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Query: UMLS:C0021051 (immunodeficiency)
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There has been a steady increase in the number of dialysis patients with human immunodeficiency viral (HIV) infection. HIV-associated nephropathy (HIVAN) is the most common cause of end-stage renal disease in this patient population. Although the major potential category of risk of HIV transmission is from the dialysis patient to staff, there are no data to indicate that this has occurred. Dialysis of patients with HIV infection is challenging and requires effective care to prolong survival.
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PMID:Patients with HIV infection and end-stage renal disease. 891 90

Patients with human immunodeficiency viral (HIV) infection who also require dialysis present a complex constellation of challenges for dialysis personnel. The major challenges that health care providers (HCPs) face when working with HIV-infected patients are related to overcoming personal fears and to adapting to HIV-specific patient care needs. Dialysis personnel who encounter these concerns do so with a background of experience that has prepared them to cope effectively with HIV disease in the dialysis setting. This article explores the problems of occupational exposure to HIV and chronic health care issues common to patients with HIV infection and renal disease.
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PMID:HIV infection: challenges for dialysis personnel. 891 91

Electron microscopy is routinely utilized in most centers in the evaluation of native renal biopsies. Several studies, primarily from the 1960s and early 1970s, provide justification for its use. Conducted by Siegel et al. (1), the largest study evaluated 213 consecutive renal biopsies and found that electron microscopy was needed for a correct diagnosis in 11%, as well as for confirmation or additional information in another 36%. However, nearly all of these studies were conducted before the use of immunofluorescence in renal biopsy diagnosis became widespread and before several new glomerular diseases and variants were described. In light of this situation and the expense of the procedure, the routine use of electron microscopy in native renal biopsies also examined by immunofluorescence and routine light microscopy was reevaluated. From January 1996 to June 1996, 288 native renal biopsies were received, and all were evaluated by the same pathologist. Of those, 233 met criteria for inclusion in this study, which were > or = 5 glomeruli for light microscopy, > or = 2 for immunofluorescence, and > or = 1 for electron microscopy, not including globally scarred glomeruli. Light microscopy (hematoxylin and eosin, periodic acid-Schiff stains) and immunofluorescence--for immunoglobulin (Ig) G, IgA, IgM, C3, C1q, fibrinogen; kappa/lambda when needed--were evaluated on each biopsy within 48 h of receipt, and a preliminary diagnosis was recorded if possible. Electron microscopy was then performed, and a final diagnosis was made. In 50 cases (21%), electron microscopy was needed to make the final diagnosis; in two of these cases, the preliminary diagnosis was incorrect, and in 48, a firm preliminary diagnosis could not be made. In the other cases, the preliminary diagnosis was correct, but in 48 (21%), ultrastructural study was felt to provide important confirmatory data, and in eight cases (3%), an additional, unrelated diagnosis was supported by the ultrastructural findings. Diagnoses most frequently requiring electron microscopy included minimal change nephropathy, early diabetic nephropathy, membranous lupus nephritis, membranoproliferative glomerulonephritis, postinfectious glomerulonephritis, thin basement membrane nephropathy (or exclusion of this in cases of otherwise unexplained hematuria), and human immunodeficiency virus-associated nephropathy (or exclusion of it in cases of collapsing glomerulopathy). Common diagnoses usually not requiring electron microscopy included IgA nephropathy, diffuse proliferative lupus nephritis, focal segmental glomerulosclerosis (not collapsing glomerulopathy variant), pauci-immune crescentic glomerulonephritis, acute interstitial nephritis, and amyloid nephropathy. This study confirms that, as was the case 20 to 30 yr ago, electron microscopy provides useful diagnostic information in nearly half of native renal biopsies. If electron microscopy cannot be performed routinely on all such biopsies, it is recommended that tissue for ultrastructural studies be set aside in each case.
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PMID:A reevaluation of routine electron microscopy in the examination of native renal biopsies. 901 50

The renal pathologic features of 120 consecutively autopsied patients affected by acquired immunodeficiency syndrome was investigated by light microscopic analysis. Variously associated renal changes were found in 82 patients (68.3%). Glomerular changes were present in 25. The following diagnoses were made: mesangial glomerulonephritis (16 patients), defined by the presence of deposits in the mesangium and/or mesangial cell proliferation; membranous glomerulonephritis (4 patients), cirrhotic glomerulosclerosis (2 patients); and lupuslike glomerulonephritis (3 patients). Glomerular diseases seemed to be significantly associated with chronic hepatitis or liver cirrhosis. Interstitial inflammation was present in 19 cases: chronic pyelonephritis (2 patients), focal nephritis (5 patients), multiple cortical abscesses (7 patients), granulomatous nephritis (5 patients). Cryptococci were found in one and undetermined microorganisms in two cases of multiple cortical abscesses. Atypical mycobacteria were found in two cases of granulomatous nephritis. Mycotic infections were identified in another 6 patients, in whom they did not elicit any inflammatory response. It is worth stressing that, although various generalized infections are common in patients with acquired immunodeficiency syndrome, only cryptococci and atypical mycobacteria also frequently involve the kidney. Focal tubular necrosis was observed in 15 patients. Benign nephrosclerosis was the most common vascular change (27 patients). Changes recalling hemolyticuremic and localized intravascular coagulation were found in three and six patients, respectively. Our data, dealing with a European Caucasian population, considerably differ from those reported in North American literature, in as much as we found no cases of human immunodeficiency virus nephropathy. Conversely, immune-mediated glomerular diseases were frequent, in agreement with recent studies on renal biopsy specimens from AIDS patients with acquired immunodeficiency syndrome. This type of infections, supplies multiple sources of antigens that may stimulate immune complex formation and, therefore, glomerular diseases.
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PMID:Renal changes in patients with acquired immunodeficiency syndrome: a post-mortem study on an unselected population in northwestern Italy. 907 21

Focal and segmental glomerulosclerosis (FSG) with endothelial tubuloreticular inclusions (TRIs) is the typical lesion of human HIV-associated glomerulopathy. Autopsy studies showed the presence of FSG in 3 of 15 macaques dying 15-120 weeks after experimental infection with a simian immunodeficiency virus (SIVMne). Ultrastructural studies generally revealed numerous endothelial TRIs (also present in normals), mesangial expansion, and evidence of mesangial cell injury. One additional animal had a small-vessel polyarteritis with a proliferative and focally crescentic glomerulonephritis; seven animals had mild, multifocal interstitial nephritis. All animals had documented viremia after infection; 14 of 15 developed antibodies to SIV postinoculation. Additional postmortem findings included severe enterocolitis, encephalitis, and opportunistic infections. In contrast, autopsy studies of macaques infected with a type D simian retrovirus (SAIDS-D/Washington, SRV-2) for similar periods of time (n = 40) showed no evidence of FSG. One SRV-infected animal had a mild proliferative glomerulonephritis. These studies indicate SIV-infected primates may provide a relevant model for study of human HIV-associated nephropathy. They also indicate the variable pathology that can be seen in primate infections of distinct retrovirus types, each of which produces a simian immunodeficiency state that resembles human AIDS.
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PMID:Focal segmental glomerulosclerosis in primates infected with a simian immunodeficiency virus. 907 83

Human immunodeficiency virus-associated nephropathy (HIVAN), characterized by heavy proteinuria, rapidly progressive renal failure, "collapsing" glomerulopathy, and tubulointerstitial abnormalities, is the most common finding in HIV-infected patients undergoing a renal biopsy and predominantly affects blacks. We describe the clinical features and renal pathologic findings of 12 intravenous drug users (IVDUs) coinfected with HIV and hepatitis C virus (HCV) who were selected for renal biopsy because they presented with features different from typical HIVAN, including hypertension, microscopic hematuria, and cryoglobulinemia. There were seven black and five Hispanic patients. Eleven patients had immune complex glomerulonephritis (ICGN); one had glomerulosclerosis with immune complex deposits. Ten individuals had evidence of past hepatitis B viral infection, but none had persistent hepatitis B surface antigenemia. No other underlying cause for immune complex glomerulonephritis was identified. Renal biopsy showed membranoproliferative glomerulonephritis in five patients, mesangial proliferative glomerulonephritis in five, membranous nephropathy in one, and "collapsing" glomerulopathy with immune complex deposits in one. Hepatitis C virus RNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) in the renal tissue and/or serum of nine of the 11 patients tested, and also in the renal biopsy tissue of four of eight patients with clinical and pathologic features of typical HIVAN without immunofluorescence evidence of immune complex deposits. One patient presented with renal failure, five patients developed end-stage renal disease (ESRD) requiring hemodialysis (mean time, 6.5 months), and six had stable renal function after a mean follow-up of 29.1 months (range, 2 to 72 months). Liver function abnormalities were present in seven of the 12 individuals, including four of the six patients who developed renal failure. These findings indicate that in some patients coinfected with HIV and HCV, the development of ICGN may dominate the clinical course of the disease. The occurrence of ICGN among black patients at risk for HIVAN may be related to the relatively high prevalence of HCV infection among IVDUs in this group.
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PMID:Immune complex glomerulonephritis in patients coinfected with human immunodeficiency virus and hepatitis C virus. 910 39

We conducted a cross-sectional survey to determine the relative course of patients with end-stage renal disease (ESRD) and human immunodeficiency virus (HIV) infection sustained on maintenance hemodialysis. All 34 patients with ESRD and HIV infection receiving hemodialysis in one hospital-based and three community-based outpatient hemodialysis facilities in Brooklyn, NY, were studied. We documented their known duration of HIV infection, duration of ESRD, and hemodialysis prescription, and noted the presence of clinical acquired immunodeficiency syndrome (AIDS). Total CD4 count, serum albumin concentration, and percent reduction of urea (predialysis blood urea nitrogen minus postdialysis blood urea nitrogen, divided by predialysis blood urea nitrogen x 100) were measured. The 34 study subjects (26 men and eight women) included 31 blacks (91%) and three Hispanics (9%) with a mean age of 42 +/- 7.5 years, 29 (85%) of whom had AIDS. Twenty subjects (59%) had a history of intravenous drug abuse. Only six subjects (18%) were receiving an antiretroviral drug (zidovudine = five, dideoxyinosine = one). In 23 subjects (68%), AIDS was diagnosed prior to ESRD and was presumed to be the cause of renal failure (HIV-associated nephropathy). The mean known duration of HIV infection was 50.5 +/- 34 months (median, 48 months); the mean duration of ESRD was 57 +/- 50 months, the mean total CD4 count was 140 +/- 150 cells/microL (median, 70 cells/microL), the mean hematocrit was 28% +/- 5%, and the mean serum albumin concentration was 3.5 +/- 0.37 g/dL. All subjects were receiving erythropoietin for anemia correction. The mean length of the prescribed thrice-weekly hemodialysis sessions was 3.5 +/- 0.4 hours. Our results suggest that the survival of many ESRD patients with HIV infection receiving hemodialysis has improved compared with the uniformly dismal survival rate reported in the 1980s. Decisions on whether to initiate renal replacement therapy in patients with AIDS and advanced renal failure should be individualized because the combination of ESRD and HIV infection does not necessarily signal near-term death.
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PMID:Uremia therapy in patients with end-stage renal disease and human immunodeficiency virus infection: has the outcome changed in the 1990s? 910 43

Human immunodeficiency virus-associated nephropathy (HIVAN) is characterized by massive proteinuria with rapidly progressive renal failure. We report an adult with HIV infection who developed nephrotic-range proteinuria and acute renal failure requiring hemodialysis. Renal biopsy findings were consistent with HIVAN, exhibiting focal and segmental glomerulosclerosis with dilated microcystic tubules filled with pale eosinophilic material. Institution of corticosteroid therapy was followed by significant improvement in renal function and proteinuria. Corticosteroids were tapered, and the patient experienced worsening of his renal failure and proteinuria. A second course of corticosteroids was again associated with improved renal function. This and other reports suggest that corticosteroids may improve the clinical course of HIVAN.
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PMID:Clinical response to prolonged corticosteroids in a patient with human immunodeficiency virus-associated nephropathy. 910 55

An etiologic agent directly linked to the development of IgA nephropathy (IgAN) has not been identified, despite the fact that various causes, including viral infections, have been implicated in the pathogenesis of this disease. Human immunodeficiency virus (HIV) infection has been linked with the development of IgAN in several clinical studies, and retroviral infection may be associated with the pathogenesis of IgAN in some patients. The incidence of IgAN has been found to possess distinct geographical distributions, and familial genetic clustering. To determine if retroviral infection is associated with IgAN in a large population of patients, genomic DNA from peripheral blood mononuclear cells from 90 patients seronegative for HIV and human T-cell leukemia virus type 1 (HTLV-1) (37 IgAN, 33 other glomerulonephritis, and 20 healthy controls) was evaluated by nested PCR using a pan-lentivirus-specific primer set (PLSPS), targeting the consensus sequence of the lentiviral pol gene. In 37.8% (14 of 37) of the patients with IgAN, the PCR products migrated in parallel with bands produced by PCR of simian immunodeficiency virus (SIV) infected cells. No products of the expected size were detected in the other patient groups (p < 0.0001, Chi-square). These results suggest that exposure to retroviral infection is more common in patients with IgAN, compared with patients with other proliferative glomerulonephritides, or patients without renal disease. These data demonstrate a possible association of IgAN with infection with non-HIV, non-HTLV-1 retrovirus.
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PMID:Retroviral infection in peripheral mononuclear cells in patients with IgA nephropathy. 912 86

Human immunodeficiency virus (HIV)-1 infection may be complicated by progressive renal glomerular disease, including focal segmental glomerulosclerosis (FSGS) and proliferative glomerulonephritis. We examined renal tissue from 71 patients, including biopsies and autopsies from patients in the presence and absence of HIV-1 infection. We assessed the extent of TGF-beta, interstitial fibrosis, and interstitial CD45-positive cellular infiltrate using immunohistochemistry. Extracellular TGF-beta 1/beta 3 was largely confined to the renal interstitium, with the highest scores in HIV-seropositive renal disease and crescentic nephritis. Among all biopsies, the TGF-beta 1/beta 3 score correlated with the fibrosis score (r = 0.79, P < 0.0001) and with the CD45 score (r = 0.60, P < 0.0001). Biopsies from HIV-infected patients, taken together, showed marginally more TGF-beta 1/beta 3 compared to biopsies from HIV-uninfected patients (P = 0.05); similarly, HIV-associated FSGS showed marginally more TGF-beta 1/beta 3 compared to FSGS biopsies obtained from HIV-uninfected patients (P = 0.05). Intracellular TGF-beta 1 and TGF-beta 3 were both expressed by renal tubular epithelial cells and in extraglomerular crescents, whereas TGF-beta 3 was also present within interstitial mononuclear cells and eosinophils, and, exclusively in HIV-infected patients, within glomerular cells. In conclusion, TGF-beta expression was increased in several progressive glomerular diseases, and was particularly but not uniquely elevated in HIV-associated renal diseases.
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PMID:Renal TGF-beta in HIV-associated kidney diseases. 915 Apr 74


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