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Chronic kidney disease

Angela C Webster, EVI NAGLER, Rachael L Morton and Philip Masson (2017) LANCET. 389(10075). p.1238-1252
abstract
The definition and classification of chronic kidney disease (CKD) have evolved over time, but current international guidelines define this condition as decreased kidney function shown by glomerular filtration rate (GFR) of less than 60 mL/min per 1.73 m(2), or markers of kidney damage, or both, of at least 3 months duration, regardless of the underlying cause. Diabetes and hypertension are the main causes of CKD in all high-income and middle-income countries, and also in many low-income countries. Incidence, prevalence, and progression of CKD also vary within countries by ethnicity and social determinants of health, possibly through epigenetic influence. Many people are asymptomatic or have nonspecific symptoms such as lethargy, itch, or loss of appetite. Diagnosis is commonly made after chance findings from screening tests (urinary dipstick or blood tests), or when symptoms become severe. The best available indicator of overall kidney function is GFR, which is measured either via exogenous markers (eg, DTPA, iohexol), or estimated using equations. Presence of proteinuria is associated with increased risk of progression of CKD and death. Kidney biopsy samples can show definitive evidence of CKD, through common changes such as glomerular sclerosis, tubular atrophy, and interstitial fibrosis. Complications include anaemia due to reduced production of erythropoietin by the kidney; reduced red blood cell survival and iron deficiency; and mineral bone disease caused by disturbed vitamin D, calcium, and phosphate metabolism. People with CKD are five to ten times more likely to die prematurely than they are to progress to end stage kidney disease. This increased risk of death rises exponentially as kidney function worsens and is largely attributable to death from cardiovascular disease, although cancer incidence and mortality are also increased. Health-related quality of life is substantially lower for people with CKD than for the general population, and falls as GFR declines. Interventions targeting specific symptoms, or aimed at supporting educational or lifestyle considerations, make a positive difference to people living with CKD. Inequity in access to services for this disease disproportionally affects disadvantaged populations, and health service provision to incentivise early intervention over provision of care only for advanced CKD is still evolving in many countries.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
GLOMERULAR-FILTRATION-RATE, QUALITY-OF-LIFE, LONGITUDINAL FOLLOW-UP, BLOOD-PRESSURE, UREMIC TOXINS, COLLABORATIVE METAANALYSIS, HEMODIALYSIS-PATIENTS, IRON SUPPLEMENTATION, POPULATION COHORTS, GENERAL-POPULATION
journal title
LANCET
Lancet
volume
389
issue
10075
pages
1238 - 1252
Web of Science type
Review
Web of Science id
000397143700036
ISSN
0140-6736
DOI
10.1016/S0140-6736(16)32064-5
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
8504025
handle
http://hdl.handle.net/1854/LU-8504025
date created
2017-01-24 09:43:20
date last changed
2017-09-08 13:35:15
@article{8504025,
  abstract     = {The definition and classification of chronic kidney disease (CKD) have evolved over time, but current international guidelines define this condition as decreased kidney function shown by glomerular filtration rate (GFR) of less than 60 mL/min per 1.73 m(2), or markers of kidney damage, or both, of at least 3 months duration, regardless of the underlying cause. Diabetes and hypertension are the main causes of CKD in all high-income and middle-income countries, and also in many low-income countries. Incidence, prevalence, and progression of CKD also vary within countries by ethnicity and social determinants of health, possibly through epigenetic influence. Many people are asymptomatic or have nonspecific symptoms such as lethargy, itch, or loss of appetite. Diagnosis is commonly made after chance findings from screening tests (urinary dipstick or blood tests), or when symptoms become severe. The best available indicator of overall kidney function is GFR, which is measured either via exogenous markers (eg, DTPA, iohexol), or estimated using equations. Presence of proteinuria is associated with increased risk of progression of CKD and death. Kidney biopsy samples can show definitive evidence of CKD, through common changes such as glomerular sclerosis, tubular atrophy, and interstitial fibrosis. Complications include anaemia due to reduced production of erythropoietin by the kidney; reduced red blood cell survival and iron deficiency; and mineral bone disease caused by disturbed vitamin D, calcium, and phosphate metabolism. People with CKD are five to ten times more likely to die prematurely than they are to progress to end stage kidney disease. This increased risk of death rises exponentially as kidney function worsens and is largely attributable to death from cardiovascular disease, although cancer incidence and mortality are also increased. Health-related quality of life is substantially lower for people with CKD than for the general population, and falls as GFR declines. Interventions targeting specific symptoms, or aimed at supporting educational or lifestyle considerations, make a positive difference to people living with CKD. Inequity in access to services for this disease disproportionally affects disadvantaged populations, and health service provision to incentivise early intervention over provision of care only for advanced CKD is still evolving in many countries.},
  author       = {Webster, Angela C and NAGLER, EVI and Morton, Rachael L and Masson, Philip},
  issn         = {0140-6736},
  journal      = {LANCET},
  keyword      = {GLOMERULAR-FILTRATION-RATE,QUALITY-OF-LIFE,LONGITUDINAL FOLLOW-UP,BLOOD-PRESSURE,UREMIC TOXINS,COLLABORATIVE METAANALYSIS,HEMODIALYSIS-PATIENTS,IRON SUPPLEMENTATION,POPULATION COHORTS,GENERAL-POPULATION},
  language     = {eng},
  number       = {10075},
  pages        = {1238--1252},
  title        = {Chronic kidney disease},
  url          = {http://dx.doi.org/10.1016/S0140-6736(16)32064-5},
  volume       = {389},
  year         = {2017},
}

Chicago
Webster, Angela C, EVI NAGLER, Rachael L Morton, and Philip Masson. 2017. “Chronic Kidney Disease.” Lancet 389 (10075): 1238–1252.
APA
Webster, A. C., NAGLER, E., Morton, R. L., & Masson, P. (2017). Chronic kidney disease. LANCET, 389(10075), 1238–1252.
Vancouver
1.
Webster AC, NAGLER E, Morton RL, Masson P. Chronic kidney disease. LANCET. 2017;389(10075):1238–52.
MLA
Webster, Angela C, EVI NAGLER, Rachael L Morton, et al. “Chronic Kidney Disease.” LANCET 389.10075 (2017): 1238–1252. Print.