RESUMO
(1) Background: It is not known whether different daily dosing schemes have different effects on colistin nephrotoxicity. We examined the effect of once- versus twice- or thrice-daily doses of colistin on renal function. (2) Methods: We performed a multicenter retrospective cohort study of hospitalized patients with a baseline glomerular filtration rate ≥ 50 mL/min who received intravenously the same colistin dose once (regimen A), twice (regimen B) or thrice daily (regimen C). The primary endpoint was acute kidney injury (AKI), defined as fulfilment of any of the RIFLE (Risk-Injury-Failure-Loss-End stage renal disease) criteria. (3) Results: We included 306 patients; 132 (43.1%) received regimen A, 151 (49.3%) regimen B, and 23 (7.5%) regimen C. Ninety-nine (32.4%) patients developed AKI; there was no difference between regimen A vs. B and C [45 (34.1%) vs. 54 (31.0%), p = 0.57]. In a propensity score−matched cohort, AKI was similar in patients receiving Regimen A, Regimen B, and Regimen C (31.6% vs. 33.3%, p = 0.78). On logistic regression analysis, diabetes was an independent predictor of AKI (OR = 4.59, 95% CI 2.03−10.39, p = 0.001) while eGFR > 80 mL/min (OR = 0.50, 95% CI 0.25−0.99, p = 0.048) was inversely associated with AKI. (4) Conclusions: Colistin once daily is not more nephrotoxic than the standard colistin regimens. The only independent predictor of nephrotoxicity was diabetes mellitus, while eGFR > 80 mL/min had a protective effect.
RESUMO
BACKGROUND: Patients infected by the human immunodeficiency virus (HIV) and receiving highly active antiretroviral therapy have a higher incidence of cardiovascular disease than healthy subjects, but little is known about cardiac function in asymptomatic and treatment-naïve patients. We sought to study cardiac function in asymptomatic HIV-infected, treatment-naïve patients. METHODS: We studied 41 HIV-infected and treatment-naïve patients and 20 age- and sex-matched healthy controls. Patients with cardiac symptoms, history of cardiac disease or NT-proBNP >100 pg/mL were excluded. We addressed cardiac function using standard echocardiography along with tissue Doppler (TDI) measurements, including strain/strain rate assessment. RESULTS: Standard echocardiographic parameters did not differ between groups, except for transmitral E wave velocity (64.8 ± 14 cm/s in HIV vs 76.1 ± 10 cm/s in controls, p = 0.002). In contrast, TDI mitral and tricuspid annulus s velocity and all strain/strain rate measurements were significantly lower in HIV patients: s lateral, 10.2 ± 2.4/11.3 ± 0.7, p = 0.011; s septal, 8.1 ± 1.6/8.7 ± 0.8, p = 0.045; s tricuspid, 13.4 ± 2.3/14.9 ± 1.3, p = 0.002; strain/strain rate, septal (strain/strain rate, 15.1 ± 5.7/-0.9 ± 0.3, 25.3 ± 1.7/-1.9 ± 0.2, p < 0.001), anterior (16.7 ± 3/-1.0 ± 0.1, 26.7 ± 1.7/-1.9 ± 0.2, p < 0.001), lateral (16.0 ± 6/-1.0 ± 0.1, 27.5 ± 1.8/-2.2 ± 0.3, p < 0.001) and posterior (15.2 ± 5.8/-1.0 ± 0.2, 26.2 ± 1.8/-2.2 ± 0.3, p < 0.001) left ventricular wall. CONCLUSIONS: HIV infection itself is accompanied by subclinical systolic dysfunction, not apparent to standard echocardiography that can be unmasked though using sensitive echocardiographic techniques.