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Article ; Online: Quality of life in pediatric chronic kidney disease: expectations and responsibilities.

Wesseling-Perry, Katherine

2023 Volume 38, Issue 12, Page(s) 3867–3869

MeSH term(s)	Humans ; Child ; Quality of Life ; Motivation ; Renal Insufficiency, Chronic/therapy ; Social Behavior
Language	English
Publishing date	2023-07-06
Publishing country	Germany
Document type	Editorial ; Comment
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-023-06070-1
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Article ; Online: Recurrent disease after pediatric renal transplantation.

Nayak, Anjali / Ettenger, Robert / Wesseling-Perry, Katherine

Pediatric transplantation

2024 Volume 28, Issue 3, Page(s) e14676

Abstract: Background: Recurrent disease after kidney transplant remains an important cause of allograft failure, accounting for 7-8% of graft loss and ranking as the fifth most common cause of allograft loss in the pediatric population. Although the ... ...

Abstract	Background: Recurrent disease after kidney transplant remains an important cause of allograft failure, accounting for 7-8% of graft loss and ranking as the fifth most common cause of allograft loss in the pediatric population. Although the pathophysiology of many recurrent diseases is incompletely understood, recent advances in basic science and therapeutics are improving outcomes and changing the course of several of these conditions. Methods: Review of the literature. Results: We discuss the diagnosis and management of recurrent disease. Conclusion: We highlight new insights into the pathophysiology and treatment of post-transplant primary hyperoxaluria, focal segmental glomerulosclerosis, immune complex glomerulonephritis, C3 glomerulopathy, lupus nephritis, atypical hemolytic uremic syndrome, and IgA nephropathy.
MeSH term(s)	Humans ; Kidney Transplantation/adverse effects ; Recurrence ; Child ; Postoperative Complications/etiology ; Postoperative Complications/diagnosis ; Kidney Diseases/etiology ; Kidney Diseases/surgery
Language	English
Publishing date	2024-04-22
Publishing country	Denmark
Document type	Journal Article ; Review
ZDB-ID	1390284-2
ISSN	1399-3046 ; 1397-3142
ISSN (online)	1399-3046
ISSN	1397-3142
DOI	10.1111/petr.14676
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Zs.A 4947: Show issues

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Article ; Online: Chromatin accessibility and epigenetic deoxyribose nucleic acid (DNA) modifications in chronic kidney disease (CKD) osteoblasts: a study of bone and osteoblasts from pediatric patients with CKD.

Martin, Aline / Kawaguchi, Riki / Wang, Qing / Salusky, Isidro B / Pereira, Renata C / Wesseling-Perry, Katherine

JBMR plus

2024 Volume 8, Issue 1, Page(s) ziad015

Abstract: Maturation defects are intrinsic features of osteoblast lineage cells in CKD patients. These defects persist ex vivo, suggesting that CKD induces epigenetic changes in bone cells. To gain insights into which signaling pathways contribute to CKD-mediated, ...

Abstract	Maturation defects are intrinsic features of osteoblast lineage cells in CKD patients. These defects persist ex vivo, suggesting that CKD induces epigenetic changes in bone cells. To gain insights into which signaling pathways contribute to CKD-mediated, epigenetically driven, impairments in osteoblast maturation, we characterized RNA expression and DNA methylation patterns by RNA-Seq and MethylationEpic in primary osteoblasts from nine adolescent and young adult dialysis patients with end-stage kidney disease and three healthy references. ATAC-Seq was also performed on a subset of osteoblasts. Bone matrix protein expression was extracted from the iliac crest and evaluated by proteomics. Gene set enrichment analysis was used to establish signaling pathways consistently altered in chromatin accessibility, DNA methylation, and RNA expression patterns. Single genes were suppressed in primary osteoblasts using shRNA and mineralization characterized in vitro. The effect of nuclear factor of activated T cells (NFAT) signaling suppression was also assessed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) incorporation. We found that signaling pathways critical for osteoblast differentiation were strongly downregulated in CKD osteoblasts. Gene set enrichment analysis identified highly significant methylation changes, differential chromatin accessibility, and altered RNA expression in NFAT signaling targets. NFAT inhibition reduced osteoblast proliferation. Combined analysis of osteoblast RNA expression and whole bone matrix composition identified 13 potential ligand-receptor pairs. In summary, epigenetic changes in CKD osteoblasts associate with altered expression of multiple osteoblast genes and signaling pathways. An increase in NFAT signaling may play a role in impaired CKD osteoblast maturation. Epigenetic changes also associate with an altered bone matrix, which may contribute to bone fragility. Further studies are necessary to elucidate the pathways affected by these genetic alterations since elucidating these pathways will be vital to correcting the underlying biology of bone disease in the CKD population.
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article
ISSN	2473-4039
ISSN (online)	2473-4039
DOI	10.1093/jbmrpl/ziad015
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Article ; Online: Comparison of estimated GFR using cystatin C versus creatinine in pediatric kidney transplant recipients.

Pizzo, Helen / Nguyen, John / Schwartz, George J / Wesseling-Perry, Katherine / Ettenger, Robert / Chambers, Eileen Tsai / Weng, Patricia

Pediatric nephrology (Berlin, Germany)

2024

Abstract: Background: An accurate, rapid estimate of glomerular filtration rate (GFR) in kidney transplant patients affords early detection of transplant deterioration and timely intervention. This study compared the performance of serum creatinine (Cr) and ... ...

Abstract	Background: An accurate, rapid estimate of glomerular filtration rate (GFR) in kidney transplant patients affords early detection of transplant deterioration and timely intervention. This study compared the performance of serum creatinine (Cr) and cystatin C (CysC)-based GFR equations to measured GFR (mGFR) using iohexol among pediatric kidney transplant recipients. Methods: CysC, Cr, and mGFR were obtained from 45 kidney transplant patients, 1-18 years old. Cr- and CysC-estimated GFR (eGFR) was compared against mGFR using the Cr-based (Bedside Schwartz, U25-Cr), CysC-based (Gentian CysC, CAPA, U25-CysC), and Cr-CysC combination (CKiD Cr-CysC, U25 Cr-CysC) equations in terms of bias, precision, and accuracy. Bland-Altman plots assessed the agreement between eGFR and mGFR. Secondary analyses evaluated the formulas in patients with biopsy-proven histological changes, and K/DOQI CKD staging. Results: Bias was small with Gentian CysC (0.1 ml/min/1.73 m Conclusions: In this small cohort, CysC-based equations with or without Cr may have better bias, precision, and accuracy in predicting GFR.
Language	English
Publishing date	2024-03-01
Publishing country	Germany
Document type	Journal Article
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-024-06316-6
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Article ; Online: Osteocyte dysfunction and renal osteodystrophy: not just calcium and phosphorus anymore.

Wesseling-Perry, Katherine

Kidney international

2017 Volume 91, Issue 6, Page(s) 1276–1278

Abstract: In an important new cross-sectional analysis in this issue, Graciolli and colleagues present bone data from 148 adult patients across the spectrum of chronic kidney disease that confirm that disrupted osteocyte function and abnormal bone histology ... ...

Abstract	In an important new cross-sectional analysis in this issue, Graciolli and colleagues present bone data from 148 adult patients across the spectrum of chronic kidney disease that confirm that disrupted osteocyte function and abnormal bone histology characterize all stages of chronic kidney disease and suggest that osteocytic Wnt signaling and osteocyte maturation may play a role in the pathogenesis of renal osteodystrophy. These concepts may alter how the skeletal, cardiovascular, and infectious complications of chronic kidney disease are managed.
Language	English
Publishing date	2017-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2017.02.026
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Zs.A 797: Show issues

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Article ; Online: Gut microbiome, parathyroid hormone, and bone.

Kermgard, Elizabeth / Chawla, Nadine Khouzam / Wesseling-Perry, Katherine

Current opinion in nephrology and hypertension

2021 Volume 30, Issue 4, Page(s) 418–423

Abstract: Purpose of review: Microorganisms in the gut (the 'microbiome') and the metabolites they produce (the 'metabolome') regulate bone mass through interactions between parathyroid hormone (PTH), the immune system, and bone. This review summarizes these data ...

Abstract	Purpose of review: Microorganisms in the gut (the 'microbiome') and the metabolites they produce (the 'metabolome') regulate bone mass through interactions between parathyroid hormone (PTH), the immune system, and bone. This review summarizes these data and details how this physiology may relate to CKD-mediated bone disease. Recent findings: The actions of PTH on bone require microbial metabolite activation of immune cells. Butyrate is necessary for CD4+ T-cell differentiation, T-reg cell expansion and CD8+ T-cell secretion of the bone-forming factor Wnt10b ligand. By contrast, mice colonized with segmented filamentous bacteria exhibit an expansion of gut Th17 cells and continuous PTH infusion increases the migration of Th17 cells to the bone marrow, contributing to bone resorption. In the context of CKD, a modified diet, frequent antibiotic therapy, altered intestinal mobility, and exposure to multiple medications together contribute to dysbiosis; the implications for an altered microbiome and metabolome on the pathogenesis of renal osteodystrophy and its treatment have not been explored. Summary: As dysregulated interactions between PTH and bone ('skeletal resistance') characterize CKD, the time is ripe for detailed, mechanistic studies into the role that gut metabolites may play in the pathogenesis of CKD-mediated bone disease.
MeSH term(s)	Animals ; Bone and Bones ; Chronic Kidney Disease-Mineral and Bone Disorder ; Dysbiosis ; Gastrointestinal Microbiome ; Humans ; Mice ; Parathyroid Hormone
Chemical Substances	Parathyroid Hormone
Language	English
Publishing date	2021-05-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1151092-4
ISSN	1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
ISSN (online)	1473-6543 ; 1535-3842
ISSN	1062-4813 ; 1062-4821
DOI	10.1097/MNH.0000000000000714
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Article ; Online: The Authors Reply.

Wesseling-Perry, Katherine

Kidney international

2015 Volume 88, Issue 3, Page(s) 640–641

MeSH term(s)	Bone and Bones/physiopathology ; Calcification, Physiologic ; Cell Proliferation ; Female ; Gene Expression ; Humans ; Kidney Failure, Chronic ; Male ; Osteoblasts/physiology
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2015.219
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Article ; Online: Racial-ethnic diversity in ambulatory blood pressure monitoring in children with chronic kidney disease.

Pagi, Reut / Yadin, Ora / Wesseling-Perry, Katherine / Norris, Keith / Laster, Marciana Lee

Pediatric nephrology (Berlin, Germany)

2022 Volume 38, Issue 3, Page(s) 819–827

Abstract: Background: Black adults with chronic kidney disease (CKD) have higher rates of hypertension as compared to White adults with CKD. Little is known of how race and ethnicity associate with the prevalence of hypertension in pediatric CKD patients. The aim ...

Abstract	Background: Black adults with chronic kidney disease (CKD) have higher rates of hypertension as compared to White adults with CKD. Little is known of how race and ethnicity associate with the prevalence of hypertension in pediatric CKD patients. The aim was to compare ambulatory blood pressure monitoring (ABPM) results for patients with CKD enrolled in the Chronic Kidney Disease in Children (CKiD) study across racial-ethnic groups. Methods: Patients from the CKiD study who identified as non-Hispanic White, non-Hispanic Black, or Hispanic were included to analyze differences in ABPM results across these racial-ethnic groups. The outcomes were fitted using 3 progressively adjusted models. Results: This study included 501 CKiD participants with at least one successful ABPM study. Compared to White participants, Black participants had 4.2 mmHg higher mean sleep systolic blood pressure and 2.7 mmHg higher mean sleep diastolic blood pressure (p = 0.001 and p = 0.004, respectively). Additionally, Black participants had higher odds of abnormal wake systolic load (OR 1.88, 1.21-2.91, p = 0.005), wake diastolic load (OR 1.68, 1.03-2.73, p = 0.04), sleep systolic load (OR 2.19, 1.36-3.5, p = 0.001), sleep diastolic load (OR 2.01, 1.28-3.15, p = 0.002), systolic non-dipping (OR 2.02, 1.31-3.10, p = 0.001), and diastolic non-dipping (OR 2.69, 1.60-4.51, p < 0.001). Compared to White participants, Hispanic participants demonstrated only a lower sleep diastolic load (OR 0.54, 0.31-0.95, p = 0.03). Conclusions: Black children with CKD have higher absolute nocturnal blood pressures and higher rates of abnormal dipping. Further studies are needed to determine the etiology of these differences and the clinical implications of racial-ethnic differences in ABPM outcomes within the pediatric CKD population. A higher resolution version of the Graphical abstract is available as Supplementary information.
MeSH term(s)	Adult ; Humans ; Child ; Blood Pressure Monitoring, Ambulatory/methods ; Circadian Rhythm ; Hypertension/diagnosis ; Blood Pressure ; Renal Insufficiency, Chronic/diagnosis
Language	English
Publishing date	2022-07-08
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-022-05659-2
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Article ; Online: Defective skeletal mineralization in pediatric CKD.

Wesseling-Perry, Katherine

Current osteoporosis reports

2015 Volume 13, Issue 2, Page(s) 98–105

Abstract: Although traditional diagnosis and treatment of renal osteodystrophy focused on changes in bone turnover, current data demonstrate that abnormalities in skeletal mineralization are also prevalent in pediatric chronic kidney disease (CKD) and likely ... ...

Abstract	Although traditional diagnosis and treatment of renal osteodystrophy focused on changes in bone turnover, current data demonstrate that abnormalities in skeletal mineralization are also prevalent in pediatric chronic kidney disease (CKD) and likely contribute to skeletal morbidities that continue to plague this population. It is now clear that alterations in osteocyte biology, manifested by changes in osteocytic protein expression, occur in early CKD before abnormalities in traditional measures of mineral metabolism are apparent and may contribute to defective skeletal mineralization. Current treatment paradigms advocate the use of 1,25(OH)2vitamin D for the control of secondary hyperparathyroidism; however, these agents fail to correct defective skeletal mineralization and may exacerbate already altered osteocyte biology. Further studies are critically needed to identify the initial trigger for abnormalities of skeletal mineralization as well as the potential effects that current therapeutic options may have on osteocyte biology and bone mineralization.
MeSH term(s)	Adolescent ; Bone and Bones/drug effects ; Bone and Bones/metabolism ; Bone and Bones/pathology ; Calcification, Physiologic/drug effects ; Calcification, Physiologic/physiology ; Calcimimetic Agents/pharmacology ; Calcimimetic Agents/therapeutic use ; Child ; Growth Hormone/pharmacology ; Growth Hormone/therapeutic use ; Humans ; Osteocytes/metabolism ; Osteocytes/pathology ; Osteogenesis/drug effects ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/physiopathology ; Rickets/drug therapy ; Rickets/etiology ; Rickets/physiopathology ; Sevelamer/pharmacology ; Sevelamer/therapeutic use ; Vitamin D/analogs & derivatives ; Vitamin D/pharmacology ; Vitamin D/therapeutic use
Chemical Substances	Calcimimetic Agents ; Vitamin D (1406-16-2) ; 1,25-dihydroxyvitamin D (66772-14-3) ; Growth Hormone (9002-72-6) ; Sevelamer (9YCX42I8IU)
Language	English
Publishing date	2015-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-015-0253-4
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Article ; Online: Pathophysiology and treatment of cardiovascular disease in pediatric chronic kidney disease.

Khouzam, Nadine / Wesseling-Perry, Katherine

Pediatric nephrology (Berlin, Germany)

2017 Volume 34, Issue 1, Page(s) 1–10

Abstract: Life expectancy in patients with all stages of chronic kidney disease (CKD) falls far short of that in the general population. Cardiovascular disease is the leading cause of mortality in pediatric patients with CKD. In contrast to the intimal ... ...

Abstract	Life expectancy in patients with all stages of chronic kidney disease (CKD) falls far short of that in the general population. Cardiovascular disease is the leading cause of mortality in pediatric patients with CKD. In contrast to the intimal atherosclerotic lesions that characterize cardiovascular disease in the general population, vascular endothelial dysfunction, medial arterial calcification, and cardiac dysfunction contribute to cardiovascular pathological conditions in CKD. The pathogenesis of these lesions, the origins of which can be identified in the absence of traditional cardiovascular risk factors, is incompletely understood. CKD-mediated vascular calcification in CKD is characterized by a transition of vascular smooth muscle cells to an osteoblast-like phenotype and altered bone and mineral metabolism are strongly linked to progressive cardiovascular disease in this population. Renal osteodystrophy therapies, including phosphate binders, vitamin D analogs, and calcimimetics, have an impact on the progression of cardiovascular disease. However, cardiovascular disease has its origins before the development of secondary hyperparathyroidism, and optimal therapeutic regimens that minimize cardiac dysfunction, vascular calcification, and early mortality remain to be defined.
MeSH term(s)	Age Factors ; Arteries/pathology ; Bone and Bones/metabolism ; Calcimimetic Agents/therapeutic use ; Cardiovascular Agents/therapeutic use ; Cardiovascular Diseases/drug therapy ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/pathology ; Chelating Agents/therapeutic use ; Child ; Chronic Kidney Disease-Mineral and Bone Disorder/drug therapy ; Chronic Kidney Disease-Mineral and Bone Disorder/etiology ; Chronic Kidney Disease-Mineral and Bone Disorder/pathology ; Disease Progression ; Endothelium, Vascular/pathology ; Humans ; Kidney Transplantation ; Minerals/metabolism ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/therapy ; Tunica Media/pathology ; Vascular Calcification/drug therapy ; Vascular Calcification/etiology ; Vascular Calcification/pathology ; Vitamin D/therapeutic use
Chemical Substances	Calcimimetic Agents ; Cardiovascular Agents ; Chelating Agents ; Minerals ; Vitamin D (1406-16-2)
Language	English
Publishing date	2017-09-22
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-017-3798-x
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