Results 21 to 30 of about 6,390,379 (302)

Sociodemographic characteristics and clinical features of patients with adult polycystic kidney disease undergoing hemodialysis [PDF]

open access: yes, 2013
Aims: To analyze the socio-demographic and clinical characteristics of patients with adult polycystic kidney disease admitted to hemodialysis services in Northwestern Paraná state, Brazil.
Tsuneto, Luiza Tamie   +13 more
core   +1 more source

Renal hemosiderosis presenting with acute kidney Injury and macroscopic hematuria in Immunoglobulin A nephropathy: a case report

open access: yesBMC Nephrology, 2021
Background Macroscopic hematuria-associated acute kidney injury (AKI) is a well-known complication of immunoglobulin A (IgA) nephropathy. In such cases, intratubular obstruction by red blood cell (RBC) casts and acute tubular necrosis are mainly observed
Shinya Taguchi   +8 more
doaj   +1 more source

Association Between Syndecan-1, Fluid Overload, and Progressive Acute Kidney Injury After Adult Cardiac Surgery

open access: yesFrontiers in Medicine, 2021
Background: Acute kidney injury (AKI) is a common complication after cardiac surgery and the prognosis of AKI worsens with the increase in AKI severity. Syndecan-1(SDC-1) is a biomarker of endothelial glycocalyx degradation.
Jiarui Xu   +31 more
doaj   +1 more source

Pyruvate kinase M2 regulates mitochondrial homeostasis in cisplatin-induced acute kidney injury

open access: yesCell Death and Disease, 2023
An important pathophysiological process of acute kidney injury (AKI) is mitochondrial fragmentation in renal tubular epithelial cells, which leads to cell death.
Wenjia Xie   +9 more
doaj   +1 more source

The Association of Syndecan-1, Hypercoagulable State and Thrombosis and in Patients With Nephrotic Syndrome

open access: yesClinical and Applied Thrombosis/Hemostasis, 2021
The aim of this study is to investigate whether Syndecan-1 (SDC-1), an indicator of endothelial glycocalyx injury, would increase the risk of hypercoagulable state and thrombosis in patients with nephrotic syndrome (NS).
Xin Chen   +8 more
doaj   +1 more source

Chemokine receptor CCR1: A new target for progressive kidney disease [PDF]

open access: yes, 2005
Infiltrating leukocytes are thought to contribute to the progression of kidney disease. Locally produced chemokines guide circulating leukocytes into the kidney, which renders therapeutic blockade of respective chemokine receptors on the leukocyte ...
Hans-Joachim Anders   +3 more
core   +1 more source

Polycystic Kidney Disease [PDF]

open access: yesAnnual Review of Medicine, 2009
A number of inherited disorders result in renal cyst development. The most common form, autosomal dominant polycystic kidney disease (ADPKD), is a disorder most often diagnosed in adults and caused by mutation in PKD1 or PKD2. The PKD1 protein, polycystin-1, is a large receptor-like protein, whereas polycystin-2 is a transient receptor potential ...
Peter C, Harris, Vicente E, Torres
openaire   +2 more sources

Chronic Kidney Disease [PDF]

open access: yesPrimary Care: Clinics in Office Practice, 2020
Chronic kidney disease is encountered by the primary care physician, in no small part owing to the high rates of hypertension and diabetes, the 2 most common etiologies of chronic kidney disease in the United States. As a primary care physician, it is important to understand the epidemiology, pathophysiology, and evaluation methods of chronic kidney ...
Cornelia, Charles, Allison H, Ferris
openaire   +6 more sources

Chronic Kidney Disease – Where Next? : Predicting Outcomes And Planning Care Pathways [PDF]

open access: yes, 2014
Peer ...
Marks, Angharad   +5 more
core   +2 more sources

Urinary proteomic biomarkers for diagnosis and risk stratification of autosomal dominant polycystic kidney disease: a multicentric study [PDF]

open access: yes, 2013
Treatment options for autosomal dominant polycystic kidney disease (ADPKD) will likely become available in the near future, hence reliable diagnostic and prognostic biomarkers for the disease are strongly needed.
Torres, Vicente E.   +101 more
core   +2 more sources

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