Kidney disease: Difference between revisions
→Notable people: add section; add Nathan W. Levin, American physician, organization founder and author |
→Diet: {{See also|Dietary acid load}} Tag: Reverted |
||
| Line 50: | Line 50: | ||
===Diet=== |
===Diet=== |
||
{{See also|Dietary acid load}} |
|||
Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for [[microalbuminuria]], a sign of kidney function decline,<ref>{{Cite journal|last1=Lin|first1=Julie|last2=Hu|first2=Frank B.|last3=Curhan|first3=Gary C.|date=2010-05-01|title=Associations of diet with albuminuria and kidney function decline|journal=Clinical Journal of the American Society of Nephrology|volume=5|issue=5|pages=836–843|doi=10.2215/CJN.08001109|issn=1555-905X|pmc=2863979|pmid=20299364}}</ref> and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.<ref>{{Cite journal|last1=Lin|first1=Julie|last2=Fung|first2=Teresa T.|last3=Hu|first3=Frank B.|last4=Curhan|first4=Gary C.|date=2011-02-01|title=Association of dietary patterns with albuminuria and kidney function decline in older white women: a subgroup analysis from the Nurses' Health Study|journal=American Journal of Kidney Diseases|volume=57|issue=2|pages=245–254|doi=10.1053/j.ajkd.2010.09.027|issn=1523-6838|pmc=3026604|pmid=21251540}}</ref> This may be because sources of animal protein, animal fat, and cholesterol, and sweets are more acid-producing, while fruits, vegetables, legumes, and whole grains are more base-producing.<ref>{{Cite journal|last1=Chen|first1=Wei|last2=Abramowitz|first2=Matthew K.|date=2014-01-01|title=Metabolic acidosis and the progression of chronic kidney disease|journal=BMC Nephrology|volume=15|pages=55|doi=10.1186/1471-2369-15-55|issn=1471-2369|pmc=4233646|pmid=24708763}}</ref><ref>{{Cite journal|last1=Sebastian|first1=Anthony|last2=Frassetto|first2=Lynda A.|last3=Sellmeyer|first3=Deborah E.|last4=Merriam|first4=Renée L.|last5=Morris|first5=R. Curtis|date=2002-12-01|title=Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors|journal=The American Journal of Clinical Nutrition|volume=76|issue=6|pages=1308–1316|issn=0002-9165|pmid=12450898|doi=10.1093/ajcn/76.6.1308|doi-access=free}}</ref><ref>{{Cite journal|last1=van den Berg|first1=Else|last2=Hospers|first2=Frédérique A. P.|last3=Navis|first3=Gerjan|last4=Engberink|first4=Marielle F.|last5=Brink|first5=Elizabeth J.|last6=Geleijnse|first6=Johanna M.|last7=van Baak|first7=Marleen A.|last8=Gans|first8=Rijk O. B.|last9=Bakker|first9=Stephan J. L.|date=2011-02-01|title=Dietary acid load and rapid progression to end-stage renal disease of diabetic nephropathy in Westernized South Asian people|journal=Journal of Nephrology|volume=24|issue=1|pages=11–17|issn=1724-6059|pmid=20872351|doi=10.5301/jn.2010.5711}}</ref><ref>{{Cite journal|last1=Brenner|first1=B. M.|last2=Meyer|first2=T. W.|last3=Hostetter|first3=T. H.|date=1982-09-09|title=Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease|journal=The New England Journal of Medicine|volume=307|issue=11|pages=652–659|doi=10.1056/NEJM198209093071104|issn=0028-4793|pmid=7050706}}</ref><ref>{{Cite journal|last1=Goraya|first1=Nimrit|last2=Wesson|first2=Donald E.|date=2014-01-01|title=Is dietary Acid a modifiable risk factor for nephropathy progression?|journal=American Journal of Nephrology|volume=39|issue=2|pages=142–144|doi=10.1159/000358602|issn=1421-9670|pmid=24513954|doi-access=free}}</ref><ref>{{Cite journal|last1=Scialla|first1=Julia J.|last2=Appel|first2=Lawrence J.|last3=Astor|first3=Brad C.|last4=Miller|first4=Edgar R.|last5=Beddhu|first5=Srinivasan|last6=Woodward|first6=Mark|last7=Parekh|first7=Rulan S.|author-link7=Rulan S. Parekh|last8=Anderson|first8=Cheryl A. M.|date=2011-07-01|title=Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease|journal=Clinical Journal of the American Society of Nephrology|volume=6|issue=7|pages=1526–1532|doi=10.2215/CJN.00150111|issn=1555-905X|pmc=3552445|pmid=21700817}}</ref><ref>{{Cite journal|last1=Kanda|first1=Eiichiro|last2=Ai|first2=Masumi|last3=Kuriyama|first3=Renjiro|last4=Yoshida|first4=Masayuki|last5=Shiigai|first5=Tatsuo|date=2014-01-01|title=Dietary acid intake and kidney disease progression in the elderly|journal=American Journal of Nephrology|volume=39|issue=2|pages=145–152|doi=10.1159/000358262|issn=1421-9670|pmid=24513976|doi-access=free}}</ref><ref>{{Cite journal|last1=Banerjee|first1=Tanushree|last2=Crews|first2=Deidra C.|last3=Wesson|first3=Donald E.|last4=Tilea|first4=Anca|last5=Saran|first5=Rajiv|last6=Rios Burrows|first6=Nilka|last7=Williams|first7=Desmond E.|last8=Powe|first8=Neil R.|last9=Centers for Disease Control and Prevention Chronic Kidney Disease Surveillance Team|date=2014-01-01|title=Dietary acid load and chronic kidney disease among adults in the United States|journal=BMC Nephrology|volume=15|pages=137|doi=10.1186/1471-2369-15-137|issn=1471-2369|pmc=4151375|pmid=25151260}}</ref><ref>{{Cite journal|last1=Goraya|first1=Nimrit|last2=Simoni|first2=Jan|last3=Jo|first3=Chan-Hee|last4=Wesson|first4=Donald E.|date=2013-03-01|title=A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate|journal=Clinical Journal of the American Society of Nephrology|volume=8|issue=3|pages=371–381|doi=10.2215/CJN.02430312|issn=1555-905X|pmc=3586961|pmid=23393104}}</ref><ref>{{Cite journal|last1=Deriemaeker|first1=Peter|last2=Aerenhouts|first2=Dirk|last3=Hebbelinck|first3=Marcel|last4=Clarys|first4=Peter|s2cid=21268495|date=2010-03-01|title=Nutrient based estimation of acid-base balance in vegetarians and non-vegetarians|journal=Plant Foods for Human Nutrition (Dordrecht, Netherlands)|volume=65|issue=1|pages=77–82|doi=10.1007/s11130-009-0149-5|issn=1573-9104|pmid=20054653}}</ref> |
Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for [[microalbuminuria]], a sign of kidney function decline,<ref>{{Cite journal|last1=Lin|first1=Julie|last2=Hu|first2=Frank B.|last3=Curhan|first3=Gary C.|date=2010-05-01|title=Associations of diet with albuminuria and kidney function decline|journal=Clinical Journal of the American Society of Nephrology|volume=5|issue=5|pages=836–843|doi=10.2215/CJN.08001109|issn=1555-905X|pmc=2863979|pmid=20299364}}</ref> and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.<ref>{{Cite journal|last1=Lin|first1=Julie|last2=Fung|first2=Teresa T.|last3=Hu|first3=Frank B.|last4=Curhan|first4=Gary C.|date=2011-02-01|title=Association of dietary patterns with albuminuria and kidney function decline in older white women: a subgroup analysis from the Nurses' Health Study|journal=American Journal of Kidney Diseases|volume=57|issue=2|pages=245–254|doi=10.1053/j.ajkd.2010.09.027|issn=1523-6838|pmc=3026604|pmid=21251540}}</ref> This may be because sources of animal protein, animal fat, and cholesterol, and sweets are more acid-producing, while fruits, vegetables, legumes, and whole grains are more base-producing.<ref>{{Cite journal|last1=Chen|first1=Wei|last2=Abramowitz|first2=Matthew K.|date=2014-01-01|title=Metabolic acidosis and the progression of chronic kidney disease|journal=BMC Nephrology|volume=15|pages=55|doi=10.1186/1471-2369-15-55|issn=1471-2369|pmc=4233646|pmid=24708763}}</ref><ref>{{Cite journal|last1=Sebastian|first1=Anthony|last2=Frassetto|first2=Lynda A.|last3=Sellmeyer|first3=Deborah E.|last4=Merriam|first4=Renée L.|last5=Morris|first5=R. Curtis|date=2002-12-01|title=Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors|journal=The American Journal of Clinical Nutrition|volume=76|issue=6|pages=1308–1316|issn=0002-9165|pmid=12450898|doi=10.1093/ajcn/76.6.1308|doi-access=free}}</ref><ref>{{Cite journal|last1=van den Berg|first1=Else|last2=Hospers|first2=Frédérique A. P.|last3=Navis|first3=Gerjan|last4=Engberink|first4=Marielle F.|last5=Brink|first5=Elizabeth J.|last6=Geleijnse|first6=Johanna M.|last7=van Baak|first7=Marleen A.|last8=Gans|first8=Rijk O. B.|last9=Bakker|first9=Stephan J. L.|date=2011-02-01|title=Dietary acid load and rapid progression to end-stage renal disease of diabetic nephropathy in Westernized South Asian people|journal=Journal of Nephrology|volume=24|issue=1|pages=11–17|issn=1724-6059|pmid=20872351|doi=10.5301/jn.2010.5711}}</ref><ref>{{Cite journal|last1=Brenner|first1=B. M.|last2=Meyer|first2=T. W.|last3=Hostetter|first3=T. H.|date=1982-09-09|title=Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease|journal=The New England Journal of Medicine|volume=307|issue=11|pages=652–659|doi=10.1056/NEJM198209093071104|issn=0028-4793|pmid=7050706}}</ref><ref>{{Cite journal|last1=Goraya|first1=Nimrit|last2=Wesson|first2=Donald E.|date=2014-01-01|title=Is dietary Acid a modifiable risk factor for nephropathy progression?|journal=American Journal of Nephrology|volume=39|issue=2|pages=142–144|doi=10.1159/000358602|issn=1421-9670|pmid=24513954|doi-access=free}}</ref><ref>{{Cite journal|last1=Scialla|first1=Julia J.|last2=Appel|first2=Lawrence J.|last3=Astor|first3=Brad C.|last4=Miller|first4=Edgar R.|last5=Beddhu|first5=Srinivasan|last6=Woodward|first6=Mark|last7=Parekh|first7=Rulan S.|author-link7=Rulan S. Parekh|last8=Anderson|first8=Cheryl A. M.|date=2011-07-01|title=Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease|journal=Clinical Journal of the American Society of Nephrology|volume=6|issue=7|pages=1526–1532|doi=10.2215/CJN.00150111|issn=1555-905X|pmc=3552445|pmid=21700817}}</ref><ref>{{Cite journal|last1=Kanda|first1=Eiichiro|last2=Ai|first2=Masumi|last3=Kuriyama|first3=Renjiro|last4=Yoshida|first4=Masayuki|last5=Shiigai|first5=Tatsuo|date=2014-01-01|title=Dietary acid intake and kidney disease progression in the elderly|journal=American Journal of Nephrology|volume=39|issue=2|pages=145–152|doi=10.1159/000358262|issn=1421-9670|pmid=24513976|doi-access=free}}</ref><ref>{{Cite journal|last1=Banerjee|first1=Tanushree|last2=Crews|first2=Deidra C.|last3=Wesson|first3=Donald E.|last4=Tilea|first4=Anca|last5=Saran|first5=Rajiv|last6=Rios Burrows|first6=Nilka|last7=Williams|first7=Desmond E.|last8=Powe|first8=Neil R.|last9=Centers for Disease Control and Prevention Chronic Kidney Disease Surveillance Team|date=2014-01-01|title=Dietary acid load and chronic kidney disease among adults in the United States|journal=BMC Nephrology|volume=15|pages=137|doi=10.1186/1471-2369-15-137|issn=1471-2369|pmc=4151375|pmid=25151260}}</ref><ref>{{Cite journal|last1=Goraya|first1=Nimrit|last2=Simoni|first2=Jan|last3=Jo|first3=Chan-Hee|last4=Wesson|first4=Donald E.|date=2013-03-01|title=A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate|journal=Clinical Journal of the American Society of Nephrology|volume=8|issue=3|pages=371–381|doi=10.2215/CJN.02430312|issn=1555-905X|pmc=3586961|pmid=23393104}}</ref><ref>{{Cite journal|last1=Deriemaeker|first1=Peter|last2=Aerenhouts|first2=Dirk|last3=Hebbelinck|first3=Marcel|last4=Clarys|first4=Peter|s2cid=21268495|date=2010-03-01|title=Nutrient based estimation of acid-base balance in vegetarians and non-vegetarians|journal=Plant Foods for Human Nutrition (Dordrecht, Netherlands)|volume=65|issue=1|pages=77–82|doi=10.1007/s11130-009-0149-5|issn=1573-9104|pmid=20054653}}</ref> |
||
Revision as of 01:54, 24 July 2022
 | This article has multiple issues. Please help improve it or discuss these issues on the talk page. (Learn how and when to remove these messages)
|
| Kidney disease | |
|---|---|
| Other names | Renal disease, nephropathy |
 | |
| Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury. | |
| Specialty | Nephrology, urology  |
| Complications | Uremia, death |
Kidney disease, or renal disease, technically referred to as nephropathy, is damage to or disease of a kidney. Nephritis is an inflammatory kidney disease and has several types according to the location of the inflammation. Inflammation can be diagnosed by blood tests. Nephrosis is non-inflammatory kidney disease. Nephritis and nephrosis can give rise to nephritic syndrome and nephrotic syndrome respectively. Kidney disease usually causes a loss of kidney function to some degree and can result in kidney failure, the complete loss of kidney function. Kidney failure is known as the end-stage of kidney disease, where dialysis or a kidney transplant is the only treatment option.
Chronic kidney disease is defined as prolonged kidney abnormalities (functional and/or structural in nature) that last for more than three months.[1] Acute kidney disease is now termed acute kidney injury and is marked by the sudden reduction in kidney function over seven days. About one in eight Americans (as of 2007) have chronic kidney disease,[2] a rate that is increasing over time.[1]
Causes
Causes of kidney disease include deposition of the Immunoglobulin A antibodies in the glomerulus, administration of analgesics, xanthine oxidase deficiency, toxicity of chemotherapy agents, and long-term exposure to lead or its salts. Chronic conditions that can produce nephropathy include systemic lupus erythematosus, diabetes mellitus and high blood pressure (hypertension), which lead to diabetic nephropathy and hypertensive nephropathy, respectively.
Analgesics
One cause of nephropathy is the long term usage of pain medications known as analgesics. The pain medicines which can cause kidney problems include aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs (NSAIDs). This form of nephropathy is "chronic analgesic nephritis," a chronic inflammatory change characterized by loss and atrophy of tubules and interstitial fibrosis and inflammation (BRS Pathology, 2nd edition).
Specifically, long-term use of the analgesic phenacetin has been linked to renal papillary necrosis (necrotizing papillitis).
Diabetes
Diabetic nephropathy is a progressive kidney disease caused by angiopathy of the capillaries in the glomeruli. It is characterized by nephrotic syndrome and diffuse scarring of the glomeruli. It is particularly associated with poorly managed diabetes mellitus and is a primary reason for dialysis in many developed countries. It is classified as a small blood vessel complication of diabetes.[3]
Diet
Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for microalbuminuria, a sign of kidney function decline,[4] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.[5] This may be because sources of animal protein, animal fat, and cholesterol, and sweets are more acid-producing, while fruits, vegetables, legumes, and whole grains are more base-producing.[6][7][8][9][10][11][12][13][14][15]
IgA nephropathy
IgA nephropathy is the most common glomerulonephritis throughout the world [16] Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. The classic presentation (in 40-50% of the cases) is episodic frank hematuria which usually starts within a day or two of a non-specific upper respiratory tract infection (hence synpharyngitic) as opposed to post-streptococcal glomerulonephritis which occurs some time (weeks) after initial infection. Less commonly gastrointestinal or urinary infection can be the inciting agent. All of these infections have in common the activation of mucosal defenses and hence IgA antibody production.
Iodinated contrast media
Kidney disease induced by iodinated contrast media (ICM) is called CIN (= contrast induced nephropathy) or contrast-induced AKI (= acute kidney injury). Currently, the underlying mechanisms are unclear. But there is a body of evidence that several factors including apoptosis-induction seem to play a role.[17]
Lithium
Lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, can cause nephrogenic diabetes insipidus; its long-term use can lead to nephropathy.[18]
Lupus
Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.[19]
Xanthine oxidase deficiency
Another possible cause of Kidney disease is due to decreased function of xanthine oxidase in the purine degradation pathway. Xanthine oxidase will degrade hypoxanthine to xanthine and then to uric acid. Xanthine is not very soluble in water; therefore, an increase in xanthine forms crystals (which can lead to kidney stones) and result in damage to the kidney. Xanthine oxidase inhibitors, like allopurinol, can cause nephropathy.
Polycystic disease of the kidneys
Additional possible cause of nephropathy is due to the formation of cysts or pockets containing fluid within the kidneys. These cysts become enlarged with the progression of aging causing renal failure. Cysts may also form in other organs including the liver, brain, and ovaries. Polycystic Kidney Disease is a genetic disease caused by mutations in the PKD1, PKD2, and PKHD1 genes. This disease affects about half a million people in the US. Polycystic kidneys are susceptible to infections and cancer.
Toxicity of chemotherapy agents
Nephropathy can be associated with some therapies used to treat cancer. The most common form of kidney disease in cancer patients is Acute Kidney Injury (AKI) which can usually be due to volume depletion from vomiting and diarrhea that occur following chemotherapy or occasionally due to kidney toxicities of chemotherapeutic agents. Kidney failure from break down of cancer cells, usually after chemotherapy, is unique to onconephrology. Several chemotherapeutic agents, for example Cisplatin, are associated with acute and chronic kidney injuries.[20] Newer agents such as anti Vascular Endothelial Growth Factor (anti VEGF) are also associated with similar injuries, as well as proteinuria, hypertension and thrombotic microangiopathy.[21]
Diagnosis
The standard diagnostic workup of suspected kidney disease includes a medical history, physical examination, a urine test, and an ultrasound of the kidneys (renal ultrasonography). An ultrasound is essential in the diagnosis and management of kidney disease.[22]
Treatment
Treatment approaches for kidney disease focus on managing the symptoms, controlling the progression, and also treating co-morbidities that a person may have.[1]
Dialysis
Transplantation
Millions of people across the world have kidney disease. Of those millions, several thousand will need dialysis or a kidney transplant at its end-stage.[23] In the United States, as of 2008, 16,500 people needed a kidney transplant.[23] Of those, 5,000 died while waiting for a transplant.[23] Currently, there is a shortage of donors, and in 2007 there were only 64,606 kidney transplants in the world.[23] This shortage of donors is causing countries to place monetary value on kidneys. Countries such as Iran and Singapore are eliminating their lists by paying their citizens to donate. Also, the black market accounts for 5-10 percent of transplants that occur worldwide.[23] The act of buying an organ through the black market is illegal in the United States.[24] To be put on the waiting list for a kidney transplant, patients must first be referred by a physician, then they must choose and contact a donor hospital. Once they choose a donor hospital, patients must then receive an evaluation to make sure they are sustainable to receive a transplant. In order to be a match for a kidney transplant, patients must match blood type and human leukocyte antigen factors with their donors. They must also have no reactions to the antibodies from the donor's kidneys.[25][23]
Prognosis
Kidney disease can have serious consequences if it cannot be controlled effectively. Generally, the progression of kidney disease is from mild to serious. Some kidney diseases can cause kidney failure.
Notable people
- Nathan W. Levin, American physician, organization founder and author
See also
- Hematologic Diseases Information Service
- Mesoamerican nephropathy, an enigmatic chronic kidney disease of Central America
- Protein toxicity
References
- ^ a b c Kim, Kun Hyung; Lee, Myeong Soo; Kim, Tae-Hun; Kang, Jung Won; Choi, Tae-Young; Lee, Jae Dong (2016-06-28). "Acupuncture and related interventions for symptoms of chronic kidney disease". The Cochrane Database of Systematic Reviews (6): CD009440. doi:10.1002/14651858.CD009440.pub2. ISSN 1469-493X. PMC 8406453. PMID 27349639.
- ^ Coresh, Josef; Selvin, Elizabeth; Stevens, Lesley A.; Manzi, Jane; Kusek, John W.; Eggers, Paul; Van Lente, Frederick; Levey, Andrew S. (2007-11-07). "Prevalence of chronic kidney disease in the United States". JAMA. 298 (17): 2038–2047. doi:10.1001/jama.298.17.2038. ISSN 1538-3598. PMID 17986697.
- ^ Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.2982
- ^ Lin, Julie; Hu, Frank B.; Curhan, Gary C. (2010-05-01). "Associations of diet with albuminuria and kidney function decline". Clinical Journal of the American Society of Nephrology. 5 (5): 836–843. doi:10.2215/CJN.08001109. ISSN 1555-905X. PMC 2863979. PMID 20299364.
- ^ Lin, Julie; Fung, Teresa T.; Hu, Frank B.; Curhan, Gary C. (2011-02-01). "Association of dietary patterns with albuminuria and kidney function decline in older white women: a subgroup analysis from the Nurses' Health Study". American Journal of Kidney Diseases. 57 (2): 245–254. doi:10.1053/j.ajkd.2010.09.027. ISSN 1523-6838. PMC 3026604. PMID 21251540.
- ^ Chen, Wei; Abramowitz, Matthew K. (2014-01-01). "Metabolic acidosis and the progression of chronic kidney disease". BMC Nephrology. 15: 55. doi:10.1186/1471-2369-15-55. ISSN 1471-2369. PMC 4233646. PMID 24708763.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Sebastian, Anthony; Frassetto, Lynda A.; Sellmeyer, Deborah E.; Merriam, Renée L.; Morris, R. Curtis (2002-12-01). "Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors". The American Journal of Clinical Nutrition. 76 (6): 1308–1316. doi:10.1093/ajcn/76.6.1308. ISSN 0002-9165. PMID 12450898.
- ^ van den Berg, Else; Hospers, Frédérique A. P.; Navis, Gerjan; Engberink, Marielle F.; Brink, Elizabeth J.; Geleijnse, Johanna M.; van Baak, Marleen A.; Gans, Rijk O. B.; Bakker, Stephan J. L. (2011-02-01). "Dietary acid load and rapid progression to end-stage renal disease of diabetic nephropathy in Westernized South Asian people". Journal of Nephrology. 24 (1): 11–17. doi:10.5301/jn.2010.5711. ISSN 1724-6059. PMID 20872351.
- ^ Brenner, B. M.; Meyer, T. W.; Hostetter, T. H. (1982-09-09). "Dietary protein intake and the progressive nature of kidney disease: the role of hemodynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease". The New England Journal of Medicine. 307 (11): 652–659. doi:10.1056/NEJM198209093071104. ISSN 0028-4793. PMID 7050706.
- ^ Goraya, Nimrit; Wesson, Donald E. (2014-01-01). "Is dietary Acid a modifiable risk factor for nephropathy progression?". American Journal of Nephrology. 39 (2): 142–144. doi:10.1159/000358602. ISSN 1421-9670. PMID 24513954.
- ^ Scialla, Julia J.; Appel, Lawrence J.; Astor, Brad C.; Miller, Edgar R.; Beddhu, Srinivasan; Woodward, Mark; Parekh, Rulan S.; Anderson, Cheryl A. M. (2011-07-01). "Estimated net endogenous acid production and serum bicarbonate in African Americans with chronic kidney disease". Clinical Journal of the American Society of Nephrology. 6 (7): 1526–1532. doi:10.2215/CJN.00150111. ISSN 1555-905X. PMC 3552445. PMID 21700817.
- ^ Kanda, Eiichiro; Ai, Masumi; Kuriyama, Renjiro; Yoshida, Masayuki; Shiigai, Tatsuo (2014-01-01). "Dietary acid intake and kidney disease progression in the elderly". American Journal of Nephrology. 39 (2): 145–152. doi:10.1159/000358262. ISSN 1421-9670. PMID 24513976.
- ^ Banerjee, Tanushree; Crews, Deidra C.; Wesson, Donald E.; Tilea, Anca; Saran, Rajiv; Rios Burrows, Nilka; Williams, Desmond E.; Powe, Neil R.; Centers for Disease Control and Prevention Chronic Kidney Disease Surveillance Team (2014-01-01). "Dietary acid load and chronic kidney disease among adults in the United States". BMC Nephrology. 15: 137. doi:10.1186/1471-2369-15-137. ISSN 1471-2369. PMC 4151375. PMID 25151260.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Goraya, Nimrit; Simoni, Jan; Jo, Chan-Hee; Wesson, Donald E. (2013-03-01). "A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate". Clinical Journal of the American Society of Nephrology. 8 (3): 371–381. doi:10.2215/CJN.02430312. ISSN 1555-905X. PMC 3586961. PMID 23393104.
- ^ Deriemaeker, Peter; Aerenhouts, Dirk; Hebbelinck, Marcel; Clarys, Peter (2010-03-01). "Nutrient based estimation of acid-base balance in vegetarians and non-vegetarians". Plant Foods for Human Nutrition (Dordrecht, Netherlands). 65 (1): 77–82. doi:10.1007/s11130-009-0149-5. ISSN 1573-9104. PMID 20054653. S2CID 21268495.
- ^ D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy". Q J Med. 64 (245): 709–727. PMID 3329736.
- ^ Idee, J.-; Boehm, J.; Prigent, P.; Ballet, S.; Corot, C. (2006). "Role of Apoptosis in the Pathogenesis of Contrast Media-induced Nephropathy and Hints for its Possible Prevention by Drug Treatment". Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry. 5 (2): 139–146. doi:10.2174/187152306776872442.
- ^ Grünfeld, JP; Rossier, BC (May 2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol. 5 (5): 270–6. doi:10.1038/nrneph.2009.43. PMID 19384328. S2CID 36253297.
- ^ Borchers, Andrea T.; Leibushor, Naama; Naguwa, Stanley M.; Cheema, Gurtej S.; Shoenfeld, Yehuda; Gershwin, M. Eric (2012-12-01). "Lupus nephritis: a critical review". Autoimmunity Reviews. 12 (2): 174–194. doi:10.1016/j.autrev.2012.08.018. ISSN 1873-0183. PMID 22982174.
- ^ Portilla D, Safar AM, Shannon ML, Penson RT. Cisplatin nephrotoxicity. In: UpToDate, Palevsky PM (Ed), UpToDate, Waltham, MA, 2013. http://www.uptodate.com/contents/cisplatin-nephrotoxicity
- ^ Robinson, Emily S.; Khankin, Eliyahu V.; Karumanchi, S. Ananth; Humphreys, Benjamin D. (1 November 2010). "Hypertension Induced by Vascular Endothelial Growth Factor Signaling Pathway Inhibition: Mechanisms and Potential Use as a Biomarker". Seminars in Nephrology. 30 (6): 591–601. doi:10.1016/j.semnephrol.2010.09.007. PMC 3058726. PMID 21146124.
- ^ Hansen, Kristoffer Lindskov; Nielsen, Michael Bachmann; Ewertsen, Caroline (2015-12-23). "Ultrasonography of the Kidney: A Pictorial Review". Diagnostics. 6 (1): 2. doi:10.3390/diagnostics6010002. ISSN 2075-4418. PMC 4808817. PMID 26838799.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b c d e f Tabarrok, Alex (January 8, 2010). "The Meat Market". Wall Street Journal.
- ^ Scheve, Tom (7 May 2008). "How Organ Donations Work". HowStuffWorks. Retrieved 9 March 2015.
- ^ "The Waiting List". www.kidneylink.org. Archived from the original on 2017-07-13. Retrieved 2015-03-09.