First‐line ritonavir/indinavir 100/800 mg twice daily plus nucleoside reverse transcriptase inhibitors in a German multicentre study: 48‐week results

Voigt, Esther; Wickesberg, A.; Wasmuth, JC; Gute, Peter; Locher, Leo; Salzberger, Bernd; Wöhrmann, A.; Adam, Axel; Weitner, Lutwin; Rockstroh, JK

doi:10.1046/j.1468-1293.2002.00123.x

Cited by 28 publications

(21 citation statements)

References 16 publications

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“…The incidence of renal colic was prospectively estimated at 23.6% over 2 years in a cohort of 555 patients treated with a HAART regimen, including indinavir [42]. In a prospective study over 48 weeks evaluating the association of ritonavir/indinavir, 100/800mg twice daily in a HAART regimen, 19 (33%) out of 57 patients discontinued study medication because of nephrolithiasis [43].…”

Section: Protease Inhibitorsmentioning

confidence: 99%

HAART-related nephropathies in HIV-infected patients

Daugas¹,

Rougier²,

Hill³

2005

Kidney International

108

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There is no doubt that highly active antiretroviral therapy (HAART) has been the most important progress in the therapy of human immunodeficiency virus (HIV)-infected patients in the last decade. A growing number of observations suggest that the beneficial effects of HAART also include improvement of HIV-related renal complications. Consequently, the cohort of HIV-infected patients requiring HAART has increased and includes patients with preexisting nephropathies, whether related or unrelated to HIV infection. However, some antiretroviral drugs may have renal- and life-threatening side-effects, especially if underlying renal abnormalities exist. In this review, we focus on those aspects that require particular attention in preventing new health complications in HIV-infected patients.

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Section: Protease Inhibitorsmentioning

confidence: 99%

HAART-related nephropathies in HIV-infected patients

Daugas¹,

Rougier²,

Hill³

2005

Kidney International

108

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“…In a series of 240 patients started on indinavir therapy, approximately 8% developed symptomatic nephrolithiasis and 20% developed crystalluria without symptoms [25]. Voigt et al [26] found a higher, 33% incidence of nephrolithiasis, in their series of 57 patients who received indinavir therapy over a 48-week observation period. Likewise, Gagnon et al [24] found a 67% prevalence of crystalluria among their study participants treated with this protease inhibitor.…”

Section: Acute Tubular Necrosismentioning

confidence: 98%

“…Likewise, Gagnon et al [24] found a 67% prevalence of crystalluria among their study participants treated with this protease inhibitor. Alkaline urine and volume depletion can lead to the formation of insoluble indinavir crystals [24][25][26]. The incidence of AKI in the setting of indinavir varies but may be as high as 25% [25,[27][28][29].…”

Section: Acute Tubular Necrosismentioning

confidence: 99%

Acute kidney injury in patients with human immunodeficiency virus infection

Cohen

Chawla

Kimmel

2008

Current Opinion in Critical Care

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“…Boosting of indinavir was not broadly implemented because of high plasma peak levels of the PI leading to enhanced renal toxicity (Voigt et al 2002;Boyd et al 2006). Boosting did not greatly enhance the bioavailability of nelfinavir.…”

Section: Second-generation Protease Inhibitor Therapy; Boosting Of Prmentioning

confidence: 99%

HIV Protease Inhibitor Resistance

Wensing

Fun

Nijhuis

2014

Handbook of Antimicrobial Resistance

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HIV protease is pivotal in the viral replication cycle and directs the formation of mature infectious virus particles. The development of highly specific HIV protease inhibitors (PIs), based on thorough understanding of the structure of HIV protease and its substrate, serves as a prime example of structure-based drug design. The introduction of first-generation PIs marked the start of combination antiretroviral therapy. However, low bioavailability, high pill burden, and toxicity ultimately reduced adherence and limited long-term viral inhibition. Therapy failure was often associated with multiple protease inhibitor resistance mutations, both in the viral protease and its substrate (HIV gag protein), displaying a broad spectrum of resistance mechanisms. Unfortunately, selection of protease inhibitor resistance mutations often resulted in cross-resistance to other PIs.Therefore, second-generation approaches were imperative. Coadministration of a cytochrome P-450 3A4 inhibitor greatly improved the plasma concentration of PIs in the patient. A second advance was the development of PIs that were efficacious against first-generation PI-resistant HIV. Both approaches increased the number of protease mutations required by the virus to develop clinically relevant resistance, thereby raising the genetic barrier towards PI resistance. These improvements greatly contributed to the success of PI-based therapy.

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First‐line ritonavir/indinavir 100/800 mg twice daily plus nucleoside reverse transcriptase inhibitors in a German multicentre study: 48‐week results

Cited by 28 publications

References 16 publications

HAART-related nephropathies in HIV-infected patients

HAART-related nephropathies in HIV-infected patients

Acute kidney injury in patients with human immunodeficiency virus infection

HIV Protease Inhibitor Resistance

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