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Determination of in Vivo Ultrafiltration Coefficient (KUF) in Patients With Chronic Kidney Disease (CKD)

2014-08-27 03:14:11 | BioPortfolio

Summary

The purpose of this study is to determine the in-vivo ultrafiltration coefficient for different sizes of xevonta High-Flux dialyzers following FDA guidelines.

Study Design

Control: Uncontrolled, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Single Group Assignment, Masking: Open Label, Primary Purpose: Basic Science

Conditions

Kidney Disease

Intervention

xevonta

Location

Georg-Haas Dialysezentrum der PHV
Gießen
Hessen
Germany
35392

Status

Recruiting

Source

B.Braun Avitum AG

Results (where available)

View Results

Links

Published on BioPortfolio: 2014-08-27T03:14:11-0400

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Medical and Biotech [MESH] Definitions

Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)

The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.

A complication of kidney diseases characterized by cell death involving KIDNEY PAPILLA in the KIDNEY MEDULLA. Damages to this area may hinder the kidney to concentrate urine resulting in POLYURIA. Sloughed off necrotic tissue may block KIDNEY PELVIS or URETER. Necrosis of multiple renal papillae can lead to KIDNEY FAILURE.

An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.

KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.

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