Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heroin-associated nephropathy (HAN), a complication of intravenous heroin abuse, was initially recognized at Kings County Hospital in Brooklyn, NY, in the early 1970s. Our recent experience indicates that after a steady incidence of new cases of HAN throughout the mid-1980s, a sharp decrease in incidence of new cases occurred starting in 1989. We sought to explore possible explanations for what amounts to disappearance of a previously prevalent disease. By means of retrospective analysis of a hospital-specific registry of new cases of end-stage renal disease (ESRD) at Kings County Hospital in Brooklyn, incidence curves from 1981 through 1993 for new cases of HAN, diabetes-induced renal disease, and human immunodeficiency virus-associated nephropathy were constructed. From hospital computer records, the number of admissions directly related to opioid abuse were extracted and charted. Unpublished surveillance records of the New York State Office of Alcoholism and Substance Abuse Services as well as reports from the New York City Department of Health, Office of AIDS Surveillance and the US Department of Justice Drug Enforcement Administration were used to determine the pattern of change in the prevalence of heroin abuse. Additionally, we used analysis of "street" heroin by the Drug Enforcement Administration to draw curves detailing drug cost and purity in New York City. There were no new cases of ESRD due to HAN for the years 1991 through 1993. The rates for new cases of ESRD due to diabetes and hypertension remained relatively constant throughout this interval.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disappearance of uremia due to heroin-associated nephropathy. 774 21

The superimposition of human immunodeficiency virus (HIV) infection, associated opportunistic infections, and anti-retroviral therapy further worsens the severity of anemia in patients also suffering from end-stage renal disease. A major cause of anemia in renal failure is a deficiency of erythropoietin. The causes of anemia in HIV disease include direct and indirect stem cell inhibition by the virus, increased peripheral destruction of red blood cells, and bone marrow suppression by various opportunistic infections and therapeutic drugs, particularly zidovudine. We compared the efficacy of recombinant human erythropoietin (rHuEPO) therapy in improving the anemia in HIV-infected end-stage renal disease patients (group I) with that in nondiabetic (group II) and diabetic (group III) hemodialysis patients without HIV infection. All three groups of patients were comparable in dialysis prescription and serum iron studies. Iron supplementation was prescribed to all patients, and none received blood transfusions. After 8 weeks of rHuEPO therapy (administered intravenously in a dose of 100 U/kg body weight thrice weekly), the mean increase in hematocrit was similar in all responders (5.8% increase in hematocrit in 23 of 30 HIV patients and 6.7% increase in 24 of 30 non-HIV patients). Response in hematocrit was noted in HIV patients despite the presence of opportunistic infections in 15 and zidovudine administration in 11. Seven HIV-positive patients and six non-HIV patients failed to respond to rHuEPO. Irrespective of the HIV status, the baseline serum EPO levels in patients responding to rHuEPO were significantly lower than those in nonresponders.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The efficacy of erythropoietin in human immunodeficiency virus-infected end-stage renal disease patients treated by maintenance hemodialysis. 777 87

Microsporidia are obligate, intracellular, spore-forming protozoal parasites. Their host range is extensive and includes most invertebrates and all classes of vertebrates. Five microsporidial genera (Enterocytozoon, Encephalitozoon, Septata, Pleistophora, and Nosema) and unclassified microsporidia have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. The majority of microsporidial infections in persons infected with human immunodeficiency virus (HIV) are attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Four cases of microsporidial infection among persons not infected with HIV who had documented or presumed cellular immunodeficiency and four cases of corneal stroma infection due to microsporidia in immunocompetent patients have been described. Furthermore, the first case of traveler's diarrhea due to E. bieneusi in an immunocompetent and otherwise healthy patient is reported in this issue. The sources of human microsporidial infections and modes of transmission are unknown.
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PMID:Microsporidial infections in immunodeficient and immunocompetent patients. 781 72

Patients with end-stage renal disease present an immunodeficiency that paradoxically coexists with activation of most immunocompetent cells, and the roles of chronic uremia and maintenance dialysis are poorly understood. We determined circulating levels of IL-1 beta and IL-1Ra, TNF-alpha and its soluble receptors (TNF-sR55 and TNF-sR75), and activation markers of T cells (soluble CD25), B cells (soluble CD23), and monocytes (neopterin) in a large cohort of undialyzed patients at various stages of chronic renal failure and in dialyzed patients on maintenance hemodialysis or chronic peritoneal dialysis. The progression of uremia was associated with a gradual increase in soluble CD25, CD23, and especially neopterin levels. Although IL-1 beta could not be detected, IL-1Ra levels were significantly increased from the earliest stage of renal failure. Plasma levels of TNF-alpha, TNF-sR55, and TNF-sR75 progressed with the severity of renal failure and correlated with soluble CD25, CD23, and neopterin levels, whereas IL-1Ra levels correlated exclusively with TNF-sR55 levels. Compared with undialyzed patients, levels of IL-1 beta were higher in patients on maintenance hemodialysis, whereas those of IL-1Ra were lower and decreased further at the end of dialysis sessions. In contrast, both TNF-sR55 and TNF-sR75 levels were significantly higher than in undialyzed patients and increased further at the end of dialysis sessions in the absence of an increase of TNF-alpha. Such an imbalance between cytokines and their inhibitors may play a pivotal role in the multifaceted process of immune dysfunction.
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PMID:Balance between IL-1 beta, TNF-alpha, and their specific inhibitors in chronic renal failure and maintenance dialysis. Relationships with activation markers of T cells, B cells, and monocytes. 781 91

Microsporidia are obligate intracellular spore-forming protozoal parasites belonging to the phylum Microspora. Their host range is extensive, including most invertebrates and all classes of vertebrates. More than 100 microsporidial genera and almost 1,000 species have now been identified. Five genera (Enterocytozoon spp., Encephalitozoon spp., Septata spp., Pleistophora sp., and Nosema spp.) and unclassified microsporidia (referred to by the collective term Microsporidium) have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. Among persons not infected with human immunodeficiency virus, ten cases of microsporidiosis have been documented. In human immunodeficiency virus-infected patients, on the other hand, over 400 cases of microsporidiosis have been identified, the majority attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Diagnosis of microsporidiosis currently depends on morphological demonstration of the organisms themselves. Initial detection of microsporidia by light microscopic examination of tissue sections and of more readily obtainable specimens such as stool, duodenal aspirates, urine, sputum, nasal discharge, bronchoalveolar lavage fluid, and conjunctival smears is now becoming routine practice. Definitive species identification is made by using the specific fluorescein-tagged antibody (immunofluorescence) technique or electron microscopy. Treatment options are limited, but symptomatic improvement of Enterocytozoon bieneusi infection may be achieved with the anthelmintic-antiprotozoal drug albendazole. Preliminary observations suggest that Septata intestinalis and Encephalitozoon infections may be cured with albendazole. Progress is being made with respect to in vitro propagation of microsporidia, which is crucial for developing antimicrosporidial drugs. Furthermore, molecular techniques are being developed for diagnostic purposes, taxonomic classification, and analysis of phylogenetic relationships of microsporidia.
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PMID:Human microsporidial infections. 783

Among a spectrum of renal disorders encountered in patients infected with the human immunodeficiency virus (HIV), the lesion studied most often has been the glomerular disease known as HIV-associated nephropathy. Of the other coincidental renal perturbations reported, the most significant are a heterogenous group encompassing potentially reversible acute renal failure (ARF), primarily acute tubular necrosis. While HIV-associated nephropathy may frequently be seen in asymptomatic HIV-seropositive individuals, acute tubular necrosis almost always is encountered in patients with clinical acquired immunodeficiency syndrome (AIDS). We analyzed our decade's experience in the management of 146 HIV disease patients with ARF (132 AIDS patients and 14 HIV-seropositive patients) and compared it with a contemporaneous group of 306 non-HIV subjects with ARF. All patients evaluated for ARF between January 1984 and December 1993 by the Renal Division at Kings County Hospital Center, Brooklyn, NY, were reviewed. Only those patients with ARF who reached a serum creatinine concentration of 530 mumol/L or higher were included in the analysis. Ninety-one percent of 146 HIV disease patients with ARF were less than 50 years old compared with only 33% of the 306 non-HIV subjects (P < 0.001). Septicemia was directly or indirectly responsible for 75% of patients with ARF in the AIDS group and for 39% in the non-HIV subjects (P < 0.006). Urinary tract obstruction was the cause of ARF in 54 of 306 (17%) non-HIV patients compared with none in the HIV group (P < 0.00001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Outcome of severe acute renal failure in patients with acquired immunodeficiency syndrome. 787 16

Polymicrobial peritonitis is a relatively uncommon, but potentially serious complication that develops in continuous ambulatory peritoneal dialysis (CAPD) patients. Its cause and optimal management remain controversial. The authors reviewed the frequency and natural history of polymicrobial peritonitis in 432 CAPD patients. Of 1,405 episodes of peritonitis, 80 were polymicrobial (6%). Patients with polymicrobial peritonitis were similar to all CAPD patients in age, gender, race, and underlying renal disease. Diabetes mellitus, human immunodeficiency virus (HIV) status, and clinically apparent gastrointestinal disease did not predisposes patients to polymicrobial peritonitis. Thirty days after the polymicrobial peritonitis, 64 patients remained on CAPD (80%), and at 180 days 48 patients continued CAPD. Prior exit-site infections were present in 12 patients (14%) with polymicrobial peritonitis. Only 22% of patients required catheter removal to treat the infection. We conclude that polymicrobial peritonitis accounts for 6% of the total episodes of peritonitis; diabetes, HIV infection, and underlying gastrointestinal disease are not more prevalent in patients with multiorganism infections. Most patients continue CAPD therapy at 30 and 180 days after the episode of polymicrobial peritonitis.
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PMID:Outcome of polymicrobial peritonitis in continuous ambulatory peritoneal dialysis patients. 787 25

This review summarizes recent progress in the immunologic aspects of parenchymal renal disease. Progress in understanding basic immune mechanisms of glomerular injury is outlined, including the roles of chemoattractants, adhesion molecules, metalloproteinases, and cytokines. Current basic and clinical studies of focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferative glomerulonephritis, minimal-change nephropathy, and IgA nephropathy are summarized. Finally, research in glomerular involvement in systemic disorders, such as lupus nephritis, antineutrophil cytoplasmic antibody-associated syndromes, and human immunodeficiency virus-associated nephropathy, is reviewed.
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PMID:Immunologic renal injury. 792 81

Familiarity with renal issues that can challenge the care of patients with human immunodeficiency virus (HIV) should expedite diagnosis and therapeutic interventions. Among the most common problems are electrolyte and acid-base imbalances from many opportunistic infections or their treatments, including hyponatremia, hyperkalemia, hypokalemia, and hypo- and hypercalcemia. Acid-base disturbances, simple or mixed, can be due to underlying sepsis, opportunistic infections, or the therapy thereof. A recent report of seven patients with HIV with type B lactic acidosis failed to identify a satisfactory etiology. Elevations in creatinine or diminishing urine output should alert the physician to the possibilities of prerenal azotemia or acute tubular necrosis, which can result from progression of prerenal azotemia or can occur secondary to administered nephrotoxins, such as certain antibiotics and radiocontrast agents. Agents associated with nephrotoxicity include aminoglycosides, antifungal, antiviral, and radiocontrast agents, and nonsteroidal anti-inflammatory pain medications. Although prerenal azotemia and acute tubular necrosis are the most frequent causes of acute renal failure, the differential diagnosis should include acute interstitial nephritis, obstructive nephropathy, and glomerulopathies such as hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, the newly described IgA nephropathy, and, in certain populations, HIV nephropathy.
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PMID:The spectrum of kidney diseases in patients with human immunodeficiency virus infection. 792 95

Several renal pathologic entities have been reported to be associated with human immunodeficiency virus (HIV) infection. The most common is focal glomerulosclerosis, but several different types of glomerulonephritis have been observed in patients with HIV infection and the acquired immunodeficiency syndrome. The mechanisms involved in the pathogenesis of the kidney disease remain obscure. We studied an HIV-infected patient treated with interferon-alpha who had developed proteinuria and membranoproliferative glomerulonephritis to determine whether the renal disease was associated with HIV infection or with chemotherapy. Circulating HIV antibodies were assessed by enzyme-linked immunosorbent assay; circulating immune complexes (CICs) were measured by C'1q assay and isolated by polyethylene glycol precipitation, then subjected to gel electrophoresis and immunochemical analysis. Renal biopsy tissue underwent acid elution, and the eluates were analyzed similarly. In addition the eluted antibody and the antibody from the CIC were assessed by immunodiffusion with eluate and immune complex antigens. A single CIC was detected, which was composed of an immunoglobulin G antibody complexed to a 26-kd protein antigen that was shown to be interferon-alpha. Eluate from the renal biopsy tissue demonstrated identical material, which cross-reacted with the components of the isolated CIC. Immune complex renal diseases, such as membranoproliferative glomerulonephritis, may be related to biologic response modifying agents in patients with HIV infection. The relative roles of their biologic response modification and the disordered immunoregulation seen in such patients in the pathogenesis of the renal disease is unclear. Renal biopsy is necessary to assess the etiology of the renal disease in HIV-infected patients.
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PMID:Membranoproliferative glomerulonephritis in a patient treated with interferon-alpha for human immunodeficiency virus infection. 797 30


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