Prevalence of HIV-associated nephropathy in autopsies of HIV-infected patients

Shahinian, Vahakn B.; Rajaraman, Srinivasan; Borucki, Michael J.; Grady, James J.; Hollander, William; Ahuja, Tejinder S.

doi:10.1016/s0272-6386(00)70259-9

Cited by 106 publications

(62 citation statements)

References 14 publications

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“…As the cause of the renal disease in this patient, HIV-associated nephropathy (HIVAN), classic type FSGS, and various types of GN that are often observed during HIV-1 infection have to be considered [1][2][3][4][5] (Table 1). HIVAN, however, is unlikely to account for the renal manifestations.…”

Section: Hiv-1 Infection and Renal Leishmaniasismentioning

confidence: 99%

“…Second, the typical histologic criteria of HIVAN (i.e., collapsing-type FSGS and cystic dilation of tubuli) were not present. [1][2][3] Classic FSGS and membranous GN could be ruled out by light microscopy and immunohistochemistry, which showed a mesangiocapillary staining pattern for IgG, C1, and C3. In addition, electron microscopy confirmed the subendothelial and intramembranous localization of the immune deposits.…”

Section: Hiv-1 Infection and Renal Leishmaniasismentioning

confidence: 99%

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Renal Leishmaniasis as Unusual Cause of Nephrotic Syndrome in an HIV Patient

Amann

Bogdan²,

Harrer³

et al. 2012

Journal of the American Society of Nephrology

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Renal involvement is a rare complication in HIV-1-infected patients leading to various pathologies and clinical symptoms. In addition to the classic HIV-1-associated nephropathy with collapsing-type focal segmental glomerulosclerosis and characteristic tubulocystic changes, which is more common in Afro-American than in Caucasian HIV-1 patients, immune complex GNs such as membranous GN and membranoproliferative GN are particularly common renal manifestations. Besides HIV-1 itself, a number of opportunistic infections may cause renal disease in HIV-1-infected patients. In this study, we report an unusual case of HIV-1 infection with a severe renal manifestation of systemic leishmaniasis that developed years after repeated visits to Mediterranean countries. The case presents several remarkable clinical, pathologic, and therapeutic aspects that may be important for daily clinical practice. 23: 586-590, 201223: 586-590, . doi: 10.1681 In April 2008, a 45-year-old Caucasian male patient was admitted to our hospital due to dyspnea and recurrent diarrhea during the past weeks. He had been known to be HIV-1 infected for 23 years, and he had been treated with various antiretroviral drug regimens since 1997. Despite therapy, he had experienced progressive immunodeficiency due to poor compliance and drug resistance. At a prior visit to our hospital in 2001, he had presented with a high viremia (500,000 copies/ml) and depleted CD4 cells (3/ml). At the current admission, he was on an antiretroviral combination regimen consisting of darunavir, low-dose ritonavir, tenofovir, and emtricitabine. J Am Soc NephrolPhysical examination revealed an elevated blood pressure of 170/110 mmHg, dyspnea, bilateral pleura effusions, gross edema of legs, scrotum, and penis, and reddish, macular and papular skin lesions on the dorsal hands, chest, abdomen, and thighs. Laboratory analyses showed abnormal renal parameters (serum creatinine 1.49 mg/dl [normal range ,1.1 mg/dl], creatinine clearance 35 ml/min [normal value 75-125 ml/min], urea 69 mg/dl [normal range 14-43 mg/dl], uric acid 7.5 mg/dl [normal range 3.5-7 mg/dl], and proteinuria of 9.6 g/24 h). Liver en-were elevated. Serum ferritin was strongly increased to 1770 ng/ml (normal range 34-310 ng/ml), and iron was slightly decreased to 28 mg/dl (normal range 40-160 mg/dl). Peripheral blood counts showed anemia (hemoglobin 8.3 mg/dl [normal range 12-16 mg/dl]), slight leukopenia (3900/ml [normal range 4000-10,000/ml]), and thrombopenia (99,000/ml [normal range 150,000-400,000/ml]). The number of CD4 + T cells was decreased to 174 cells/ml. Quantitative PCR analyses demonstrated low HIV-1 viremia (790 copies/ml), a low cytomegalovirus viremia (6 copies/10 5 cells), and shedding of BK virus in the urine (4400 copies/ml). PCR analyses yielded negative results for hepatitis C virus in serum and for adenovirus and John Cunningham virus in the urine. All other laboratory parameters including the complement factors C3 and C4, antinuclear antibodies, cryoglobulins, anti-dsDNA antibodies, ...

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Section: Hiv-1 Infection and Renal Leishmaniasismentioning

confidence: 99%

Section: Hiv-1 Infection and Renal Leishmaniasismentioning

confidence: 99%

Renal Leishmaniasis as Unusual Cause of Nephrotic Syndrome in an HIV Patient

Amann

Bogdan²,

Harrer³

et al. 2012

Journal of the American Society of Nephrology

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“…8 The effect of APOL1 variants has not been determined for HIVAN, affecting approximately 10% of HIVinfected African Americans before the initiation of combined antiretroviral therapy. 9 APOL1 and MYH9 are adjacent genes on Chromosome 22, in a region that shows signatures of both historical selection at the time of human and nonhuman divergence and more recent selection within certain African populations. 8,10 -14 APOL1 is unique to certain higher primates but is not found in nonprimate species.…”

mentioning

confidence: 99%

APOL1 Genetic Variants in Focal Segmental Glomerulosclerosis and HIV-Associated Nephropathy

Kopp

Nelson

Sampath

et al. 2011

Journal of the American Society of Nephrology

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822

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Trypanolytic variants in APOL1, which encodes apolipoprotein L1, associate with kidney disease in African Americans, but whether APOL1-associated glomerular disease has a distinct clinical phenotype is unknown. Here we determined APOL1 genotypes for 271 African American cases, 168 European American cases, and 939 control subjects. In a recessive model, APOL1 variants conferred seventeenfold higher odds (95% CI 11 to 26) for focal segmental glomerulosclerosis (FSGS) and twenty-ninefold higher odds (95% CI 13 to 68) for HIV-associated nephropathy (HIVAN). FSGS associated with two APOL1 risk alleles associated with earlier age of onset (P ϭ 0.01) and faster progression to ESRD (P Ͻ 0.01) but similar sensitivity to steroids compared with other subjects. Individuals with two APOL1 risk alleles have an estimated 4% lifetime risk for developing FSGS, and untreated HIVinfected individuals have a 50% risk for developing HIVAN. The effect of carrying two APOL1 risk alleles explains 18% of FSGS and 35% of HIVAN; alternatively, eliminating this effect would reduce FSGS and HIVAN by 67%. A survey of world populations indicated that the APOL1 kidney risk alleles are present only on African chromosomes. In summary, African Americans carrying two APOL1 risk alleles have a greatly increased risk for glomerular disease, and APOL1-associated FSGS occurs earlier and progresses to ESRD more rapidly. These data add to the evidence base required to determine whether genetic testing for APOL1 has a use in clinical practice.

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“…[2][3][4] The prevalence of HIVAN may be as high as 15% of HIV patients (based upon autopsy data), and 4232 new cases of HIVAN reached ESRD between 2002 and 2006 in the United States. 5 HIVAN is a rapidly progressive form of chronic kidney disease (CKD) characterized by nephrotic range proteinuria. Kidney biopsies demonstrate histologic abnormalities in both glomeruli and tubules, including collapsing FSGS, podocyte proliferation and dedifferentiation, tubular dilation, microcyst formation, and tubulointerstitial inflammation.…”

mentioning

confidence: 99%