Acquired Immunodeficiency Syndrome and the Kidney

Seney, Frank D.; Burns, Dennis K.; Silva, Fred G.

doi:10.1016/s0272-6386(12)80779-7

Cited by 109 publications

(35 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Every increase in serum creatinine must lead to careful consideration of other causes of nephropathy, whether they are drug induced or disease associated (10,20). Although the cooccurrence is rare, HIV infection has been shown to coincide with different glomerular and extraglomerular nephropathies (6,21).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pyrimethamine inhibits renal secretion of creatinine

Opravil

Keusch

Lüthy

1993

Antimicrob Agents Chemother

View full text Add to dashboard Cite

The mechanism of increased serum creatinine after administration of pyrimethamine and dapsone was evaluated for six healthy volunteers. Serum parameters, urine sediment, and clearances of creatinine, inulin, and para-aminohippurate were assessed prior to and 28 h after the ingestion of a single, combined dose of 100 mg of pyrimethamine and 200 mg of dapsone. In a second series, the same renal function tests were performed for nine human immunodeficiency virus-infected men before and after 1 month of prophylactic treatment with a weekly dose of 75 mg of pyrimethamine and 200 mg of dapsone to evaluate sustained effects on renal function. Serum creatinine increased within 28 h from 81 14 to 102 + 16 ,umol/liter (P = 0.002) in the healthy volunteers. Blood urea nitrogen, 132-microglobulin, and urine remained normal. Creatinine clearance decreased from 125 + 27 to 91 ± 26 ml/min (P < 0.02) without changes in inulin clearance. The effect was reversible within 21 days and attributable to pyrimethamine, as determined by administration of each drug alone. The sustained effect of four doses of pyrimethamine and dapsone in human immunodeficiency virus-infected patients consisted of an analogous rise in serum creatinine from 69 17 to 87 + 32 ,umol/liter (P < 0.05). Both creatinine and inulin clearances, however, were unchanged, representing a new equilibrium between creatinine production and elimination at a higher level in serum. Pyrimethamine, thus, may reversibly inhibit renal tubular secretion of creatinine without affecting the glomerular filtration rate. This physiologic effect in pyrimethamine-treated patients must be differentiated from possible organ-related nephropathies.

show abstract

Section: Discussionmentioning

confidence: 99%

“…1). Thereafter, serum creatinine fell continuously from day 6 to day 21 after drug intake, normalizing at 104 20 ,umol/liter on day 21. The highest individual value observed was 150 ,umol/liter on day 1.…”

mentioning

confidence: 97%

Pyrimethamine inhibits renal secretion of creatinine

Opravil

Keusch

Lüthy

1993

Antimicrob Agents Chemother

View full text Add to dashboard Cite

show abstract

“…In addition, glomerular changes are observed and often represent segmental glomerulosclerosis. Kidney disease such as tubulointerstitial nephritis and focal and segmental glomerulosclerosis are relatively frequent in SIV-infected macaques (417) and in AIDS patients, especially in children (352,394,418). The early expression of the Tg along with the specific C3H/HeN background may explain the high penetrance of this phenotype in the CD4C/HIV Tg mice.…”

Section: Aids-like Disease In Transgenic Mice Expressing Hiv-1mentioning

confidence: 99%

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

2004

View full text Add to dashboard Cite

Oropharyngeal and esophageal candidiases remain significant causes of morbidity in human immunodeficiency virus (HIV)-infected patients, despite the dramatic ability of antiretroviral therapy to reconstitute immunity. Notable advances have been achieved in understanding, at the molecular level, the relationships between the progression of HIV infection, the acquisition, maintenance, and clonality of oral candidal populations, and the emergence of antifungal resistance. However, the critical immunological defects which are responsible for the onset and maintenance of mucosal candidiasis in patients with HIV infection have not been elucidated. The devastating impact of HIV infection on mucosal Langerhans' cell and CD4+ cell populations is most probably central to the pathogenesis of mucosal candidiasis in HIV-infected patients. However, these defects may be partly compensated by preserved host defense mechanisms (calprotectin, keratinocytes, CD8+ T cells, and phagocytes) which, individually or together, may limit Candida albicans proliferation to the superficial mucosa. The availability of CD4C/HIV transgenic mice expressing HIV-1 in immune cells has provided the opportunity to devise a novel model of mucosal candidiasis that closely mimics the clinical and pathological features of candidal infection in human HIV infection. These transgenic mice allow, for the first time, a precise cause-and-effect analysis of the immunopathogenesis of mucosal candidiasis in HIV infection under controlled conditions in a small laboratory animal

show abstract

“…1,2 Specific phenotypes have been observed in the lymphoid organs, [1][2][3] lung, 4,5 kidney, 6,7 bone marrow, 8 striated muscle, 9 peripheral 10 and central 11,12 nervous system, and heart. 13 Cardiac disease in AIDS was under-appreciated early in the course of the epidemic, but is now recognized as one of the most frequent complications of infection with HIV-1.…”

mentioning

confidence: 99%

Cardiac Disease in Transgenic Mice Expressing Human Immunodeficiency Virus-1 Nef in Cells of the Immune System

Kay

Yue

Hanna

et al. 2002

The American Journal of Pathology

View full text Add to dashboard Cite

We previously reported that a severe acquired immune deficiency syndrome-like disease develops in transgenic (Tg) mice expressing the human immunodeficiency virus-1 in its natural target cells: immature and mature CD4 ؉ T cells and cells of the macrophage/ dendritic lineage. Here, we show that these mice also develop cardiac disease, characterized most prominently by a focal myocytolysis, occasionally by myocarditis and by deposition of endogenous immunoglobulin on cardiomyocytes. Microfil perfusion demonstrated widespread coronary arteriospasm and echocardiographic analysis revealed depressed cardiac function in Tg mice. A higher (but still modest) level of cardiomyocyte apoptosis was detected in Tg as compared to non-Tg hearts. Tg expression was detected in some of the infiltrating mononuclear cells, but not in cardiomyocytes or in cells of the heart vessels, suggesting a human immunodeficiency virus-1-induced disease process mediated by cells of the immune system. The similarity of the heart disease observed in these Tg mice to that observed in acquired immune deficiency syndrome patients suggests a common pathogenesis.

show abstract

Acquired Immunodeficiency Syndrome and the Kidney

Cited by 109 publications

References 60 publications

Pyrimethamine inhibits renal secretion of creatinine

Pyrimethamine inhibits renal secretion of creatinine

Immunopathogenesis of Oropharyngeal Candidiasis in Human Immunodeficiency Virus Infection

Cardiac Disease in Transgenic Mice Expressing Human Immunodeficiency Virus-1 Nef in Cells of the Immune System

Contact Info

Product

Resources

About