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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal consequences of HIV disease are diverse: some unique attributable to HIV infection per se and some coincidental reflecting the nature and severity of underlying primary illness. In addition, renal sequelae may also be iatrogenic, owing to a variety of therapeutic agents employed in the management of HIV infection. Renal failure from any cause, both reversible (acute) and irreversible (ESRD), contributes greatly to morbidity and mortality in HIV-infected patients. An understanding of the spectrum of renal derangements is essential for clinicians to manage patients with HIV disease better.
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PMID:Renal complications in HIV disease. 894 Dec 30

HIV-infected patients may present with a variety of patterns of renal involvement. Acute renal failure is common and most often a result of sepsis, hypotension, and nephrotoxic agents. It is potentially avoidable, and support through the period of renal failure may lead to resolution of the renal dysfunction. HIV-associated nephropathy is a unique pattern of sclerosing glomerulopathy that ranges in prevalence from 1 to 10% of the HIV-infected population in different geographic locales. This complication of HIV infection will likely present a growing challenge to the medical community as HIV infection continues to spread worldwide. Deciphering the pathogenetic mechanisms of this most rapidly progressive form of focal segmental sclerosis is not only clinically relevant, but will hopefully provide valuable insights into the mediation of the more common idiopathic form of the disease. The potential for improved renal survival of patients with HIV-associated nephropathy has become more realistic with the development and use of antiretroviral agents, as well as studies on the role of immunosuppression and ACE inhibition in this population. An awareness of other glomerular lesion and tubulointerstitial lesions has broadened our understanding of populations with renal disease who have been infected by HIV. Moreover, as prolonged survival of HIV-infected individuals is being achieved with modern antiviral therapy, the percentage of patients surviving with nephropathy will likely grow in coming years. Awareness of the growth of this population and those requiring short- and long-term hemodialysis and peritoneal dialysis will allow appropriate planning for ESRD in the HIV-infected population.
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PMID:HIV infection and the kidney. 901 59

HIV-associated nephropathy (HIVAN) is a progressive glomerular and tubular disease that is increasingly common in AIDS patients and one of the leading causes of end stage renal disease in African Americans. A major unresolved issue in the pathogenesis of HIVAN is whether the kidney disease is due to renal cell infection or a "bystander" phenomenon mediated by systemically dysregulated cytokines. To address this issue, we have used two different experimental approaches and an HIV-1 transgenic mouse line that develops a progressive renal disease histologically similar to HIVAN in humans. In the murine model, kidney tissue expresses the transgene and in heterozygous adults, renal disease develops shortly thereafter. We demonstrate by terminal deoxynucleotide transferase-mediated dUTP-biotin nick-end labeling assay that similar to the disease in humans, apoptosis of renal tubular epithelial cells is a component of the molecular pathogenesis. To determine whether apoptosis is due to transgene expression or environmental factors, we treated fetal kidney explants (normal and transgenic) with UV light to induce transgene expression. Apoptosis occurred in transgenic but not normal littermates after stimulation of transgene expression. To confirm a direct effect of HIV expression on the production of HIVAN, we transplanted kidneys between normal and transgenic mice. HIVAN developed in transgenic kidneys transplanted into nontransgenic littermates. Normal kidneys remained disease free when transplanted into transgenic littermates. Thus, the renal disease in the murine model is intrinsic to the kidney. Using two different experimental approaches, we demonstrate a direct effect of transgene expression on the development of HIVAN in the mouse. These studies suggest that in humans, a direct effect of HIV-1 expression is likely the essential cause of HIVAN, rather than an indirect effect of cytokine dysregulation.
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PMID:Nephropathy in human immunodeficiency virus-1 transgenic mice is due to renal transgene expression. 920 60

Chronic infections contribute significantly to morbidity and mortality in dialysis patients. These infections are acquired either before or after initiation of dialysis, and the latter may be via nosocomial modes of transmission. Consequently, policies that deal with infection control in dialysis units have assumed increasing importance. The incidence and prevalence of hepatitis C virus (HCV) infection among patients on dialysis is steadily declining. Nonetheless, the 0.4% to 15% incidence of anti-HCV in hemodialysis (HD) units continues to be a cause for concern. Although nosocomial transmission of HCV infection in HD units has been demonstrated, the Centers for Disease Control and Prevention (CDC), Atlanta, GA, does not recommend dedicated machines, patient isolation, or a ban on reuse in HD patients with HCV infection. Conventional cleansing and sterilization procedures for reprocessing the dialyzers appear to be adequate to inactivate the virus. Over the years, there has been a steady increase in the number of human immunodeficiency virus (HIV)-infected patients entering end-stage renal disease (ESRD) programs. Transmission of HIV infection is extremely unlikely in dialysis units that conform to the standard practice guidelines. Dedicated machines or isolation from other patients are not recommended for patients with HIV infection. Risk of acquiring HIV infection after an occupational exposure is approximately 0.32%. Nonetheless, a combination of zidovudine and lamuvidine for most parenteral exposures, and the addition of a protease inhibitor in high-risk exposures, is recommended. The wide range of immunological derangements in chronic renal failure have been postulated to be the cause for the increased susceptibility of dialysis patients to tuberculosis (TB). The high incidence of extrapulmonary disease may be a significant factor in the delay in diagnosis of TB in these patients. In view of their high-risk for exposure to TB, the purified protein derivative (PPD) skin test is recommended on an annual basis in the staff of dialysis units.
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PMID:A 1990s perspective of hepatitis C, human immunodeficiency virus, and tuberculosis infections in dialysis patients. 924 19

Recombinant human erythropoietin has been available for clinical use since 1985. It was an immediate success in treating the anemia of chronic renal failure and has also enjoyed some objective success in the treatment of other anemias in either a therapeutic or prophylactic setting, but the issues of appropriate patient selection and cost-benefit ratios are still unresolved. This review discusses the most recent literature concerning the use of recombinant human erythropoietin for the anemia associated with cancer, HIV infection, myelodysplasia, prematurity, autologous blood transfusion, bone marrow transplantation, and chronic renal failure.
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PMID:Clinical use of erythropoietin. 937 81

Human immunodeficiency virus-associated nephropathy (HIVAN) is the third leading cause of end-stage renal failure in Blacks between the ages of 20 and 64. Because the incidence of HIV infection has continued to increase in Blacks as survival has improved, the pool of patients alive and at risk for developing HIVAN has vastly expanded. This suggests that HIVAN will continue to increase in importance to the end-stage renal disease program. The racial predilection for the disease in Blacks implies that genetic or environmental cofactors are involved. Evidence in human and animal models has shown that proliferation of renal epithelial cells is the predominant feature of the disease and that apoptosis occurs. The prospect that renal infection is necessary to stimulate cells to proliferate remains a possibility but is not yet proven. Cytokine dysregulation may also be involved in disease progression, but evidence is lacking that altered cytokine production is the proximate cause of HIVAN. Many issues remain to be resolved including the potential for renal infection in vivo, the mechanisms responsible for proliferation and apoptosis, and factors that provide racial susceptibility to HIVAN. Advances in our understanding of pathogenesis will be required to control the growth of HIV-related renal diseases in the ESRD population.
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PMID:Pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy. 969 55

We studied 92 HIV-positive patients retrospectively between January 1994 and December 1996 and prospectively from January to July 1997. We determined serum creatinine and 24-hour proteinuria. The median age of the patients was 22 (+/- 4) years and most patients were aged between 25 and 45 years. The sex ratio was 2.17 and most patients were infected with HIV-1 (67.39%). Renal failure occurred in 27.16% of cases, due to changes in blood pressure and infectious diseases. Three patients had a nephrotic syndrome caused by HIV. Thirty-eight cases of lung infection, ten of urinary infection, twelve infections of the digestive system and fifteen cases of skin infection were recorded. The median duration of stay in hospital was 23 (+/- 8) days and the median cost of hospitalization was 147,450 F CFA (+/- 31,057). The treatment given was purely symptomatic and three patients died during the study. One patient suffered chronic renal failure and is now undergoing hemodialysis. Preventive treatment would be of great value.
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PMID:[Renal complications associated with human acquired immunodeficiency virus infection in a population of hospital patients at the Hospital and University National Center in Cotonou]. 979 39

Diseases in other organs may impair the male reproductive system. Acute critical conditions such as severe trauma, surgery, myocardial infarction, burns, liver failure, intoxication, or starvation are associated with suppression of gonadotropin secretion and secondary hypogonadism. With chronic illnesses, a primary testicular disorder with elevated gonadotropin levels may occur. This may be associated with increased peripheral conversion of androgens to estrogens, resulting in clinical presentation of combined androgen deficiency and estrogen excess. The association of hypogonadism and feminization with cirrhosis of the liver is a classic example. Types of hypogonadism that may occur with chronic anemia, chronic renal failure, chronic spinal cord injury, thyroid diseases, Cushing's syndrome, diabetes mellitus, obesity, HIV infection, neoplasia, and other chronic illnesses are also described. Numerous drugs have side effects on the reproductive system.
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PMID:Reproductive effects of nontesticular illness. 992 10

In 1986, Weiss et al reported a group of patients with nephrotic syndrome, progressive chronic renal failure, and the histopathologic features of glomerular capillary collapse. Similar lesions are often described in human immunodeficiency virus (HIV) nephropathy. We evaluated 893 consecutive nontransplant renal biopsies performed in our department and the follow-up of the patients at our outpatient service. Sixteen specimens were identified with the pathological features of collapsing glomerulopathy (focal segmental or global glomerular capillary collapse and visceral epithelial cell hyperplasia), with no evidence of HIV infection and/or intravenous drug abuse. Their clinical characteristics were analyzed and compared with a group of 29 patients with noncollapsing focal segmental glomerulosclerosis (FSGS). The follow-up period of both patient groups was 5 +/- 1.46 years. The Kaplan-Meier life table method was used to present survival of the patients. The age of both groups was similar, 34 +/- 4 years (mean +/- standard error of the mean) for patients with collapsing glomerulopathy and 35 +/- 3 years for those with FSGS. The serum creatinine level was greater in patients with collapsing glomerulopathy (183 +/- 31 micromol/L) compared with those with FSGS (115 +/- 18 micromol/L), but the difference was not significant (P = 0.0504). The difference in proteinuria was not significant (P = 0.7668); it was 5.83 +/- 0.74 g/d in patients with collapsing glomerulopathy and 5.42 +/- 0.84 g/d in those with focal sclerosing glomerulonephritis. The difference in systolic (P = 0.4) and diastolic blood pressure (P = 0.556) was also not significant. Survival of the patients with collapsing glomerulopathy was worse than that of patients with FSGS (P = 0.025). Renal function survived 5 years in 40% of the patients with FSGS, but patients with collapsing glomerulopathy had no renal function survival. Our data suggest that idiopathic collapsing glomerulopathy is a distinct clinicopathologic entity with similar clinical features to focal sclerosing glomerulonephritis, but a worse prognosis and a rapidly progressive course toward end-stage renal disease.
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PMID:Collapsing glomerulopathy: clinical characteristics and follow-up. 1019 29

This study evaluated the role of serum cardiac troponin I as a biochemical marker for the diagnosis of acute coronary syndromes in the presence of noncardiac diseases. Diagnostic characteristics were examined in 102 consecutive patients who were found to have serum cardiac troponin I levels higher than the upper reference limit of 0.6 ng/mL. Of 102 patients with cardiac troponin I levels of >0.6 ng/mL, 35 did not have the final diagnoses of acute coronary syndromes (myocardial infarction or unstable angina) but had various other final diagnoses, including nonischemic dilated cardiomyopathy, muscular disorders, central nervous system disorders, HIV disease, chronic renal failure, sepsis, lung diseases, and endocrine disorders. The mean value of serum cardiac troponin I in the patients with diseases other than acute coronary syndromes was significantly lesser than in those with acute coronary syndromes (2.0+/-1.9 [SD] v. 24.7+/-28.2 ng/mL; P<.0001). There were significantly fewer histories of chest pain and prior myocardial infarction in patients with diseases other than acute coronary syndromes than in those with acute coronary syndromes (history of chest pain, 3 v. 48 patients [P<.001]; history of prior myocardial infarction, 0 v. 30 patients [P<.001]). In conclusion, elevated serum levels of cardiac troponin I, especially in the lower ranges, should be interpreted with caution, particularly in patients suffering from acute illnesses who lack other diagnostic features suggestive of acute coronary ischemic events.
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PMID:Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes. 1033 75


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