William L Clapp
· ProfessorVerifiedUniversity of Florida · Pathology, Immunology and Laboratory Medicine
Active 1974–2026
About
Dr. William L. Clapp serves as Professor and Director of Renal Pathology in the Department of Pathology, Immunology and Laboratory Medicine at the University of Florida College of Medicine. He oversees the Renal Pathology service, which is one of the busiest in the southeastern United States, evaluating native and transplant renal biopsies from UF Health and numerous other institutions across Florida. His teaching responsibilities include directing the Kidney and Urinary Tract (KUT) course for medical students and teaching renal pathology and cell and molecular biology of cancer at UF College of Medicine. Dr. Clapp's research interests focus on diagnostic aspects and underlying mechanisms of kidney diseases, especially autoimmune diseases, as well as renal development and structural-functional correlates. His work includes active involvement in research projects utilizing artificial intelligence and computational imaging to improve diagnosis and prognosis of kidney-related conditions.
Research topics
- Biology
- Immunology
- Internal medicine
- Medicine
- Pathology
- Endocrinology
- Genetics
- Chemistry
- Virology
- Cancer research
Selected publications
A Comprehensive Benchmark of Histopathology Foundation Models for Kidney Digital Pathology Images
ArXiv.org · 2026-03-16
articleOpen accessHistopathology foundation models (HFMs), pretrained on large-scale cancer datasets, have advanced computational pathology. However, their applicability to non-cancerous chronic kidney disease remains underexplored, despite coexistence of renal pathology with malignancies such as renal cell and urothelial carcinoma. We systematically evaluate 11 publicly available HFMs across 11 kidney-specific downstream tasks spanning multiple stains (PAS, H&E, PASM, and IHC), spatial scales (tile and slide-level), task types (classification, regression, and copy detection), and clinical objectives, including detection, diagnosis, and prognosis. Tile-level performance is assessed using repeated stratified group cross-validation, while slide-level tasks are evaluated using repeated nested stratified cross-validation. Statistical significance is examined using Friedman test followed by pairwise Wilcoxon signed-rank testing with Holm-Bonferroni correction and compact letter display visualization. To promote reproducibility, we release an open-source Python package, kidney-hfm-eval, available at https://pypi.org/project/kidney-hfm-eval/ , that reproduces the evaluation pipelines. Results show moderate to strong performance on tasks driven by coarse meso-scale renal morphology, including diagnostic classification and detection of prominent structural alterations. In contrast, performance consistently declines for tasks requiring fine-grained microstructural discrimination, complex biological phenotypes, or slide-level prognostic inference, largely independent of stain type. Overall, current HFMs appear to encode predominantly static meso-scale representations and may have limited capacity to capture subtle renal pathology or prognosis-related signals. Our results highlight the need for kidney-specific, multi-stain, and multimodal foundation models to support clinically reliable decision-making in nephrology.
Clinical Kidney Journal · 2026-03-25
articleOpen accessA Comprehensive Benchmark of Histopathology Foundation Models for Kidney Digital Pathology Images
arXiv (Cornell University) · 2026-03-16
preprintOpen accessHistopathology foundation models (HFMs), pretrained on large-scale cancer datasets, have advanced computational pathology. However, their applicability to non-cancerous chronic kidney disease remains underexplored, despite coexistence of renal pathology with malignancies such as renal cell and urothelial carcinoma. We systematically evaluate 11 publicly available HFMs across 11 kidney-specific downstream tasks spanning multiple stains (PAS, H&E, PASM, and IHC), spatial scales (tile and slide-level), task types (classification, regression, and copy detection), and clinical objectives, including detection, diagnosis, and prognosis. Tile-level performance is assessed using repeated stratified group cross-validation, while slide-level tasks are evaluated using repeated nested stratified cross-validation. Statistical significance is examined using Friedman test followed by pairwise Wilcoxon signed-rank testing with Holm-Bonferroni correction and compact letter display visualization. To promote reproducibility, we release an open-source Python package, kidney-hfm-eval, available at https://pypi.org/project/kidney-hfm-eval/ , that reproduces the evaluation pipelines. Results show moderate to strong performance on tasks driven by coarse meso-scale renal morphology, including diagnostic classification and detection of prominent structural alterations. In contrast, performance consistently declines for tasks requiring fine-grained microstructural discrimination, complex biological phenotypes, or slide-level prognostic inference, largely independent of stain type. Overall, current HFMs appear to encode predominantly static meso-scale representations and may have limited capacity to capture subtle renal pathology or prognosis-related signals. Our results highlight the need for kidney-specific, multi-stain, and multimodal foundation models to support clinically reliable decision-making in nephrology.
BMJ Case Reports · 2025-09-01 · 1 citations
articleOpen accessWe present a case of a pregnant woman in her 40 s diagnosed with primary Sjögren's disease (pSjD) complicated by distal type I renal tubular acidosis. At 12 weeks' gestation, she exhibited dry eyes, dry mouth and renal dysfunction for the first time. Electrolyte studies confirmed hyperchloraemic normal anion gap metabolic acidosis with elevated urine pH. Positive serologies included +ANA, +SSA and +RF. Schirmer's test was positive. Renal biopsy indicated chronic tubulointerstitial nephritis with 40% interstitial fibrosis. Hydroxychloroquine and prednisone (60 mg daily) improved renal function, but rapid tapering led to mild worsening in renal function, sicca symptoms and fetal growth restriction. Steroid dose escalation and azathioprine initiation led to clinical improvements. At 35 weeks' gestation, she delivered preterm due to pre-eclampsia and intrahepatic cholestasis. The neonate had cutaneous neonatal lupus but was otherwise healthy. This case highlights the clinical complexity of managing distal renal tubular acidosis in pregnant patients with pSjD and the need for evidence-based treatment guidelines.
Journal of the American Society of Nephrology · 2025-10-01
articleIntroduction: Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare glomerulonephritis caused by deposition of a monoclonal immunoglobulin within the glomeruli. The triggers and management for PGNMID are incompletely understood, particularly when associated with rapidly progressive glomerulonephritis (RPGN). Case Description: A 40-year-old woman, who had pre-eclampsia two years prior, presented to the hospital with hypertensive emergency and fatigue. Her serum creatinine was at 4.2 mg/dL (0.98 mg/dL six months prior) and albuminuria at 8.7 g/g. In the previous month, she was taking 600-1200 mg of ibuprofen daily for flu-like symptoms. Her creatinine rose to 8.6 mg/dL at 7 days and to 12.27 mg/dL at 10 days after the admission. She received intravenous methylprednisolone followed by 40 mg of prednisone daily. Kidney biopsy revealed PGNMID with IgG-3-lambda deposits and prominent cellular crescents (76%) as well as acute tubular injury. Serum protein electrophoresis showed no abnormal bands and free light chain ratio was normal at 1.04. Antibodies against myeloperoxidase, proteinase 3, glomerular basement membrane, antinuclear, and complements C3 and C4 were unremarkable. Parvovirus was positive. There was no identifiable malignancy. Bone marrow biopsy showed no identifiable clone. Since empiric clone-directed therapy had shown benefit in some cases of PGNMID, the patient received 1 g of rituximab. Unfortunately, her kidney function did not improve, and she was transitioned to hemodialysis with monitoring for renal recovery and possible second dose of rituximab with daratumumab. Discussion: This rare case of RPGN in the setting of PGNMID is possibly related to an infection, including parvovirus. Other possible associations include pregnancy, although it concluded two years prior to the onset of RPGN, and ibuprofen. More data is needed to effectively manage this rare glomerulonephritis.
Monoclonal gammopathy-associated dense deposit disease
Kidney International · 2025-05-20
articleKidney International Reports · 2025-04-21 · 1 citations
articleOpen accessSenior authorJournal of the American Society of Nephrology · 2025-10-01
articleIntroduction: Anti-phospholipase A2 receptor antibodies (anti-PLA2R) are detected in 70-80% of patients with primary membranous nephropathy (pMN). The presence of pretransplant anti-PLA2R increases the risk of recurrent anti-PLA2R MN post KT but might be not associated with disease activity post KT. Case Description: A 51-year-old male with kidney failure due to anti-PLA2R MN who received a cadaveric KT presents with worsening proteinuria. Serum anti-PLA2R titer (IFA) was 1:2560 at listing 6 months prior to KT. Induction was with Alemtuzumab and maintenance with Tacrolimus (TAC), Mycophenolate (MMF), and Prednisone. His post KT course was complicated by DGF, followed by hypogammaglobinemia and disseminated Nocardia 2 months post KT treated with long-term antibiotics, reduction in TAC, and withdrawal of MMF. 6 weeks post KT he started to have worsening proteinuria. Donor-derived cell-free DNA was 0.43% with absent donor-specific antibodies. Given anti-PLA2R titer 1:80, recurrent MN was presumed. Due to active disseminated Nocardia precluding therapy, KT biopsy was deferred. He was conservatively managed with Losartan. By 12 months post KT patient had complete (clinical and serological) remission with serum creatinine (SCr) 1.7-1.9 mg/dl (baseline), urine PCR down to 70 mg/g, and undetected anti-PLA2R. Patient started again to have worsening albuminuria and proteinuria 3760 mg/g and 4290 mg/g, respectively with SCr up to 2.2 mg/dl at 16 months post KT. Anti-PLA2R remained undetected. KT biopsy yielded findings consistent with PLA2R-positive MN (Figure 1). The patient received Rituximab with improved SCr and proteinuria. Discussion: This case of anti-PLA2R MN recurring after complete remission post KT is illustrative of evaluating proteinuria and kidney function with KT biopsy to monitor disease activity rather than solely relying upon anti-PLA2R titer. Literature supports the correlation of anti-PLA2R levels with disease activity and remission before KT and with recurrence post KT. However, data on anti-PLA2R to monitor disease activity in recurrent anti-PLA2R MN post KT is limited.
Prediction of Kidney Graft Inflammation Using Self-Supervised Learning
Journal of the American Society of Nephrology · 2025-10-01
articleTervaert-Guided Integration of Histology and Clinical Data for Diabetic Kidney Disease Distinction
Journal of the American Society of Nephrology · 2025-10-01
article
Frequent coauthors
- 31 shared
I. David Weiner
University of Florida
- 28 shared
Dara Wakefield
University of Florida
- 19 shared
Sriram Ambadapadi
Arizona State University
- 18 shared
Hyun‐Wook Lee
University of Florida
- 17 shared
Alexandra Lucas
University of Florida
- 16 shared
Byron P. Croker
University of Florida
- 15 shared
Hao Chen
Nanjing Medical University
- 15 shared
Jill W. Verlander
University of Florida
Education
M.D., Pathology
University of Florida College of Medicine
Awards & honors
- Basic Science Teacher of the Year 2015 University of Florida…
- Exemplary Teacher Award 2004 University of Florida College o…
- Basic Science Teacher of the Year 2002 University of Florida…
- Teaching Excellence Awards 1995-2020 UF COM student classes
- Individual National Research Service Award, NIH (1984-1987)
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