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)

Uncontrolled or refractory nephrotic syndrome (NS), seen in a variety of glomerular disorders, leads to end-stage renal disease (ESRD). This study describes the use and efficacy of cyclosporine (CSA) for the treatment of refractory NS in 83 children seen over a 10-year period. The histological diagnosis leading to the NS was focal segmental glomerulosclerosis (FSGS) in 51% (n = 42), IgM nephropathy in 20% (n = 17), membranoproliferative glomerulonephritis in 10% (n = 8), lupus nephritis in 6% (n = 5), human immunodeficiency virus (HIV) nephropathy in 5% (n = 4), minimal change disease in 7% (n = 6), and membranous nephropathy in 1% (n = 1) of patients. During CSA therapy the mean proteinuria of the study population decreased from 5.14 g/24 h (4.80 g/m2 per 24 h) to 1.23 g/24 h (0.92 g/m2 per 24 h) (P < 0.001), the mean serum albumin increased from 2.13 g/dl to 3.53 g/dl (P < 0.001), the mean serum cholesterol decreased from 364 mg/dl to 223 mg/dl (P < 0.001), and the mean serum creatinine increased from 0.77 mg/dl to 1.2 mg/dl (P < 0.01). When analyzed by histological diagnosis, similar significant trends of reduction in proteinuria were seen in all but the lupus group. There was a rise in serum creatinine following the use of CSA in patients with FSGS, lupus nephritis, and HIV nephropathy; however the elevated serum creatinine was only significant in patients with FSGS. At the end of the study period, 20 patients had reached ESRD, of which 11 had FSGS, 5 had lupus nephritis, and 4 were patients with HIV nephropathy. Fifty-four patients were in remission at the end of the study period (48 with proteinuria < 100 mg/24 h and 6 with proteinuria < 500 mg/24 h). In conclusion, among children with refractory NS, CSA induced a remission in a large proportion. However toxicity, as noted by the rise in serum creatinine, was observed in several patients. Since this toxicity may be drug induced or a natural progression of the disease, careful monitoring and close follow-up are essential.
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PMID:One-center experience with cyclosporine in refractory nephrotic syndrome in children. 1010 Feb 85

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

Human immunodeficiency virus-associated nephropathy (HIVAN) develops more often in HIV-infected blacks than whites. Blacks also show marked familial clustering of other causes of end-stage renal disease (ESRD), particularly diabetes mellitus-, hypertension-, and systemic lupus erythematosus-associated ESRD. We compared the family history of ESRD in 201 blacks with ESRD caused by HIVAN (cases) to that of 50 HIV-infected blacks without renal disease (controls) to determine whether HIV-associated ESRD shows familial aggregation. Cases were identified using the Southeastern Kidney Council/ESRD Network 6 Family History of ESRD database. Cases initiated dialysis between September 1993 and October 1998. Controls were consecutively identified, HIV-infected blacks with serum creatinine concentrations of 1.3 mg/dL or less and no proteinuria, treated in an infectious disease clinic during September 1998. Cases and controls had similar mean ages and family sizes. First- or second-degree relatives with ESRD were reported by 24.4% of the cases compared with 6% of the controls (P = 0.004). Logistic regression analysis, controlling for sex, family size, and age, showed cases were 5.4 times more likely than controls to have close relatives with ESRD (P = 0.007). The 49 HIVAN cases who reported a positive family history had a mean of 1.2 additional relatives with ESRD per case (60 total relatives with ESRD). HIVAN was not listed as the cause of ESRD in any of the 27 relatives who underwent dialysis in Network 6 facilities. We conclude that ESRD clusters in the families of nearly 25% of blacks initiating renal replacement therapy for HIVAN. This familial aggregation of ESRD appears to be independent of HIV infection. Although environmental factors cannot be excluded, it is possible an inherited susceptibility to renal failure is present in many blacks with HIV infection who subsequently develop nephropathy.
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PMID:Familial clustering of end-stage renal disease in blacks with HIV-associated nephropathy. 1043 Sep 71

We retrospectively reviewed the charts of 54 human immunodeficiency virus (HIV) infected patients or acquired immunodeficiency syndrome (AIDS), who were hospitalized at the Bronx-Lebanon Hospital Center with acute pancreatitis between January 1993 and December 1995. Nineteen were female and 35 were male patients. Thirty-five (65%) of 54 patients were younger than 40 years (average age, 42 years). Forty-eight (89%) of the patients had a CD4 count of <200 units/ml of blood. Seventeen (32%) patients died either of complications of acute pancreatitis or of underlying disease. The conventional prognostic criteria used to assess the severity of pancreatitis, including Ranson's and Imrie's criteria and the APACHE II system, were applied. We determined that these criteria were not appropriate to our HIV/AIDS patients. Only serum calcium levels at 48 h after admission and serum creatinine and blood urea nitrogen (BUN) at admission and at 48 h after admission had significant p values (<0.05). We believe that the predictors commonly used to identify the severity of pancreatitis were not useful in these patients because of their low CD4 counts and preexisting liver and renal disease.
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PMID:Predictors of the severity of acute pancreatitis in patients with HIV infection or AIDS. 1043 59

Lamivudine population pharmacokinetics were investigated by using nonlinear mixed-effect modelling (NONMEM) analysis of data from 394 human immunodeficiency virus (HIV)-infected patients treated with lamivudine (150 to 300 mg every 12 h) in two large, phase III clinical efficacy-safety trials, NUCA3001 and NUCA3002. Analyses of 1,477 serum lamivudine concentration determinations showed that population estimates for lamivudine oral clearance (CL/F; 25.1 liters/h) and volume of distribution (V/F; 128 liters) were similar to values previously reported for HIV-infected patients in phase I pharmacokinetic studies. Lamivudine CL/F was significantly influenced by the covariates creatinine clearance and weight and not affected by age, Centers for Disease Control and Prevention (CDC) classification, CD4(+) cell count, HIV type 1 (HIV-1) RNA PCR, or gender and race when CL/F was corrected for differences in patient weight. The population estimate for lamivudine V/F was not significantly influenced by the covariates gender, race, age, weight, renal function, HIV-1 RNA PCR, or CDC classification and CD4(+) cell count when creatinine clearance was included with CL/F in the model. Lamivudine disposition was significantly influenced by renal function. However, as only three patients had an estimated creatinine clearance of <60 ml/min, dosage adjustments for patients with impaired renal function should not be determined based on the population parameters derived in this analysis.
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PMID:Population pharmacokinetics of lamivudine in adult human immunodeficiency virus-infected patients enrolled in two phase III clinical trials. 1058 4

Pentachlorophenol (PCP) was, and still is, one of the most frequently used fungicides and pesticides. The use of PCP has been more restricted during the last few years. PCP's most important industrial application is as a wood preservative. The pentachlorophenol can be absorbed into the body by all the routes of occupational exposure. Some epidemiological observations suggest that exposure to PCP solutions may result in an increased risk for certain diseases in humans, e.g., immunodeficiency, blood disorders, malignancies, congenital anomalies. Chronic poisoning is difficult to detect since symptoms are often vague. Acute poisoning is due to interference with oxidative phosphorylation and can present itself as an unexpected case of sudden death. Four cases of PCP poisoning, including one fatalitie, occurred in two small wood preservative plants. All cases presented with increased serum creatinine phosphokinasa. The clinical finding are reported, and treatment modalities commented. At present there is no antidote for PCP. The basis for treatment is intensive supportive care to maintain vital bodily function. In one patient plasmapheresis was used and rapid recover was obtained. It is suggested that such therapy may be lifesaving in such intoxications.
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PMID:[Pentachlorophenol poisoning. Report of 4 cases and review of the literature]. 1085 27

Indinavir is a potent protease inhibitor widely used in combination with reverse-transcriptase inhibitors to treat human immunodeficiency virus (HIV) disease. Individuals treated with indinavir are prone to develop urinary complications, including renal colic, renal calculi, lower urinary tract symptoms, and indinavir crystalluria. Although renal stones secondary to indinavir have been described and characterized, little is known about the onset, frequency, and significance of the crystalluria. To document the longitudinal characteristics of indinavir crystalluria and associated urine abnormalities, 54 asymptomatic indinavir-naive HIV-positive individuals had urinalysis testing initially weekly and then monthly during the first year of indinavir treatment. Six hundred eight urinalyses were performed (11 +/- 2 urinalysis/subject), including 579 microscopy examinations performed by a nephrologist (10 +/- 2 examinations/subject). Baseline urinalysis results were essentially normal. After the start of treatment, indinavir crystalluria was frequently observed (67% of subjects). After the first 2 weeks, indinavir crystalluria remained constant at a frequency of approximately 25% of urine sediments examined at each test point. Other urine abnormalities, principally leukocytes (>/=10/high-power field) and casts, were observed in 39% of subjects. These abnormalities were more severe in five subjects, with concomitant increasing serum creatinine levels in three of them. Additional urine findings include the predominance of low pH (</=5. 5 in 72% of urinalyses) and high specific gravity (>/=1.025 in 66% of urinalyses). In conclusion, abnormal urinalysis results were noted frequently during the first year of treatment with indinavir. The main findings were the high proportion of subjects with crystalluria and the relatively high frequency of crystalluria observed consistently throughout. These findings may occasionally be associated with other urine abnormalities, presumably secondary to indinavir crystalluria.
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PMID:Prospective study of urinalysis abnormalities in HIV-positive individuals treated with indinavir. 1097 82

Chronic diarrhoea of the adult is defined as diarrhea during 30 days or longer. Frequent causes of chronic diarrhea in the immunocompetent adult without recent travel to developing countries are noninfectious processes, including laxatives misuse, diseases causing chronic maldigestion, osmotically active artificial sweeteners (i.e. sorbitol), hormonal disorders or drugs with intestinal side effects. Infectious agents as the cause of chronic diarrhea are important in two populations, namely in travelers returning from tropical countries bearing a significant risk of intestinal parasitic infections and in immunocompromised patients, especially AIDS patients with CD4 cell counts below 50 per microliter. Intestinal parasites and C. difficile, Y. enterocolitica, Shigellae and Cytomegalovirus are the most important causative agents of chronic diarrhea. Intestinal pathogens were identified in 46% of chronic, but only in 16.5% of acute diarrhea episodes of HIV-infected patients. An extensive medical history including recent travel as well as the detailed characteristics of onset of symptoms and of their time course is essential for the diagnosis. All patients should have a complete differential blood count, ESR, determination of electrolytes, liver enzymes, creatinine, blood glucose, and serum albumin. Tests to exclude hyperthyriodism, or pancreatic insufficiency as well as a d-xylose absorption test can be included, if appropriate. Microbiological-parasitological investigations are obligatory in patients with chronic diarrhea returning from countries with increased risk of traveler diarrhea, in cases of suspected immunodeficiency, if sudden onset of symptoms with fever is reported, after antibiotic treatment, and in children below six years of age. As a rule, stool specimens are appropriate, for the detection of cytomegalovirus colonic biopsies are necessary. In the latter case colonosigmoidoscopy has no diagnostic advantage. One single stool specimen is sufficient for the detection of bacteria or toxins, in contrast to parasitological investigations, where only three consecutive specimens provide sufficient diagnostic sensitivity.
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PMID:[Chronic diarrhea: value of microbiology in diagnosis]. 1106 10

Multiple endocrine and metabolic consequences of human immunodeficiency virus (HIV) infection exist that may contribute to bone loss in men with the acquired immune deficiency syndrome (AIDS) wasting syndrome. Recent studies suggest that anabolic strategies can increase lean body mass in men with AIDS wasting. Prior studies have not examined the effects of anabolic agents on bone mineral density (BMD) or bone turnover in these men. To determine the effects of testosterone and progressive resistance training on BMD and bone turnover in eugonadal men with AIDS wasting, we randomly assigned 54 eugonadal men with AIDS wasting (weight < 90% IBW or weight loss >10% from preillness baseline) to receive either testosterone enanthate (200 mg/week, im) or placebo and to progressive resistance training (3 times/week) or no training in a 2 x 2 factorial study design for 3 months. The BMD of the lumbar spine, proximal femur, and total body; lean body mass; and fat mass were measured by dual energy x-ray absorptiometry. Total body scans were repeated after 12 weeks of therapy. Baseline bone turnover and BMD were compared with those in 35 age-matched healthy non-HIV-infected control subjects. Compared with controls, lumbar spine BMD (1.021 +/- 0.018 vs. 1.084 +/- 0.025 g/cm(2); P = 0.04) and total hip BMD (0.951 +/- 0.017 vs. 1.070 +/- 0.019 g/cm(2); P < 0.0001) were reduced in men with AIDS wasting. T-scores were lower in men with AIDS wasting at the lumbar spine (-0.62 +/- 0.17 vs. -0.07 +/- 0.23, P = 0.05) and total hip (-0.65 +/- 0.11 vs. +0.20 +/- 0.014, P < 0.0001). Total hip T scores were less than -1.0 in 33% of men with AIDS wasting. Neither the use of protease inhibitors nor the duration of protease inhibitors use correlated with BMD. Serum osteocalcin levels were lower (3.63 +/- 0.29 vs. 4.54 +/- 0.31 nmol/L; P < 0.04) and urinary N-telopeptide excretion was higher (45.4 +/- 4.5 vs. 26.8 +/- 3.0 nmol BCE/mmol creatinine; P = 0.004) in men with AIDS wasting than in controls. Lumbar spine BMD, as assessed on regional total body dual energy x-ray absorptiometry scan, increased over the 12-week treatment period in response to testosterone (+2.4 +/- 1.3 vs. -1.3 +/- 1.0%, testosterone vs. placebo, respectively; P = 0.02), but not in response to training (+0.8 +/- 1.0 vs. +0.4 +/- 1.3%, training vs. no training; P = 0.70). Lumbar spine and total hip BMD are reduced in eugonadal men with AIDS wasting. Biochemical markers of bone turnover suggest that bone formation and bone resorption are uncoupled in these men. Testosterone administration, but not resistance training, over 3 months increases lumbar spine BMD in eugonadal men with AIDS wasting.
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PMID:Osteopenia in eugonadal men with acquired immune deficiency syndrome wasting syndrome. 1134 1


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