Bio


Dr. Aron is a board-certified, fellowship-trained nephrologist and a clinical assistant professor in the Department of Medicine, Division of Nephrology at Stanford University School of Medicine.

He provides care for patients with a wide range of kidney-related conditions, such as kidney disease and failure, lupus nephritis, diabetic kidney disorder, renal insufficiency, and more. His consistent goal is to work with each patient to develop a personalized and comprehensive care plan that strives to achieve the best possible kidney health and quality of life.

Dr. Aron’s research experience includes participation in the investigation of a gene panel created to support the management of chronic kidney disease. He also took part in the study of an electronic dashboard and decision support tool developed to help clinicians improve the efficiency of care for people with chronic kidney disease.

He has published articles on genetic testing for kidney disorders, immune system suppression in nephropathy, diagnosis of acute kidney injury, and other topics. His work has appeared in journals such as Kidney360 and he has been a peer reviewer for the Clinical Journal of the American Society of Nephrology.

Dr. Aron has made presentations to his peers at the American Society of Nephrology Kidney Week and other meetings. He educates the kidney specialists of the future, and has led workshops and delivered many lectures. He also contributed to the textbook Tubulointerstitial Nephritis.

Dr. Aron is a member of the American Society of Nephrology.

Clinical Focus


  • Nephrology

Academic Appointments


Professional Education


  • Board Certification: American Board of Internal Medicine, Nephrology (2021)
  • Fellowship: Yale New Haven Hospital Nephrology Fellowship (2021) CT
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2018)
  • Residency: Beth Israel Deaconess Medical Center Internal Medicine Residency (2018) MA
  • Medical Education: University of Connecticut School of Medicine Registrar (2015) CT

All Publications


  • Is There a Role for More Intense Immunosuppression in IgA Nephropathy? KIDNEY360 Aron, A. W. 2022; 3 (3): 410-412

    View details for DOI 10.34067/KID.0000512022

    View details for Web of Science ID 000793823800002

    View details for PubMedID 35582174

    View details for PubMedCentralID PMC9034818

  • Compensatory Fetal Membrane Mechanisms Between Biglycan and Decorin in Inflammation MOLECULAR REPRODUCTION AND DEVELOPMENT de Araujo, L., Horgan, C. E., Aron, A., Iozzo, R. V., Lechner, B. E. 2015; 82 (5): 387-396

    Abstract

    Preterm premature rupture of fetal membranes (PPROM) is associated with infection, and is one of the most common causes of preterm birth. Abnormal expression of biglycan and decorin, two extracellular matrix proteoglycans, leads to preterm birth and aberrant fetal membrane morphology and signaling in the mouse. In humans and mice, decorin dysregulation is associated with inflammation in PPROM. We therefore investigated the link between biglycan and decorin and inflammation in fetal membranes using mouse models of intraperitoneal Escherichia coli injections superimposed on genetic biglycan and decorin deficiencies. We assessed outcomes in vivo as well as in vitro using quantitative PCR, Western blotting, and enzyme-linked immunosorbent assays. Our results suggest that biglycan and decorin compensate for each other in the fetal membranes, but lose the ability to do so under inflammation, leading to decreased latency to preterm birth. Furthermore, our findings suggest that biglycan and decorin play discrete roles in fetal membrane signaling pathways during inflammation, leading to changes in the abundance of MMP8 and collagen α1VI, two components of the fetal membrane extracellular matrix that influence the pathophysiology of PPROM. In summary, these findings underline the importance of biglycan and decorin as targets for the manipulation of fetal membrane extracellular matrix stability in the context of inflammation.

    View details for DOI 10.1002/mrd.22488

    View details for Web of Science ID 000354627600008

    View details for PubMedID 25914258

    View details for PubMedCentralID PMC4439295

  • Prestroke Living Situation and Depression Contribute to Initial Stroke Severity and Stroke Recovery JOURNAL OF STROKE & CEREBROVASCULAR DISEASES Aron, A. W., Staff, I., Fortunato, G., McCullough, L. D. 2015; 24 (2): 492-499

    Abstract

    Substantial evidence from both experimental and clinical studies has demonstrated that social isolation can increase stroke incidence and impair recovery. Social isolation leads to higher rates of recurrent stroke but is often not reported as a risk factor. We examined prospectively collected stroke center database variables, which included prestroke living situation, to determine if social isolation could be determined from existing data using living arrangement as a proxy. Patients were categorized into 4 groups hypothesized to represent increasing levels of social isolation: living with spouse, living with family, living alone with visiting services, and living alone. Initial stroke severity and recovery were measured using the National Institutes of Health Stroke Scale and Barthel Index, respectively. A multivariate model was used to determine the relationship among prestroke living situation, stroke severity, and functional outcome. Patients living alone had less severe strokes on admission and better recovery at 3 months compared with the other cohorts. Patients living alone or those who lived with a spouse had less severe strokes on presentation and better recovery at both 3 and 12 months after stroke compared with the other cohorts. However, on detailed examination, it was found that these patients also had significantly higher prestroke function. Pre-existing depression was significantly higher in women, and depressed patients had poorer outcomes 3 months after stroke. Information regarding isolation is notably absent from most large stroke databases. A more comprehensive evaluation of social interaction should be obtained to more accurately measure social isolation.

    View details for DOI 10.1016/j.jstrokecerebrovasdis.2014.09.024

    View details for Web of Science ID 000349177300035

    View details for PubMedID 25524014

    View details for PubMedCentralID PMC4315755

  • Fate Mapping by PiggyBac Transposase Reveals That Neocortical GLAST+ Progenitors Generate More Astrocytes Than Nestin+ Progenitors in Rat Neocortex CEREBRAL CORTEX Siddiqi, F., Chen, F., Aron, A. W., Fiondella, C. G., Patel, K., LoTurco, J. J. 2014; 24 (2): 508-520

    Abstract

    Progenitors within the neocortical ventricular zone (VZ) first generate pyramidal neurons and then astrocytes. We applied novel piggyBac transposase lineage tracking methods to fate-map progenitor populations positive for Nestin or glutamate and aspartate transpoter (GLAST) promoter activities in the rat neocortex. GLAST+ and Nestin+ progenitors at embryonic day 13 (E13) produce lineages containing similar rations of neurons and astrocytes. By E15, the GLAST+ progenitor population diverges significantly to produce lineages with 5-10-fold more astrocytes relative to neurons than generated by the Nestin+ population. To determine when birth-dated progeny within GLAST+ and Nestin+ populations diverge, we used a Cre/loxP fate-mapping system in which plasmids are lost after a cell division. By E18, birth-dated progeny of GLAST+ progenitors give rise to 2-3-fold more neocortical astrocytes than do Nestin+ progenitors. Finally, we used a multicolor clonal labeling method to show that the GLAST+ population labeled at E15 generates astrocyte progenitors that produce larger, spatially restricted, clonal clusters than the Nestin+ population. This study provides in vivo evidence that by mid-corticogenesis (E15), VZ progenitor populations have significantly diversified in terms of their potential to generate astrocytes and neurons.

    View details for DOI 10.1093/cercor/bhs332

    View details for Web of Science ID 000329840900022

    View details for PubMedID 23118195

    View details for PubMedCentralID PMC3888371

  • Lower NIH Stroke Scale Scores Are Required to Accurately Predict a Good Prognosis in Posterior Circulation Stroke CEREBROVASCULAR DISEASES Inoa, V., Aron, A. W., Staff, I., Fortunato, G., Sansing, L. H. 2014; 37 (4): 251-255

    Abstract

    The NIH stroke scale (NIHSS) is an indispensable tool that aids in the determination of acute stroke prognosis and decision making. Patients with posterior circulation (PC) strokes often present with lower NIHSS scores, which may result in the withholding of thrombolytic treatment from these patients. However, whether these lower initial NIHSS scores predict better long-term prognoses is uncertain. We aimed to assess the utility of the NIHSS at presentation for predicting the functional outcome at 3 months in anterior circulation (AC) versus PC strokes.This was a retrospective analysis of a large prospectively collected database of adults with acute ischemic stroke. Univariate and multivariate analyses were conducted to identify factors associated with outcome. Additional analyses were performed to determine the receiver operating characteristic (ROC) curves for NIHSS scores and outcomes in AC and PC infarctions. Both the optimal cutoffs for maximal diagnostic accuracy and the cutoffs to obtain >80% sensitivity for poor outcomes were determined in AC and PC strokes.The analysis included 1,197 patients with AC stroke and 372 with PC stroke. The median initial NIHSS score for patients with AC strokes was 7 and for PC strokes it was 2. The majority (71%) of PC stroke patients had baseline NIHSS scores ≤4, and 15% of these 'minor' stroke patients had a poor outcome at 3 months. ROC analysis identified that the optimal NIHSS cutoff for outcome prediction after infarction in the AC was 8 and for infarction in the PC it was 4. To achieve >80% sensitivity for detecting patients with a subsequent poor outcome, the NIHSS cutoff for infarctions in the AC was 4 and for infarctions in the PC it was 2.The NIHSS cutoff that most accurately predicts outcomes is 4 points higher in AC compared to PC infarctions. There is potential for poor outcomes in patients with PC strokes and low NIHSS scores, suggesting that thrombolytic treatment should not be withheld from these patients based solely on the NIHSS. © 2014 S. Karger AG, Basel.

    View details for DOI 10.1159/000358869

    View details for Web of Science ID 000337036300003

    View details for PubMedID 24686370

    View details for PubMedCentralID PMC4956480

  • Uterine Dysfunction in Biglycan and Decorin Deficient Mice Leads to Dystocia during Parturition PLOS ONE Wu, Z., Aron, A. W., Macksoud, E. E., Iozzo, R. V., Hai, C., Lechner, B. E. 2012; 7 (1): e29627

    Abstract

    Cesarean birth rates are rising. Uterine dysfunction, the exact mechanism of which is unknown, is a common indication for Cesarean delivery. Biglycan and decorin are two small leucine-rich proteoglycans expressed in the extracellular matrix of reproductive tissues and muscle. Mice deficient in biglycan display a mild muscular dystrophy, and, along with mice deficient in decorin, are models of Ehlers-Danlos Syndrome, a connective tissue anomaly associated with uterine rupture. As a variant of Ehlers-Danlos Syndrome is caused by a genetic mutation resulting in abnormal biglycan and decorin secretion, we hypothesized that biglycan and decorin play a role in uterine function. Thus, we assessed wild-type, biglycan, decorin and double knockout pregnancies for timing of birth and uterine function. Uteri were harvested at embryonic days 12, 15 and 18. Nonpregnant uterine samples of the same genotypes were assessed for tissue failure rate and spontaneous and oxytocin-induced contractility. We discovered that biglycan/decorin mixed double-knockout dams displayed dystocia, were at increased risk of delayed labor onset, and showed increased tissue failure in a predominantly decorin-dependent manner. In vitro spontaneous uterine contractile amplitude and oxytocin-induced contractile force were decreased in all biglycan and decorin knockout genotypes compared to wild-type. Notably, we found no significant compensation between biglycan and decorin using quantitative real time PCR or immunohistochemistry. We conclude that the biglycan/decorin mixed double knockout mouse is a model of dystocia and delayed labor onset. Moreover, decorin is necessary for uterine function in a dose-dependent manner, while biglycan exhibits partial compensatory mechanisms in vivo. Thus, this model is poised for use as a model for testing novel targets for preventive or therapeutic manipulation of uterine dysfunction.

    View details for DOI 10.1371/journal.pone.0029627

    View details for Web of Science ID 000301361500015

    View details for PubMedID 22253749

    View details for PubMedCentralID PMC3258236