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

The mechanism of the binding of IgA to the mesangium in IgA nephropathy (IgAN) is unknown. Interactions between IgA and components of the mesangial matrix may contribute. We measured by enzyme-linked immunosorbent assay the binding of serum IgA, IgG, and IgM from patients with IgAN, human immunodeficiency virus type I (HIV) infection, and healthy controls to purified native collagen types I to VI, and to an extract of normal kidney tissue. HIV infection is an appropriate disease control because of the lack of mesangial IgA deposits, despite high serum levels of IgA and IgA1-containing immune complexes. Increased levels of IgA-binding to collagen types I and V and the kidney extract were found only in IgAN. Both IgAN and HIV-infected patients had increased IgA-binding to collagen types II, III, and VI. Preabsorption of the sera with gelatin substantially reduced the IgA-binding to collagen types I to IV, but not to types V and VI. This finding suggests that the binding to collagen type V is not fibronectin-mediated, but may reflect autoantibody formation. Thus, fibronectin-mediated IgA-collagen interactions are not specific for IgAN, and their pathogenetic role is questionable. The role of IgA anti-collagen type V antibodies requires further study.
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PMID:Binding of serum immunoglobulins to collagens in IgA nephropathy and HIV infection. 140 20

A 9-year-old boy is presented who was antibody positive for human immunodeficiency virus (HIV) and who had recurrent episodes of gross hematuria. Renal biopsy revealed findings typical of IgA nephropathy but also showed electron-microscopic abnormalities seen with HIV-associated nephropathy. In addition, IgA antibodies to multiple HIV proteins were detected in serum by Western blot analysis, and circulating immune complexes of the IgA class were present. Although HIV-associated nephropathy and IgA nephropathy are thought to be distinct conditions, five adults with a similar combination of findings have been reported, and our patient adds to the evidence for a link between these two entities in some patients. We propose that the histological parallels between the conditions may merely represent the limited renal responses available to multiple types of injuries, and we support the attempts underway to probe renal tissue for the HIV genome.
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PMID:IgA nephritis in a child with human immunodeficiency virus: a unique form of human immunodeficiency virus-associated nephropathy? 153 39

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

A 37-year-old Caucasian male homosexual presented with hematuria and rapidly progressive acute renal failure. He was found to have proteinuria and microscopic hematuria as well as RBC casts. Investigations revealed polyclonal gammopathy with five times normal serum IgA levels as well as elevated serum IgG. Renal biopsy showed evidence of crescentic IgA nephropathy with ultrastructural changes of tubuloreticular inclusions described in HIV nephropathy. He was found to be positive for human immunodeficiency viral antibodies. Renal function improved during follow-up after two doses of 1 g each of methylprednisone. In our opinion, this is the first case of HIV-related crescentic IgA nephropathy. HIV testing should be performed more frequently in patients presenting with acute glomerular diseases.
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PMID:Crescentic IgA nephropathy as a manifestation of human immune deficiency virus infection. 180 45

The problems in the diagnosis and especially the pathogenetic mechanism of IgA nephropathy are discussed and suggestions are made that this entity may not be a renal disease of primary renal immunogenetic origin but may be a disease of disturbed mesangial transport mechanism for IgA. Suggestions are made for intensive studies on the pathogenesis and differential diagnosis of focal glomerulosclerosis vs. minimal change disease (lipoid nephrosis) especially by immunohistology and T Cell sub-set abnormalities. It is suggested to study minimal change disease from the viewpoint of a T Cell immunodeficiency with lymphokines as a permeability changing factor. Depressed antibody formation in such partially immunodeficient patients may be important for differential diagnosis from other nephrotic stages. The immunology of acute glomerulonephritis as caused by cytoplasmic streptococcal antigens requires further study together with resultant chronic glomerulonephritis on an auto-antibody basis. The disputed merits of plasmapheresis require further detailed studies. The investigation of the suggested importance of nephrectomies on the renal function of kidney donors is of utmost importance in view of its relation to the future of live donor transplantations.
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PMID:The future of nephrologic research: significance and urgent problems. 623 Nov 48

Antineutrophil cytoplasmic autoantibodies (ANCA) have been used as markers of systemic vasculitides, including microscopic polyarteritis (MPA) and Wegener's granulomatosis. The diagnostic potential of ANCA assays together with antibodies against the neutrophil enzymes myeloperoxidase (MPO) and proteinase 3 for detecting a systemic vasculitis was tested in a Chinese patient population. 672 sera were received for ANCA assay, and ANCA detected by indirect immunofluorescence was positive in 73 sera from 42 patients. Of the 42 patients, 3 had cytoplasmic ANCA, while 39 had a perinuclear pattern. There was no patient with Wegener's granulomatosis. Two cytoplasmic ANCA positive patients suffered from ulcerative colitis. Another cytoplasmic ANCA positive patient was a carrier of human immunodeficiency virus. Of the 39 perinuclear ANCA positive patients, 10 had MPA. Eight of them were tested for anti-MPO antibody, and all were positive. Other immune disorders that were perinuclear ANCA positive included: 13 patients with systemic lupus erythematosus, 3 with mixed connective tissue disease, 1 with Goodpasture's syndrome, 2 with inflammatory bowel disease, and 2 patients with IgA nephropathy. Anti-MPO antibody was not specific for MPA, and 7 out of the 13 patients with systemic lupus erythematosus were anti-MPO antibody positive. Our study suggests that ANCA and anti-MPO antibody are not specific for MPA in a Chinese population. They would alert the clinician of the possibility of vasculitis, but a clinicopathological correlation is essential in making the diagnosis.
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PMID:Use of antineutrophil cytoplasmic autoantibodies in diagnosing vasculitis in a Chinese patient population. 791 85

This review summarizes recent progress in the immunologic aspects of parenchymal renal disease. Progress in understanding basic immune mechanisms of glomerular injury is outlined, including the roles of chemoattractants, adhesion molecules, metalloproteinases, and cytokines. Current basic and clinical studies of focal segmental glomerulosclerosis, membranous nephropathy, membranoproliferative glomerulonephritis, minimal-change nephropathy, and IgA nephropathy are summarized. Finally, research in glomerular involvement in systemic disorders, such as lupus nephritis, antineutrophil cytoplasmic antibody-associated syndromes, and human immunodeficiency virus-associated nephropathy, is reviewed.
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PMID:Immunologic renal injury. 792 81

Familiarity with renal issues that can challenge the care of patients with human immunodeficiency virus (HIV) should expedite diagnosis and therapeutic interventions. Among the most common problems are electrolyte and acid-base imbalances from many opportunistic infections or their treatments, including hyponatremia, hyperkalemia, hypokalemia, and hypo- and hypercalcemia. Acid-base disturbances, simple or mixed, can be due to underlying sepsis, opportunistic infections, or the therapy thereof. A recent report of seven patients with HIV with type B lactic acidosis failed to identify a satisfactory etiology. Elevations in creatinine or diminishing urine output should alert the physician to the possibilities of prerenal azotemia or acute tubular necrosis, which can result from progression of prerenal azotemia or can occur secondary to administered nephrotoxins, such as certain antibiotics and radiocontrast agents. Agents associated with nephrotoxicity include aminoglycosides, antifungal, antiviral, and radiocontrast agents, and nonsteroidal anti-inflammatory pain medications. Although prerenal azotemia and acute tubular necrosis are the most frequent causes of acute renal failure, the differential diagnosis should include acute interstitial nephritis, obstructive nephropathy, and glomerulopathies such as hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, the newly described IgA nephropathy, and, in certain populations, HIV nephropathy.
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PMID:The spectrum of kidney diseases in patients with human immunodeficiency virus infection. 792 95

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

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


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