About

Josephine D. Abraham, MD, MPH, is a Nephrologist and Professor of Medicine at the University of Utah School of Medicine. She began her undergraduate and medical training at the University of Madras, India, in 1981, completing her studies in 1987. After training briefly in the United Kingdom and earning a Master of Public Health at the University of Utah, she completed her Internal Medicine Residency at the University of Utah School of Medicine in 2004 and a Nephrology Fellowship in 2006. She practiced nephrology for five years before returning to the University of Utah in 2011. Dr. Abraham is the Clinical Chief for the Division of Nephrology and has served as the Nephrology Fellowship Training Program Director. She is the Medical Director of the Home Dialysis Program and the Acute Dialysis Program at the University Hospital. Her clinical interests include various aspects of kidney disease, particularly Glomerulonephritis, Vasculitis, Secondary hypertension, Onco nephrology including Amyloidosis, and Home Dialysis. She is board certified in Internal Medicine and Nephrology, and her work emphasizes improving patient care through clinical expertise and leadership in nephrology.

Research topics

• Medicine
• Internal medicine
• Radiology
• Immunology
• Surgery
• Remote sensing
• Anesthesia
• Pharmacology
• Oncology
• Biology
• Neuroscience

Selected publications

• Double Trouble: A Patient with Light-Chain Amyloidosis and Apolipoprotein A-IV Amyloidosis

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

  articleSenior author
  PublisherDOI

• Hyperammonemia and Fatal Cerebral Edema: A Complication of Gastric Bypass Surgery

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

  articleSenior author

  Introduction: Hyperammonemia is characteristic of few disease processes including liver failure, urea cycle disorders, inborn errors of metabolism, drugs and infection with urea-splitting organisms in lung transplant.Renal replacement therapy(RRT) is indicated in acute liver failure with grade 2 or higher encephalopathy even in the absence of renal failure. We present a case of hyperammonemia in a patient with gastric bypass which resulted in fatal cerebral edema despite prompt initiation of continuous RRT(CRRT). Case Description: A 50-year-old woman with history of Protein C and S deficiency complicated by venous thromboembolism and gastric bypass surgery was brought to the emergency department due to confusion following a gastrointestinal illness. Laboratory studies revealed a large anion gap and hyperammonemia to 169 umol/L with normal liver tests. Patient was admitted to intensive care unit and intubated for progressive encephalopathy and ammonia levels rose to 478 umol/L. Nephrology was consulted, CRRT was initiated, and she was started on a high-caloric/low-protein enteral diet. On hospital day two she developed progressive cerebral edema and her family decided to transition to comfort care.Studies for Ureaplasma and Mycoplasma PCR were negative and Valproic acid levels were undetectable.Evaluation for inborn errors of the urea cycle revealed elevated levels of plasma glutamine and acylcarnitine species but low levels of free carnitine. Genetic studies for urea cycle defects and hyperammonemia revealed a heterozygote variant of uncertain significance in the CYC1 gene. Discussion: Hyperammonemia is an uncommon under-recognized complication of bariatric surgery. Bariatric surgery may unmask latent urea cycle enzyme deficiencies or impair citrulline synthesis in the intestinal wall which leads to depletion of urea cycle substrates. The associated weight loss, hyperinsulinemia and zinc deficiency may downregulate urea cycle enzymes and interfere with ornithine transcarbamylase function. Post-surgical proliferation of urea-splitting microbiota may also raise ammonia levels. Hemodialysis is effective in reducing ammonia levels and continuous dialysis strategy is often employed to avoid rebound hyperammonemia. This case illustrates a rare complication of bariatric surgery and highlights the role for renal replacement therapy in the management of cerebral edema.

  PublisherDOI

• Hyperkalemic? Don't Miss the Mag!

  Journal of the American Society of Nephrology · 2025-10-01 · 1 citations

  articleSenior author
  PublisherDOI

• Influence of Baseline Kidney Function on Patient and Kidney Outcomes in Patients with COVID-19: A Multi-National Observational Study

  Journal of Clinical Medicine · 2025-02-12 · 1 citations

  articleOpen access

  Background/Objectives: Acute kidney injury (AKI) is a common complication of coronavirus disease-19 (COVID-19), but the impact of baseline kidney function and care processes on outcomes is not well understood. We hypothesized that baseline kidney health status may influence courses and outcomes of AKI. Methods: This is a multinational, multicenter, retrospective cohort study. We included hospitalized adult COVID-19 patients with kidney disease (AKI, end-stage kidney disease (ESKD), chronic kidney disease (CKD), or kidney transplant (KT) recipients) from 1 January 2020 to 31 March 2022, across 52 centers in 23 countries. Patients with no prior kidney function information were classified as acute kidney disease (AKD) if estimated glomerular filtration rate (eGFR) at admission was <60 mL/min/1.73 m2 and as no known kidney disease (NKD) if eGFR was ≥60 mL/min/1.73 m2. We defined combined outcome as death or non-kidney recovery at hospital discharge. Multivariable binary regression models were applied. Results: Among 4158 patients, 882 had ESKD, and 3038 developed AKI. AKI patients were categorized as NKD (31.8%), AKD (38.6%), CKD (23.3%), and KT recipients (3.3%). NKD patients had higher AKI severity and more intensive care unit care needs. In the multivariable analyses, the risk of the combined outcome was higher in AKD (OR 1.459 [1.061, 2.005]) or CKD (OR 1.705 [1.206, 2.410]) patients, although the risk of in-hospital mortality was similar to NKD. Among the survivors at hospital discharge, the risk of partial or non-recovery was higher in CKD (OR 5.445 [3.864, 7.672]) or KT recipients (OR 4.208 [2.383, 7.429]) compared to NKD. These findings were consistent across income categories. Conclusions: Among AKI patients with COVID-19, nearly two-thirds had underlying kidney dysfunction, with 55% identified as having baseline AKD, which had higher risk of death or non-kidney recovery at discharge compared to NKD.

  PublisherOA PDFDOI

• Electroencephalography (EEG) - Based Neuromarketing: Predicting Favourable and Unfavourable Consumer Reactions Using ML Techniques

  BRAIN BROAD RESEARCH IN ARTIFICIAL INTELLIGENCE AND NEUROSCIENCE · 2025-09-08

  articleOpen access

  Neuromarketing is an emerging field that combines neuroscience with marketing to gain insights into unconscious consumer behaviour. Traditional methods like surveys often fail to capture real-time emotional and cognitive responses. To address this gap, this study employs EEG signal analysis to predict favourable and unfavourable consumer reactions to advertisements and products. The theoretical foundation is based on the dual-process theory, which distinguishes between fast, emotional decision-making (System 1), and slow, rational thinking (System 2). EEG markers such as alpha, beta, and theta bands are used to assess attention, engagement, and decision conflict. EEG data was collected using a single-channel Neurosky Mindwave headset from 14 participants aged 18–22. A total of 80 ads were shown, categorised by product and design type. Subject-dependent and subject-independent analyses were conducted. In the SD study, Naïve Bayes and SVM classifiers achieved a maximum accuracy of 0.62. In the SI analysis, SVM showed strong performance across product and gender-based classification. A deep learning model also produced comparable accuracy. These findings demonstrate the potential of EEG-based neuromarketing to provide deeper insights into consumer behaviour, with possible implications for both commercial and clinical applications.

  PublisherOA PDFDOI

• A Diagnostic Challenge: Distinguishing Complement-Mediated and Hypertension-Induced Thrombotic Microangiopathy

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

  article

  Introduction: Thrombotic Microangiopathy (TMA) is a serious condition characterized by microangiopathic anemia, thrombocytopenia, and end organ damage. Prompt initiation of treatment for TMA is important in preventing irreversible damage, though tests can take multiple days to result and sometimes a clear diagnosis is not made. In particular, several articles have suggested links between malignant hypertension and genetic mutations in the complement pathway, making the distinction between the two very difficult. Case Description: A 39-year-old female presented with hypertensive emergency and was found to have acute kidney injury with creatinine of 12 mg/dl. Workup revealed hemolytic anemia, thrombocytopenia, proteinuria, and hematuria but broad serologic work-up was negative. She became oliguric and required dialysis shortly after admission. She had evidence of hypertensive damage including left ventricular hypertrophy and hypertensive retinopathy. The patient’s anemia, thrombocytopenia, and general symptoms improved with blood pressure control. Kidney biopsy was consistent with TMA with evidence of hypertensive damage including “onion skinning” and marked arteriosclerosis. Her renal function failed to improve despite adequate blood pressure management. Genetic testing revealed a heterozygous variant in C3AR1 gene, a variant of undetermined significant that has been associated with complement mediated TMA. She was started on eculizumab for potential complement mediated TMA. Discussion: The potential overlap in pathophysiology between complement mediated TMA and hypertension induced TMA is less recognized. Genetic abnormalities are not discovered in a significant proportion of cases of complement mediated TMA. Meanwhile, approximately 50% of cases of hypertension induced TMA reveal abnormalities in complement genes. Case reports have shown renal function improvement in cases of refractory hypertension induced TMA, even months after diagnosis, after eculizumab treatment. With the relatively efficacious treatment for complement mediated HUS with anti-complement therapy and the diagnostic ambiguity in these cases, the decision to initiate eculizumab therapy remains difficult. Fortunately, there is growing research into tests that may help identify patients that would benefit from eculizumab therapy.Fibrin Deposition and Luminal Occlusion

  PublisherDOI

• Delayed Onset Euglycemic Diabetic Ketoacidosis Following SGLT2 Inhibitor Discontinuation

  Journal of the American Society of Nephrology · 2025-10-01 · 1 citations

  articleSenior author

  Introduction: Euglycemic diabetic ketoacidosis (euDKA) is a serious complication of sodium-glucose cotransporter-2 inhibitors. While most cases present shortly after exposure, delayed-onset euDKA after drug discontinuation is rare. Due to its late presentation of acidosis without marked hyperglycemia the diagnosis may be missed or delayed. We report a case of euDKA occurring four days after cessation of dapagliflozin. Case Description: A 49-year-old man with quadriplegia, autonomic dysreflexia, hypertension, and type 2 diabetes presented to the hospital with hypotension and possible small bowel pneumatosis. He underwent exploratory laparotomy on hospital day (HOD) 0 which was unrevealing. His course was complicated by undifferentiated shock requiring vasoactive support, and acute hypoxic respiratory failure requiring intubation and mechanical ventilation. By HOD 4, he developed persistent high anion gap metabolic acidosis, hypokalemia, hypophosphatemia, and polyuria. Labs revealed blood glucose of 151 mg/dL, bicarbonate 14 mEq/L, anion gap 19 with normal lactate and an elevated beta-hydroxybutyrate (β-HB) 5.44 mmoL/L with urine glucose >1000. With the worsening acidosis, positive ketones and euglycemia the patient was diagnosed with euDKA and promptly started on an insulin drip with concurrent dextrose. The anion gap normalized and metabolic acidosis resolved within 24 hours of starting the insulin drip and the patient was then transitioned to subcutaneous insulin. Discussion: This case highlights delayed-onset euDKA, presenting four days after dapagliflozin discontinuation. Although the drug's half-life is 13 hours, its pharmacodynamic effects including persistent glycosuria, suppressed insulin, and increased glucagon can persist well beyond drug clearance. Clinicians should recognize that the risk of euDKA does not end with the last dose of an SGLT2 inhibitor. Even in the absence of active therapy or hyperglycemia, patients recently exposed to these agents remain at risk, particularly during periods of physiologic stress. Prompt recognition of euDKA and early initiation of insulin with glucose are critical to prevent morbidity. This case underscores the need for heightened clinical suspicion in patients with recent SGLT2i use who develop unexplained anion gap acidosis.

  PublisherDOI

• #3084 Familial nephropathy associated with a combined mutations of Alport and Nail Patella syndrome genes in the same family

  Nephrology Dialysis Transplantation · 2024-05-01

  articleOpen access1st authorCorresponding

  Abstract Introduction Alport syndrome is a genetic condition stemming from mutation in Type IV collagen and is characterized by kidney disease and frequently hearing loss and ocular abnormalities. Renal involvement is from an abnormality of the glomerular basement membrane with hematuria and proteinuria progressing eventually to renal failure. In the vast majority, the inheritance is X- linked affecting the alpha 5 chain of type IV collagen while in about 15 percent of the patients the inheritance is autosomal recessive or dominant with mutations affecting alpha 3 or 4 chains of type IV collagen. Sensorineural deafness is common and ocular abnormalities may include lenticonus, corneal opacities, fleck retinopathy and temporal retinal thinning. Nail Patella syndrome (NPS) is a rare genetic condition from mutation in the LMX1B gene on chromosome 9 with an autosomal dominant inheritance. Glomerular disease is from characteristic glomerular basement membrane changes and is associated with nail, pelvic girdle and limb abnormalities. A forme fruste with glomerular lesions but lacking extrarenal features is recognized but uncommon. We present a family with mutations in both COL4A5 and LMX1B presenting with hematuria and proteinuria Case Presentation A 23 year old female was evaluated for hematuria and proteinuria. Her history was notable for kidney biopsy at the age thirteen showing focal and segmental glomerulosclerosis (FSGS). She was treated with tacrolimus for four years from age thirteen through seventeen. Patient was reportedly diagnosed with Nail Patella Syndrome after genetic testing. Her family history was notable for hematuria in her brother and hematuria and proteinuria in her mother. On physical examination she was noted to have no nail or skeletal abnormalities associated with Nail Patella Syndrome. Her labs were notable for a serum creatinine of 0.6 mg/dl and proteinuria of 155 mg/g creatinine of proteinuria. Urine microscopy revealed dysmorphic hematuria. Radiological imaging did not show skeletal abnormalities observed in Nail Patella Syndrome but genetic testing identified a pathogenic variant in COL4A5 c.919G>A (p.Gly307Ser) in addition to a variant of uncertain significance in LMX1B c.349G>A (p.Gly117Ser). Her brother aged 20 had a creatinine of 0.87 mg/dl with dysmorphic hematuria and no proteinuria. Genetic testing showed the same pathogenic variant in COL4A5 as in his sibling. His mother aged 55 was subsequently evaluated and had a creatinine 0.73 mg/dl with dysmorphic hematuria and 152 mg/g of proteinuria. Genetic testing was with the same variant in COL4A5 noted in her two children. Renal biopsy was extensive thinning and segmental lamellation of the glomerular basement membrane with eight percent FSGS. The typical “moth-eaten” appearance of the glomerular basement membrane characteristic of NPS was not evident. Segmental staining was observed with alpha 5 unit of Type IV collagen. Audiology and retinal optical coherence optometry studies are pending. Discussion Alport syndrome and Nail Patella Syndrome are rare genetic disorders that cause variable degrees of renal insufficiency from glomerular base membrane defects and are associated with characteristic extra renal manifestations. This is the first report of an inherited nephritis with combined mutations in COL4A5 and LMX1B. The clinical features and renal biopsy are compatible with Alport Syndrome and the significance of the mutation in LMX1B is uncertain. Conclusion This is the first case report of a combined mutation in COL4A5 and LMX1B gene presenting with hematuria and minimal proteinuria with preserved kidney function.

  PublisherOA PDFDOI

• A Rare Cause of Collapsing FSGS: Hemophagocytic Lymphohistiocytosis-Associated with Epstein-Barr Virus

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

  article

  Introduction: Hemophagocytic lymphohistiocytosis (HLH) is a severe, life-threating syndrome of pathologic immune system activation. Viral infection, such as Epstein Bar Virus (EBV) infection, is a known trigger of HLH. Collapsing focal segmental glomerulosclerosis (FSGS), an aggressive variant of FSGS, that may be idiopathic or occur with infectious or inflammatory conditions. Here we present a case of a patient who presented with AKI (acute kidney injury) requiring hemodialysis who was later diagnosed with HLH associated EBV and collapsing FSGS/ATN on renal biopsy. Case Description: A 42-year-old Somalian male with hypertension and new diagnosis of ESRD presented to the emergency department for hemodialysis (HD). He had presented two weeks prior at an outside hospital with renal failure ultimately thought to be ESRD from hypertension as his serologies were negative and ultrasound did not show obstruction. He had no prior baseline renal function as he did not follow routinely with primary care. During HD, he was found to be tachycardic and febrile, requiring admission. He underwent extensive workup for infectious etiologies and was ultimately diagnosed with HLH associated EBV. Genetic HLH panel was negative. He also underwent renal biopsy during this admission with evidence of FSGS with collapsing features and extensive ATN. He was started on rituximab and dexamethasone with improving results in his EBV titers from 21,000 to 10,000 after dose #4 and was discharged in stable condition. He remained on hemodialysis without evidence of renal recovery. Unfortunately, he presented a month later and was found to be hypotensive, febrile and tachycardic on dialysis. There was evidence of relapse with EBV PCR >110,000 and ferritin >40,000. He was also found to have disseminated cryptococcal infection, encephalopathy, and shock requiring multiple pressors and CRRT and eventually passed during admission. Discussion: Collapsing FSGS may be idiopathic or occur with infectious or inflammatory conditions. HLH secondary to EBV infectious resulting in collapsing FSGS is rare and the exact mechanism is unknown. This case highlights the important association between HLH associated EBV, and collapsing FSGS in a rapidly progressive course leading to ESRD as well as the need for thorough evaluation of patients with presumed hypertensive kidney disease

  PublisherDOI

• A Rare Cause of Kidney Failure: Native Kidney BK Polyomavirus Nephropathy after Lung Transplant

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

  article

  Introduction: BK polyomavirus nephropathy (BKVN) is a common complication of kidney transplantation, affecting 1-10% of renal transplant patients. It is rare in the native kidneys and is most often reported following hematopoietic stem cell transplantation. We present a case of native kidney BKVN leading to end-stage kidney disease (ESKD) in a lung transplant recipient. Case Description: A 71-year-old woman with history of obliterative bronchiolitis who received a bilateral lung transplant in 2021 (on everolimus, mycophenolate mofetil, and prednisone) with course complicated by ischemic stroke, intermittent hypotension, and frequent urinary tract infections was referred to the renal clinic with progressive renal failure in 2023. At the time of referral her serum creatinine had risen from 1 to 2 mg/dl over 12 months. Workup was remarkable for pyuria with positive urine culture. Kidney ultrasound was without obstruction and serologies were negative. She underwent a kidney biopsy which revealed BK polyomavirus nephropathy with 40% interstitial fibrosis and tubular atrophy. Despite minimizing immunosuppression, her kidney function continued to worsen. She was started on cidofovir and, though her BK serum viral load improved, her renal function deteriorated and she developed ESKD. She is now on peritoneal dialysis undergoing evaluation for kidney transplant. Discussion: BK nephropathy of the native kidneys in non-kidney solid organ transplant recipients is gaining recognition as an important cause of renal failure and progression to ESKD. Patients with unexplained renal failure after non-renal solid organ transplant may benefit from screening for BK virus to facilitate early diagnosis of BK polyomavirus nephropathy.Viral inclusions within the tubuler epithelial cells.Postive SV40 staining of tubular epithelial cells.

  PublisherDOI

Frequent coauthors

• Michel Azizi

  Hôpital Européen Georges-Pompidou

  104 shared

• Ajay J. Kirtane

  Cardiovascular Research Foundation

  89 shared

• Ajay Jain

  St Bartholomew's Hospital

  47 shared

• Felix Mahfoud

  Universitätsklinikum des Saarlandes

  45 shared

• Melvin D. Lobo

  Barts Health NHS Trust

  43 shared

• Manish Saxena

  Barts Health NHS Trust

  43 shared

• Desmond Jay

  42 shared

• Jan Basile

  Medical University of South Carolina

  34 shared

Education

• M.D.

  University of Utah School of Medicine

  2004

• M.A., Public Health

  University of Utah

• B.S.

  University of Madras, India

  1987