About

Sarah Gilligan grew up in Maine and completed her undergraduate degree in Psychology at Tufts University. She then moved to California, where she met her husband while working on her MS in Kinesiology. After graduate school, she worked in Denver as a research assistant studying exercise in patients with diabetes and peripheral artery disease (PAD) before returning to Tufts for medical school through the Maine Track program, which included a rural hospital experience on Longitudinal Integrated Curriculum pathway. She moved to Utah for her residency and continued there for her nephrology fellowship and faculty position. Her professional interests are clinical nephrology and education. Dr. Gilligan is board-certified by the American Board of Internal Medicine in Internal Medicine and Nephrology. She specializes in transitions of care from pediatrics, sarcoidosis, plasmapheresis, and kidney and hypertension nephrology. She is highly regarded by patients for her thoroughness, kindness, and ability to explain complex medical information clearly. Her dedication to patient care and education underscores her contributions to improving health outcomes in nephrology.

Research topics

• Internal medicine
• Medicine
• Pathology
• Gastroenterology
• Urology
• Virology
• Dermatology
• Endocrinology
• Immunology

Selected publications

• IgG4-Related Kidney Disease Following Autologous Bone Marrow Transplant: A Case Report

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

  article

  Introduction: IgG4-related disease (IgG4-RD) is a chronic relapsing autoimmune disease characterized by increased production of IgG-4 and tissue infiltration of IgG4 positive plasma cells. It can co-exist with or contribute to the pathogenesis of several autoimmune diseases. A systematic review of literature reveals no established relationship between autologous bone marrow transplant (ABMT) and IgG-4 RD. Our case explores a potential link between IgG4-RD and ABMT. Recognizing this association is key due to the treatable nature of early stage IgG4-RD Case Description: A 76-year-old man with history of multiple myeloma status post ABMT in 2017 and off all treatment for myeloma presented with an AKI and sub-nephrotic range proteinuria (UPCR 679 mg/g). Initial creatinine was 4.0 mg/dl, up from a baseline of 0.9 six months prior, and peaked at 5.8 during the hospitalization. He had no systemic signs or infectious symptoms. Autoimmune workup was remarkable for a weakly positive ANA, borderline positive dsDNA, low C3/C4, elevated IgG4, and positive IgM/IgG cryoglobulins. Kidney biopsy showed: marked lymphoplasmacytic interstitial nephritis characterized by > 10/HPF IgG4-positive plasma cells, with mesangial immune complex glomerulonephritis. IF showed full-house staining. Bone marrow biopsy performed 10 days prior to hospitalization showed 7% plasma cells. He was treated with prednisone 60mg daily, with a slow taper over 3 months followed by reinitiation of myeloma treatment for 4 months. Creatinine improved to 4.8 at discharge and further declined to 1.7 by five months follow up. Proteinuria decreased to 286 mg/g, and autoimmune markers—normalized or became negative within two weeks post-discharge Discussion: This case suggests a possible link between IgG4-related disease (IgG4-RD) and autologous bone marrow transplant (ABMT). Early recognition and prompt treatment with steroids led to marked improvement in renal function. We suspect IgG4-RD in this patient based on biopsy findings consistent with the disease, elevated serum IgG4 levels, absence of clinical another autoimmune condition, and the typical steroid-responsive course. While ABMT is known to cause immune dysregulation and has been associated with various autoimmune conditions, to our knowledge, no prior reports have described a connection between ABMT and IgG4-RDLight microscopy showing significant interstitial inflammation

  PublisherDOI

• Fast and Furious: IgAN with Rapidly Progressive Glomerulonephritis

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

  articleSenior author

  Introduction: IgA Nephropathy (IgAN) is the most common cause of glomerulonephritis and can manifest with a wide range of kidney impairment, ranging from asymptomatic hematuria to Rapidly Progressive Glomerulonephritis (RPGN). This later entity is uncommon, encompassing <10% of IgAN presentations, and generally leads to poor renal outcomes. Despite the many recent advances in the field of IgAN management, the optimal management of IgAN with RPGN remains unclear and current guidelines recommend treating these patients with cyclophosphamide and glucocorticoids similar to patients with renal ANCA-associated vasculitis. Case Description: A 21-year-old man presented after a month of fevers, chills, pharyngitis, non-productive cough, edema, and lower extremity palpable purpura and was found to have AKI with nephrotic range proteinuria and hematuria. History was notable for an AKI with hematuria and proteinuria shortly after an episode of pharyngitis two years earlier, though repeat labs found normal renal function with bland urine soon after and he was later lost to follow up. On his current presentation serologic testing and renal imaging was unremarkable. Renal biopsy was obtained which showed findings of a crescentic glomerulonephritis with IgA dominant deposits. He received treatment with pulse dose steroids and cyclophosphamide. He required hemodialysis due to hypervolemia and hyperkalemia, and unfortunately has remained dialysis-dependent four months out from his presentation. Discussion: This case of IgAN with RPGN demonstrates the rapid development of kidney failure in a young patient despite prompt and intensive immunosuppression. The current recommendations for treatment of IgAN with RPGN are based on limited prospective data as there are no randomized controlled trials studying this entity. Ongoing research is needed to better inform management of this uncommon but devastating IgAN presentation.

  PublisherDOI

• Crescentic Phase of Alport Syndrome: A Rare Glimpse into Rapid Progression

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

  articleSenior author

  Introduction: Crescentic glomerulonephritis (GN) represents a rare histologic finding in Alport syndrome, especially among adults. We report a rare case of progressive chronic kidney disease (CKD) due to crescentic GN in a 22-year-old man with Alport syndrome. Case Description: This 22-year-old man with Alport syndrome complicated by bilateral hearing loss and CKD first presented to the hospital with hyperkalemia. He was diagnosed at age 8 via kidney biopsy showing glomerular basement membrane abnormalities consistent with Alport syndrome. He presented to Nephrology at his baseline serum creatinine of 1.8 mg/dL with estimated glomerular filtration rate (eGFR) of 51 ml/min due to hyperkalemia of 6.7 mmol/L. His hyperkalemia was medically managed without stopping enalapril. Over the next 12 months, his kidney function steadily declined with stable proteinuria of 5 g/g without nephrotic syndrome. He often missed clinic appointments and laboratory draws, which complicated management. Within 12 months, his serum creatinine rose to 9 mg/dL with eGFR was 7 ml/min, prompting admission to the hospital for initiation of dialysis. While hospitalized, he underwent kidney biopsy which revealed early segmental fibrocellular crescents, marked interstitial fibrosis and tubular atrophy (80%), and electron microscopy findings of extensive thinning and lamellation of the glomerular basement membranes consistent with Alport syndrome. Genetic testing confirmed hemizygous COL4A5 mutation. Serum antineutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibodies were sent and resulted negative. The relatively rapid progression of CKD to end-stage kidney disease was attributed to crescentic GN secondary to Alport syndrome, and he is currently awaiting kidney transplantation. Discussion: Crescentic GN is a rare histologic finding among patients with Alport syndrome. The few existing case reports often describe pediatric patients with nephritic or nephrotic syndrome. This patient had a more gradual presentation with progressively worsening CKD without nephritic or nephrotic syndrome. Crescentic GN is likely underdiagnosed in this population as patients don’t usually require biopsy for diagnosis and rarely undergo repeat biopsy. Given its rarity, it is unclear whether this entity should be treated different than non-crescentic Alport syndrome.Native kidney biopsy specimen demonstrating glomerulus with mesangial expansion, mesangial hypercellularity, and an early fibrocelluar crescent by light microscopy with Periodic acid–Schiff stain.

  PublisherDOI

• Dual Molecular Diagnosis: COL4A3 and PKD1

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

  articleSenior author
  PublisherDOI

• A Double Dip: Concurrent Hypocalcemia and Hypophosphatemia After Denosumab in a Patient with CKD

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

  articleSenior author

  Introduction: Hypocalcemia is a commonly reported adverse event following denosumab infusion, especially among patients with chronic kidney disease (CKD). Hypophosphatemia is a lesser reported but equally important risk following denosumab. We report a case of severe hypophosphatemia and hypocalcemia after the administration of denosumab in a patient with CKD. Case Description: A 71-year-old woman with history of bilateral lung transplant, hypertension, and CKD stage 4 due to biopsy proven calcineurin inhibitor toxicity presented for routine follow up and was found to have calcium 7.7 mg/dL and phosphorus 1.1 mg/dL. Ten days prior to the visit she had received a denosumab infusion and had recently stopped her daily calcium supplement. Additional evaluation revealed creatinine within baseline range at 2.0 mg/dl, increase in PTH from 38 pg/ml 2 months prior to 572 pg/ml, normal 25-hydroxy vitamin D of 31 mg/mL, and elevated 1,25-dihydroxy vitamin D of 115 pg/ml. Urine studies confirmed urinary phosphorus wasting with urine phosphorus to creatinine ratio of 534 mg/g and fractional excretion of phosphorus of 49%. As she was asymptomatic, she declined hospital admission for IV phosphorus infusion. She was prescribed oral phosphorus and calcium supplementation with frequent outpatient labs until her calcium and phosphorus normalized while tapering her supplements. Subsequently, her serum calcium and phosphorus levels remained stable within normal limits off supplementation and PTH improved to 109 pg/ml. Discussion: Hypocalcemia is frequently reported after denosumab infusion, especially among patients with CKD, but hypophosphatemia is rarely reported. A small proportion of patients with CKD were included in the initial trials studying denosumab and hypocalcemia was not a statistically significant adverse event in those trials, though this has since been described in multiple case reports. There are fewer case reports of hypophosphatemia after denosumab infusion, but this represents an important adverse event. The proposed mechanism involves reduction in serum calcium (due to decreased osteoclast activity) leading to hyperparathyroidism and subsequent urinary phosphorus wasting. We recommend clinicians proactively supplement calcium and vitamin D in patients with CKD receiving denosumab and monitor serum calcium and phosphorus levels around 10-14 days after denosumab administration.

  PublisherDOI

• Kidney Cysts and Uncontrolled Hypertension: A Dissecting Diagnosis

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

  article

  Introduction: Autosomal dominant polycystic kidney disease (ADPKD), the most common genetic cause of kidney disease, is associated with cardiovascular complications. There are guidelines for screening for intracranial aneurysm (ICA), however, a paucity of research regarding the risk of extracranial aneurysms and other vascular abnormalities. Here we discuss the case of a young patient without known medical problems diagnosed simultaneously with aortic dissection and ADPKD. Case Description: A 30-year-old male presented to the ED with severe back pain. A CT scan revealed thoracic aortic abdominal dissection (TAAD) and massive enlargement of bilateral kidneys measuring 30cm and 26cm with a variety of cysts consistent with ADPKD. Of note, creatinine was 3.4 mg/dL and eGFR was 23 ml/min with unknown baseline. His blood pressure required 5 agents for control but he was in normal health prior to admission with no known medical issues. He was unaware of ADPKD diagnosis but his mom and two cousins have ADPKD and/or end-stage renal disease. During admission he underwent aortic repair and recovered well. His eGFR was 17 ml/min at the time of discharge but was unfortunately lost to follow up. Of note, our patient lacked many known risk factors of aortic dissection including hypertension, collagen disorders, or trauma but did report a history of cigarette smoking. Discussion: ADPKD is often caused by PKD1 and PKD2 genes and affects multiple organ systems. Notably the expression of PKD1 in vascular smooth muscle and PKD2 in endothelium creates risk factors for ICA, TAAD, and aortic root dilation. Our patient lacked risk factors of vascular dissection upon presentation, raising suspicion of association with his ADPKD. Studies have shown an increased risk of aortic dissection in patients with ADPKD, including a cohort study in Taiwan that found a 5-fold risk increase. This case brings to light the risks and benefits of preemptive screening for vascular anomalies beyond ICA in patients with ADPKD.

  PublisherDOI

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

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

  articleSenior author

  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

• A Periodic Curveball: Collagenofibrotic Glomerulopathy

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

  article

  Introduction: Collagenofibrotic Glomerulopathy is a rare idiopathic disease with unknown pathogenesis and no treatment. Case Description: A 65-year-old man with hypertension and tobacco use disorder was hospitalized after 5 months of fevers, rigors, weight loss, malaise and one week of heavy acetaminophen and ibuprofen use. He was treated for acetaminophen toxicity and received extensive infectious and hematologic workup, which revealed multiple hypermetabolic lymph nodes on PET CT with necrotizing lymphadenitis on biopsy and prostatomegaly with intermittent bleeding on cystoscopy. Nephrology was consulted for microscopic hematuria, spot urine protein:creatinine ratio 524 mg/g, and 117 mg/g albuminuria. Creatinine was 0.9 mg/dL with estimated glomerular filtration rate 90 ml/min/1.73m2. Serologic workup was negative aside from antinuclear antibody titer of 1:80. Urine microscopy showed acanthocytes. Subsequent renal biopsy showed mesangial and subendothelial deposits of curved fibrils with frayed edges and transverse banding at 60 nm periodicity, consistent with collagenofibrotic glomerulopathy (Figure). Two years later, renal function remains preserved with mild proteinuria and microscopic hematuria. The etiology of his B-symptoms remains unconfirmed. He has been treated with valsartan and dapagliflozin. Rheumatology initiated methotrexate for suspected systemic autoimmune inflammatory syndrome. A recent repeat bone marrow biopsy revealed chronic monomyelocytic leukemia stage 0. Discussion: Collagenofibrotic glomerulopathy is identified by atypical type III collagen deposition in the mesangium and subendothelium. Limited case reports note hypertension, mild proteinuria, microscopic hematuria and typically preserved renal function, consistent with this case. Interestingly, this mysterious disease was found amid a mysterious constellation of symptoms. It is classically not linked with extrarenal symptoms at diagnosis, but re-evaluation of known cases should be considered for later development of hematologic or rheumatologic disease.Electron Microscopy

  PublisherDOI

• OMg! What Links Hypomagnesemia, Kidney Stones, and Arrhythmia

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

  articleSenior author

  Introduction: Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is an autosomal recessive disease that usually presents during early childhood and is known to be caused by mutations of claudin-16 and claudin-19. We discuss an atypical presentation of an adult patient with kidney stones and hypomagnesemia with genetic testing remarkable for heterozygous mutation in claudin-16 (c235C>G). Case Description: 23 year old female with history of kidney stones presented to the ED with ventricular fibrillation cardiac arrest. After successful resuscitation, she recovered quickly with intact neurological function. Initial workup revealed low-normal magnesium of 1.7 mg/dL which dropped to 1.5 mg/dL during hospitalization despite 4g of intravenous magnesium per day in addition to oral supplementation. Admission labs were also significant for a calcium of 7.8 mg/dL, albumin of 3.7 mg/dL and serum creatinine of 1.02 mg/dL, which improved during hospitalization. Laboratory values prior to this admission were not available. Medication history was unrevealing for culprit medications, including loop or thiazide diuretics. Urine studies revealed a fractional excretion of magnesium at 16%. Patient was supplemented with magnesium and discharged. During outpatient follow up, a 24 hour urine collection was obtained. She was found to have hypocitraturia, however with a normal urine calcium. Genetic testing was obtained which was negative for pathogenic variants but positive for a variant of unknown significance; a c235C>G heterozygous mutation in claudin-16. Upon outpatient clinic follow up, she continued to require magnesium oxide supplementation, currently at 400mg twice daily, with a corresponding magnesium level of 1.8 mg/dL. Discussion: FHHNC has over 50 known mutations in the claudin-16 gene, and presents in early childhood leading to progressive kidney failure. Our adult patient had significant renal magnesium wasting during hospitalization that continued as an outpatient, and required ongoing supplementation. Although clinical history and urine magnesium studies were consistent with FHHNC, she did not have hypercalciuria or family history of kidney stones or kidney failure. As genetic testing has become more common in clinical practice, this case highlights the need to critically assess variants of uncertain significance and monitor for any potential clinical manifestations.

  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

  articleSenior author

  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

• Kalani L. Raphael

  VA Salt Lake City Healthcare System

  10 shared

• Josephine Abraham

  9 shared

• Divya Raghavan

  University of Utah

  8 shared

• Isaac E. Hall

  University of Utah

  8 shared

• Monica P. Revelo Penafiel

  5 shared

• Laith Al‐Rabadi

  5 shared

• Şuayp Oygen

  University of Utah

  5 shared

• Miklos Z. Molnar

  5 shared

Labs

• University of Utah Health NephrologyPI

Education

• B.A., Psychology

  Tufts University

• M.S., Kinesiology

  California

• M.D.

  Tufts University