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Item Comparison of Tissue Injury from Focused Ultrasonic Propulsion of Kidney Stones Versus Extracorporeal Shock Wave Lithotripsy(Elsevier, 2014-01) Connors, Bret A.; Evan, Andrew P.; Blomgren, Philip M.; Hsi, Ryan S.; Harper, Jonathan D.; Sorensen, Mathew D.; Wang, Yak-Nam; Simon, Julianna C.; Paun, Marla; Starr, Frank; Cunitz, Bryan W.; Bailey, Michael R.; Lingeman, James E.; Department of Anatomy & Cell Biology, IU School of MedicinePurpose Focused ultrasonic propulsion is a new non-invasive technique designed to move kidney stones and stone fragments out of the urinary collecting system. However, the extent of tissue injury associated with this technique is not known. As such, we quantitated the amount of tissue injury produced by focused ultrasonic propulsion under simulated clinical treatment conditions, and under conditions of higher power or continuous duty cycles, and compared those results to SWL injury. Materials and Methods A human calcium oxalate monohydrate stone and/or nickel beads were implanted (with ureteroscopy) into 3 kidneys of live pigs (45–55 kg) and repositioned using focused ultrasonic propulsion. Additional pig kidneys were exposed to SWL level pulse intensities or continuous ultrasound exposure of 10 minutes duration (ultrasound probe either transcutaneous or on the kidney). These kidneys were compared to 6 kidneys treated with an unmodified Dornier HM3 Lithotripter (2400 shocks, 120 SWs/min and 24 kV). Histological analysis was performed to assess the volume of hemorrhagic tissue injury created by each technique (% functional renal volume, FRV). Results SWL produced a lesion of 1.56±0.45% FRV. Ultrasonic propulsion produced no detectable lesion with the simulated clinical treatment. A lesion of 0.46±0.37% FRV or 1.15±0.49% FRV could be produced if excessive treatment parameters were used while the ultrasound probe was placed on the kidney. Conclusions Focused ultrasonic propulsion produced no detectable morphological injury to the renal parenchyma when using clinical treatment parameters and produced injury comparable in size to SWL when using excessive treatment parameters.Item Effect of lisinopril and atenolol on aortic stiffness in patients on hemodialysis(American Society of Nephrology (ASN), 2015-04-07) Georgianos, Panagiotis I.; Agarwal, Rajiv; Department of Medicine, IU School of MedicineBACKGROUND AND OBJECTIVES: Whether improvements in arterial compliance with BP lowering are because of BP reduction alone or if pleiotropic effects of antihypertensive agents contribute remains unclear. It was hypothesized that, among patients on hemodialysis, compared with a β-blocker (atenolol), a lisinopril-based therapy will better reduce arterial stiffness. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Among 200 participants of the Hypertension in Hemodialysis Patients Treated with Atenolol or Lisinopril Trial, 179 patients with valid assessment of aortic pulse wave velocity at baseline (89 patients randomly assigned to open-label lisinopril and 90 patients randomly assigned to atenolol three times a week after dialysis) were included in the secondary analysis. Among them, 109 patients had a valid pulse wave velocity measurement at 6 months. Monthly measured home BP was targeted to <140/90 mmHg by addition of antihypertensive drugs and dry weight adjustment. The difference between drugs in percentage change of aortic pulse wave velocity from baseline to 6 months was analyzed. RESULTS: Contrary to the hypothesis, atenolol-based treatment induced greater reduction in aortic pulse wave velocity relative to lisinopril (between drug difference, 14.8%; 95% confidence interval, 1.5% to 28.5%; P=0.03). Reduction in 44-hour ambulatory systolic and diastolic BP was no different between groups (median [25th, 75th percentile]; atenolol: -21.5 [-37.7, -7.6] versus lisinopril: -15.8 [-28.8, -1.5] mmHg; P=0.27 for systolic BP; -14.1 [-22.6, -5.3] versus -10.9 [-18.4, -0.9] mmHg, respectively; P=0.30 for diastolic BP). Between-drug difference in change of aortic pulse wave velocity persisted after adjustments for age, sex, race, other cardiovascular risk factors, and baseline ambulatory systolic BP but disappeared after adjustment for change in ambulatory systolic BP (11.8%; 95% confidence interval, -2.3% to 25.9%; P=0.10). CONCLUSIONS: Among patients on dialysis, atenolol was superior in improving arterial stiffness. However, differences between atenolol and lisinopril in improving aortic stiffness among patients on hemodialysis may be explained by BP-lowering effects of drugs.Item Markers of renal disease and function are associated with systemic inflammation in HIV infection: Renal and inflammatory markers in HIV infection(Wiley Blackwell (Blackwell Publishing), 2015-11) Gupta, Samir K; Kitch, Douglas; Tierney, Camlin; Melbourne, Kathleen; Ha, Belinda; McComsey, Grace A; AIDS Clinical Trials Group Study A5224s Team; Department of Medicine, IU School of MedicineOBJECTIVES: Both renal disease and systemic inflammation predict non-AIDS-defining events and overall mortality in HIV-infected patients. Here, we sought to determine the relationships between renal disease and circulating inflammation markers. METHODS: We performed a secondary analysis of AIDS Clinical Trials Group Study A5224s to determine if markers of renal disease [urine protein:creatinine ratio (uPCR), urine albumin:creatinine ratio (uACR), and estimated glomerular filtration rate (eGFR), using Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine and cystatin C-creatinine] were associated with markers of systemic inflammation [high-sensitivity C-reactive protein, interleukin-6, tumour necrosis factor (TNF)-α, soluble TNF-α receptor I (sTNFRI), sTNFRII, and soluble vascular cellular and intercellular adhesion molecules]. We correlated these renal and inflammatory markers prior to antiretroviral initiation and after 96 weeks of therapy. RESULTS: We found that eGFR (estimated using CKD-EPI cystatin C-creatinine), uPCR, and uACR were significantly correlated with most assessed markers of systemic inflammation prior to antiretroviral initiation. uPCR and eGFR (using CKD-EPI cystatin C-creatinine), but not uACR, remained significantly correlated with most of the assessed inflammatory markers after 96 weeks of antiretroviral therapy (ART). Most of these correlations, although statistically significant, were < 0.50. eGFR using CKD-EPI creatinine was much less frequently associated with inflammation markers and only significantly correlated with sTNFR1 at week 0 and with sTNFRI and II at week 96. CONCLUSIONS: Renal disease and function were associated with systemic inflammation in HIV infection, both before and after ART. Systemic inflammation may partially explain the relationships between proteinuria, albuminuria, and reduced renal function and future adverse outcomes.Item Mezlocillin pharmacokinetics in renal impairment(1983) Aronoff, George R.Item Relationships between renal parameters and serum and urine markers of inflammation in those with and without HIV infection(Mary Ann Liebert, 2015-04) Shinha, Takashi; Mi, Deming; Liu, Ziyue; Orschell, Christie M.; Lederman, Michael M.; Gupta, Samir K.; Department of Medicine, IU School of MedicineWe sought to determine the relationships among intrarenal and systemic inflammation and renal disease in HIV. We compared paired serum and urinary levels (normalized to urine creatinine) of monocyte chemotactic protein-1 (MCP-1), regulated on activation normal T cell expressed and secreted (RANTES), interferon-γ-induced protein-10 (IP-10), interleukin-8 (IL-8), and β2-microglobulin (B2M) between two groups of HIV-infected subjects not receiving antiretroviral therapy (ART) [A: not expecting to initiate ART immediately due to having CD4 cell counts ≥350/μl, N=26; B: about to initiate ART, N=19], a group of HIV-infected subjects receiving virologically suppressive antiretroviral therapy [C, N=30], and a group of HIV-uninfected, healthy volunteers [D, N=45]. We then correlated these inflammatory biomarker levels with urine protein/creatinine ratios (uPCR), urine albumin/creatinine ratios (uACR), and estimated glomerular filtration rates (eGFR). Urine inflammatory biomarker levels were highest in Group B. When combining all four study groups, statistically significant positive correlations included uPCR with urine IL-8, urine MCP-1, urine IP-10, and serum IP-10 and uACR with urine IL-8, urine B2M, serum IP-10, and serum B2M. eGFR was statistically significantly negatively correlated with serum MCP-1 and serum B2M. Paired serum and urine levels of IP-10 and B2M (but not IL-8, RANTES, or MCP-1) were significantly correlated with each other in the overall group. The levels of urine inflammatory markers tested differed by HIV status and use of virologically suppressive ART. These urine and serum inflammatory markers were differentially correlated with uPCR, uACR, and eGFR, suggesting that different intrarenal and systemic inflammatory pathways may contribute to different measures of nephropathy.Item Sodium chloride transport by Madin Darby canine kidney cyst epithelial cells(1991) Macias, William Louis