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 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and pathologic findings in the kidneys of 30 consecutive acquired immunodeficiency syndrome (AIDS) autopsies and in 34 consecutive renal biopsies performed on HIV infected patients at our institution between 1983 and 1987 were studied. To determine if the lesions of HIV-associated nephropathy have morphologic specificity, a subgroup of 13 biopsies with a diagnosis of HIV-associated nephropathy (HIVN) were compared to 13 biopsies each of heroin-associated nephropathy (HAN) and of idiopathic focal segmental glomerulosclerosis (IFSGS) matched for patient age, proteinuria and serum creatinine. A diagnosis of HIVN was made in 1 of 30 (3.3%) AIDS autopsies and 26 of 34 (76.5%) renal biopsies. When compared to HAN and IFSGS, HIVN had more globally "collapsed" glomeruli (P less than 0.001), less glomerular hyalinosis (P less than 0.02), more severe visceral epithelial cell swelling (P less than 0.05), more numerous visceral epithelial cell droplets (P less than 0.002), more prevalent and severe tubular microcystic dilatation (P less than 0.02), and tubular cell degenerative changes (P less than 0.001). Focal glomerular electron-dense deposits were present in 14 of 26 cases. Tubuloreticular inclusions were extremely numerous in glomerular and interstitial capillary endothelial cells as well as in interstitial leukocytes (P less than 0.001). Granular degeneration of nuclear chromatin was present in 10 of 26 cases. Nuclear bodies were more numerous in tubular and interstitial cells of HIVN (P less than 0.01), particularly type 3 (P less than 0.001). Reversal of tissue T4/T8 ratio was observed. We conclude that while no single morphologic feature of HIVN is specific, the combination of clinical and pathologic findings is quite distinctive and permits a presumptive diagnosis of HIVN in otherwise asymptomatic carriers.
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PMID:Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study. 277 Jan 14

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

AIDS-associated nephropathy (AAN) causing acute renal failure has been described in patients with AIDS. It is characterized by massive proteinuria and focal segmental glomerulosclerosis. From 1982 until 1987, 177 patients with AIDS were seen in our center. Most of them were homosexual or bisexual men. One patient was also an intravenous drug addict. One patient was a black female. None suffered from a nephrotic syndrome or needed hemodialysis during their illness. In 47 of the 110 patients who died an autopsy was performed. On microscopical examination of kidney tissue obtained at autopsy, no abnormalities were seen in 12 patients and slight abnormalities were found in 35 patients. Glomerular changes, mostly fibrous caps in Bowman's space, were present in 22 patients. Mesangial and intracapillary lesions were seen in only 5 patients. Tubular atrophy was found in 14 patients and sparse interstitial inflammation in 15 patients. A renal localisation of disseminated opportunistic infections was found in 11 patients: CMV (n = 4), tuberculosis (n = 2), Mycobacterium avium intracellulare (n = 1) and Cryptococcal infection (n = 4). In one patient a renal localisation of a Kaposi sarcoma and in another patient a renal localisation of a disseminated non-Hodgkin lymphoma was found. In conclusion the clinical picture of AAN with acute renal failure was not found in our center. As is the case with heroin associated nephropathy, AAN seems to be confined to certain areas in the USA, suggesting that racial or local co-factors, are important for the pathogenesis of AAN in AIDS.
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PMID:Glomerular lesions and opportunistic infections of the kidney in AIDS: an autopsy study of 47 cases. 278 96

Tubuloreticular inclusions (TRI) and cylindrical confronting cisternae (CCC) are present in cells of patients with the acquired immunodeficiency syndrome (AIDS) and have also been detected in the kidneys of individuals with AIDS and heavy proteinuria. We examined renal biopsy tissue from 13 patients with proteinuria and/or renal insufficiency. At the time of biopsy, two of the patients had AIDS (group A), four had AIDS-related complex (ARC) (group B), and seven presented without any clinical signs or symptoms characteristic of AIDS or ARC. These seven had risk factors for AIDS, and systemic lupus erythematosus (SLE) was excluded in all. Abundant TRI were present in the renal endothelial and fibroblastic interstitial cells in all patients from group A and B and in four patients who had no evidence for AIDS or ARC at the time of biopsy (group C). These individuals were followed, and all developed AIDS within a period of 3 to 14 months. CCC were detected in two of two patients in group A, one of four in group B, and one of four in group C. TRI and CCC were not present in the renal tissue of the remaining three patients; they did not develop ARC or AIDS over a prolonged observation period. Our findings suggest that TRI and TRF are ultrastructural markers for human immunodeficiency virus (HIV) associated nephropathy and can be seen before AIDS has manifested itself. These structures may be of predictive value for the future development of AIDS in patients presenting with apparent idiopathic renal disease.
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PMID:Renal cytomembranous inclusions in idiopathic renal disease as predictive markers for the acquired immunodeficiency syndrome. 284 54

The existence of an HIV-related nephropathy as a distinct disease entity is controversial. We observed a high incidence of renal disease in our AIDS patients. Of 182 patients, 59 patients (32.4%) were found to have heavy proteinuria (greater than 2 g/24 h). Of these, 24 patients had slow progression of renal insufficiency and 2 patients had rapid deterioration to end stage renal disease. There was a notable absence of hypertension in these cases. The incidence of proteinuria was similar in blacks and hispanics; however 22.8% of blacks had renal insufficiency as compared to 6.9% of hispanics. There was no difference in the incidence of heavy proteinuria between intravenous drug abusers (32.3%) and nonabusers (33.3%). Renal morphology when examined showed characteristic changes, including cytomembranous structures and virus-like particles. These changes were similar in patients with heavy or light proteinuria, though they were less severe in the latter. We conclude that a HIV-related nephropathy exist and the presence of cytomembranous structures and virus-like particles in the renal tissue raises the possibility of a viral etiology for this disorder.
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PMID:Evidence for an HIV-related nephropathy: a clinico-pathological study. 291 6

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

Although a variety of renal lesions may occur in acquired immune deficiency syndrome (AIDS), a rare but aggressive form of focal and segmental glomerulosclerosis with capillary collapse has been considered a possible component of this disorder. It is manifested by heavy proteinuria and progression to renal failure in a short time. We studied renal biopsies from nine patients with HIV infection and the above clinical features and compared the renal tissues to biopsies from HIV-positive individuals with immune complex glomerulonephritis and to biopsies from patients with heroin abuse nephropathy. The HIV-associated nephropathy was characterized by a combination of lesions: focal and segmental glomerulosclerosis, often in an early stage of evolution and with prominent degenerative changes of visceral epithelium; tubular necrosis without identifiable nephrotoxic or hemodynamic etiology; interstitial edema; large plasma protein-containing tubular casts in all segments of the nephron associated with marked tubular dilatation; and widespread tubuloreticular structures in vascular endothelium. In contrast, neither the sclerosing glomerular changes nor the tubulointerstitial abnormalities were present in HIV-infected patients with immune complex glomerulonephritis. Similarly, the tubular and interstitial changes and widespread tubuloreticular structures were absent in heroin-abuse nephropathy. The lesions of HIV-associated nephropathy occurred in patients with AIDS, AIDS-related complex, and in individuals clinically asymptomatic for HIV infection. Their morphological features in asymptomatic patients are sufficiently specific to allow for accurate diagnosis of HIV infection.
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PMID:HIV-associated nephropathy. A unique combined glomerular, tubular, and interstitial lesion. 307 May 50

Five children with acquired immunodeficiency syndrome (AIDS) and clinically significant renal disease had detailed pathologic examination of renal tissue (biopsy specimens, autopsy specimens, or both). All patients had proteinuria, hypoalbuminemia, and edema; one patient had persistent azotemia. In two cases, renal disease was the first manifestation of human immunodeficiency virus (HIV) infection. All patients had progressive renal disease, and four of the five died. Pathologic studies revealed focal glomerulosclerosis and mesangial proliferative glomerulonephritis with deposits of immunoglobulins and complement demonstrated by immunofluorescence and electron microscopy. Characteristic tubuloreticular structures were also demonstrated in the glomerular endothelial or epithelial cells in two cases. Renal disease is part of the multisystem involvement in children with AIDS. The pathogenesis of renal disease is not known, but circulating immune complexes are known to occur in children with HIV infection and may be involved.
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PMID:Acquired immunodeficiency syndrome-associated renal disease in children. 338 27

Renal tissues from two groups of patients with acquired immune deficiency syndrome (AIDS) were examined: Group A had severe proteinuria and varying degrees of renal insufficiency, designated AIDS-associated nephropathy (AAN), and Group B had no renal involvement. Control Group C consisted of patients with heroin-associated nephropathy (HAN) with proteinuria comparable to patients in Group A but without AIDS or its related complex (ARC). The most frequent finding, common to both AAN and HAN, was focal glomerular sclerosis. In contrast to HAN, AAN tissue showed mesangial hypocellularity, sparse interstitial infiltrates, severe tubular degenerative changes, tubular microcystic ectasia, Bowman's space dilatation, and presence of multiple complex inclusions both in the nuclei and cytoplasm in a variety of cells. Abundant tubuloreticular inclusions were found in the endothelial and occasionally in the interstitial cell cytoplasm. Nuclear bodies (NBs) were seen in greater frequency, complexity, size, and heterogeneity, and of budding configuration in Group A as compared with Groups B and C; NBs in Group C were mostly of simple types (I and II). In addition, a peculiar granulofibrillary transformation in many tubular and interstitial cell nuclei was observed in Group A. This transformation was rarely present in Group B and was never seen in Group C. Because complex NBs (Types III to V) and various intracytoplasmic and intranuclear inclusions present in Group A are often associated with viral invasion, their presence in kidneys of AIDS patients with proteinuria suggests a viral etiology for AAN.
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PMID:Renal ultrastructural markers in AIDS-associated nephropathy. 354 10

Between January 1982 and December 1986, among the 750 patients with the acquired immunodeficiency syndrome (AIDS) who were treated at two adjacent hospitals in New York City, 78 (10.4 percent) needed evaluation for renal disorders. Reversible acute renal failure due to nephrotoxic injury, ischemic injury, or both was present in 23 patients (30 percent) (Group I). The remaining 55 (70 percent) had massive proteinuria, azotemia, or both (AIDS-associated nephropathy; Group II), and irreversible uremia developed in 43. In an additional 18 patients, all of whom had a history of intravenous narcotic drug use, AIDS was diagnosed after the initiation of maintenance hemodialysis for chronic renal failure (Group III). Survival for more than six months after the onset of chronic uremia occurred in only two subjects in Group II; all patients in Group III died within three months of the diagnosis of AIDS. Death in the patients in Groups II and III followed a syndrome of "failure to thrive" characterized by inanition unresponsive to intensive nutritional support and hemodialysis. In contrast, 8 of 17 patients with acute renal failure (Group I) and a serum creatinine concentration above 6 mg per deciliter regained renal function (serum creatinine level, less than 2.0 mg per deciliter). Four of the seven lived for 10 to 24 months, whereas the other four died of sepsis within a month. Our observations suggest that maintenance hemodialysis is not effective in prolonging life either in patients with AIDS-associated nephropathy and uremia or in patients with end-stage renal failure in whom AIDS develops during the course of maintenance dialysis. Hemodialysis may be useful in the management of potentially reversible acute renal failure in patients with AIDS.
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PMID:The types of renal disease in the acquired immunodeficiency syndrome. 356 58


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