A5055238958- Renal Diseases and Glomerulopathies
- HIV Research and Treatment
- Chronic Kidney Disease and Diabetes
- HIV/AIDS drug development and treatment
- Acute Kidney Injury Research
- HIV-related health complications and treatments
- Electrolyte and hormonal disorders
- Renin-Angiotensin System Studies
- Fibroblast Growth Factor Research
- Neonatal Respiratory Health Research
- Virus-based gene therapy research
- Neonatal Health and Biochemistry
- HIV/AIDS Research and Interventions
- Renal and related cancers
- Ion Transport and Channel Regulation
- Trauma, Hemostasis, Coagulopathy, Resuscitation
- CRISPR and Genetic Engineering
- Receptor Mechanisms and Signaling
- Nitric Oxide and Endothelin Effects
- Chronic Lymphocytic Leukemia Research
- Phagocytosis and Immune Regulation
- Pregnancy and preeclampsia studies
- Renal function and acid-base balance
- Genetic and Kidney Cyst Diseases
- Sodium Intake and Health
University of Virginia
2020-2025
Albemarle (United States)
2025
Colorado Kidney Care
2024
University of Virginia Medical Center
2024
George Washington University
2012-2023
Children's National
2013-2023
Georgetown University
2001-2017
Zhejiang University
2017
Kanti Children's Hospital
2016
National Academy of Medical Sciences
2016
In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) published a guideline on the classification and management of acute kidney injury (AKI). The was derived from evidence available through February 2011. Since then, new has emerged that important implications for clinical practice in diagnosing managing AKI. April 2019, KDIGO held controversies conference entitled Acute Injury with following goals: determine best practices areas uncertainty treating AKI; review key relevant literature...
Abstract It is important to realize that guidelines cannot always account for individual variation among patients. They are not intended supplant physician judgment with respect particular patients or special clinical situations. IDSA considers adherence these be voluntary, the ultimate determination regarding their application made by in light of each patient's circumstances.
HIV-positive individuals are at increased risk for kidney disease, including HIV-associated nephropathy, noncollapsing focal segmental glomerulosclerosis, immune-complex and comorbid as well injury resulting from prolonged exposure to antiretroviral therapy or opportunistic infections. Clinical guidelines disease prevention treatment in largely extrapolated studies the general population, do not fully incorporate existing knowledge of unique HIV-related pathways genetic factors that...
We report, to our knowledge, the first HIV type 1 (HIV-1) transgenic (Tg) rat. Expression of transgene, consisting an HIV-1 provirus with a functional deletion gag and pol , is regulated by viral long terminal repeat. Spliced unspliced transcripts were expressed in lymph nodes, thymus, liver, kidney, spleen, suggesting that Tat Rev are functional. Viral proteins identified spleen tissue sections immunohistochemistry gp120 was present splenic macrophages, T B cells, serum. Clinical signs...
Antiretroviral therapy (ART) has decreased HIV-1 associated morbidity. However, despite ART, immune cells remain latently infected leading to chronic inflammation and comorbidities. New strategies are needed target viral proteins inflammation. We found activation of Notch3 in renal the mouse model (HIV-Tg26) patients with HIV nephropathy. hypothesized that targeting constitutes an effective for HIV-related kidney diseases (HIV-CKD). generated HIV-Tg26 mice knocked out (Tg-N3KO). Compared at...
APOL1 risk alleles associate with chronic kidney disease in African Americans, but the mechanisms remain to be fully understood. We show that activate protein kinase R (PKR) cultured cells and transgenic mice. This effect is preserved when a premature stop codon introduced alleles, suggesting RNA not required for effect. Podocyte expression of allele RNA, protein, mice induces glomerular injury proteinuria. Structural analysis shows variants possess secondary structure serving as scaffold...
People of African ancestry carrying certain APOL1 mutant alleles are at elevated risk developing renal diseases. However, the mechanisms underlying APOL1-associated diseases unknown. Because gene is unique to humans and some primates, new animal models needed understand function in vivo We generated transgenic Drosophila fly lines expressing human wild type allele (G0) or predominant (G1) different tissues. Ubiquitous expression G0 G1 induced lethal phenotypes, was more toxic than G0....
IntroductionIndividuals with focal segmental glomerular sclerosis (FSGS) typically undergo kidney biopsy only once, which limits the ability to characterize cell gene expression over time.MethodsWe used single-cell RNA sequencing (scRNA-seq) explore disease-related molecular signatures in urine cells from subjects FSGS. We collected 17 samples 12 FSGS and captured these as 23 samples. The inflammatory renal epithelial immune were evaluated bulk data sets of minimal change disease (MCD) (The...
Importance The incidence and associated outcomes of recurrent acute kidney injury (rAKI) in neonates remain largely unknown. Objective To determine the incidence, risk factors, clinical with rAKI critically ill neonates. Design, Setting, Participants This cohort study was a secondary analysis multicenter, international Assessment Worldwide Acute Kidney Injury Epidemiology Neonates retrospective study. Comparisons were made among no AKI, single AKI episode (sAKI), rAKI. All younger than 14...
We investigated the hypothesis that hypokalemia might induce renal injury via a mechanism involves subtle and alterations in local vasoactive mediators would favor sodium retention. To test this hypothesis, we conducted studies rats with diet-induced K + deficiency. also determined whether hypokalemic nephropathy show salt sensitivity. Twelve weeks of resulted decrease creatinine clearance, tubulointerstitial macrophage infiltration, interstitial collagen type III deposition, an increase...
HIV-1 transcription is activated by Tat protein, which recruits cyclin-dependent kinase 9 (CDK9)/cyclin T1 and other host transcriptional coactivators to the <i>HIV-1</i> promoter. itself phosphorylated CDK2, inhibition of CDK2 small interfering RNA, iron chelator 2-hydroxy-1-naphthylaldehyde isonicotinoyl hydrazone (<i>311</i>), deferasirox (ICL670) inhibits transcription. Here we have analyzed a group novel di-2-pyridylketone thiosemicarbazone- 2-benzoylpyridine thiosemicarbazone-based...