Ajay Kumar at 21:31, 29 August 2023

2023-08-29T21:31:51Z

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{{Short description|Damage to or disease of a kidney}}
{{Distinguish|neuropathy}}
{{Multiple issues|
{{update|date=August 2017}}
{{More medical citations needed|date=August 2019}}
}}

{{Infobox medical condition (new)
| name = Kidney disease
| synonyms = Renal disease, nephropathy
| image = Kidney – acute cortical necrosis.jpg
| caption = 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]].
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| complications = [[Uremia]], [[death]]
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'''Kidney disease''', or '''renal disease''', technically referred to as '''nephropathy''', is damage to or [[disease]] of a [[kidney]]. [[Nephritis]] is an [[Inflammation|inflammatory]] kidney disease and has several types according to the location of the inflammation. Inflammation can be diagnosed by [[blood test]]s. [[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 [[Assessment of kidney function|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 [[Kidney dialysis|dialysis]] or a [[Kidney transplantation|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.<ref name=":0">{{Cite journal|last1=Kim|first1=Kun Hyung|last2=Lee|first2=Myeong Soo|last3=Kim|first3=Tae-Hun|last4=Kang|first4=Jung Won|last5=Choi|first5=Tae-Young|last6=Lee|first6=Jae Dong|date=2016-06-28|title=Acupuncture and related interventions for symptoms of chronic kidney disease|journal=The Cochrane Database of Systematic Reviews|volume=2016 |issue=6|pages=CD009440|doi=10.1002/14651858.CD009440.pub2|issn=1469-493X|pmid=27349639|pmc=8406453}}</ref> Acute kidney disease is now termed [[acute kidney injury]] and is marked by the sudden reduction in kidney function over seven days. In 2007, about one in eight Americans had chronic kidney disease.<ref>{{Cite journal|last1=Coresh|first1=Josef|last2=Selvin|first2=Elizabeth|last3=Stevens|first3=Lesley A.|last4=Manzi|first4=Jane|last5=Kusek|first5=John W.|last6=Eggers|first6=Paul|last7=Van Lente|first7=Frederick|last8=Levey|first8=Andrew S.|date=2007-11-07|title=Prevalence of chronic kidney disease in the United States|journal=JAMA|volume=298|issue=17|pages=2038–2047|doi=10.1001/jama.298.17.2038|issn=1538-3598|pmid=17986697|doi-access=}}</ref> This rate is increasing over time<ref name=":0" /> to where about 1 in 7 Americans are estimated to have CKD as of 2021.<ref>{{Cite web |date=2022-08-02 |title=Chronic Kidney Disease in the United States, 2021 |url=https://www.cdc.gov/kidneydisease/publications-resources/ckd-national-facts.html |access-date=2022-10-09 |website=www.cdc.gov |language=en-us}}</ref>

==Causes==
[[File:Kidney diseases world map-Deaths per million persons-WHO2012.svg|thumb|upright=1.3|Deaths due to kidney diseases per million persons in 2012 {{refbegin|3}}{{legend|#ffff20|16-61}}{{legend|#ffe820|62-79}}{{legend|#ffd820|80-88}}{{legend|#ffc020|89-95}}{{legend|#ffa020|96-110}}{{legend|#ff9a20|111-120}}{{legend|#f08015|121-135}}{{legend|#e06815|136-160}}{{legend|#d85010|161-186}}{{legend|#d02010|187-343}}{{refend}}]]

Causes of kidney disease include deposition of the [[Immunoglobulin A]] [[Antibody|antibodies]] in the [[glomerulus]], administration of [[analgesic]]s, [[xanthine oxidase deficiency]], [[Cytotoxicity|toxicity]] of [[chemotherapeutic agents|chemotherapy agents]], and a 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===
{{Main article|Analgesic nephropathy}}
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 drug]]s ([[NSAID]]s). 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===
{{Main article|Diabetic nephropathy}}
Diabetic nephropathy is a progressive kidney disease caused by [[angiopathy]] of the [[capillary|capillaries]] in the [[Glomerulus (kidney)|glomeruli]]. It is characterized by [[nephrotic syndrome]] and diffuse [[glomerulosclerosis|scarring of the glomeruli]]. It is particularly associated with poorly managed [[diabetes mellitus]] and is a primary reason for [[Kidney dialysis|dialysis]] in many developed countries. It is classified as a [[Microangiopathy|small blood vessel complication]] of diabetes.<ref>Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.2982</ref>

=== Autosomal dominant polycystic kidney disease ===
Gabow 1990 talks about Autosomal Dominant Polycystic Kidney disease and how this disease is genetic. They go on to say "Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic disease, affecting a half million Americans. The clinical phenotype can result from at least two different gene defects. One gene that can cause ADPKD has been located on the short arm of chromosome 16."<ref>{{cite journal |last1=Gabow |first1=Patricia A. |title=Autosomal Dominant Polycystic Kidney Disease—More Than a Renal Disease |journal=American Journal of Kidney Diseases |date=1 November 1990 |volume=16 |issue=5 |pages=403–413 |doi=10.1016/S0272-6386(12)80051-5 |pmid=2239929 }}</ref> The same article also goes on to say that millions of Americans are effected by this disease and is very common.

=== Long COVID and Kidney Disease ===
Yende & Parikh 2021 talk about the effects that [[COVID-19|COVID]] can have on a person that has a pre-existing health issue regarding kidney diseases. "frailty, chronic diseases, disability and immunodeficiency are at increased risk of kidney disease and progression to kidney failure, and infection with [[SARS-CoV-2]] can further increase this risk" (Long COVID and Kidney Disease, 2021).<ref>{{cite journal |last1=Yende |first1=Sachin |last2=Parikh |first2=Chirag R. |title=Long COVID and kidney disease |journal=Nature Reviews Nephrology |date=December 2021 |volume=17 |issue=12 |pages=792–793 |doi=10.1038/s41581-021-00487-3 |pmid=34504319 |pmc=8427150 }}</ref>

===Diet===
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 [[Candy|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 (chemistry)|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>

===IgA nephropathy===
{{Main article|IgA nephropathy}}
IgA nephropathy is the most common [[glomerulonephritis]] throughout the world <ref>{{cite journal |last=D'Amico |first=G | year= 1987 | title= The commonest glomerulonephritis in the world: IgA nephropathy.|journal= Q J Med |volume=64 | issue=245 | pages=709–727 | pmid=3329736 }}</ref> 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===
{{Main article|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.<ref>{{cite journal |doi=10.2174/187152306776872442 |title=Role of Apoptosis in the Pathogenesis of Contrast Media-induced Nephropathy and Hints for its Possible Prevention by Drug Treatment |journal=Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry |volume=5 |issue=2 |pages=139–146 |year=2006 |last1=Idee |first1=J.- |last2=Boehm |first2=J. |last3=Prigent |first3=P. |last4=Ballet |first4=S. |last5=Corot |first5=C. }}</ref>

===Lithium===
[[Lithium (medication)|Lithium]], a medication commonly used to treat [[bipolar disorder]] and [[schizoaffective disorder]]s, can cause [[nephrogenic diabetes insipidus]]; its long-term use can lead to nephropathy.<ref>{{cite journal |last1=Grünfeld |first1=JP |last2=Rossier |first2=BC |s2cid=36253297 |title=Lithium nephrotoxicity revisited |journal=Nat Rev Nephrol |date=May 2009 |volume=5 |issue=5 |pages=270–6 |doi=10.1038/nrneph.2009.43 |pmid=19384328}}</ref>

===Lupus===
Despite expensive treatments, [[lupus nephritis]] remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.<ref>{{Cite journal|last1=Borchers|first1=Andrea T.|last2=Leibushor|first2=Naama|last3=Naguwa|first3=Stanley M.|last4=Cheema|first4=Gurtej S.|last5=Shoenfeld|first5=Yehuda|last6=Gershwin|first6=M. Eric|date=2012-12-01|title=Lupus nephritis: a critical review|journal=Autoimmunity Reviews|volume=12|issue=2|pages=174–194|doi=10.1016/j.autrev.2012.08.018|issn=1873-0183|pmid=22982174}}</ref>

===Xanthine oxidase deficiency===
{{Main article|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 stone]]s) and result in damage to the kidney. [[Xanthine oxidase]] inhibitors, like [[allopurinol]], can cause nephropathy.

===Polycystic disease of the kidneys===
{{Main article|Polycystic kidney disease}}
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===
{{Main article|Onconephrology}}
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|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.<ref>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</ref> 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]].<ref name="pmid21146124">{{cite journal|last=Robinson|first=Emily S.|author2=Khankin, Eliyahu V. |author3=Karumanchi, S. Ananth |author4= Humphreys, Benjamin D. |title=Hypertension Induced by Vascular Endothelial Growth Factor Signaling Pathway Inhibition: Mechanisms and Potential Use as a Biomarker|journal=Seminars in Nephrology|date=1 November 2010|volume=30|issue=6|pages=591–601|doi=10.1016/j.semnephrol.2010.09.007|pmc=3058726|pmid=21146124}}</ref>

==Diagnosis==
The standard [[Medical diagnosis#Other diagnostic procedure methods|diagnostic workup]] of suspected kidney disease includes a [[medical history]], [[physical examination]], a [[Urine test strip|urine test]], and an [[Medical ultrasound|ultrasound]] of the kidneys ([[renal ultrasonography]]). An ultrasound is essential in the diagnosis and management of kidney disease.<ref>{{Cite journal|last1=Hansen|first1=Kristoffer Lindskov|last2=Nielsen|first2=Michael Bachmann|last3=Ewertsen|first3=Caroline|date=2015-12-23|title=Ultrasonography of the Kidney: A Pictorial Review|journal= Diagnostics|volume=6|issue=1|page=2|doi=10.3390/diagnostics6010002|issn=2075-4418|pmc=4808817|pmid=26838799|doi-access=free }}</ref>

== Treatment ==
Treatment approaches for kidney disease focus on managing the symptoms, controlling the progression, and also treating co-morbidities that a person may have.<ref name=":0" />

=== Dialysis ===
{{main|Kidney dialysis}}

=== Transplantation ===
{{main|Kidney transplantation}}
Millions of people across the world have kidney disease. Of those millions, several thousand will need [[renal replacement therapy|dialysis]] or a [[kidney transplantation|kidney transplant]] at its [[kidney failure|end-stage]].<ref name="MeatMarketWSJ">{{cite news|last1=Tabarrok|first1=Alex|title=The Meat Market|date=January 8, 2010|newspaper=Wall Street Journal}}</ref> In the United States, as of 2008, 16,500 people needed a kidney transplant.<ref name="MeatMarketWSJ" /> Of those, 5,000 died while waiting for a transplant.<ref name="MeatMarketWSJ" /> Currently, there is a shortage of donors, and in 2007 there were only 64,606 kidney transplants in the world.<ref name="MeatMarketWSJ" /> 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.<ref name="MeatMarketWSJ" /> The act of buying an organ through the black market is illegal in the United States.<ref>{{cite web|last1=Scheve|first1=Tom|title=How Organ Donations Work|date=7 May 2008|url=http://health.howstuffworks.com/medicine/modern-treatments/organ-donation7.htm|publisher=HowStuffWorks|access-date=9 March 2015}}</ref> 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 [[Antibody|antibodies]] from the donor's kidneys.<ref name="kidneylink">{{cite web|title=The Waiting List|url=http://www.kidneylink.org/TheWaitingList.aspx|website=www.kidneylink.org|access-date=2015-03-09|archive-url=https://web.archive.org/web/20170713113505/http://www.kidneylink.org/TheWaitingList.aspx|archive-date=2017-07-13|url-status=dead}}</ref><ref name="MeatMarketWSJ" />

==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]].

==See also==
* [[Hematologic Diseases Information Service]]
* [[Mesoamerican nephropathy]], an enigmatic chronic kidney disease of Central America
* [[Protein toxicity]]

==References==
{{Reflist}}

== External links ==
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{{Nephrology}}
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[[Category:Kidney diseases]]

Kidney disease - Revision history

Ajay Kumar at 21:31, 29 August 2023