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Book ; Online ; E-Book: Biomarkers of kidney disease

Edelstein, Charles L.

2017

Author's details	edited by Charles L. Edelstein, MD, PhD
Keywords	Kidney Diseases / diagnosis ; Biomarkers
Language	English
Size	1 Online-Ressource (xvii, 613 Seiten), Illustrationen
Edition	Second edition
Publisher	Elsevier AP
Publishing place	Amsterdam
Publishing country	Netherlands
Document type	Book ; Online ; E-Book
Remark	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019476712
ISBN	978-0-12-803035-6 ; 9780128030141 ; 0-12-803035-6 ; 0128030143
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Book: Biomarkers in kidney disease

Edelstein, Charles L.

2011

Title variant	Kidney disease
Author's details	ed. by Charles L. Edelstein
Language	English
Size	XVI, 437 S. : Ill., graph. Darst., 23 cm
Edition	1. ed.
Publisher	Elsevier Acad. Press
Publishing place	Amsterdam u.a.
Publishing country	Netherlands
Document type	Book
HBZ-ID	HT016580005
ISBN	978-0-12-375672-5 ; 0-12-375672-3
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: The Pathophysiology of Left Ventricular Hypertrophy, beyond Hypertension, in Autosomal Dominant Polycystic Kidney Disease.

Oto, Ozgur A / Edelstein, Charles L

Nephron

2022 Volume 148, Issue 4, Page(s) 215–223

Abstract: Heart disease is one of the leading causes of death in autosomal dominant polycystic kidney disease (ADPKD) patients. Left ventricular hypertrophy (LVH) is an early and severe complication in ADPKD patients. Two decades ago, the prevalence of LVH on ... ...

Abstract	Heart disease is one of the leading causes of death in autosomal dominant polycystic kidney disease (ADPKD) patients. Left ventricular hypertrophy (LVH) is an early and severe complication in ADPKD patients. Two decades ago, the prevalence of LVH on echocardiography in hypertensive ADPKD patients was shown to be as high as 46%. Recent studies using cardiac magnetic resonance imaging have shown that the prevalence of LVH in ADPKD patients may be lower. The true prevalence of LVH in ADPKD patients is controversial. There is evidence that factors other than hypertension contribute to LVH in ADPKD patients. Studies have shown that young normotensive ADPKD adults and children have a higher left ventricular mass index compared to controls and that the prevalence of LVH is high in patients with ADPKD whose blood pressure is well controlled. Polycystin-1 (PC-1) and polycystin-2 (PC-2) control intracellular signaling pathways that can influence cardiac function. Perturbations of PC-1 or PC-2 in the heart can lead to profound changes in cardiac structure and function independently of kidney function or blood pressure. PC-1 can influence mammalian target of rapamycin and mitophagy and PC-2 can influence autophagy, processes that play a role in LVH. Polymorphisms in the angiotensin-converting enzyme gene may play a role in LVH in ADPKD. This review will detail the pathophysiology of LVH, beyond hypertension, in ADPKD.
MeSH term(s)	Adult ; Child ; Humans ; Polycystic Kidney, Autosomal Dominant/pathology ; TRPP Cation Channels/genetics ; Hypertrophy, Left Ventricular/complications ; Hypertension/complications ; Hypertension/epidemiology ; Blood Pressure/physiology
Chemical Substances	TRPP Cation Channels
Language	English
Publishing date	2022-07-27
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, U.S. Gov't, P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	207121-6
ISSN	2235-3186 ; 1423-0186 ; 1660-8151 ; 0028-2766
ISSN (online)	2235-3186 ; 1423-0186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000525944
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Article ; Online: Overview of Antibiotic-Induced Nephrotoxicity.

Campbell, Ruth E / Chen, Chang Huei / Edelstein, Charles L

Kidney international reports

2023 Volume 8, Issue 11, Page(s) 2211–2225

Abstract: Drug-induced nephrotoxicity accounts for up to 60% of cases of acute kidney injury (AKI) in hospitalized patients and is associated with increased morbidity and mortality in both adults and children. Antibiotics are one of the most common causes of drug- ... ...

Abstract	Drug-induced nephrotoxicity accounts for up to 60% of cases of acute kidney injury (AKI) in hospitalized patients and is associated with increased morbidity and mortality in both adults and children. Antibiotics are one of the most common causes of drug-induced nephrotoxicity. Mechanisms of antibiotic-induced nephrotoxicity include glomerular injury, tubular injury or dysfunction, distal tubular obstruction from casts, and acute interstitial nephritis (AIN) mediated by a type IV (delayed-type) hypersensitivity response. Clinical manifestations of antibiotic-induced nephrotoxicity include acute tubular necrosis (ATN), AIN, and Fanconi syndrome. Given the potential nephrotoxic effects of antibiotics on critically ill patients, the use of novel biomarkers can provide information to optimize dosing and duration of treatment and can help prevent nephrotoxicity when traditional markers, such as creatinine, are unreliable. Use of novel kidney specific biomarkers, such as cystatin C and urinary kidney injury molecule-1 (KIM-1), may result in earlier detection of AKI, dose adjustment, or discontinuation of antibiotic and development of nonnephrotoxic antibiotics.
Language	English
Publishing date	2023-08-25
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2023.08.031
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Biomarkers of kidney disease

Edelstein, Charles L

2017

Author's details	edited by Charles L. Edelstein
MeSH term(s)	Kidney Diseases/diagnosis ; Biomarkers
Language	English
Size	xvii, 613 pages :, illustrations
Edition	Second edition.
Document type	Book
Note	Preceded by Biomarkers in kidney disease / edited by Charles L. Edelstein. 2011.
ISBN	9780128030141 ; 0128030143
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Apoptosis and autophagy in polycystic kidney disease (PKD).

Nowak, Kristen L / Edelstein, Charles L

Cellular signalling

2019 Volume 68, Page(s) 109518

Abstract: Apoptosis in the cystic epithelium is observed in most rodent models of polycystic kidney disease (PKD) and in human autosomal dominant PKD (ADPKD). Apoptosis inhibition decreases cyst growth, whereas induction of apoptosis in the kidney of Bcl-2 ... ...

Abstract	Apoptosis in the cystic epithelium is observed in most rodent models of polycystic kidney disease (PKD) and in human autosomal dominant PKD (ADPKD). Apoptosis inhibition decreases cyst growth, whereas induction of apoptosis in the kidney of Bcl-2 deficient mice increases proliferation of the tubular epithelium and subsequent cyst formation. However, alternative evidence indicates that both induction of apoptosis as well as increased overall rates of apoptosis are associated with decreased cyst growth. Autophagic flux is suppressed in cell, zebra fish and mouse models of PKD and suppressed autophagy is known to be associated with increased apoptosis. There may be a link between apoptosis and autophagy in PKD. The mammalian target of rapamycin (mTOR), B-cell lymphoma 2 (Bcl-2) and caspase pathways that are known to be dysregulated in PKD, are also known to regulate both autophagy and apoptosis. Induction of autophagy in cell and zebrafish models of PKD results in suppression of apoptosis and reduced cyst growth supporting the hypothesis autophagy induction may have a therapeutic role in decreasing cyst growth, perhaps by decreasing apoptosis and proliferation in PKD. Future research is needed to evaluate the effects of direct autophagy inducers on apoptosis in rodent PKD models, as well as the cause and effect relationship between autophagy, apoptosis and cyst growth in PKD.
MeSH term(s)	Animals ; Apoptosis ; Autophagy ; Caspase Inhibitors/pharmacology ; Caspases/metabolism ; Humans ; Polycystic Kidney Diseases/pathology ; Polycystic Kidney Diseases/therapy ; Signal Transduction
Chemical Substances	Caspase Inhibitors ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2019-12-24
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2019.109518
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Article ; Online: Raising serum uric acid with a uricase inhibitor worsens PKD in rat and mouse models.

Chaudhary, Anjana / He, Zhibin / Atwood, Daniel J / Miyazaki, Makoto / Oto, Ozgur A / Davidoff, Allen / Edelstein, Charles L

American journal of physiology. Renal physiology

2024

Abstract: Humans are predisposed to gout because they lack uricase that converts uric acid to allantoin. Rodents have uricase, resulting in low basal serum uric acid. A uricase inhibitor raises serum uric acid in rodents. There were 2 aims of the study in ... ...

Abstract	Humans are predisposed to gout because they lack uricase that converts uric acid to allantoin. Rodents have uricase, resulting in low basal serum uric acid. A uricase inhibitor raises serum uric acid in rodents. There were 2 aims of the study in polycystic kidney disease (PKD): 1) to determine whether increasing serum uric acid with the uricase inhibitor, oxonic acid, resulted in faster cyst growth and 2) to determine whether treatment with the xanthine oxidase inhibitor, oxypurinol, reduced the cyst growth caused by oxonic acid. Orthologous models of human PKD were used: PCK rats, a polycystic kidney and hepatic disease 1 (Pkhd1) gene model of autosomal recessive PKD (ARPKD) and
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00372.2023
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Article ; Online: Autophagy inhibition by chloroquine and hydroxychloroquine could adversely affect acute kidney injury and other organ injury in critically ill patients with COVID-19.

Edelstein, Charles L / Venkatachalam, Manjeri A / Dong, Zheng

Kidney international

2020 Volume 98, Issue 1, Page(s) 234–235

MeSH term(s)	Acute Kidney Injury ; Autophagy ; Betacoronavirus ; COVID-19 ; Chloroquine ; Coronavirus Infections ; Critical Illness ; Humans ; Hydroxychloroquine ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2
Chemical Substances	Hydroxychloroquine (4QWG6N8QKH) ; Chloroquine (886U3H6UFF)
Keywords	covid19
Language	English
Publishing date	2020-05-08
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2020.05.001
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Article ; Online: A case report of pre-eclampsia-like endothelial injury in the kidney of an 85-year-old man treated with ibrutinib.

Li, Amy / Ambruso, Sophia L / Oto, Ozgur Akin / Barry, Marc / Edelstein, Charles L

BMC nephrology

2022 Volume 23, Issue 1, Page(s) 264

Abstract: Background: Glomerular endotheliosis is the pathognomonic glomerular lesion in pre-eclampsia that has also been described in those taking tyrosine kinase inhibitors for cancer treatment. Ibrutinib is a Bruton's tyrosine kinase inhibitor used to treat ... ...

Abstract	Background: Glomerular endotheliosis is the pathognomonic glomerular lesion in pre-eclampsia that has also been described in those taking tyrosine kinase inhibitors for cancer treatment. Ibrutinib is a Bruton's tyrosine kinase inhibitor used to treat chronic lymphocytic leukemia (CLL). We report the first known case of glomerular endotheliosis on kidney biopsy in a patient on ibrutinib monotherapy. Case presentation: The patient presented with acute on chronic kidney disease, proteinuria, low C3 and C4 and a high rheumatoid factor titer. A kidney biopsy was performed to confirm a preliminary diagnosis of membranoproliferative glomerulonephritis (MPGN), the most common glomerular disease in patients with CLL. Unexpectedly, the kidney biopsy showed pre-eclampsia-like lesions on light and electron microscopy: occlusion of glomerular peripheral capillary lumens by swollen reactive endothelial cells. Findings of glomerulonephritis were not seen, and there were no specific glomerular immune deposits by immunofluorescence or electron microscopy. Conclusions: CLL is known to cause glomerular lesions, mainly MPGN. There is increasing evidence that ibrutinib, a major treatment for CLL, can cause kidney disease, but the precise pathology is not characterized. We present a patient with CLL on ibrutinib with signs of glomerular endotheliosis. Based on the absence of CLL-induced kidney pathologies typically seen on the kidney biopsy and the non-selectivity of ibrutinib, we attributed the glomerular endotheliosis to ibrutinib. In pre-eclampsia, increased soluble fms-like tyrosine kinase 1 (sFlt1) levels induce endothelial dysfunction by decreasing vascular endothelial growth factor (VEGF). Ibrutinib has been demonstrated to have non-selective tyrosine kinase inhibition, including inhibition of VEGF receptor (VEGFR) and epidermal growth factor receptor (EGFR). VEGFR and EGFR inhibitors have recently been described in the literature to cause hypertension, proteinuria, and glomerular endotheliosis. Kidney biopsy should be performed in CLL patients on ibrutinib that present with acute kidney injury (AKI) or proteinuria to determine whether the clinical picture is attributable to the disease itself or a complication of the therapy.
MeSH term(s)	Adenine/adverse effects ; Adenine/analogs & derivatives ; Aged, 80 and over ; Endothelial Cells ; ErbB Receptors ; Glomerulonephritis, Membranoproliferative/chemically induced ; Glomerulonephritis, Membranoproliferative/diagnosis ; Humans ; Hypertension ; Kidney/pathology ; Kidney Diseases/chemically induced ; Kidney Diseases/diagnosis ; Leukemia, Lymphocytic, Chronic, B-Cell/complications ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Male ; Piperidines/adverse effects ; Proteinuria/complications ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1
Chemical Substances	Piperidines ; Vascular Endothelial Growth Factor A ; ibrutinib (1X70OSD4VX) ; ErbB Receptors (EC 2.7.10.1) ; FLT1 protein, human (EC 2.7.10.1) ; Vascular Endothelial Growth Factor Receptor-1 (EC 2.7.10.1) ; Adenine (JAC85A2161)
Language	English
Publishing date	2022-07-23
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	2041348-8
ISSN	1471-2369 ; 1471-2369
ISSN (online)	1471-2369
ISSN	1471-2369
DOI	10.1186/s12882-022-02873-w
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Article ; Online: Metformin does not slow cyst growth in the PCK rat model of polycystic kidney disease.

Oto, Ozgur A / Atwood, Daniel J / Chaudhary, Anjana / He, Zhibin / Li, Amy S / Wempe, Michael F / Edelstein, Charles L

Physiological reports

2023 Volume 11, Issue 17, Page(s) e15776

Abstract: Metformin (MET) has the potential to activate p-AMPK and block mTORC1-induced proliferation of tubular cells in PKD kidneys. The aim of this study was to determine the effects of MET on cyst growth, kidney function, AMPK and mTOR signaling, and lactate ... ...

Abstract	Metformin (MET) has the potential to activate p-AMPK and block mTORC1-induced proliferation of tubular cells in PKD kidneys. The aim of this study was to determine the effects of MET on cyst growth, kidney function, AMPK and mTOR signaling, and lactate levels in male PCK rats, a Pkhd1 gene mutation model of human autosomal recessive polycystic kidney disease (ARPKD). MET 300 mg/kg/day IP from days 28 to 84 of age resulted in a mean serum metformin level that was 10 times the upper limit of therapeutic, no effect on cyst indices, nephrotoxicity, and increased serum lactate. MET 150 mg/kg resulted in a therapeutic serum metformin level but had no effect on kidney weight, cyst indices, kidney function, or mTOR and autophagy proteins. In summary, a standard dose of MET was ineffective in reducing PKD, did not activate p-AMPK or suppress mTOR and the higher dose resulted in increased lactate levels and nephrotoxicity. In conclusion, the study dampens enthusiasm for human studies of MET in PKD. Doubling the metformin dose resulted in a 10-fold increase in mean blood levels and toxicity suggesting that the dosage range between therapeutic and toxic is narrow.
MeSH term(s)	Humans ; Animals ; Male ; Rats ; AMP-Activated Protein Kinases ; Polycystic Kidney Diseases/drug therapy ; Cysts ; Metformin/pharmacology ; Metformin/therapeutic use ; Renal Insufficiency ; Lactates
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31) ; Metformin (9100L32L2N) ; Lactates
Language	English
Publishing date	2023-08-27
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.15776
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