Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Springer Science and Business Media LLC  

DOI： 10.1007/s13730-022-00766-3

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Other Link： https://link.springer.com/article/10.1007/s13730-022-00766-3/fulltext.html

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：Oxford University Press (OUP)  

Abstract

Background

Immunoglobulin A nephropathy (IgAN) is the most common glomerulonephritis worldwide, characterized by mesangial polymeric IgA1 deposition. IgAN is believed to develop owing to aberrant mucosal immunoreaction against commensals in the tonsils. However, the exact interrelation between pathogenic IgA and mucosal microbiota in IgAN patients is unclear.

Methods

Biopsy-proven IgAN or recurrent tonsillitis (RT) patients who had undergone tonsillectomy were enrolled. We used 16S ribosomal RNA gene amplicon sequencing with a flow cytometry-based bacterial cell sorting technique) and immunoglobulin repertoire sequencing of the IgA heavy chain to characterize IgA-coated bacteria of the tonsillar microbiota (IgA-SEQ) and their corresponding IgA repertoire. Furthermore, we fractionated patient serum using gel-filtration chromatography and performed flow cytometry-based analysis of IgA binding to bacteria cultured from incised tonsils.

Results

Tonsillar proliferation-inducing ligand and B-cell activating factor levels were significantly higher in IgAN than in RT patients. IgA-SEQ for tonsillar microbiota revealed the preferential binding ability of IgA to Bacteroidetes in IgAN tonsils compared with those from RT patients. Expression of immunoglobulin heavy (IGH) constant alpha 1 with IGH variable 3–30 was significantly higher in IgAN than that in RT, and positively correlated with the IgA-coated enrichment score of Bacteroidetes. Serum polymeric IgA, comprising high levels of GdIgA1, exhibited considerable binding to Bacteroidetes strains cultured from the tonsils of IgAN patients.

Conclusions

These findings provide evidence that aberrant mucosal immune responses to tonsillar anaerobic microbiota, primarily consisting of members of the phylum Bacteroidetes, are involved in IgAN pathophysiology.

DOI： 10.1093/ndt/gfaa223

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Authorship：Lead author,　Corresponding author   Publishing type：Research paper (scientific journal)   Publisher：Japanese Society for Dialysis Therapy  

DOI： 10.4009/jsdt.54.513

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Authorship：Lead author,　Corresponding author   Language：English   Publishing type：Research paper (scientific journal)  

Hypermagnesemia is generally considered an exceptional iatrogenic condition usually caused by magnesium-containing cathartics. In particular, this condition often develops when magnesium-containing cathartics are administered to elderly patients with renal insufficiency or bowel movement dysfunction. Although magnesium oxide (MgO) is widely prescribed as a laxative, serum magnesium concentration has not been examined in most cases. In this report, we present the cases of four elderly patients with constipation and symptomatic hypermagnesemia caused by MgO ingestion, one of which had a lethal course. All of the patients were older than 65 years and with renal dysfunction. In addition, they had difficulties in expressing their symptoms because of cerebrovascular events or dementia. These cases suggest that hypermagnesemia caused by magnesium-containing cathartics is more likely to develop than previously recognized and that physicians should be aware that patients with chronic kidney disease and the elderly are at risk of hypermagnesemia on magnesium administration. We recommend serum magnesium monitoring for high-risk patients after initial prescription or dose increase.

DOI： 10.1007/s13730-018-0359-5

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Publishing type：Research paper (scientific journal)   Publisher：Portland Press Ltd.  

Chronic inhibition of the renin–angiotensin–aldosterone system (RAAS) causes progressive renal vascular disease characterized by concentric arterial and arteriolar hypertrophy (CAAH), driven by sustained activation of renin-producing cells. However, the mechanisms linking impaired RAAS signaling to vascular remodeling remain unclear. Using a Ren1c-T2A knock-in mouse, we identified a mechanistic link between defective renin function and progressive vascular disease. The T2A insertion generates a hypomorphic renin allele, and homozygous mice develop progressive CAAH accompanied by markedly reduced levels of enzymatically active renin in the circulation. In response to reduced renin activity, mice activate a robust compensatory program characterized by increased Ren1 mRNA expression, depletion of renal renin stores, accumulation of catalytically impaired renin in the circulation, and extensive recruitment of renin-lineage cells along the renal arteriolar tree. Despite this response, RAAS activity remains insufficient, and homozygous mice develop progressive hypotension and renal dysfunction following the onset of CAAH. To define the basis of impaired renin function, molecular dynamics simulations revealed that the C-terminal T2A peptide alters the renin catalytic pocket, disrupting key aspartate residues and electrostatic interactions required for efficient angiotensinogen cleavage. These findings demonstrate that chronic renin deficiency is sufficient to drive renal arteriolar remodeling and functional decline in the absence of overt glomerular injury. Our results provide a mechanistic framework linking chronic RAAS suppression to progressive renal vascular disease and establish this model as a platform for investigating the long-term consequences of RAAS inhibition and pathogenic renin variants.

DOI： 10.1042/cs20261291

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Publishing type：Research paper (scientific journal)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

Background:

Aberrant mucosal immune responses are underlying causes of Immunoglobulin A nephropathy (IgAN), the most prevalent type of chronic glomerulonephritis. However, the role of T cells in IgAN pathogenesis remains elusive. To address this knowledge gap, we profiled the T-cell receptor (TCR) repertoire in the tonsils of patients with IgAN.

Methods:

This study included 27 and 20 patients with biopsy-confirmed IgAN and recurrent tonsillitis (RT), respectively, who underwent tonsillectomy. The TCR repertoire was determined by high-throughput sequencing coupled with unbiased adaptor ligation polymerase chain reaction (PCR). Furthermore, the usage of variable and joining regions in TCRα (TRA) and β (TRB) genes in each group was assessed. TRA clonotypes shared among the patients were characterized by complementary determining region 3 (CDR3) lengths, types of mucosal-associated invariant T (MAIT) cells, hydrophobicity, and their relationships with tonsillar galactose-deficient IgA1 (Gd-IgA1) and tonsillar IgA-binding indices of tonsillar bacteria.

Results:

The TRA repertoire exhibited significantly lower similarity in patients with IgAN than did in RT cases ( P < 0.001). Sharing TRA clonotypes among patients with IgAN was significantly sparser than that among RT cases. The relative abundance of shared TRA clonotypes with shorter CDR3 lengths was significantly increased in patients with IgAN ( P_adj = 0.041), which was characterized by low MAIT match scores. Significant negative correlations were observed between the MAIT scores and hydrophobicity for these TRA clonotypes in patients with IgAN. The relative abundances of these clonotypes significantly and positively correlated with the IgA binding indices of the phylum Bacteroidetes ( P_adj = 0.008) in both groups and tonsillar Gd-IgA1 levels in patients with IgAN ( P = 0.035).

Conclusions:

The results in this study suggest aberrant T-cell subsets involvement in tonsillar immunity in patients with IgAN.

DOI： 10.34067/kid.0000001154

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Publisher：Cold Spring Harbor Laboratory  

Chronic inhibition of the renin-angiotensin system (RAS), while widely used to treat hypertension, can lead to an underrecognized form of vascular disease marked by concentric arteriolar and arterial hypertrophy (CAAH). Here, using two lineage-traced mouse models of genetic renin deletion and sustained RAS blockade, we uncover a pathogenic cascade initiated by renin-lineage cell fate reprogramming. Loss of endocrine identity and transformation of smooth muscle cells drives a shift toward a fibrotic, inflammatory, and secretory phenotype that remodels the extracellular matrix and promotes vascular thickening and luminal narrowing. Integrated transcriptomic, proteomic, and metabolomic profiling revealed a hypoxia-linked metabolic switch—characterized by succinate accumulation and NAD⁺ depletion—coupled to Hif activation and disease progression. We identify Cdh13 and collagens (including Col1a1 and Col12a1) as early urinary biomarkers and define a 10-gene molecular signature of CAAH with potential clinical application. These findings establish renin-lineage cell plasticity and metabolic dysfunction as central drivers of CAAH and nominate candidate biomarkers for early detection and therapeutic targeting in RAS-inhibited patients.

DOI： 10.1101/2025.07.09.663881

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Publisher：Cold Spring Harbor Laboratory  

Renin cells synthesize and release the hormone-enzyme renin to regulate blood pressure and fluid-electrolyte homeostasis. Their function and identity depend on communication with surrounding cells and nerve fibers within complex kidney structure. Because renin cells are rare -0.01 % of kidney cells- conventional histological approaches cannot capture their interaction with nerve fibers and surrounding cells within the nephron and its vasculature. Using a novel ultrabright renin cell-specific tdTomato reporter mouse, high-resolution 3D imaging, and single-cell RNA-Seq, we mapped the interactions of renin cells with growing axons during normal kidney vascular development, in response to threats to homeostasis, and a severe arterial disease caused by a defective renin enzyme. During embryonic kidney development, stromal and renin cell progenitors assemble the arterioles, express axon attractants and neurotrophins that establish the precise innervation of renin cells and arterioles in a centrifugal pattern. Hypotension and sodium depletion led to an increase in the volume and number of renin cells along the arterioles. Renin enzymatic deficiency led to hypertrophy and endocrine transformation of renal arterioles, aberrant axon sprouting and sympathetic hyperinnervation suggesting a feed-forward mechanism whereby renin cells and axons co-induce each other, orchestrate neurovascular development and arteriolar remodeling when renin cells are over stimulated.

DOI： 10.1101/2025.07.08.663706

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Publisher：Cold Spring Harbor Laboratory  

Juxtaglomerular (JG) cells are crucial regulators of blood pressure and fluid-electrolyte homeostasis. Under normal conditions, renin secretion by JG cells is sufficient to maintain homeostasis. However, under physiological stress such as narrowing of one of the renal arteries, heart failure, dehydration, or chronic administration of renin-angiotensin system (RAS) inhibitors, additional cells along the renal arterioles are transformed to the renin phenotype to meet the demands for renin and regain homeostasis. In cases of prolonged and persistent stimulation of renin cells, concentric arteriolar hypertrophy develops. The study of renin cell identity, plasticity and function often requires the isolation of this rare cell type. Here, we report on the generation of a mouse model to label renin-expressing cells with a bright fluorescent reporter under control of the Ren1c locus for the tracking and isolation of renin cells. Kidneys from adult heterozygous (Het) Ren1ctdTomato/+ mice showed tdTomato signal confined to the JG area under basal conditions, and extending along the afferent arterioles and in the intraglomerular mesangium upon treatment with captopril + low-salt diet to induce the endocrine transformation of renin cells. Unexpectedly, homozygous (Homo) Ren1ctdTomato/tdTomato mice exhibited increased tdTomato signal that extended along the afferent arterioles and into the mesangium even under normal physiological conditions, with progressive thickening of the kidney arterioles with age. Despite reduced renin immunostaining in the renal cortex, Ren1ctdTomato/tdTomato Homo mice exhibited significantly higher kidney Ren1 mRNA and circulating renin levels when compared to Het controls. Moreover, Homo mice showed significantly lower blood pressure measured under anesthesia and angiotensin I (Ang I) plasma levels, indicating compromised renin activity. In addition, Homo mice developed interstitial fibrosis and compromised kidney function. The concentric arteriolar hypertrophy phenotype observed in these mice is identical to that described when RAS is genetically or pharmacologically inhibited, including the presence of mutations in the renin gene. Unlike mice with global deletion of renin, these animals did not require neonatal saline injections to survive and did not develop other kidney abnormalities, indicating that the bicistronic approach rendered a renin hypomorphic mouse. Ren1ctdTomato mice constitute an excellent model for the bright and strong labeling of renin-expressing cells and for the study of the mechanisms involved in the development of concentric vascular hypertrophy under RAS inhibition. In addition, this model may provide a better understanding of factors controlling renin protein folding, stability, packaging, and release.

DOI： 10.1101/2025.05.02.651896

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Language：English   Publishing type：Research paper (scientific journal)   Publisher：American Physiological Society  

Fate mapping and genetic manipulation are important tools to study the identity of renin cells. Here, we report on a novel Cre mouse model, Akr1b7^CreERT2, for the spatial and temporal regulation of gene expression in renin cells. Cre is properly expressed in renin cells during development and in the adult under basal conditions and under physiological stress. Moreover, renin can be efficiently deleted in the adult, leading to the development of concentric vascular hypertrophy.

DOI： 10.1152/ajprenal.00129.2024

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Authorship：Lead author   Publishing type：Research paper (international conference proceedings)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

Background: Renin secretion from the juxtaglomerular (JG) cells controls circulating Angiotensin II (AngII), a critical blood pressure determinant. AngII is believed to suppress renin release from JG cells to prevent excessive blood pressure elevation. However, a direct negative feedback mechanism has yet to be established in JG cells. In JG cells, Ca²⁺ is a crucial second messenger that governs renin secretion by suppressing cAMP, a potent renin secretion stimulator. Thus, in contrast to most secretory cells, renin secretion from JG cells is inversely related to the intracellular Ca²⁺ level. However, the role of AngII in modulating JG cell Ca²⁺dynamics remains unclear.

Objective: Define intracellular Ca²⁺ responses to AngII and identify the critical channels to suppress renin secretion in JG cells.

Methods: Kidney slices from mice expressing JG-specific GCaMP6f, a genetically encoded Ca²⁺ indicator under the control of the Ren1c promoter, were imaged ex vivo on a widefield fluorescent microscope for 30 min per experiment (n = 5). In each experiment, slices were continuously perfused with buffer containing variable Ca²⁺ and AngII concentrations, ± specific Ca²⁺ channel inhibitors. Images were captured at 10 Hz and analyzed using Mesmerize Ca²⁺ imaging software to identify and plot fluorescent intensity over time for each JG cell. Additional kidney slices were incubated in 24-well plates with buffer containing vehicle or AngII ± Ca²⁺channel inhibitors for 30 min. ELISA determined renin concentration.

Results: 1) AngII dose-dependently evoked robust and periodic Ca²⁺-oscillations (Ca²⁺ spikes) in JG cells (mean spikes/min; 50 pM: 5.4, 300 pM: 7.7, 3 nM: 13.2, and 300 nM: 17.6). 2) AngII-elicited Ca²⁺ activity was markedly reduced with “Ca²⁺-free” buffer. 3) L-type voltage-dependent Ca²⁺ channel (VDCC) blocker nifedipine moderately decreased AngII-elicited Ca²⁺ spikes, while T-type VDCC blocker TTA-P2 did not. 4) Blocking endoplasmic reticulum (ER) Ca²⁺-release drastically reduced Ca²⁺ activity. 5) AngII dose-dependently decreased renin secretion in kidney slices, congruent with the AngII-elicited Ca²⁺ activity in imaging studies.

Conclusion: AngII dose-dependently and directly elicited large, periodic Ca²⁺-oscillations in JG cells that suppressed renin release. Both extracellular Ca²⁺ influx and intracellular Ca²⁺ release from ER stores are required for sustained Ca²⁺ activity. L-type, but not T-type, Ca²⁺ channels participate in JG cell Ca²⁺-oscillations.

DOI： 10.1161/hyp.81.suppl_1.mp17

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Publishing type：Research paper (international conference proceedings)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

Background: Chronic stimulation of renin cells by long-term use of renin-angiotensin system (RAS) inhibitors or renin deletion leads to concentric renal arteriolar hypertrophy frequently surrounded by immune-inflammatory cells. The disease is caused by the renin cells which increase in number and adopt an embryonic-secretory phenotype and induce the accumulation of smooth muscle cells that obstruct the vessels leading to ischemia. Normally, renin cells are innervated but it is unclear whether innervation of the renal arterial tree is affected under RAS inhibition.

Hypothesis: Long-term RAS inhibition increases renal arteriolar innervation.

Methods: We used two models of RAS inhibition: 1) Ren1c-/-; Ren1c-Cre; R26RmTmG mice studied at 3 months of age; 2) SMMHCCreERT2; R26RtdTomato; Ren1cYFP mice were treated with captopril for 6 months. We performed tissue clearing and 3D staining with an anti-tubulin β3 antibody. The expression of neurogenesis-related genes in renin lineage cells was examined using our previous single-cell RNA sequencing (scRNA-seq) data from mouse kidneys. We compared RNA expression of nerve growth factor (NGF) between Ren1c−/− mice and control mice by qPCR and in situ hybridization (ISH). T cell infiltration was observed by immunostaining with anti-CD3 antibody.

Results: 3-D imaging revealed that in both RAS inhibition models there was marked hyperinnervation. Renin cells expanded along and around the renal arterioles, and covered the glomeruli. Axons grew in numerous branches surrounding thickened afferent arterioles, bound tightly to renin cells and encasing the glomeruli. Our scRNA-seq data showed that Ngf, a gene important for neurogenesis and produced by immune cells, was highly expressed in renin cells. In Ren1c−/− mice, expression of Ngf was significantly increased compared to controls (p=0.0054). ISH revealed that Ngf was highly expressed in Ren1c−/− mice in the juxtaglomerular area and in the renal cortical stroma. Infiltration of T cells around affected arterioles was prominent in both models of RAS inhibition.

Conclusion: Long-term inhibition of RAS leads to renal hyperinnervation, infiltration of immune cells and arteriolar hypertrophy. The identification of this neuro-immune-endocrine arterioles may help understand and treat vascular disease and hypertension.

DOI： 10.1161/hyp.81.suppl_1.aw12

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Publishing type：Research paper (scientific journal)   Publisher：Wiley  

Abstract

Introduction

Atypical hemolytic uremic syndrome (aHUS) is a rare form of thrombotic microangiopathy. Personal genome analyses have revealed numerous aHUS‐causing variants, mainly complement‐related genes. However, not all aHUS‐causing variants have been functionally validated.

Methods

An exome sequence analysis of a Japanese multiplex family composed of three patients diagnosed with aHUS in infancy and showing frequent relapses clustered in a dominant transmission mode was performed. Protein interaction between the C3d and C‐terminal domains of factor H was analyzed using a quartz crystal microbalance.

Results

Following filtering by heterozygous variants, amino acid substitutions, and allele frequency, the analysis revealed eight rare variants shared by the affected individuals. Variant prioritization listed C3 p.W1034R as the most likely candidate gene mutation in the affected individuals, despite being classified as a variant of uncertain significance. Binding of recombinant C3d harboring 1034R to recombinant short consensus repeats 15 to 20 of factor H was significantly suppressed compared with that of C3 with 1034W.

Conclusion

C3 p.W1034R results in an inherited form of aHUS that often presents with recurrent episodes, possibly because of impaired interactions between the C3d and C‐terminal domains of factor H. Following comprehensive genomic analysis, functional validation of C3 p.W1034R strengthens the molecular basis for aHUS pathophysiology.

DOI： 10.1002/mgg3.2288

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Authorship：Lead author   Publishing type：Research paper (conference, symposium, etc.)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

Background: Renin regulates blood pressure (BP) and fluid homeostasis. Renin cells harbor a pressure sensor, the renin cell baroreceptor that controls renin synthesis and release. We recently discovered that the renin cell baroreceptor is a nuclear mechanotransducer within the renin cells that transmits external pressures to chromatin and regulates Ren1 expression. However, which transcription factors (TF) regulate renin expression during pressure sensing remains unclear.

Objective: Define the responsible TFs for Ren1 as part of the renin cell baroreceptor.

Methods: Forkhead box protein D1 (FoxD1) expressing stromal cells are the progenitors for juxtaglomerular cells (JG), mesangial cells (MC), pericytes (PC), and vascular smooth muscle cells (VSMC) of the renal arteriole. We generated FoxD1-GC; R26R ^TdTomato mice, in which all FoxD1 ⁺ cells and their descendants are labeled with tdTomato reporter. We applied a surgical model of aortic coarctation (AoCo) between the roots of the left and right renal arteries and sorted tdTomato ⁺ cells from the cortices of the left kidney (LK, low pressure) and the right kidney (RK, high pressure). Then, we performed single-cell RNA-seq to identify candidate TFs activated at low pressure. Candidates were then validated and deleted in the renin cells of mice exposed to hypotensive conditions.

Results: 1) By single-cell RNA-seq, FoxD1 ⁺ cells were clustered into JG, VSMC, MC and PC, and other cell types. Differentially expressed gene (DEG) analysis in LK compared to RK showed that Ren1 was the highest DEG in JG. In VSMC, DEG includes Ren1 and Kruppel-like factor 2 ( Klf2) , which showed the highest Log ₂ fold change (0.36) among the major TFs. 2) We generated Klf2 ^fl/fl ; Ren1 ^dCre ( Klf2 cKO) mice, and found a 55.1% decrease of kidney cortices Ren1 mRNA expression by qPCR (n = 5, P=0.022) and reduced plasma renin levels by ELISA (40.1 ± 9.6 vs 15.1 ± 7.3 ng/mL, n = 12, P<0.001) compared to wild type mice. Klf2 cKO mice treated with captopril-added water (0.5 g/L) and a low Na ⁺ diet for 7 days displayed reduced renin immunostaining in the JG and along the afferent arterioles.

Conclusion: We identified Klf2 as a key TF for Ren1 as a part of the renin cell baroreceptor. Experiments for Klf2 cKO mice with AoCo surgery are ongoing.

DOI： 10.1161/hyp.80.suppl_1.069

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Publishing type：Research paper (international conference proceedings)   Publisher：Ovid Technologies (Wolters Kluwer Health)  

Background: Renin cells are essential for the regulation of blood pressure (BP). In adult mammals, renin cells are present in small numbers in the juxtaglomerular area, but when homeostasis is threatened, such as by hypotension, additional cells along the renal arterioles are recruited to synthesize and release renin. However, there have been no studies to date that have shown changes in the distribution of renin cells in response to changes in BP by three-dimensional (3D) imaging.

Objective: Establish a method to visualize and measure renin cells, and comparison of renin expression differences in kidneys exposed to hypo- or hypertension in 3D.

Methods: We used our new mouse model ( Ren1 ^c-tdTomato ) that expresses renin and the fluorescent tdTomato under the control of the endogenous renin gene environment. To test whether we could detect differences in the distribution of renin in response to changes in BP, we subjected Ren1 ^c-tdTomato mice to aortic coarctation at 3 months of life. The right and left kidneys (RK, LK) are exposed to high and low BPs, respectively. We harvested kidneys after 72 hours and performed tissue-clearing. We used light sheet microscopy for imaging and the Imaris software for 3D reconstruction and data analysis. We defined the 3D renin cell index (3D-RI) as total volume of renin cells (μm ³ ) divided by total number of glomeruli. We extracted 10 cubes of 500 μm square each from the L and R renal cortex, calculated their individual 3D-RI and compared them.

Results: With tissue-clearing-based 3D imaging, renin cells were clearly visualized, allowing observation of their distribution and appearance at a one-cell resolution. In the LK exposed to hypotension, several afferent arterioles were identified where renin cells extended close to their branching point. Further, the average value of the 3D-RI was significantly higher in LK (21460 ±6303) than in RK (12838 ± 4632; p = 0.003).

Conclusion: Using our new Ren1 ^c-tdTomato mouse and 3D imaging technology we detected differences in renin cells appearance and distribution in kidneys exposed to hypo- or hypertension. Combined with spatial single cell multiomics, 3D visualization of renin cells will open new avenues for understanding how vascular cells acquire their positional identity in health and disease.

DOI： 10.1161/hyp.80.suppl_1.026

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Language：English   Publishing type：Research paper (scientific journal)  

INTRODUCTION: Levetiracetam is a newer second-generation anticonvulsant for the treatment of generalized and partial seizure disorders. Common adverse effects are rhabdomyolysis and neuropsychiatric problems, such as somnolence, dizziness, and mood changes. The present report describes the first case, to our knowledge, of levetiracetam overdose resulting in acute kidney injury for which hemodialysis was required. PATIENT CONCERNS: A 51-year-old man presented with hypotension and disturbance of consciousness with subsequent development of oliguria and elevated creatinine. Based on his history of ingesting a large dose of levetiracetam and the course of the disease, he was considered to have been poisoned by levetiracetam. DIAGNOSIS: Acute kidney injury induced by levetiracetam poisoning. INTERVENTIONS/OUTCOMES: Dialysis was performed for the rapidly progressing renal failure. His renal function improved, and he was weaned from dialysis and discharged home on the 19th day. CONCLUSION: We should be aware of the possibility that severe renal function deterioration may occur in some patients with levetiracetam overdose. It is possible that clinicians underestimate the occurrence of this problem. In cases of acute renal failure in levetiracetam poisoning, induction of dialysis is beneficial.

DOI： 10.1097/MD.0000000000030884

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Authorship：Lead author   Publishing type：Doctoral thesis  

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Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1093/ndt/gfaa319

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Language：English   Presentation type：Oral presentation (general)  

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Language：English  

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Venue：東京  

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Venue：東京  

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Venue：静岡  

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Venue：新潟  

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Venue：神奈川  

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Venue：茨城  

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Venue：新潟  

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Language：English  

Venue：Washington DC   Country：United States  

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Venue：愛知  

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Language：English  

Venue：San Diego   Country：United States  

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Venue：東京  

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Language：English   Presentation type：Oral presentation (general)  

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Venue：東京  

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Language：English  

Venue：New Orleans   Country：United States  

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Venue：東京  

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Venue：東京  

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Venue：新潟  

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