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)

Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN), the single most common cause of end-stage renal failure in seropositive patients, has increased in incidence by 30% each year since 1991. Occurring almost exclusively in blacks, HIVAN became the third leading cause of ESRD in blacks, ages 20 to 64, in 1995. During that year, the absolute number of new acquired immune deficiency syndrome (AIDS) cases declined for the first time since the epidemic began. The decrease occurred predominantly in white males, whereas in blacks with heterosexual exposures for risk factors, the incidence actually increased. Also in 1995, the number of AIDS-related deaths declined for the first time. If these trends continue, we can expect a continued increase in the number of blacks living with AIDS. We estimate that 1% to 4% will develop renal failure from HIVAN. The incidence of HIVAN can be expected to increase unless new approaches are successful in preventing the spread of HIV-1 in all segments of the population or in treating the renal complications of HIV-1 infection.
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PMID:The human immunodeficiency virus (HIV) epidemic and HIV-associated nephropathy. 969 50

Human immunodeficiency virus-associated nephropathy (HIVAN) is the third leading cause of end-stage renal failure in Blacks between the ages of 20 and 64. Because the incidence of HIV infection has continued to increase in Blacks as survival has improved, the pool of patients alive and at risk for developing HIVAN has vastly expanded. This suggests that HIVAN will continue to increase in importance to the end-stage renal disease program. The racial predilection for the disease in Blacks implies that genetic or environmental cofactors are involved. Evidence in human and animal models has shown that proliferation of renal epithelial cells is the predominant feature of the disease and that apoptosis occurs. The prospect that renal infection is necessary to stimulate cells to proliferate remains a possibility but is not yet proven. Cytokine dysregulation may also be involved in disease progression, but evidence is lacking that altered cytokine production is the proximate cause of HIVAN. Many issues remain to be resolved including the potential for renal infection in vivo, the mechanisms responsible for proliferation and apoptosis, and factors that provide racial susceptibility to HIVAN. Advances in our understanding of pathogenesis will be required to control the growth of HIV-related renal diseases in the ESRD population.
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PMID:Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy. 969 55

Patients with human immunodeficiency virus (HIV) nephropathy (HIVN) face improved outlooks both before and after starting renal replacement therapy for end-stage renal disease, compared with the situation a little over a decade and a half before, when the disease was first recognized. Therapy with cyclosporin, glucocorticoids, and angiotensin-converting enzyme inhibitors provides the prospect of longer courses of renal insufficiency for patients with HIVN, and perhaps the hope of blunting progression of the disease when patients are treated early. Trials of patients with biopsy-proven HIVN are important to evaluate further the role of such newer therapies. HIV-infected patients with end-stage renal disease have been treated with hemodialysis, peritoneal dialysis, and renal transplantation. The course of therapy for dialysis patients may be improving, but ultimately depends on the stage of the viral illness. The disparities in the demographic composition of the patient populations probably underlies findings reported from different centers. Transplantation is currently a low-priority treatment option for HIV-infected patients with ESRD, but several studies provide fascinating insights into viral-host interactions.
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PMID:Treatment of human immunodeficiency virus (HIV)-associated nephropathy. 969 56

This study was designed to determine whether there was any difference in the T-cell subset counts and serum immunoglobulin concentrations in patients with chronic renal failure as compared to normal controls. Ninety individuals participated in the study. These were divided into three groups as follows; (i) 30 subjects with normal renal function; (ii) 30 subjects with chronic renal failure (CRF)(creatinine clearance 10-50 mls/min), not requiring haemodialysis and; (iii) 30 subjects with end stage renal disease (creatinine clearance < 10 mls/min) on haemodialysis. The subjects in the three groups were matched for age and sex. In addition, it was ascertained that none of the subjects was on any medication or suffered from any ailment known to interfere with the immune system. The T-cell subset counts were carried out using flow cytometry while the serum concentration of immunoglobulins was measured using the radio-immunodiffusion method. Patients with CRF, whether on haemodialysis or not, had significantly lower lymphocyte counts as a proportion of total white cell count (19% and 19.2% respectively versus 39%) and low absolute CD4 cell counts per mm3 (337 +/- 94 and 449 +/- 116 respectively versus 891 +/- 360) and CD8 cell counts per mm3 (437 +/- 234 and 490 +/- 176 respectively versus 644 +/- 228) as compared to normals, with no statistically significant difference between the two groups with CRF. The CD4: CD8 ratios in the three groups studied were 1.487 +/- 0.233, 0.961 +/- 0.326 and 0.751 +/- 0.167 respectively, being significantly higher in normal controls than in any of the groups with CRF (p < 0.05) and in the group with CRF not requiring dialysis than in those requiring it (p < 0.05). The serum concentration of immunoglobulins in the two groups with CRF were similar to those in the group with normal renal function. It is concluded that CRF represents a state of immunodeficiency not significantly corrected by haemodialysis.
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PMID:T-cell subset counts and serum immunoglobulin concentrations in patients with chronic renal failure at the Kenyatta National Hospital. 974 96

We clinically investigated a total of 288 cases of bacteremia for the past ten years, from January 1986 to December 1995, at the Second Department of Internal Medicine in the jikei University Hospital. All of the subjects who had a positive reaction to blood culture or catheter tip culture were investigated for their basic disease, complications, and detected bacteria. Malignant tumors, chronic renal failure, diabetes mellitus, and hematologic disease were frequent by noted. The cases due to primary infection were mainly respiratory organ infection or urinary tract infection, which were 47.8% of the total. In 31.3% of the total, catheter tip cultures were positive. Except for catheter related infection, Gram-positive coccus were detected in 40.3%, which was most frequent. Methicillin resistant Staphylococcus aureus (MRSA) were 8.1% and Staphylococcus epidermidis were 11.2%. In catheter related infection, Gram-positive coccus were detected in 59.9%, which was most frequent amongst them, MRSA was 17.2%, S. epidermidis was 16.2%. The mortality of bacteremia was 12.5%, mainly from hematologic diseases, immunodeficiency due to long term steroid administration etc. Accordingly, the more the advance of chemotherapy, the better the prognosis of septicemia is. Appearance of catheter related infection was unexpected frequent. Increase of immunocompromised host is thought to be one of the main factors in the outbreak of bacteremia.
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PMID:[A clinical investigation of bacteremia for the past ten years at the Second Department of Internal Medicine, Jikei University Hospital]. 978 May 85

Hemodialysis permits a long term survival to patients with End Stage Renal Disease (E.S.R.D.). However the patients ongoing hemodialysis presented a immunodeficiency and a important modification of drugs biodisponibility. Tuberculosis is an endemic disease in our countries. Extrapulmonary tuberculosis is reported from these two cases among 13 patients treated in C.H.U.A. Le Dantec hemodialysis center. Clinical symptoms are not specific bacteria is not found. Diagnosis is obtained by a bundle of arguments. Antituberculosis treatment need to be adjusted in this field. Even if Rifampicine can be administrated at normal dose. The others drugs must be adapted on their clearance and the underlying disease. The two patients presented psychiatrical symptoms motivating a reduction of isoniazide dose witch threshold toxicity is lowered by renal failure state. These observations must increase watchfulness on nephrologist of undeveloping countries, confronted with tuberculosis renewed out break.
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PMID:[Tuberculosis among hemodialysis patients in Dakar, apropos of 2 cases]. 987 94

In 1986, Weiss et al reported a group of patients with nephrotic syndrome, progressive chronic renal failure, and the histopathologic features of glomerular capillary collapse. Similar lesions are often described in human immunodeficiency virus (HIV) nephropathy. We evaluated 893 consecutive nontransplant renal biopsies performed in our department and the follow-up of the patients at our outpatient service. Sixteen specimens were identified with the pathological features of collapsing glomerulopathy (focal segmental or global glomerular capillary collapse and visceral epithelial cell hyperplasia), with no evidence of HIV infection and/or intravenous drug abuse. Their clinical characteristics were analyzed and compared with a group of 29 patients with noncollapsing focal segmental glomerulosclerosis (FSGS). The follow-up period of both patient groups was 5 +/- 1.46 years. The Kaplan-Meier life table method was used to present survival of the patients. The age of both groups was similar, 34 +/- 4 years (mean +/- standard error of the mean) for patients with collapsing glomerulopathy and 35 +/- 3 years for those with FSGS. The serum creatinine level was greater in patients with collapsing glomerulopathy (183 +/- 31 micromol/L) compared with those with FSGS (115 +/- 18 micromol/L), but the difference was not significant (P = 0.0504). The difference in proteinuria was not significant (P = 0.7668); it was 5.83 +/- 0.74 g/d in patients with collapsing glomerulopathy and 5.42 +/- 0.84 g/d in those with focal sclerosing glomerulonephritis. The difference in systolic (P = 0.4) and diastolic blood pressure (P = 0.556) was also not significant. Survival of the patients with collapsing glomerulopathy was worse than that of patients with FSGS (P = 0.025). Renal function survived 5 years in 40% of the patients with FSGS, but patients with collapsing glomerulopathy had no renal function survival. Our data suggest that idiopathic collapsing glomerulopathy is a distinct clinicopathologic entity with similar clinical features to focal sclerosing glomerulonephritis, but a worse prognosis and a rapidly progressive course toward end-stage renal disease.
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PMID:Collapsing glomerulopathy: clinical characteristics and follow-up. 1019 29

CD40 and its ligand CD40L are key players in T cell-B cell interaction and T cell-antigen-presenting cell (APC) interaction. Inhibition of CD40-CD40L interaction leads to severe humoral and cellular immunodeficiency. In this study we examined the presence of soluble CD40 (sCD40) in the serum of haemodialysis (HD) patients, CAPD patients, chronic renal failure (CRF) patients and healthy donors in order to evaluate the possible involvement of CD40 in uraemic immunodeficiency. Soluble CD40 was detected in the serum of healthy donors (n = 41) with a mean of 0.14 +/- 0.12 ng/ml and in the urine of healthy donors with a mean of 1.80 +/- 0.74 ng/ml. Soluble CD40 was highly elevated in all patients with impaired renal function. HD patients (n = 22) had up to 100-fold elevated sCD40 levels with a mean concentration of 8.32 +/- 4.11 ng/ml, whereas CAPD patients (n = 10) had considerably lower levels of sCD40 with a mean of 3.58 +/- 2.40 ng/ml. A strong correlation between sCD40 and serum creatinine levels was noted in CRF patients (n = 66). The highly elevated levels of sCD40 may point to the involvement of CD40 and its ligand CD40L in the clinical manifestation of uraemic immunodeficiency.
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PMID:Soluble CD40 in the serum of healthy donors, patients with chronic renal failure, haemodialysis and chronic ambulatory peritoneal dialysis (CAPD) patients. 1040 29

The response to vaccination with recombinant hepatitis B virus (HBV) vaccine is poor in haemodialysis patients. A defect in the antigen-presenting cells may be responsible for this hyporesponsiveness. To overcome this and to improve the response to HBV vaccine in dialysis patients, we used granulocyte-macrophage colony-stimulating factor (GM-CSF) as a vaccine adjuvant. Fifteen consecutive patients with chronic renal failure (CRF), commenced on dialysis, were stratified to receive either 40microg HBV vaccine (Engerix-B) at 0, 1, 2 and 6 months (group A, n=9) or 3microg kg-1 GM-CSF (Leucomax) on day 1 followed by the vaccination schedule described above (group B, n=6). All patients were negative for hepatitis B surface antigen (HBsAg), antibodies to hepatitis C virus (anti-HCV) and human immunodeficiency virus (HIV) serology. Titres of antibody to HBsAg (HBsAb) were quantitatively assayed, using enzyme-linked immunosorbent assay (ELISA), at 1, 2, 6 and 7 months from the first dose of vaccination. Only 44% of the patients in group A developed protective antibody levels (mean HBsAb: 22 IU l-1) Fifty per cent of responders developed protective antibody levels (HBsAb >10 IU l-1) only after the fourth dose of vaccination. In contrast, all six patients (100%) in group B developed protective levels of HBsAb (mean HBsAb: 70 IU l-1) (P<0.02). Sixty-seven per cent of the responders were protected after only the second dose of vaccination (P=0.046). No serious adverse effects of GM-CSF were observed in group B. Hence, haemodialysis patients respond poorly to HBV vaccine. GM-CSF is a safe vaccine adjuvant capable of stimulating an earlier and a stronger antibody response to HBV vaccine in haemodialysis patients.
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PMID:Granulocyte-macrophage colony-stimulating factor enhances the efficacy of hepatitis B virus vaccine in previously unvaccinated haemodialysis patients. 1060 57

Patients with chronic renal failure show an immunodeficiency characterized by frequent infectious complications and a low response to vaccinations. This is paralleled in vitro by a low T-cell proliferation on mitogenic stimuli because of an impaired costimulation by accessory cells. Furthermore, alterations of the cytokine profile are correlated with impaired immune function. The immune system is influenced by both uremia and renal replacement therapy. To evaluate the influence of hemodialysis on immune parameters, we studied patients before and after the initiation of chronic hemodialysis therapy. Fourteen patients with end-stage renal failure were tested before dialysis initiation and during the first 6 weeks of hemodialysis treatment. We determined the in vitro T-cell proliferation, as well as plasma levels of interleukin-6 (IL-6) and the release of IL-6 and IL-10 into culture supernatant poststimulation with lipopolysaccharide. After 6 weeks of intermittent hemodialysis, in vitro T-cell proliferation on stimulation improved significantly (stimulation index, 21.6 +/- 18.5 versus 58.1 +/- 45.5; P < 0.01). This improvement occurred regardless of whether synthetic dialyzers or cellulosic membranes were used for the initiation of dialysis. Plasma IL-6 levels, as well as IL-6 and IL-10 secretion, did not change during the study period. In patients with end-stage renal disease, the initiation of hemodialysis led to a significant improvement of in vitro T-cell proliferation. This effect may have a role for an improvement of immune function in vivo. The expected normalization of IL-6 and IL-10 production may be masked by cytokine induction through hemodialysis membranes.
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PMID:Initiation of hemodialysis treatment leads to improvement of T-cell activation in patients with end-stage renal disease. 1073 80


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