/- 1.3% apoptotic cells/field). LDL also induced a similar effect on human mesangial cells. These studies were further confirmed by DNA fragment assays and ELISA for programmed cell death. LDL treated cells also showed enhanced mRNA expression for RSG-2, a marker for active cell death. These in vitro results provide a basis for the speculation that LDL has the potential to cause an initial hypercellular and subsequent hypocellular mesangium in the course of the development of glomerulosclerosis.

Animals↗
PubMed1996

Increased applied pressure enhances the uptake of IgG complexes by macrophages.

Increased pressure, as may occur with hypertension, may alter cellular function by inducing repetitive mechanical strain. However, increased pressure itself may directly alter cellular function independent of stretching of cells. We undertook the present study to determine whether increased applied pressure could alter uptake of IgG complexes by macrophages. Increased pressure was applied to confluent macrophages grown on plastic culture plates using a pressure chamber apparatus kept inside the incubator at 37 degrees C and pressure regulated using a rotator pump and adjustable outlet valve. Macrophages that were subjected to increased pressure were found to have a significantly greater uptake of IgG complexes in a dose-dependent manner. The effect of increased pressure could be abrogated by carrying out experiments in calcium-free medium while this exerted no effect on uptake by macrophages under control conditions. Increased uptake of IgG complexes by macrophages subjected to increased applied pressure could also be attenuated by incubation with the calcium channel blockers amlodipine and cinnarizine. To determine whether the effect of increased pressure was related to the plastic substrate on which the cells are grown, cells were also seeded onto type I collagen gels and uptake of IgG complexes was measured. Uptake by macrophages on the type I collagen substrate was significantly enhanced with increased applied pressure compared to control (p < 0.01). These studies demonstrate that exposure of macrophages to increased pressure enhances their uptake of IgG complexes via a mechanism that appears to involve an increase in intracellular calcium. This effect might play a role in some of the consequences of systemic arterial and glomerular capillary hypertension.

Amlodipine↗
PubMed1996

Predictors of survival in HIV-infected patients on hemodialysis.

We undertook the present study to determine whether there might be variables other than CD4 counts which might help predict survival of HIV-infected patients who are placed on chronic hemodialysis, survival which often is extremely poor. We studied prospectively (n = 18) and retrospectively (n = 6) 24 consecutive HIV-positive patients on chronic hemodialysis at our institution over a 7-year period and recorded clinical and laboratory variables at the time of initiation of dialysis. The mean survival for the group as a whole was 11 +/- 8 (range 2-32) months. A highly significant positive correlation was found between survival and CD4 counts (p < 0.001) and blood pressure (systolic, p < 0.02; diastolic, p < 0.05; mean arterial, p < 0.05). Infection rate and urine protein excretion both had significant negative correlations with survival (p < 0.01 and p < 0.02, respectively). The presence of edema appeared to have a positive effect on survival (p < 0.01). The use of antiretroviral therapy resulted in significantly greater survival of HIV-infected patients (15.2 +/- 2.2 vs. 6.2 +/- 1.2 months, p < 0.01). Using a general linear model, it was found that CD4 count and systolic, diastolic, and mean arterial blood pressures and infection rate all were independent estimators of survival. We conclude that variables other than CD4 counts might also be useful in predicting survival in HIV-infected patients on chronic hemodialysis.

AIDS-Associated Nephropathy↗
PubMed1996

Renal cell carcinoma presenting as a solitary anterior superior mediastinal mass.

Lesions of the anterior mediastinum typically include neoplasms of the thymus or thyroid, hemangioma, germ cell neoplasms, lymphoma and others. Renal cell carcinoma often presents with flank pain, hematuria, abdominal pain and/or fever. Chest cavity involvement by renal cell carcinoma typically manifests as pulmonary parenchymal disease with or without hilar lymph node involvement. We report an unusual presentation of renal cell carcinoma in a patient who presented with symptoms secondary to a large anterior mediastinal mass. A 64-year-old woman came to the hospital complaining of malaise, cough, dyspnea, weight loss and night sweats. Chest roentgenogram and computed tomography revealed a large anterior superior mediastinal mass without significant pulmonary parenchymal disease. She was also noted to have microscopic hematuria and a renal mass was found. Histology of both masses revealed renal cell carcinoma. This case suggests that renal cell carcinoma may merit consideration in the differential diagnosis of an anterior mediastinal mass and illustrates an unusual manner by which this lesion may present.

Carcinoma, Renal Cell↗
PubMed1995

Oxidation of mesangial matrix using a mixed function oxidase system augments adhesion of macrophages: possible role of macrophage scavenger receptors.

Oxygen radicals are believed to play a role in the pathogenesis of aging and glomerular injury. Changes in cellular function may result from modification of the extracellular matrix with which they interact. We produced oxidized mesangial matrix protein using a mixed function oxidase system. Carbonyl content of the oxidized matrix was significantly increased. Adhesion of macrophages to the oxidized mesangial matrix was significantly enhanced, an effect which was significantly abrogated by scavenger receptor blockade with polyinosinic acid or dextran sulfate. Neither polyinosinic acid nor dextran sulfate diminished macrophage adhesion to unmodified matrix. These data demonstrate for the first time that mesangial matrix can undergo oxidation and that such oxidation may promote accumulation of macrophages in the mesangium via interaction of macrophage scavenger receptors with oxidized matrix proteins.

Analysis of Variance↗
PubMed1995

Applied pressure modulates mesangial cell proliferation and matrix synthesis.

Substantial in vivo evidence suggests a significant role for glomerular capillary pressure in the pathogenesis of progressive glomerulosclerosis. One presently available in vitro system allows one to study cells while undergoing stretch. However, no comparable system is available to allow one to study in an in vitro system how direct application of pressure to glomerular mesangial cells might result in the development of glomerulosclerosis. We constructed a pressure chamber in which mesangial cells could be subjected to an applied pressure by means of a roller pump and adjustable outlet valve. Mesangial cells were grown either under control conditions or under an applied pressure of 40 to 50 mm Hg corresponding to physiologic intraglomerular pressure. Application of pressure significantly decreased mesangial cell number in prolonged culture though no discernable effect on cell proliferation could be detected after only short-term exposure. Long-term exposure to increased pressure significantly enhanced mesangial cell [3H] proline incorporation, a marker for synthesis of the matrix component collagen, an event considered to be a precursor to the development of glomerulosclerosis. Mesangial cell matrix synthesis was significantly greater for cells subjected to 50 to 60 mm Hg pressure compared to 40 to 50 mm Hg pressure. Secretory products from macrophages subjected to 40 to 50 mm Hg of applied pressure were found to significantly enhance mesangial cell proliferation compared to secretory products from macrophages grown under normal pressure. The enhancement of mesangial cell matrix synthesis by pressure could not be attributed to any change in partial pressure of oxygen in the media nor pH. These data suggest that the direct application of pressure to mesangial cells may result in the development of glomerulosclerosis by increasing mesangial cell matrix synthesis. These in vitro data support a role for glomerular capillary pressure in the pathogenesis of progressive glomerulosclerosis.

Animals↗