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

After cardiovascular diseases and bacterial infections viral hepatitis is the most frequent disease which complicates haemodialyzation treatment of patients with chronic renal failure. Substitution of renal function is for these patients a life saving procedure. It is, however, complicated treatment associated with various risks of acute and chronic complications. The prevalence of parenterally transmitted viral hepatitis in the population of haemodialyzed patients is by far higher than the prevalence of these diseases in the general population. There are several reasons for this condition. In addition to the character of this treatment there is also the fact that for reasons of immunodeficiency the course proper of infetious hepatitis in haemodialyzed patients is markedly more often terminated by development of the chronic state of the disease with permanent viraemia. These patients become a possible source of infection of the other patients and possibly also the staff of haemodialyzation centres. Vaccination against viral hepatitis B reduces the risk of transmission of the disease. However a large proportion of patients is enlisted in the haemodialyzation programme acutely without the possibility of previous vaccination. Some patients who are vaccinated during the predialyzation period do not respond by antibody formation. Viral hepatitis complicates or makes it impossible in some cases to include the patient in the transplantation programme. The prevalence of viral hepatitis in patients in the haemodialyzation programme was significantly reduced despite all mentioned facts. During the last three years a certain stagnation of this positive trend was recorded. New therapeutic possibilities (the use of interferon and new antiviral properations--analogues of nucleoside bases) offer a chance of a further decrease of the number of these serious diseases.
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PMID:[Viral hepatitis of patients in a regular haemodialysis programme]. 1563 69

A retrospective study of Streptococcus pneumoniae bacteraemia among adult patients in two large teaching hospitals in Spain identified 108 (10.6%) of 1,020 episodes as nosocomial pneumococcal bloodstream infections (NPBIs). Seventy-seven clinical records with sufficient data were available for analysis. The interval between admission and a positive blood culture was 3--135 days (median 17 days; interquartile range 8--27). The main underlying and predisposing conditions for NPBI were malignancy (31%), chronic obstructive pulmonary disease (28.6%), heart failure (16.9%), chronic renal failure (15.6%), liver cirrhosis (13%) and infection with human immunodeficiency virus (13%). Overall, 31.2% of patients developed severe sepsis, 11.7% septic shock, and 3.9% multi-organ failure. The main portals of entry were pneumonia (70.1%), meningitis (5.2%) and primary peritonitis (5.2%). Of the responsible serogroups, 78% were included in the 23-valent polysaccharide vaccine. Thirty-five (45.5%) patients died, with death considered to be related to the NPBI in 21 (27.3%) cases. Following multivariate analysis, factors that independently predicted death after adjusting for age were: ultimately fatal underlying disease (OR, 8.9; 95% CI, 0.8--94.3; p<0.001); rapidly fatal underlying disease (OR, 15.0; 95% CI, 2.8--81.3; p<0.001); heart failure (OR, 8.11; 95% CI, 1.1--60.8; p<0.03); inadequate empirical therapy (OR, 10.6; 95% CI, 1.2--97; p<0.003); a severe sepsis score (OR, 9.5; 95% CI, 1.9--47.0; p<0.001); and septic shock or multi-organ failure (OR, 63.7; 95% CI, 4.9--820.7; p<0.001). Adequate empirical therapy was an independent protective factor (OR, 0.05; 95% CI, 0.04--0.58; p<0.005), but the use of more than one antimicrobial agent was not.
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PMID:Nosocomial bloodstream infections caused by Streptococcus pneumoniae. 1621 9

Chronic granulomatous disease (CGD) is a genetic disease caused by structural mutations in the enzyme NADPH oxidase that results in severe immunodeficiency. End-stage renal disease occurs in this patient population, and is often attributed to the necessary use of nephrotoxic anti-infectives. In this report, we present the experiences of two centers in transplantation of three patients with CGD: one transplanted with CGD, one cured of his CGD with bone marrow transplantation who subsequently underwent kidney transplantation and one that received a kidney transplant prior to being cured of CGD via a sequential peripheral blood stem cell transplant (SCT). All three recipients have enjoyed excellent outcomes. Their courses demonstrate the absolute requirements for a multidisciplinary and compulsive approach before, during and after transplantation. These case reports also highlight the unexpectedly benign effects of immunosuppressive therapy in this patient population.
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PMID:Successful renal transplantation in patients with chronic granulomatous disease. 1646 77

Renal disease is becoming an increasingly prevalent entity in human immunodeficiency virus (HIV)-infected patients; it occurs in a variety of clinical settings and is associated with histopathological changes. HIV-related renal impairment can present as acute or chronic kidney disease; it can be caused directly or indirectly by HIV and/or by drug-related effects that are directly nephrotoxic or lead to changes in renal function by inducing metabolic vaculopathy and renal damage. Acute renal failure is frequently caused by the toxic effects of antiretroviral therapy or nephrotoxic antimicrobial substances used in the treatment of opportunistic infections. Chronic renal disease can be caused by multiple pathophysiological mechanisms, leading to HIV-associated nephropathy, a form of collapsing focal glomerulosclerosis, thrombotic microangiopathy, and various forms of immune complex glomerulonephritis. The increase in life expectancy and alteration of lipid metabolism due to receipt of highly active antiretroviral therapy are expected to result in an increased prevalence of diabetes and hypertension and, thus, to secondary diabetic and hypertensive renal damage. Antiretroviral agents, such as indinavir and tenofovir, have been associated with nephrotoxic drug effects that have been shown to be reversible in most cases. In this article, we review the current knowledge about acute and chronic HIV-associated renal disease, metabolic alterations and related nephropathies, and toxic drug effects of combination antiretroviral pharmacotherapy.
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PMID:HIV-associated renal diseases and highly active antiretroviral therapy-induced nephropathy. 1661 64

Human immunodeficiency virus (HIV)-related renal disease is the third-leading cause of end-stage renal disease (ESRD) among African Americans aged 20-64 years. The number of HIV-infected (HIV+) patients reaching ESRD will increase exponentially over the next decade. Because of significant improvements in therapy and management during the last ten years, survival of HIV+ patients has improved. The survival experience of very long-term HIV+ peritoneal dialysis (PD) patients remains to be investigated. The objective of the present study was to examine the important differences in clinical and laboratory parameters between HIV+ and HIV-negative (HIV-) PD patients. To assess the factors associated with better survival in HIV+ PD patients, we retrospectively reviewed the charts of 488 PD patients, including 53 HIV+ patients, for the period 1987 to September 2004. We collected demographic, clinical, and laboratory data, including CD4 cell counts and history of hospitalizations and peritonitis. Maximum survival of HIV+ PD patients was 12.5 years as compared with 15.87 years in HIV-patients. Not surprisingly, HIV was a strong independent predictor of mortality in PD patients [relative risk (RR) = 3.09, p < 0.0001]. In HIV+ patients, higher CD4 counts at the initiation of dialysis were strongly associated with better survival (RR = 0.10 and p < 0.0001, > or =200 cells/mm3 vs. < or =50 cells/mm3). In univariate analysis, use of highly active antiretroviral therapy (HAART) was associated with significantly improved survival in HIV+ PD patients. Patients treated with I or 2 drugs had a 4.3-times higher mortality risk than those who received HAART therapy (p = 0.012). Independent associations were seen between HIV and younger age, African American race, male sex, and lower serum albumin. The rates of hospitalization (p < 0.0001) and peritonitis (p < 0.01) were significantly higher in HIV+ patients than in HIV-patients. Very long-term survival of HIV+ patients with chronic renal failure is possible on PD therapy. Morbidity and mortality of these patients may be improved with HAART therapy, better nutrition, and treatment of peritonitis.
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PMID:Survival experience of peritoneal dialysis patients with human immunodeficiency virus: a 17-year retrospective study. 1668 10

Human immunodeficiency virus-associated nephropathy (HIVAN) is a very distinct, unique, clinico-pathological syndrome, and a structural type of renal failure that is the most common cause of chronic renal failure in patients who are HIV-seropositive. Early referral and a long-term, primary care approach can improve patient outcomes. Careful adjustments of prescription doses with regularly scheduled, and at times frequent, laboratory testing will yield, optimal health, improve the quality of life, and most importantly, will decrease the incidence of morbidity and mortality in those individuals afflicted with both HIV and HIVAN.
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PMID:Human immunodeficiency virus-1 associated nephropathy (HIVAN): epidemiology, pathogenesis, histology, diagnosis, and medical management. 1685 98

Chronic renal failure (CRF) patients display an immunodeficiency state, and uremic solutes that accumulate during CRF may be involved in this immunodeficiency. In this study, we examined whether the uremic solute para-cresol (p-cresol), at concentrations similar to those found in patients, alters leukocyte transmigration in vitro. We found that p-cresol significantly inhibited monocyte THP-1 cell line and PBMCs transmigration across IL-1beta-stimulated human umbilical vein endothelial cell (HUVEC) in a static two-compartment model. This inhibitory effect of p-cresol persisted in the presence of a physiologic concentration of human serum albumin. In order to investigate the mechanism involved, expression of endothelial chemokines, fractalkine, monocyte chemoattractant protein 1 (MCP-1) and IL-8 and membrane expression of junctional adhesion molecule A (JAM-A or JAM-1) were studied. We found that p-cresol decreased mRNA expression of the chemokine fractalkine in IL-1beta-stimulated HUVEC, without modifying mRNA expression of MCP-1 and IL-8. In addition, p-cresol decreased IL-1beta-induced expression of membrane-bound and soluble forms of fractalkine and impaired the membrane expression of JAM-A. Taken together, these results suggest that p-cresol, by impairing leukocyte transendothelial migration, plays a role in the immune dysfunction of uremic patients.
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PMID:The uremic solute p-cresol decreases leukocyte transendothelial migration in vitro. 1695 66

Previous studies have documented that sustained virologic response (SVR) is significantly reduced in African Americans with chronic HCV genotype 1 following treatment with interferon and ribavirin when compared with Caucasians. The specific aim of the present retrospective study was to assess virologic response to interferon and ribavirin in African Americans with HCV genotypes 2 and 3. A review of our database identified 42 African Americans and 334 Caucasians with HCV genotypes 2 and 3. Patients coinfected with hepatitis B or human immunodeficiency virus, chronic renal failure, and recipients of an organ transplant were excluded. Thirty of the African Americans were treated with either standard interferon or peginterferon and ribavirin as initial treatment for chronic HCV. Ninety of the 334 Caucasians were matched to the African Americans with regards to genotype, cirrhosis, treatment regimen, sex, age, and body weight for comparison of virologic response. The proportion of patients with HCV genotype 2 was significantly greater (P < 0.001) in African Americans compared with Caucasians (81%vs 52%). End-of-treatment virologic response was observed in 94% of Caucasians compared with 80% in African Americans (P= 0.036). SVR was observed in 82% and 57% of Caucasians and African Americans, respectively (P= 0.012). Similar results were observed when patients who had been treated with only peginterferon and ribavirin were assessed. These results suggest that African Americans have a global defect in their ability to eradicate HCV infection following treatment with interferon and ribavirin which transcends across all genotypes.
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PMID:Treatment of chronic hepatitis C virus in African Americans with genotypes 2 and 3. 1731 33

This review looks at the clinical performance of Immunodeficiency Virus (HIV) infected individuals with end stage renal disease (ESRD) treated using continuous ambulatory peritoneal dialysis (CAPD). It also considers the potential infectious nature of the peritoneal dialysis effluent (PDE) and offers suggestions on how to circumvent this risk.
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PMID:Continuous ambulatory peritoneal dialysis and the human immunodeficiency virus. 1758 75

The number of people living with human immunodeficiency virus (HIV) worldwide was estimated to be 39.5 million in 2006, 2.6 million more than in 2004. The manifestations of HIV infection in the kidney are multiple and varied, highlighting the complexity of the disease process. There is a wide spectrum of renal disease that occurs in the course of HIV infection. Biopsy studies reveal varying frequencies of histological patterns. HIV-associated nephropathy (HIVAN) is most common. A biopsy study at Chris Baragwanath Hospital in Soweto, South Africa showed that HIVAN was present in 27% and immune complex disease in 21%. Han et al. studied HIV-positive patients in Durban, South Africa and screened for proteinuria, including microalbuminuria. They found persistent proteinuria in 6%; HIVAN in 21/30 (72.4%) and the prevalence of HIVAN in patients with persistent microalbuminuria was 85.7%. Studies in black patients have shown a higher prevalence of both severe glomerular lesions (focal glomerulosclerosis) and nephrotic range proteinuria with renal dysfunction in the presence of normo-hypotension. There have been no prospective randomised controlled studies with any form of therapy for HIVAN to date. Therapy of HIVAN has included corticosteroids, cyclosporine and antiretroviral therapy (ART). ART appears to be a logical choice in the management of HIV-associated renal disease. Regimens containing protease inhibitors have been shown to be associated with significant slowing of the decline in creatinine clearance. Both peritoneal dialysis and haemodialysis are appropriate treatment modalities for HIV-infected patients with end stage renal disease. The choice of dialysis modality between haemodialysis and peritoneal dialysis is not a factor in predicting survival, if patients are stable on ART. Preliminary short-term data in case reports and small cohorts of liver, kidney, and heart transplant recipients suggest that patient survival rates may be similar to those in HIV-uninfected transplant recipients. However, high rates of acute and chronic rejection have been observed among HIV-infected kidney transplant recipients. The Infectious Diseases Society of America (IDSA) published guidelines in 2005, recommending that all individuals be assessed for kidney disease at the time of diagnosis of HIV infection with a screening urinalysis for proteinuria and a calculated estimate of renal function. Therefore any patient with persistent proteinuria, persistent haematuria or glomerular filtration rate < 60 mL/min per 1.73 m(2) should be referred to an institution where a specialist can evaluate this patient for further investigations. An integrated plan to reduce the progression to kidney failure together with lifestyle measures, focusing also on high risk groups with effective management at all levels of chronic kidney disease remains essential.
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PMID:Chronic kidney disease in human immunodeficiency virus infection. 1762 82


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