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)

Patients infected with human immunodeficiency virus type 1 (HIV-1) develop a renal syndrome characterized by proteinuria, renal failure, and focal segmental glomerulosclerosis. By using a noninfectious HIV-1 DNA construct lacking the gag and pol genes, three transgenic mouse lines have been generated that develop a syndrome remarkably similar to the human disease. In the present study, we have characterized in detail one of these lines, Tg26. In Tg26 mice, proteinuria was detectable at approximately 24 days of age, followed by severe nephrotic syndrome and rapid progression to end-stage renal failure. Renal histology showed focal segmental glomerulosclerosis and microcystic tubular dilatation. Indirect immunofluorescence studies demonstrated increased accumulation of the basement membrane components laminin, collagen type IV, and heparan sulfate proteoglycan. The viral protein Rev was present in sclerotic glomeruli. Northern blot analysis of total renal RNA showed expression of viral genes prior to the appearance of histologic renal disease, with greatly diminished viral gene expression late in the disease course. Kidneys from transgenic mice expressed increased steady-state levels of collagen alpha 1(IV) mRNA when glomerulosclerosis was present. We conclude that the presence of HIV-1 genes is associated with progressive renal dysfunction and glomerulosclerosis in transgenic mice.
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PMID:Progressive glomerulosclerosis and enhanced renal accumulation of basement membrane components in mice transgenic for human immunodeficiency virus type 1 genes. 154 49

Infection with the human immunodeficiency virus type 1 (HIV-1) can cause a spectrum of renal disease, termed acquired immunodeficiency syndrome (AIDS) nephropathy. The most common clinical manifestations of kidney involvement in HIV-1-infected patients are proteinuria and/or nephrotic syndrome, and the histopathological pattern usually reveals focal segmental glomerulosclerosis. We describe an 8-year-old child with AIDS who presented with recurrent gross hematuria. A kidney biopsy demonstrated IgA nephropathy. This unique case indicates that the range of kidney disease in HIV-infected children may be broader than originally thought, and that these patients warrant a complete evaluation of any renal abnormality.
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PMID:IgA nephropathy in a child with human immunodeficiency virus type 1 infection. 176 86

We report here the cases of 15 children in whom nephrotic syndrome developed, from among 164 children (55% male, 90% black) followed in our acquired immunodeficiency syndrome clinic from 1984 through 1990. Mean age at onset of nephrotic syndrome was 4.9 +/- 2.6 years. Fourteen patients were black and one was Hispanic. Seventy-three percent of our patients with nephrotic syndrome were girls. The mean duration of clinical acquired immunodeficiency syndrome before development of nephrotic syndrome was 1.7 +/- 1.1 years. In eight patients, nephrotic syndrome appeared between 3 and 11 months after intravenous infusions of immune globulin or albumin were administered as part of a research protocol; this incidence (8/47) was higher than the incidence of nephrotic syndrome among those who did not receive intravenous infusions (7/117, p less than 0.05). Tissue for histologic examination was available for 80% of the patients, and histologic examination demonstrated mesangial hypercellularity (5 patients), focal segmental glomerulosclerosis (4 patients), minimal change disease (2 patients), and IgM nephropathy (1 patient). Deposition of one or more immunoglobulins was noted in all but one patient studied with immunofluorescence. Corresponding electron-dense deposits were seen by electron microscopy in 78% of specimens. Prednisone did not induce a remission of nephrotic syndrome in the 13 patients treated, whereas cyclosporine did so in the 3 patients to whom it was administered. Five patients were in the end stage of renal disease within 8 months. Successful maintenance peritoneal dialysis was performed in three patients, but 80% of patients have died of human immunodeficiency virus-related complications; one patient was lost to follow-up. We conclude that immune-complex deposition is consistently seen in children with human immunodeficiency virus-associated nephrotic syndrome. This nephrotic syndrome is resistant to steroid therapy, but we observed a remission of the proteinuria with cyclosporine therapy in three patients. For patients with end-stage renal disease, maintenance peritoneal dialysis may improve the quality of life.
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PMID:Nephrotic syndrome associated with acquired immunodeficiency syndrome in children. 194 75

A survey of consultations to the Division of Nephrology at San Francisco General Hospital from 1982 to 1988 found only seven cases of proven or possible renal disease matching that described for human immunodeficiency virus (HIV)-associated nephropathy (nephrotic proteinuria, rapidly progressive renal insufficiency, and focal and segmental glomerulosclerosis [FSGS] histologically). In the period from April 1, 1988 (the conclusion of the original survey) through December 31, 1990, a roughly 11-fold increase in the incidence of such cases among referrals of HIV-infected patients to the Division occurred compared with the initial experience. The patients were nearly exclusively black men, only about half of whom had intravenous drug abuse (IVDA) as an HIV risk factor. This striking increase was associated with a progressive increase in the number of black patients with acquired immunodeficiency syndrome (AIDS) in San Francisco, and in the percentage of patients with an AIDS diagnosis discharged from San Francisco General Hospital (SFGH) who were black. These data support other evidence indicating a particular vulnerability of blacks to this form of renal disease and help to reconcile data from our division with the experience reported from other centers.
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PMID:Increasing incidence of human immunodeficiency virus-associated nephropathy at San Francisco General Hospital. 196 49

Initial autopsy studies concerned primarily with the systemic manifestations of the acquired immunodeficiency syndrome (AIDS) did not indicate that significant renal problems were likely to occur in AIDS patients. However, several recent studies have suggested that important renal and electrolyte disorders develop frequently in at least some groups of AIDS patients. In this report, we review current information concerning such disorders and describe our study of the frequency and types of renal lesions in the first 50 AIDS patients undergoing autopsy at this institution. We conclude that a number of renal lesions and electrolyte abnormalities occur in AIDS patients, although the frequency and nature of these problems vary considerably from center to center. Studies from several centers, including our own, indicate that AIDS patients are particularly likely to develop tubulointerstitial lesions (such as nephrocalcinosis and interstitial nephritis) and electrolyte disorders. Additional studies from specific centers in New York City, Miami, Detroit, and Los Angeles indicate that AIDS patients can also develop glomerular lesions, including a variant of focal and segmental glomerulosclerosis (FSGS) associated with heavy proteinuria and rapidly progressive renal failure. Although FSGS is not commonly observed in all centers, AIDS patients with this lesion appear to have a distinctive combination of clinical and pathological features, suggesting that they have a specific "human immunodeficiency virus (HIV)-associated" nephropathy. Preliminary evidence suggests that this lesion may be related to direct renal HIV infection, although confirmation of this possibility is needed. The approach to the AIDS patient with renal disease should involve correction of reversible disorders and consideration of dialysis as necessary.
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PMID:Acquired immunodeficiency syndrome and the kidney. 219 75

A spectrum of renal abnormalities has been described in patients infected with the human immunodeficiency virus (HIV) with or without signs of the acquired immunodeficiency syndrome (AIDS). In particular, attention has been focused on a nephropathy characterized clinically by nephrotic proteinuria and rapidly advancing renal insufficiency, and histologically by focal and segmental glomerulosclerosis (FSGS). To evaluate the relationship between HIV infection and structural renal disease, we reviewed all consultations between January 1982 and March 1988 to the Division of Nephrology at San Francisco General Hospital (SFGH), a municipal hospital treating approximately one-third of AIDS cases in San Francisco. Seventy-three consultation requests were received during this period regarding patients with AIDS (48), AIDS-Related Complex (23), or asymptomatic HIV infection (2). Of these, 27 gave evidence of structural renal disease (Group I): 14 had chronic renal insufficiency, in 10 of whom nephrotic proteinuria was also present. However, progression of renal insufficiency to end-stage renal disease (ESRD) in this group did not follow the rapid course described for HIV-associated nephropathy. Renal tissue was examined in 11 Group I patients and showed FSGS in four and a variety of acute and chronic glomerular and tubulointerstitial changes in the others. In 46 Group II patients, consultation was requested for acute renal failure or fluid, electrolyte, and acid-base disturbances. We also reviewed 91 consecutive autopsies performed in patients dying with AIDS at SFGH between 1981 and 1986.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal involvement in patients infected with HIV: experience at San Francisco General Hospital. 234 28

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

Of 155 children with the acquired immunodeficiency syndrome (AIDS) whom we evaluated during a 6 1/2-year period, 12 were found to have proteinuria. Histologic studies of tissue from these 12 patients revealed a wide spectrum of renal disease: focal glomerulosclerosis in 5, mesangial hyperplasia in 5, segmental necrotizing glomerulonephritis in 1, and minimal change disease in 1. In addition, 6 had tubulointerstitial infiltrates, and 10 had glomerular dense deposits. All 10 renal specimens studied by electron microscopy contained endothelial tubuloreticular inclusions. The mean age (+/- SD) of the five patients with focal glomerulosclerosis when this condition was identified was 27 +/- 19 months. All five had severe renal failure within a year and died of other causes during the following year. The mean age of the five patients with mesangial hyperplasia was 38 +/- 31 months. Although none of them went on to have renal failure, four died within 8 +/- 7 months. Ten of the 12 patients with proteinuria died during the study period. Of the two surviving, one had mesangial hyperplasia and the other had minimal change disease. We conclude that children who acquire human immunodeficiency virus (HIV) infection during the perinatal period may have renal disease, most often focal glomerulosclerosis, as is the case in adults, or mesangial hyperplasia. Although 5 of the 12 children we studied had renal failure during the study period, none died of it. Further studies are needed to determine the correlations between clinical and pathological features and the pathophysiology of AIDS nephropathy in children.
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PMID:Renal disease in children with the acquired immunodeficiency syndrome. 277 Jul 91

Lesions induced in rhesus monkeys by different isolates of simian immunodeficiency virus (SIV)/Delta were studied at necropsy. Four groups of monkeys were inoculated with SIV/Delta isolated from other experimentally infected rhesus monkeys, while one group was inoculated with SIV/Delta from an asymptomatic mangabey monkey. Three rhesus isolates and the mangabey isolate were virulent, killing 75-100% of infected monkeys. One rhesus isolate, which had been extensively passaged in vitro, was attenuated but was restored to virulence by single animal passage. Clinically, infected monkeys had lymphadenopathy, splenomegaly, diarrhea, and a rash. Most monkeys died of enteric disease. The following lesions were seen: weight loss, thymic atrophy, lymphoid atrophy, bone marrow hyperplasia, encephalitis, colitis, amyloidosis, hepatitis, glomerulosclerosis, and the presence of syncytial cells. One Rh Epstein-Barr virus (EBV)-related lymphoma occurred. Opportunistic agents were identified: cytomegalovirus, adenovirus, Cryptosporidia, and Pneumocystis. Shigella and Campylobacter often caused colitis.
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PMID:Necropsy findings in rhesus monkeys experimentally infected with cultured simian immunodeficiency virus (SIV)/delta. 285 Jun 50

A nephrology consultation was called on 100 adult patients of 1,635 (6.1%) patients with human immunodeficiency virus (HIV) infection seen between 1982 and 1987 at the University of Miami/Jackson Memorial Medical Center. Renal disease was observed in all groups of patients with a risk factor for HIV infection with a lesser incidence, however, among homosexuals. Intravenous drug (IVD) use and possibly race appear to be important factors in the development of renal complications. Renal disease was the dominant clinical feature in eight asymptomatic HIV carriers and in 34 patients with AIDS-related complex (ARC) who had not developed the opportunistic infections and/or malignancies associated with acquired immunodeficiency syndrome (AIDS). Ninety-one percent of consultations were requested for evaluation of proteinuria and/or renal failure. Nephrotic range proteinuria, in excess of 3 g/24 h, was present in 52 patients, and was less prevalent in homosexuals than in other groups at risk. Renal failure (serum creatinine greater than or equal to 5 mg/dL), initially present in 32 patients, eventually developed in 69 and improved in only 18 of them. A renal biopsy, obtained for work-up of nephrotic syndrome (22 patients) or renal insufficiency (3 patients), uncovered a picture of focal and segmental glomerulosclerosis in all 25 instances. Overall, 76 patients are dead, seven are lost to follow-up, and 17 are alive, of whom eight (four HIV carriers, two patients with ARC, and two with AIDS) are on maintenance hemodialysis with a mean survival time of 217 days.
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PMID:The clinical spectrum of renal disease associated with human immunodeficiency virus. 304


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