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Query: UMLS:C0021051 (immunodeficiency)
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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

Sixteen adolescent specific pathogen free cats were inoculated with the Petaluma strain of feline immunodeficiency virus (FIV) and two cats were then necropsied at each of 5, 10, 21, 28, 42, 56, 70, and 84 day time points following infection. Lymphadenopathy gradually increased starting at Day 10 and persisted for the duration. Gross clinical signs of fever, mild to severe malaise, anorexia, diarrhea, dehydration, and generalized soreness appeared around Day 42, peaked at Day 56, and disappeared by Days 70-84 post-infection. Leukopenia, associated initially with a mild lymphopenia and later by both a mild lymphopenia and a severe neutropenia, appeared 14-28 days following infection, troughed at Day 56, and persisted thereafter. The CD4+:CD8+ T cell ratio started to decrease around Day 28, reaching a nadir at Days 56-70. This decrease was due to a decline in the absolute numbers and percentage of CD4+ T cells and an increase in the percentage of CD8+ T cells. Significant histopathologic lesions included myeloid hyperplasia between Days 56-70 post-infection; thymitis with cortical involution and follicular hyperplasia starting at Day 42; lymphoid hyperplasia of peripheral and mesenteric nodes, spleen and tonsils beginning around Day 42; typhlitis most evident from Day 56 onward, and an interstitial nephritis and pneumonitis that was most intense after Day 42. Virus was isolated from peripheral blood mononuclear cells (PBMC) beginning 2 weeks post-infection, and plasma viremia appeared 1 week later. Plasma and PBMC-associated viremia peaked at 42-56 days following infection and decreased abruptly thereafter. Proviral DNA was detectable as early as 5 days after infection in blood leukocytes and after 10 days in other organs. The central nervous system, lungs, thymus, tonsils and mesenteric lymph nodes were the earliest sites of virus localization. Antibodies to the FIV capsid protein appeared 14 days following infection and reached peak levels by Days 42-56. Abnormalities occurring during the primary stage of FIV infection were consistent with those described for acute simian and human immunodeficiency virus-induced disease.
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PMID:An experimental study of primary feline immunodeficiency virus infection in cats and a historical comparison to acute simian and human immunodeficiency virus diseases. 785 70

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

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

Fourteen three-month-old rabbits spontaneously-infected with the microsporidium Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923 were inoculated intravenously with lymphocytes (Ly) from seropositive bovine leukemia virus infected cattle (Ly/BLV) or with fetal lamb kidney cells infected with bovine fetal leukemia (FLK/BLV). Thirteen rabbits were seropositive to BLV at least for a period of three months. Six rabbits died of pulmonary lesions. Chronic inflammatory lesions of encephalitozoonosis were found in six rabbits killed between 454 and 548 days of the observation period. Five animals bore subcutaneous granulomas. Immunohistochemically, E. cuniculi was demonstrated in the inflammatory lesions of rabbits studied. Control animals also spontaneously infected with E. cuniculi did not show clinical signs of encephalitozoonosis. Morphological changes were found incidentally in the form of small glial foci and focal interstitial nephritis in these animals. The combined action of BLV-E. cuniculi on the bodies of rabbits is proposed as a suitable model for the study of encephalitozoonosis in man with human immunodeficiency virus (HIV) infection.
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PMID:Bovine leukemia virus-induced clinical signs and morphological changes of encephalitozoonosis in rabbits. 943 37

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

Indinavir sulfate has been reported to cause asymptomatic crystalluria and nephrolithiasis in patients with human immunodeficiency virus (HIV) infection. Patients taking indinavir may present with asymptomatic crystalluria, nephrolithiasis with frank renal colic and obstruction, flank pain in the absence of nephrolithiasis, and dysuria or urgency. Asymptomatic crystalluria has been described as benign. Discontinuation of the drug has not been recommended in the absence of nephrolithiasis. We report two HIV-positive patients receiving indinavir who developed acute interstitial nephritis with foreign body giant cell reaction on renal biopsies. Both patients had asymptomatic crystalluria, although crystals were associated with clumps of white blood cells (WBCs) on urinalysis in one patient. Both cases show that the inflammatory response was significant enough to lead to tubular injury and acute renal impairment. Our findings suggest that asymptomatic crystalluria attributable to indinavir may illicit an inflammatory response with acute renal insufficiency, warranting monitoring of renal function, especially in patients with crystalluria.
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PMID:Acute tubulointerstitial nephritis attributable to indinavir therapy. 1073 9

We report a case of a 31-year-old woman with common variable immunodeficiency (CVID) complicated with intractable diarrhea and the functional disorder of renal tubules. The patient became hypogammaglobulinemic after she suffered from measles at 6 years of age. She also suffered from lupus-like syndrome at 7 years of age. The complete remission was obtained by glucocorticosteroid treatment. An intravenous immunoglobulin replacement therapy was introduced at 11 years of age, since then her general condition was stable for more than 20 years. When she was 29 years old, she suffered from generalized malaise, anorexia with body weight loss, and numbness of face. The intractable diarrhea as protein loosing syndrome, and the severe abnormality of electrolyte balance with metabolic acidosis as the functional disorder of renal tubules were found. Her condition was not improved by the electrolytes or alkali replacement therapy. She was admitted for further evaluation and treatment. The intractable diarrhea and the functional disorder of renal tubules were dramatically improved after absolute restriction of food intake under hyperalimentation. When she began to take food, the symptom and sign became worse again. The interstitial nephritis and nonspecific inflammation of intestine were found by the tissue biopsy. The most characteristic finding was the infiltration of lymphocytes (predominantly CD 8 + T lymphocytes) in both intestinal mucosa and renal interstitium. The introduction of glucocorticosteroids improved her general condition and biochemical findings. This CVID case is complicated with intractable diarrhea and the functional disorder of renal tubules which is associated with the infiltration of CD 8 + lymphocytes in intestine and kidney. We consider that such case is very rare and valuable to report.
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PMID:[A case of common variable immunodeficiency with intractable diarrhea and the functional disorder of renal tubules]. 1086 33

Introduction of several classes of antiviral agents for the treatment of immunodeficiency virus has led to increased survival and improved quality of life for patients with HIV infection. Protease inhibitors have become the mainstays of current therapy in patient with AIDS. Renal intolerance of indinavir is a rare but important complication in HIV positive patients. The renal function of patients receiving indinavir should be closely monitored. Benign and asymptomatic crystalluria occurs in 4-13% of HIV positive patients. Several cases of acute renal failure, renal atrophy and interstitial nephritis have also been reported. A hydration protocol consisting of one to two liters of fluid should be initiated three hours after each indinavir dose. If significant renal insufficiency persists, temporary indinavir withdrawal or switching to another protease inhibitor should be considered.
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PMID:Renal toxicity of protease inhibitors. 1099 Mar 64


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