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Book: Proteinuria in nephrotic syndrome

Tumlin, James A.

mechanistic and clinical considerations in optimizing management

(American journal of nephrology ; vol. 47, suppl. 1 (2018))

2018

Author's details	guest editors James A. Tumlin, Kirk N. Campbell
Series title	American journal of nephrology ; vol. 47, suppl. 1 (2018)
Collection
Language	English
Size	52 Seiten, Illustrationen
Publisher	Karger
Publishing place	Basel
Publishing country	Switzerland
Document type	Book
HBZ-ID	HT019723503
ISBN	978-3-318-06210-6 ; 9783318062113 ; 3-318-06210-3 ; 3318062111
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

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Article ; Online: Proteinuria in Nephrotic Syndrome: Mechanistic and Clinical Considerations in Optimizing Management.

Tumlin, James A / Campbell, Kirk N

American journal of nephrology

2018 Volume 47 Suppl 1, Page(s) 1–2

MeSH term(s)	Humans ; Nephrotic Syndrome/complications ; Nephrotic Syndrome/therapy ; Proteinuria/etiology ; Proteinuria/therapy
Language	English
Publishing date	2018-05-31
Publishing country	Switzerland
Document type	Introductory Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000481632
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Comparative Levels of Urinary Biomarkers of Renal Injury and Inflammation Among Patients With Diabetic Nephropathy With or Without Hyperuricemia.

Alex, Ryan / Press, Ella / Sanchez, Lorin / Whitson, Jeremy / Marder, Brad / Tumlin, James Alan

Journal of clinical rheumatology : practical reports on rheumatic & musculoskeletal diseases

2024

Abstract: Background: The association between hyperuricemia and development of progressive chronic kidney disease has received increasing attention in recent years. Recent preclinical studies have shown that non-crystalline uric acid can induce renal-specific ... ...

Abstract	Background: The association between hyperuricemia and development of progressive chronic kidney disease has received increasing attention in recent years. Recent preclinical studies have shown that non-crystalline uric acid can induce renal-specific arteriolopathy, leading to renal injury and tubulointerstitial inflammation. Methods: We conducted a open-label cross-sectional study of 25 patients with chronic kidney disease stage III (estimated glomerular filtration rate [eGFR], 7.0 mg/dL) levels of serum uric acid. To determine the correlation between hyperuricemia on urinary protein levels and renal disease progression, we retrospectively compared urine protein and eGFR data between the 2 groups. Results: Eleven patients with normal uric acid levels and 14 with hyperuricemia were enrolled. Urinary levels of both kidney injury molecule-1 (KIM-1) and monocyte chemoattractant protein-1 (MCP-1) were significantly higher in patients with hyperuricemia. Among the normouricemic White and African American (AA) subgroups, there was no difference in KIM-1 or MCP-1 levels, whereas KIM-1 levels were significantly higher among hyperuricemic AA patients with hyperuricemia. Urinary protein was significantly higher between Whites and AA patients with serum uric acid level >7.0 mg/dL as well as patients with urinary KIM-1 levels >1000 pg/mg Cr. A trend toward a more rapid decline in eGFR was noted among hyperuricemic AAs; however, this trend was not statistically significant. Conclusions: Patients with type 2 diabetic nephropathy and persistently elevated serum uric acid levels express higher levels of both KIM-1 and MCP-1 reflective of on-going renal injury and inflammation.
Language	English
Publishing date	2024-02-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	1283266-2
ISSN	1536-7355 ; 1076-1608
ISSN (online)	1536-7355
ISSN	1076-1608
DOI	10.1097/RHU.0000000000002068
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Zs.A 4815: Show issues

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Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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Article ; Online: Protecting Podocytes: A Key Target for Therapy of Focal Segmental Glomerulosclerosis.

Campbell, Kirk N / Tumlin, James A

American journal of nephrology

2018 Volume 47 Suppl 1, Page(s) 14–29

Abstract: Background: Focal segmental glomerulosclerosis (FSGS) is a histologic pattern of injury demonstrated by renal biopsy that can arise from a diverse range of causes and mechanisms. It has an estimated incidence of 7 per 1 million and is the most common ... ...

Abstract	Background: Focal segmental glomerulosclerosis (FSGS) is a histologic pattern of injury demonstrated by renal biopsy that can arise from a diverse range of causes and mechanisms. It has an estimated incidence of 7 per 1 million and is the most common primary glomerular disorder leading to end-stage renal disease in the United States. This review focuses on damage to the podocyte and the consequences of this injury in patients with FSGS, the genetics of FSGS, and approaches to treatment with a focus on the effects on podocytes. Summary: The podocyte is central to the glomerular filtration barrier and is particularly vulnerable because of its highly differentiated post-mitotic phenotype. The progressive structural changes involved in the pathology of FSGS include podocyte foot process effacement, death of podocytes and exposure of the glomerular basement membrane, filtration of nonspecific plasma proteins, expansion of capillaries, misdirected filtration at points of synechiae, and mesangial matrix proliferation. Although damage to and death of podocytes can result from single-gene disorders, evidence also suggests a role for soluble factors, such as soluble urokinase-type plasminogen activator receptor, cardiotrophin-like cytokine-1, and anti-CD40 antibodies, that promote FSGS recurrence post transplant. Several classes of medications, including corticosteroids, calcineurin inhibitors, endothelin receptor antagonists, adrenocorticotropic hormone, and rituximab, have been shown to be effective for the treatment of FSGS and have been demonstrated to have significant protective effects on podocytes. Key Messages: Greater understanding of podocyte biology is essential to the identification of new treatment targets and medications for the management of patients with FSGS.
MeSH term(s)	Glomerulosclerosis, Focal Segmental/drug therapy ; Glomerulosclerosis, Focal Segmental/genetics ; Humans ; Mutation ; Podocytes/drug effects ; Practice Guidelines as Topic
Language	English
Publishing date	2018-05-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604540-6
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000481634
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

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Location:
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Article ; Online: IgA nephropathy: the lectin pathway and implications for targeted therapy.

Barratt, Jonathan / Lafayette, Richard A / Zhang, Hong / Tesar, Vladimir / Rovin, Brad H / Tumlin, James A / Reich, Heather N / Floege, Jürgen

Kidney international

2023 Volume 104, Issue 2, Page(s) 254–264

Abstract: Many patients with immunoglobulin A nephropathy (IgAN) progress to kidney failure even with optimal supportive care. An improved understanding of the pathophysiology of IgAN in recent years has led to the investigation of targeted therapies with ... ...

Abstract	Many patients with immunoglobulin A nephropathy (IgAN) progress to kidney failure even with optimal supportive care. An improved understanding of the pathophysiology of IgAN in recent years has led to the investigation of targeted therapies with acceptable tolerability that may address the underlying causes of IgAN or the pathogenesis of kidney injury. The complement system-particularly the lectin and alternative pathways of complement-has emerged as a key mediator of kidney injury in IgAN and a possible target for investigational therapy. This review will focus on the lectin pathway. The examination of kidney biopsies has consistently shown glomerular deposition of mannan-binding lectin (1 of 6 pattern-recognition molecules that activate the lectin pathway) together with IgA1 in up to 50% of patients with IgAN. Glomerular deposition of pattern-recognition molecules for the lectin pathway is associated with more severe glomerular damage and more severe proteinuria and hematuria. Emerging research suggests that the lectin pathway may also contribute to tubulointerstitial fibrosis in IgAN and that collectin-11 is a key mediator of this association. This review summarizes the growing scientific and clinical evidence supporting the role of the lectin pathway in IgAN and examines the possible therapeutic role of lectin pathway inhibition for these patients.
MeSH term(s)	Humans ; Glomerulonephritis, IGA/pathology ; Lectins/metabolism ; Kidney Glomerulus/pathology ; Kidney/pathology ; Immunoglobulin A/metabolism
Chemical Substances	Lectins ; Immunoglobulin A
Language	English
Publishing date	2023-05-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.04.029
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Zs.A 797: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Arrhythmia and Time of Day in Maintenance Hemodialysis: Secondary Analysis of the Monitoring in Dialysis Study.

Soomro, Qandeel H / Koplan, Bruce A / Costea, Alexandru I / Roy-Chaudhury, Prabir / Tumlin, James A / Kher, Vijay / Williamson, Don E / Pokhariyal, Saurabh / McClure, Candace K / Charytan, David M

Kidney medicine

2024 Volume 6, Issue 4, Page(s) 100799

Abstract: Rationale & objective: The incidence of arrhythmia varies by time of day. How this affects individuals on maintenance dialysis is uncertain. Our objective was to quantify the relationship of arrhythmia with the time of day and timing of dialysis.: ... ...

Abstract	Rationale & objective: The incidence of arrhythmia varies by time of day. How this affects individuals on maintenance dialysis is uncertain. Our objective was to quantify the relationship of arrhythmia with the time of day and timing of dialysis. Study design: Secondary analysis of the Monitoring in Dialysis study, a multicenter prospective cohort study. Settings & participants: Loop recorders were implanted for continuous cardiac monitoring in 66 participants on maintenance dialysis with a follow up of 6 months. Exposure: Time of day based on 6-hour intervals. Outcomes: Event rates of clinically significant arrhythmia. Analytical approach: Negative binomial mixed effects regression models for repeated measures were used to evaluate data from the Monitoring in Dialysis study for differences in diurnal patterns of clinically significant arrhythmia among those with end-stage kidney disease with heart failure and end-stage kidney disease alone. We additionally analyzed rates according to presence of heart failure, time of dialysis shift, and dialysis versus nondialysis day. Results: Rates of clinically significant arrhythmia peaked between 12:00 AM and 5:59 AM and were more than 1.5-fold as frequent during this interval than the rest of the day. In contrast, variations in atrial fibrillation peaked between 6:00 AM and 11:59 AM, but variations across the day were qualitatively small. Clinically significant arrhythmia occurred at numerically higher rate in individuals with end-stage kidney disease and heart failure (5.9 events/mo; 95% CI, 1.3-26.8) than those without heart failure (4.0 events/mo; 95% CI, 0.9-17.9). Although differences in overall rate were not significant, their periodicity was significantly different ( Limitations: Post hoc analysis, unable to account for unmeasured confounders. Conclusion: Clinically significant arrhythmias showed strong diurnal patterns with a maximal peak between 12:00 AM and 5:59 AM and noon. Although overall arrhythmia rates were similar, the peak rate occurred overnight in individuals without heart failure and during the morning in individuals with heart failure. Further exploration of the influence of circadian rhythm on arrhythmia in the setting of hemodialysis is needed.
Language	English
Publishing date	2024-02-20
Publishing country	United States
Document type	Journal Article
ISSN	2590-0595
ISSN (online)	2590-0595
DOI	10.1016/j.xkme.2024.100799
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Randomized Phase II JANUS Study of Atacicept in Patients With IgA Nephropathy and Persistent Proteinuria.

Barratt, Jonathan / Tumlin, James / Suzuki, Yusuke / Kao, Amy / Aydemir, Aida / Pudota, Kishore / Jin, Hulin / Gühring, Hans / Appel, Gerald

Kidney international reports

2022 Volume 7, Issue 8, Page(s) 1831–1841

Abstract: Introduction: Patients with IgA nephropathy (IgAN) and persistent proteinuria are at risk of progression to kidney failure. Atacicept is a novel B-cell-targeted immunomodulator, shown to reduce immunoglobulin levels in patients with autoimmune diseases.! ...

Abstract	Introduction: Patients with IgA nephropathy (IgAN) and persistent proteinuria are at risk of progression to kidney failure. Atacicept is a novel B-cell-targeted immunomodulator, shown to reduce immunoglobulin levels in patients with autoimmune diseases. Methods: JANUS (NCT02808429) was a phase II study that assessed the safety, pharmacodynamic effects, and efficacy of atacicept in patients with IgAN and proteinuria ≥1 g/d or 0.75 mg/mg on 24-hour UPCR despite maximal standard of care therapy. Results: A total of 16 patients were randomized 1:1:1 to placebo ( Conclusion: Atacicept has an acceptable safety profile in patients with IgAN and is effective at reducing the levels of pathogenic factor Gd-IgA1, with potential improvements in proteinuria and renal function.
Language	English
Publishing date	2022-05-26
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2022.05.017
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Proteinuria in Nephrotic Syndrome: Mechanistic and Clinical Considerations in Optimizing Management

Tumlin, James A. / Campbell, Kirk N.

American Journal of Nephrology

2018 Volume 47, Issue Suppl 1, Page(s) 1–2

Institution	Department of Medicine, UT College of Medicine, University of Tennessee, Chattanooga, Tennessee, USA Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA
Language	English
Publishing date	2018-05-31
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Introduction
ZDB-ID	604540-6
ISBN	978-3-318-06210-6 ; 3-318-06210-3
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000481632
Database	Karger publisher's database

In stock of ZB MED Cologne/Königswinter

Zs.A 1635: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article: Protecting Podocytes: A Key Target for Therapy of Focal Segmental Glomerulosclerosis

Campbell, Kirk N. / Tumlin, James A.

American Journal of Nephrology

2018 Volume 47, Issue Suppl 1, Page(s) 14–29

Institution	Division of Nephrology, Icahn School of Medicine at Mount Sinai, New York, New York, USA Department of Medicine, UT College of Medicine, University of Tennessee, Chattanooga, Tennessee, USA
Abstract	Background: Focal segmental glomerulosclerosis (FSGS) is a histologic pattern of injury demonstrated by renal biopsy that can arise from a diverse range of causes and mechanisms. It has an estimated incidence of 7 per 1 million and is the most common primary glomerular disorder leading to end-stage renal disease in the United States. This review focuses on damage to the podocyte and the consequences of this injury in patients with FSGS, the genetics of FSGS, and approaches to treatment with a focus on the effects on podocytes. Summary: The podocyte is central to the glomerular filtration barrier and is particularly vulnerable because of its highly differentiated post-mitotic phenotype. The progressive structural changes involved in the pathology of FSGS include podocyte foot process effacement, death of podocytes and exposure of the glomerular basement membrane, filtration of nonspecific plasma proteins, expansion of capillaries, misdirected filtration at points of synechiae, and mesangial matrix proliferation. Although damage to and death of podocytes can result from single-gene disorders, evidence also suggests a role for soluble factors, such as soluble urokinase-type plasminogen activator receptor, cardiotrophin-like cytokine-1, and anti-CD40 antibodies, that promote FSGS recurrence post transplant. Several classes of medications, including corticosteroids, calcineurin inhibitors, endothelin receptor antagonists, adrenocorticotropic hormone, and rituximab, have been shown to be effective for the treatment of FSGS and have been demonstrated to have significant protective effects on podocytes. Key Messages: Greater understanding of podocyte biology is essential to the identification of new treatment targets and medications for the management of patients with FSGS.
Keywords	Adrenocorticotropic hormone ; Calcineurin ; Corticosteroid ; Podocyte ; Proteinuria ; Renal ; Sclerosis
Language	English
Publishing date	2018-05-31
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Review Article
ZDB-ID	604540-6
ISBN	978-3-318-06210-6 ; 3-318-06210-3
ISSN	1421-9670 ; 0250-8095
ISSN (online)	1421-9670
ISSN	0250-8095
DOI	10.1159/000481634
Database	Karger publisher's database

In stock of ZB MED Cologne/Königswinter

Zs.A 1635: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Impaired blood flow in acute kidney injury: pathophysiology and potential efficacy of intrarenal vasodilator therapy.

Tumlin, James A

Current opinion in critical care

2009 Volume 15, Issue 6, Page(s) 514–519

Abstract: Purpose of review: Acute kidney injury (AKI) is a common complication of hospitalized patients and associated with significant morbidity and mortality. Numerous studies have documented that acute reductions in glomerular filtration rates are associated ... ...

Abstract	Purpose of review: Acute kidney injury (AKI) is a common complication of hospitalized patients and associated with significant morbidity and mortality. Numerous studies have documented that acute reductions in glomerular filtration rates are associated with significant in-hospital mortality. Moreover, patients progressing to dialysis-dependent AKI can have mortality rates that exceed 60%. The pathophysiology of AKI is unknown, but marked reductions in corticomedullary blood flow leads to significant reductions in glomerular filtration rate during early phases of the disease. The recognition that hypoperfusion of the outer medulla is common to many forms of AKI and contributes to tubular ischemia has led many investigators to re-examine the use of vasodilators to restore blood flow and stabilize renal function. Recent findings: Numerous prospective trials have studied the efficacy of various vasoactive compounds with primarily negative results. However, trial designs that failed to fully examine the dose response of many investigational agents contributed to the development of systemic hypotension, thus offsetting potential benefits of the treatment. Emerging devices that allow for intrarenal administration of drugs have led to the concept of 'targeted renal' prophylaxis and treatment. The rationale is that local renal administration can improve the safety profile of many vasoactive agents. Recent studies confirm that higher doses of fenoldopam or other vasodilators can be administered intrarenally without the development of systemic hypotension. Summary: Previous trials utilizing vasodilator therapy to stabilize renal function in AKI have given conflicting results. This study will critically review trial design and dose selection used in previous studies of vasodilator therapy in AKI. Lastly, the potential for high-dose therapy using intrarenal drug delivery systems will be discussed.
MeSH term(s)	Acute Kidney Injury/blood ; Acute Kidney Injury/physiopathology ; Catheterization ; Fenoldopam/administration & dosage ; Fenoldopam/pharmacology ; Fenoldopam/therapeutic use ; Humans ; Renal Circulation/drug effects ; Vasodilator Agents/administration & dosage ; Vasodilator Agents/pharmacology ; Vasodilator Agents/therapeutic use
Chemical Substances	Vasodilator Agents ; Fenoldopam (INU8H2KAWG)
Language	English
Publishing date	2009-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1235629-3
ISSN	1531-7072 ; 1070-5295
ISSN (online)	1531-7072
ISSN	1070-5295
DOI	10.1097/MCC.0b013e328332f6f9
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