About

Justin Belcher, MD, PhD, FASN, is an Associate Professor of Medicine (Nephrology) at Yale School of Medicine. He grew up in Connecticut and graduated cum laude with a degree in history from Williams College. He attended Drexel University College of Medicine, where he was elected to Alpha Omega Alpha, and completed his internship, residency, and Chief Residency in Internal Medicine at George Washington University. During his research fellowship in nephrology at Yale, he earned a PhD in 2014 from the Investigative Medicine Program. His primary research focus is on acute kidney injury in patients with cirrhosis, including the use of novel biomarkers to improve diagnosis, therapeutic decisions, and prognosis. Dr. Belcher has clinical expertise in caring for patients with a wide variety of kidney-related ailments, with particular interests in acute kidney injury, complex acid-base and electrolyte abnormalities, critical care nephrology, and chronic kidney disease. He is actively engaged in education at Yale and its affiliate hospital system, instructing medical students, residents, and fellows through formal and informal didactics, lectures, and workshops.

Research topics

• Medicine
• Internal medicine
• Gastroenterology
• Urology

Selected publications

• Biomarkers of inflammation and risk of adverse events in patients with cirrhosis

  Liver Transplantation · 2026-03-27

  article

  Acute kidney injury (AKI) is a frequent and severe complication in patients with cirrhosis. Identifying patients at high risk for AKI progression and in-hospital complications could enable timely targeted interventions. Given the central role of inflammation in AKI and cirrhosis, we investigated whether inflammatory biomarkers could provide prognostic insights. In this multicenter, prospective cohort study, we enrolled 188 patients with cirrhosis and AKI from 4 tertiary care centers. Urine and plasma samples were analyzed for 4 biomarkers: urine monocyte chemoattractant protein-1 (MCP-1), urine YKL-40, and plasma tumor necrosis factor receptors 1 and 2 (TNFR-1, TNFR-2). Biomarkers were assessed for their associations with AKI progression, mortality, and in-hospital complications using multivariate analyses adjusted for demographics, baseline kidney function, and MELD score. Urine MCP-1, plasma TNFR-1, and plasma TNFR-2 were each associated with increased odds of AKI progression and mortality: urine MCP-1 had odds ratio (OR) 2.35 (95% CI, 1.26-5.65), plasma TNFR-1 OR 6.90 (95% CI, 2.45-25.50), and plasma TNFR-2 OR 2.69 (95% CI, 1.34-6.17) per standard deviation (SD) higher biomarker level. Plasma TNFR-1 had the strongest associations with in-hospital complications. Each SD higher plasma TNFR-1 was associated with developing hepatic encephalopathy (OR 2.53; 95% CI, 1.37-5.06), developing spontaneous bacterial peritonitis (OR 2.20; 95% CI, 1.14-4.47), variceal bleeding during admission (OR 3.47; 95% CI, 1.05-14.46), and requiring dialysis (OR 2.81; 95% CI, 1.39-6.23). Inflammatory biomarkers effectively identify high-risk patients with AKI and cirrhosis. Incorporating these biomarkers into clinical decision-making has the potential to guide treatment.

  PublisherDOI

• Predicting the Use of Dialysis for Acute Kidney Injury in Patients with Cirrhosis—Does Diagnosis Matter?

  Digestive Diseases and Sciences · 2025-06-05

  editorialOpen access1st authorCorresponding
  PublisherOA PDFDOI

• To Stay or to Fold: Biomarkers and the Management of Potentially Hemodynamic Acute Kidney Injury

  American Journal of Kidney Diseases · 2025-06-11

  editorial1st authorCorresponding
  PublisherDOI

• Outcomes of Acute Tubular Necrosis in Hospitalized Patients with Cirrhosis: Results from the HRS-HARMONY Consortium

  Journal of the American Society of Nephrology · 2025-10-01

  article1st authorCorresponding
  PublisherDOI

• The heart–kidney axis in cirrhosis: rethinking hepatorenal and cardiorenal syndromes—authors’ reply

  Intensive Care Medicine · 2025-02-01

  letter
  PublisherDOI

• Kidney Tubule Secretion Can Discriminate the Cause of Acute Kidney Injury in Cirrhosis

  Clinical Journal of the American Society of Nephrology · 2025-09-16

  article

  Key Points In cirrhotic patients with AKI, tubular secretion differentiates those with acute tubular necrosis versus other causes. Different secretory function by cause of AKI may affect treatment approaches and drug dosing in patients with cirrhosis and AKI. Background AKI is a common and severe complication among hospitalized patients with cirrhosis. The most common causes of AKI in cirrhosis are prerenal azotemia (PRA), hepatorenal syndrome (HRS), and acute tubular necrosis (ATN), and treatment depends on its causes. Kidney proximal tubular secretion is an essential mechanism for elimination of many drugs and toxins and may be affected in AKI. We hypothesized that assessing secretion would help distinguish between structural tubular injury (ATN) and hemodynamic perturbations (PRA and HRS). Methods We collected paired plasma and spot urine specimens from 76 hospitalized patients with cirrhosis and AKI from four tertiary care centers in North America. A panel of endogenous metabolites known to be secreted was measured in blood and urine by tandem mass spectrometry, and a summary secretion score was calculated by averaging the standardized spot urine-to-plasma ratios of the endogenous secretion markers, with higher urine-to-plasma ratios reflecting greater tubular secretion. The summary secretion score was assessed for its ability to discriminate ATN from non-ATN. Results Among the 76 patients with cirrhosis and AKI, 39 (51%) had PRA, 13 (17%) had HRS, and 24 (32%) had ATN. Median secretion scores were significantly lower in ATN (50.3; 95% confidence intervals [CIs], 42.2 to 61.2) compared with PRA (61.7; 95% CI, 55.4 to 75.4) or HRS (62.5; 95% CI, 55.6 to 66.5; P = 0.007). In models adjusted for clinical characteristics, baseline eGFR, and model for end stage liver disease score, higher summary secretion score was associated with lower odds of ATN (odds ratio per SD higher secretion score, 0.34; 95% CI, 0.15 to 0.67). The summary secretion score showed good discriminative ability in diagnosing ATN versus other causes of AKI (area under the receiver operating curve, 0.73; 95% CI, 0.60 to 0.85). Conclusions In patients with cirrhosis and AKI, substantially lower tubular secretion was observed among inpatients with ATN relative to those with PRA and HRS. These results support the use of tubular secretion for the differential diagnosis of AKI in cirrhosis and may have important therapeutic and prognostic implications.

  PublisherDOI

• OS-038-YI Urinary neutrophil gelatinase-associated lipocalin (NGAL) as a diagnostic and prognostic biomarker of acute kidney injury in patients with decompensated cirrhosis: an individual patient data meta-analysis

  Journal of Hepatology · 2025-05-01

  article
  PublisherDOI

• Association of Hepatorenal Syndrome-Acute Kidney Injury with Mortality in Patients with Cirrhosis Requiring Renal Replacement Therapy

  Kidney360 · 2024-09-30 · 7 citations

  articleOpen accessSenior authorCorresponding

  Key Points In patients with cirrhosis and AKI requiring renal replacement therapy (RRT), hepatorenal syndrome-AKI was not associated with an increased 90-day mortality when compared with other AKI etiologies. Etiology of AKI may not be a critical factor regarding decisions to trial RRT in acutely ill patients with cirrhosis and AKI. Although elevated, mortality rates in this study are comparable with those reported in general hospitalized patients with AKI requiring RRT. Background While AKI requiring renal replacement therapy (AKI-RRT) is associated with increased mortality in heterogeneous inpatient populations, the epidemiology of AKI-RRT in hospitalized patients with cirrhosis is not fully known. Herein, we evaluated the association of etiology of AKI with mortality in hospitalized patients with cirrhosis and AKI-RRT in a multicentric contemporary cohort. Methods This is a multicenter retrospective cohort study using data from the HRS-HARMONY consortium, which included 11 US hospital network systems. Consecutive adult patients admitted in 2019 with cirrhosis and AKI-RRT were included. The primary outcome was 90-day mortality, and the main independent variable was AKI etiology, classified as hepatorenal syndrome (HRS-AKI) versus other (non–HRS-AKI). AKI etiology was determined by at least two independent adjudicators. We performed Fine and Gray subdistribution hazard analyses adjusting for relevant clinical variables. Results Of 2063 hospitalized patients with cirrhosis and AKI, 374 (18.1%) had AKI-RRT. Among them, 65 (17.4%) had HRS-AKI and 309 (82.6%) had non–HRS-AKI, which included acute tubular necrosis in most cases (62.6%). Continuous renal replacement therapy was used as the initial modality in 264 (71%) of patients, while intermittent hemodialysis was used in 108 (29%). The HRS-AKI (versus non–HRS-AKI) group received more vasoconstrictors for HRS management (81.5% versus 67.9%), whereas the non–HRS-AKI group received more mechanical ventilation (64.3% versus 50.8%) and more continuous renal replacement therapy (versus intermittent hemodialysis) as the initial RRT modality (73.9% versus 56.9%). In the adjusted model, HRS-AKI (versus non–HRS-AKI) was not independently associated with increased 90-day mortality (subdistribution hazard ratio, 1.36; 95% confidence interval, 0.95 to 1.94). Conclusions In this multicenter contemporary cohort of hospitalized adult patients with cirrhosis and AKI-RRT, HRS-AKI was not independently associated with an increased risk of 90-day mortality when compared with other AKI etiologies. The etiology of AKI appears less relevant than previously considered when evaluating the prognosis of hospitalized adult patients with cirrhosis and AKI requiring RRT.

  PublisherDOI

• Acute kidney injury in patients with cirrhosis: Acute Disease Quality Initiative (ADQI) and International Club of Ascites (ICA) joint multidisciplinary consensus meeting

  Journal of Hepatology · 2024-03-26 · 172 citations

  reviewOpen access

  Patients with cirrhosis are prone to developing acute kidney injury (AKI), a complication associated with a markedly increased in-hospital morbidity and mortality, along with a risk of progression to chronic kidney disease. Whereas patients with cirrhosis are at increased risk of developing any phenotype of AKI, hepatorenal syndrome (HRS), a specific form of AKI (HRS-AKI) in patients with advanced cirrhosis and ascites, carries an especially high mortality risk. Early recognition of HRS-AKI is crucial since administration of splanchnic vasoconstrictors may reverse the AKI and serve as a bridge to liver transplantation, the only curative option. In 2023, a joint meeting of the International Club of Ascites (ICA) and the Acute Disease Quality Initiative (ADQI) was convened to develop new diagnostic criteria for HRS-AKI, to provide graded recommendations for the work-up, management and post-discharge follow-up of patients with cirrhosis and AKI, and to highlight priorities for further research.

  PublisherOA PDFDOI

• Hepatorenal Syndrome-AKI Reversal and Liver Transplant Rates in Patients Treated with Terlipressin

  Journal of the American Society of Nephrology · 2024-10-01

  article1st authorCorresponding
  PublisherDOI

Frequent coauthors

• Andrew S. Allegretti

  28 shared

• Chirag R. Parikh

  Johns Hopkins University

  27 shared

• Kavish R. Patidar

  27 shared

• Hani M. Wadei

  Mayo Clinic in Florida

  24 shared

• Eric S. Orman

  Michael E. DeBakey VA Medical Center

  22 shared

• Kevin R. Regner

  Medical College of Wisconsin

  20 shared

• Guadalupe García‐Tsao

  Yale University

  20 shared

• Juan Carlos Q. Velez

  University of Illinois Chicago

  19 shared

Education

• B.A., History

  Williams College

• M.D.

  Medical School

Awards & honors

• Alpha Omega Alpha (at Drexel University College of Medicine)