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)

Nephropathies associated with human immunodeficiency syndrome (HIVAN) are characterized by gross proteinuria, lack of change in blood pressure, and various histologic lesions. The present study prospectively measured microalbuminuria in 72 HIV-seropositive patients (3 asymptomatic, 32 AIDS-related complex, 37 AIDS) screened for Phase I clinical pharmacology studies. There were 14 patients (19.4%) that had abnormal urinary levels of microalbumin; 7 of these patients (50%) had proteinuria similar to those values found in diabetic nephrotic syndrome. Microalbumin levels were not correlated with race, sex, risk factors of AIDS, disease history, or concurrent drug therapy. In contrast, urinary microalbumin levels were correlated with CD 4 T-cell and WBC counts, tumor necrosis factor alpha and beta 2-microglobulin levels, suggesting an association between AIDS progression and microalbuminuria. By monitoring urinary microalbumin levels, those patients susceptible to the development of nephrotic syndrome could be identified and prophylactic measures initiated.
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PMID:Incidence of microalbuminuria in ambulatory patients with acquired immunodeficiency syndrome. 151 82

More than 87,000 patients with acquired immunodeficiency syndrome (AIDS) were reported to the Centers for Disease Control in the United States, of whom more than half died through January 1989. When the AIDS epidemic is considered worldwide, these numbers should be doubled at least [27]. Whereas electrolyte disorders and acute renal complications were recognized early on in the AIDS epidemic, it was not until 1984 that a nephropathy was described in patients with human immunodeficiency virus-Type 1 (HIV-1) (formerly called LAV/HTLV-III) infection [18, 30, 36]. This nephropathy was characterized, clinically, by heavy proteinuria or the nephrotic syndrome and a rapid progression to end-stage chronic renal failure and, pathologically, by an aggressive form of focal segmental glomerulosclerosis. The existence of an AIDS-related nephropathy was not readily accepted because of its uneven geographic distribution amongst areas severely affected by the AIDS epidemic [24, 48]. This brief review summarizes the clinical and pathologic features of AIDS-related nephropathy.
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PMID:Acquired immunodeficiency syndrome (AIDS)--related renal disease. 268 68

Human immunodeficiency virus-associated nephropathy (HI-VAN) is a common form of nephropathy present in HIV-infected individuals that clinically presents with proteinuria that is frequently in the nephrotic range, less often with hematuria, and with a course that may evolve to irreversible azotemia ultimately resulting in renal failure. Pediatric and adult HIV-positive patients both experience HIVAN morphologically after displaying focal segmental glomerulosclerosis, diffuse mesangial hyperplasia, microcystic tubular dilatation, interstitial inflammation, edema, and fibrosis. There is minimal information regarding the interstitial inflammatory cell infiltrate, despite the possibility that these cells may play an important role in the etiology of HIVAN. This study was designed to characterize and compare several morphological and immunopathological features of clearly established HIVAN, particularly the hematopoietic cell markers present on the interstitial inflammatory cells and the state of T-lymphocyte activation (ie, class II expression). Quantitative grading of HIVAN kidneys showed that CD4-positive and CD8-positive T cells comprised the major cell populations in the interstitium, often with CD4-positive T cells exceeding or being equivalent in number to CD8-positive T cells. B cells and macrophages were negligible components of the infiltrate. Human leukocyte antigen-DR class II molecules were found to be increased on the interstitial T cells as well as on all glomerular cells and endothelial cells. There was no significant relationship established between the immunophenotype of the interstitial inflammatory cells and other morphological, ultrastructural, immunofluorescent, or clinical features. These data imply that the inflammatory infiltrate in HIVAN is largely composed of activated T cells. At this point the role of these interstitial T cells in HIVAN is undetermined, although it can be speculated that they may be participating as antiviral or autoreactive immune effector cells imparting renal injury in this entity.
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PMID:Immunopathological characteristics of in situ T-cell subpopulations in human immunodeficiency virus-associated nephropathy. 770 20

A 43-year-old man with rapidly evolving renal failure from biopsy-proven human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) and superimposed thrombotic microangiopathic changes was treated with prednisone. His serum creatinine decreased from 7.5 to 3.9 mg/dL, and the 24-hour protein excretion decreased from 15.7 to 6.1 g over 6 to 8 weeks. As the prednisone was tapered, however, the creatinine began to increase, and a repeat biopsy was done to assist with therapeutic decisions. The major differences from the pretreatment biopsy were marked reductions in interstitial lymphocytes and macrophages and absence of thrombotic microangiopathic lesions. This is the first report comparing pretreatment and posttreatment renal biopsy specimens and the findings provide some insight into the means by which prednisone exerts its beneficial clinical effects acutely on this disease.
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PMID:Clinicopathologic correlates of prednisone treatment of human immunodeficiency virus-associated nephropathy. 884 Sep 56

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 (HIV)-associated nephropathy (HIVAN) is a clinicopathologic entity that includes proteinuria, azotemia, focal segmental glomerulosclerosis or mesangial hyperplasia, and tubulointerstitial disease. The incidence of HIVAN is increased in black patients and variable depending on the age and geographic area. The objective of this study was to describe relevant clinical and pathological findings in 30 children with HIVAN followed at the Children's National Medical Center in Washington, D.C. Our experience of the last 12 years showed a spectrum of HIVAN that seems to be coincident with the degree of acquired immunodeficiency syndrome (AIDS) symptomatology. By renal sonograms and frequent urinalysis, we identified children undergoing the early stages of HIVAN with enlarged echogenic kidneys, proteinuria, and "urine microcysts". HIVAN did not necessarily progress rapidly to end-stage renal disease. Nephrotic syndrome or chronic renal insufficiency were late manifestations of HIVAN. Children with HIVAN were likely to develop transient electrolyte disorders, heavy proteinuria, and acute renal failure due to systemic infectious episodes or nephrotoxic drugs. HIVAN was associated with other HIV-induced illnesses and high mortality rates. Early detection and careful clinical follow-up of children with HIVAN may reduce the incidence of renal-cardiovascular complications and improve their quality of life.
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PMID:Human immunodeficiency virus (HIV)-associated nephropathy in children from the Washington, D.C. area: 12 years' experience. 969 52

The existence of a human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) as a distinct disease entity characterized by glomerulosclerosis is well established in North America and Western Europe. Although the large number of HIV-infected cases overwhelm the Asian countries, no cases of HIVAN are documented in the literature. We studied 26 cases of HIV-infected Thai patients with proteinuria greater than 1.5 g/d of protein during 1995 and 1996. None of the patients were treated with antiretroviral drugs at the time of renal biopsy. Intravenous drug addiction and sexual transmission were risk factors in 11 and 15 patients, respectively. Pathological examinations were performed by light microscopic and immunoperoxidase study. Mesangial proliferative glomerulonephritis was found in 17 cases, immunoglobulin A (IgA) nephropathy in 2 cases, and diffuse proliferative glomerulonephritis and interstitial nephritis secondary to cryptococcal infection in 2 cases each. One case each had membranous glomerulopathy, membranoproliferative glomerulonephritis, and granulomatous interstitial nephritis secondary to tuberculosis. The renal pathological findings of HIVAN with the unique features described in previous literature were not evident in these patients. Although the data in this study are limited to 26 HIV-infected Thai patients, we believe that HIVAN is uncommon in the Asian HIV-infected population.
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PMID:Renal pathology and HIV infection in Thailand. 1002 39

A number of chimeric simian-human immunodeficiency virus (SHIV) viruses containing tat, rev, vpu, and env from HIV-1 (strain HXBc2) in a genetic background of simian immunodeficiency virus (SIV(mac)239) have been derived from the parental nonpathogenic SHIV-4 virus. In this article we examine the renal pathology associated with the derivation of these pathogenic SHIV strains. The first of the pathogenic SHIVs, SHIV(KU-1), is associated with rapid CD4(+) T cell loss and opportunistic infections associated with AIDS, but only one of four infected pigtail macaques examined has developed significant renal pathology. The renal pathology in this macaque consists of a diffuse increase in matrix in the core of each lobule with collapsed glomerular capillries, which is similar to the renal changes reported in HIVAN. Passage of this virus into rhesus macaques yielded SHIV(KU-2), which results in renal pathology in three of four inoculated rhesus macaques in which <10% of the glomeruli are involved. A molecular clone of SHIV(KU-2) was derived (SHIV(KU-2MC4)) that causes neurologic and renal pathology with more than 60% of the glomeruli involved and results in uremic level BUN concentrations. These results indicate that SHIV(KU-2MC4) causes severe significant glomerular pathology and should permit a detailed analysis of the molecular determinants associated with the development of SHIV-associated glomerulosclerosis in rhesus macaques.
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PMID:Simian-human immunodeficiency virus-associated nephropathy in macaques. 1095 26

Human immunodeficiency virus (HIV)--associated nephropathy (HIVAN) and other glomerular lesions (e.g., immunoglobulin A nephropathy and immune complex glomerulonephritis) are frequent complications of HIV infection. These renal diseases usually present as a nephrotic syndrome with progressive loss of renal function and an increased risk of mortality. The prevalence and epidemiology of these renal lesions remain largely undefined; however, most studies agree that black race is a major risk factor for HIVAN. Observational studies have suggested that antiretroviral medications and angiotensin-converting enzyme inhibitors have beneficial effects on slowing the progression of renal disease among patients with HIVAN; however, little is known about the effect of these therapies on other renal lesions. Future research should focus on gaining a better understanding of the distribution and determinants of renal disease among HIV-infected patients as well as on performing controlled studies to test treatment strategies.
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PMID:Renal diseases associated with human immunodeficiency virus infection: epidemiology, clinical course, and management. 1138 4

Human immunodeficiency virus (HIV) associated nephropathy (HIVAN) is the most common disease delineated in biopsy series of patients with HIV infection and renal disease. Although the renal histologic lesions in patients with HIV infection present a spectrum of findings, several groups have emphasized characteristic clinical and pathologic features of HIVAN. Consensus has since been reached that HIVAN has a distinctive pathology, consistent with focal segmental glomerulosclerosis, but involving all subunits of the kidney. Several studies have linked the pathogenesis of focal glomerulosclerosis to abnormalities of the glomerular epithelial cell. Recent advances in molecular histologic studies and treatment link the pathogenesis of HIVAN to factors associated with the viral lifecycle. Cytopathic effects of HIV gene products, apoptosis mediated by HIV infection, the elaboration of chemokines and cytokines as a result of viral or host protein synthesis in patients with genetic susceptibility to nephropathy, and the subversion of the host metabolic and synthetic machinery by the virus might be sufficient to create a rapidly progressive disease. If HIV infects and has cytopathic effects on glomerular epithelial cells, and dysfunction of these cells is intimately related to the pathogenesis and progression of renal disease, a reasonable pathogenic mechanism for the development of HIVAN may be inferred. The similarities of HIVAN and the collapsing variant of focal segmental glomerulosclerosis pose the intriguing possibility that the latter is a viral illness as well. The disease is marked by glomerular sclerosis with varying degrees of collapse, tubular epithelial cell degeneration, simplification, microcystic dilatation, interstitial fibrosis and immune cell infiltration. At the level of electron microscopy, tubular reticular inclusions in renal endothelial cells are a typical, but not pathognomonic feature of HIVAN.
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PMID:HIV-associated nephropathy: virologic issues related to renal sclerosis. 1295 44


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