Kidney disease

Short description: Pathological conditions of the kidney, impairing the organ's ability to filter blood

"Nephropathy" redirects here. It is not to be confused with neuropathy.

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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.
Complications| Uremia, death

Kidney diseases, or renal diseases, technically referred to as nephropathies, are pathological conditions affecting the kidneys—the organs that facilitate removal of waste products and toxins from the bloodstream, regulate the body's concentration of electrolytes, maintain the appropriate acid-base balance of plasma, and produce urine as a byproduct of metabolism.[1]

When used colloquially, the term kidney disease may refer to chronic kidney disease (CKD), an umbrella term for any progressive loss of kidney function over at least three months, from any cause.[2] In contrast, kidney damage over a shorter period of time is known as acute kidney injury.[1]

From a technical standpoint, the heterogenous group of kidney diseases can be broadly divided into categories based on which anatomical structures are involved: the glomeruli, the filtering capillaries of the kidney; tubules, which carry filtered blood; the renal interstitium, the fluid-filled space between these structures; and the renal blood vessels, which deliver blood towards and away from the kidney.[1] Glomerular disease, or glomerulonephritis, can be further divided into the nephritic and nephrotic syndromes, which are respectively characterized by blood and protein leaking into the urine.[3]

All forms of kidney disease, glomerular or otherwise, have the potential to damage all four components of the kidney, culminating in end-stage renal disease—the stage of disease at which dialysis or a kidney transplant are necessary.[4]

Rates for both chronic kidney disease and mortality have increased, associated with the rising prevalence of diabetes and the aging global population.[5][6] The World Health Organization has reported that "kidney diseases have risen from the world's nineteenth leading cause of death to the ninth, with the number of deaths increasing by 95% between 2000 and 2021."[7] In the United States, prevalence has risen from about one in eight in 2007,[8] to one in seven in 2021.[9]

## Contents

* 1 Causes
* 1.1 Autosomal dominant polycystic kidney disease
* 1.2 IgA nephropathy
* 1.3 Polycystic disease of the kidneys
* 1.4 Xanthine oxidase deficiency
* 1.5 Diabetes
* 1.6 Lupus
* 1.7 COVID-19
* 1.8 Analgesics
* 1.9 Iodinated contrast media
* 1.10 Toxicity of chemotherapy agents
* 1.11 Lithium
* 1.12 Anabolic-androgenic steroids
* 1.13 Diet
* 2 Diagnosis
* 3 Treatment
* 3.1 Transplantation
* 3.2 Dialysis
* 4 Prognosis
* 5 See also
* 6 References

## Causes

Deaths due to kidney diseases per million persons in 2012

16–61

62–79

80–88

89–95

96–110

111–120

121–135

136–160

161–186

187–343

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 a long-term exposure to lead or its salts. Chronic conditions that can produce nephropathy include systemic lupus erythematosus, as well as diabetes mellitus and high blood pressure (hypertension), which lead to diabetic nephropathy and hypertensive nephropathy, respectively.[citation needed]

### Autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic disease, affecting a half million Americans.[10] 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.[11]

### IgA nephropathy

IgA nephropathy is the most common glomerulonephritis throughout the world [12] 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.

### 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.

### 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.

### 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.[13]

### Lupus

Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.[14]

### COVID-19

COVID-19 is associated with kidney disease. In patients hospitalized with COVID-19, the prevalence of acute kidney injury is estimated to be 28%, and the prevalence of renal replacement therapy is estimated to be 9%.[15]

### Analgesics

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One cause of nephropathy is the long term usage of pain medications known as analgesics.[16][17] The pain medicines which can cause kidney problems include Tylenol, aspirin, acetaminophen, paracetamol,[18] and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen.[19] This form of nephropathy is "chronic analgesic nephritis" or Analgesic Nephropathy,[17] a chronic inflammatory change characterized by loss and atrophy of tubules and interstitial fibrosis[20] and inflammation (BRS Pathology, 2nd ed.).

Specifically, long-term use of the analgesic phenacetin has been linked to renal papillary necrosis (necrotizing papillitis).[17]

### Iodinated contrast media

Kidney disease induced by iodinated contrast media (ICM) is called contrast induced nephropathy (CIN) or contrast-induced acute kidney injury (AKI). Currently, the underlying mechanisms are unclear. But there is a body of evidence that several factors including apoptosis-induction seem to play a role.[21]

### 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.[22] 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.[23]

### 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.[24] Long term lithium treatment is known to cause chronic kidney disease after 10-20 years of treatment in 1-5% of people.[25][26] End-stage renal disease due to lithium occurs in 0.53% of people versus 0.2% in the general population.[27][28][29] Dosing lithium more than once per day is associated with more kidney damage.[30] Kidney harm can be mitigated by dosing lithium once per day at night and keeping the dose as low as possible.[31] Dosing lithium once per day allows for long periods where the kidney is exposed to low levels of lithium, which minimizes kidney harm.[32]

### Anabolic-androgenic steroids

Regular and long-term use of anabolic-androgenic steroids (AAS) can cause both acute and chronic kidney disease through several direct and indirect mechanisms.[33][34][35] Focal segmental glomerulosclerosis is the most common condition arising in such cases.[36][37] Discontinuation of AAS in the early stage of Kidney Disease can result in a reversal of the kidney damage.[38][39]

### Diet

Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for microalbuminuria, a sign of kidney function decline,[40] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.[41] 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.[42][43][44][45][46][47][48][49][50][51][excessive citations]

## 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.[52]

## Treatment

Treatment approaches for kidney disease focus on managing the symptoms, controlling the progression, and also treating co-morbidities that a person may have.[53]

### Transplantation

Main article: Medicine:Kidney 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.[54] In the United States, as of 2008, 16,500 people needed a kidney transplant.[54] Of those, 5,000 died while waiting for a transplant.[54] Currently, there is a shortage of donors, and in 2007 there were only 64,606 kidney transplants in the world.[54] 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.[54] The act of buying an organ through the black market is illegal in the United States.[55] 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.[56][54]

### Dialysis

Main article: Engineering:Kidney dialysis

Because of the shortage of kidney donors, kidney dialysis is the most common method of renal replacement therapy for patients with kidney failure. Usually it is started at Stage 5 of chronic kidney failure, when the glomerular filtration rate is less than 15% of the normal.

For most patients, a kidney transplant offers a significant survival advantage and improved quality of life compared to remaining on dialysis, often adding years to life expectancy, though early risks exist, especially with certain donor types or in the elderly, but long-term outcomes favor transplant. Studies consistently show better long-term survival rates for transplant recipients, with one-year survival rates often above 90-95% for transplant, while dialysis patients face higher mortality.[57][58][59]

## 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

1. ↑ 1.0 1.1 1.2 Chang, Anthony; Laszik, Zoltan (2021) (in en). Robbins & Coltran Pathologic Basis of Disease (10th ed.). Philadelphia, PA: Elsevier. pp. 895–952. ISBN 978-0-323-60992-0.
2. ↑ "Kidney Disease: Fact Sheet | National Kidney Foundation" (in en). https://www.kidney.org/about/kidney-disease-fact-sheet.
3. ↑ "Patient education: Glomerular disease (Beyond the Basics), UpToDate". https://www.uptodate.com/contents/glomerular-disease-beyond-the-basics.
4. ↑ "Definition and staging of chronic kidney disease in adults, UpToDate". https://www.uptodate.com/contents/definition-and-staging-of-chronic-kidney-disease-in-adults#H27258404.
5. ↑ Imai, Enyu; Matsuo, Seiichi (28 June 2008). "Chronic kidney disease in Asia". The Lancet 371 (9631): 2147–2148. doi:10.1016/S0140-6736(08)60928-9. PMID 18586155. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(08)60928-9/abstract. Retrieved 12 August 2024.
6. ↑ James, Matthew T; Hemmelgarn, Brenda R; Tonelli, Marcello (10 April 2010). "Early recognition and prevention of chronic kidney disease". The Lancet 375 (9722): 1296–1309. doi:10.1016/S0140-6736(09)62004-3. PMID 20382326. https://www.sciencedirect.com/science/article/pii/S0140673609620043. Retrieved 12 August 2024.
7. ↑ "The top 10 causes of death" (in en). https://www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death.
8. ↑ Coresh, Josef; Selvin, Elizabeth; Stevens, Lesley A.; Manzi, Jane; Kusek, John W.; Eggers, Paul; Van Lente, Frederick; Levey, Andrew S. (7 November 2007). "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. Bibcode: 2007JAMA..298.2038C.
9. ↑ "Chronic Kidney Disease in the United States, 2023" (in en-us). 15 May 2024. https://www.cdc.gov/kidney-disease/php/data-research/.
10. ↑ "Polycystic Kidney Disease, Autosomal Dominant". https://www.ucsfhealth.org/conditions/polycystic-kidney-disease-autosomal-dominant.
11. ↑ Gabow, Patricia A. (1 November 1990). "Autosomal Dominant Polycystic Kidney Disease – More Than a Renal Disease". American Journal of Kidney Diseases 16 (5): 403–413. doi:10.1016/S0272-6386(12)80051-5. PMID 2239929.
12. ↑ D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy.". Q J Med 64 (245): 709–727. PMID 3329736.
13. ↑ Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p. 2982
14. ↑ Borchers, Andrea T.; Leibushor, Naama; Naguwa, Stanley M.; Cheema, Gurtej S.; Shoenfeld, Yehuda; Gershwin, M. Eric (1 December 2012). "Lupus nephritis: a critical review". Autoimmunity Reviews 12 (2): 174–194. doi:10.1016/j.autrev.2012.08.018. ISSN 1873-0183. PMID 22982174.
15. ↑ Silver, Samuel; Beaubien-Souligny, William; Shah, Prakesh; Harel, Shai; Blum, Daniel; Kishibe, Teruko; Meraz-Muñoz, Alejandro; Wald, Ron et al. (8 December 2020). "The Prevalence of Acute Kidney Injury in Patients Hospitalized With COVID-19 Infection: A Systematic Review and Meta-analysis". Kidney Medicine 3 (1): 83–98.e1. doi:10.1016/j.xkme.2020.11.008. PMID 33319190. PMC 7723763. https://www.kidneymedicinejournal.org/article/S2590-0595(20)30257-0/fulltext. Retrieved 5 April 2024.
16. ↑ De Broe, Marc E.; Elseviers, Monique M. (12 February 1998). "Analgesic Nephropathy" (in en). New England Journal of Medicine 338 (7): 446–452. doi:10.1056/NEJM199802123380707. ISSN 0028-4793. PMID 9459649. http://www.nejm.org/doi/abs/10.1056/NEJM199802123380707.
17. ↑ 17.0 17.1 17.2 Roy, Neil; Bennet, David (Nov 2007). Essentials : Renal, Gastrointestinal and Hepatobiliary Systems. iUniverse, Incorporated. pp. 23. ISBN 9780595465125.
18. ↑ Papich, Mark (2005). "Drugs and the kidneys: preventing and managing their potential adverse effects" (in en). p. 858. https://www.cabidigitallibrary.org/doi/full/10.5555/20053197348.
19. ↑ Prescott, L. F. (1 January 1982). "Analgesic Nephropathy: A Reassessment of the Role of Phenacetin and Other Analgesics" (in en). Drugs 23 (1): 75–149. doi:10.2165/00003495-198223010-00004. ISSN 1179-1950. PMID 7035123. https://doi.org/10.2165/00003495-198223010-00004.
20. ↑ "Tubulointerstitial Diseases" (in en-US), Practical Renal Pathology (W.B. Saunders): pp. 127–158, 1 January 2013, doi:10.1016/B978-0-443-06966-6.00009-X, ISBN 978-0-443-06966-6, https://www.sciencedirect.com/science/chapter/edited-volume/abs/pii/B978044306966600009X, retrieved 23 March 2026
21. ↑ 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.
22. ↑ 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
23. ↑ 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. PMID 21146124.
24. ↑ Grünfeld, JP; Rossier, BC (May 2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol 5 (5): 270–276. doi:10.1038/nrneph.2009.43. PMID 19384328.
25. ↑ Malhi, Gin S; Tanious, Michelle; Das, Pritha; Berk, Michael (1 March 2012). "The science and practice of lithium therapy" (in EN). Australian & New Zealand Journal of Psychiatry 46 (3): 192–211. doi:10.1177/0004867412437346. ISSN 0004-8674. PMID 22391277. https://doi.org/10.1177/0004867412437346.
26. ↑ Tondo, Leonardo; Alda, Martin; Bauer, Michael; Bergink, Veerle; Grof, Paul; Hajek, Tomas; Lewitka, Ute; Licht, Rasmus W. et al. (22 July 2019). "Clinical use of lithium salts: guide for users and prescribers" (in en). International Journal of Bipolar Disorders 7 (1): 16. doi:10.1186/s40345-019-0151-2. ISSN 2194-7511. PMID 31328245.
27. ↑ Presne, Claire; Fakhouri, Fadi; Noël, Laure-Hélène; Stengel, Bénédicte; Even, Christian; Kreis, Henri; Mignon, Françoise; Grünfeld, Jean-Pierre (August 2003). "Lithium-induced nephropathy: Rate of progression and prognostic factors". Kidney International 64 (2): 585–592. doi:10.1046/j.1523-1755.2003.00096.x. ISSN 0085-2538. PMID 12846754. https://linkinghub.elsevier.com/retrieve/pii/S0085253815493652.
28. ↑ Tondo, Leonardo; Abramowicz, Maria; Alda, Martin; Bauer, Michael; Bocchetta, Alberto; Bolzani, Lorenza; Calkin, Cynthia V.; Chillotti, Caterina et al. (1 August 2017). "Long-term lithium treatment in bipolar disorder: effects on glomerular filtration rate and other metabolic parameters" (in en). International Journal of Bipolar Disorders 5 (1): 27. doi:10.1186/s40345-017-0096-2. ISSN 2194-7511. PMID 28480485.
29. ↑ Barroilhet, S. A.; Ghaemi, S. N. (2020). "When and how to use lithium" (in en). Acta Psychiatrica Scandinavica 142 (3): 161–172. doi:10.1111/acps.13202. ISSN 1600-0447. PMID 32526812. https://onlinelibrary.wiley.com/doi/abs/10.1111/acps.13202.
30. ↑ Carter, Lorie; Zolezzi, Monica; Lewczyk, Andrea (1 October 2013). "An Updated Review of the Optimal Lithium Dosage Regimen for Renal Protection" (in EN). The Canadian Journal of Psychiatry 58 (10): 595–600. doi:10.1177/070674371305801009. ISSN 0706-7437. PMID 24165107. https://doi.org/10.1177/070674371305801009.
31. ↑ MD, Chris Aiken (19 January 2026). "6 Ways to Protect the Kidneys While Prescribing Lithium" (in en). https://www.psychiatrictimes.com/view/6-ways-protect-kidneys-while-prescribing-lithium.
32. ↑ Barroilhet, S. A.; Ghaemi, S. N. (2020). "When and how to use lithium" (in en). Acta Psychiatrica Scandinavica 142 (3): 161–172. doi:10.1111/acps.13202. ISSN 1600-0447. PMID 32526812. https://onlinelibrary.wiley.com/doi/abs/10.1111/acps.13202.
33. ↑ Parente Filho, Sérgio Luiz Arruda; Gomes, Pedro Eduardo Andrade de Carvalho; Forte, Guilherme Aguiar; Lima, Laio Ladislau Lopes; Silva Júnior, Geraldo Bezerra da; Meneses, Gdayllon Cavalcante; Martins, Alice Maria Costa; Daher, Elizabeth De Francesco (January 2020). "Kidney disease associated with androgenic–anabolic steroids and vitamin supplements abuse: Be aware!" (in en). Nefrología 40 (1): 26–31. doi:10.1016/j.nefro.2019.06.003. PMID 31585781.
34. ↑ Davani-Davari, Dorna; Karimzadeh, Iman; Khalili, Hossein (December 2019). "The potential effects of anabolic-androgenic steroids and growth hormone as commonly used sport supplements on the kidney: a systematic review" (in en). BMC Nephrology 20 (1). doi:10.1186/s12882-019-1384-0. ISSN 1471-2369. PMID 31151420.
35. ↑ "Weightlifters Bulking Up With Anabolic Steroids Also Do Serious Harm To Kidneys" (in en). 10 December 2009. https://www.cuimc.columbia.edu/news/weightlifters-bulking-anabolic-steroids-also-do-serious-harm-kidneys.
36. ↑ "Bodybuilding With Steroids Damages Kidneys". https://www.sciencedaily.com/releases/2009/10/091029141202.htm.
37. ↑ Ireland, Rebecca (March 2010). "Anabolic steroid abuse can lead to focal segmental glomerulosclerosis" (in en). Nature Reviews Nephrology 6 (3): 130. doi:10.1038/nrneph.2010.5. ISSN 1759-5061. https://www.nature.com/articles/nrneph.2010.5.
38. ↑ Davani-Davari, Dorna; Karimzadeh, Iman; Khalili, Hossein (December 2019). "The potential effects of anabolic-androgenic steroids and growth hormone as commonly used sport supplements on the kidney: a systematic review" (in en). BMC Nephrology 20 (1). doi:10.1186/s12882-019-1384-0. ISSN 1471-2369. PMID 31151420.
39. ↑ "Using steroids to bulk up? Watch for kidney damage". Reuters. https://www.reuters.com/article/business/healthcare-pharmaceuticals/using-steroids-to-bulk-up-watch-for-kidney-damage-idUSTRE59T446.
40. ↑ Lin, Julie; Hu, Frank B.; Curhan, Gary C. (1 May 2010). "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. PMID 20299364.
41. ↑ Lin, Julie; Fung, Teresa T.; Hu, Frank B.; Curhan, Gary C. (1 February 2011). "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. PMID 21251540.
42. ↑ Chen, Wei; Abramowitz, Matthew K. (1 January 2014). "Metabolic acidosis and the progression of chronic kidney disease". BMC Nephrology 15. doi:10.1186/1471-2369-15-55. ISSN 1471-2369. PMID 24708763.
43. ↑ Sebastian, Anthony; Frassetto, Lynda A.; Sellmeyer, Deborah E.; Merriam, Renée L.; Morris, R. Curtis (1 December 2002). "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.
44. ↑ 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. et al. (1 February 2011). "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.
45. ↑ Brenner, B. M.; Meyer, T. W.; Hostetter, T. H. (9 September 1982). "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.
46. ↑ Goraya, Nimrit; Wesson, Donald E. (1 January 2014). "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.
47. ↑ Scialla, Julia J.; Appel, Lawrence J.; Astor, Brad C.; Miller, Edgar R.; Beddhu, Srinivasan; Woodward, Mark; Parekh, Rulan S.; Anderson, Cheryl A. M. (1 July 2011). "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. PMID 21700817.
48. ↑ Kanda, Eiichiro; Ai, Masumi; Kuriyama, Renjiro; Yoshida, Masayuki; Shiigai, Tatsuo (1 January 2014). "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.
49. ↑ Banerjee, Tanushree; Crews, Deidra C.; Wesson, Donald E.; Tilea, Anca; Saran, Rajiv; Rios Burrows, Nilka; Williams, Desmond E.; Powe, Neil R. et al. (1 January 2014). "Dietary acid load and chronic kidney disease among adults in the United States". BMC Nephrology 15. doi:10.1186/1471-2369-15-137. ISSN 1471-2369. PMID 25151260.
50. ↑ Goraya, Nimrit; Simoni, Jan; Jo, Chan-Hee; Wesson, Donald E. (1 March 2013). "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. PMID 23393104.
51. ↑ Deriemaeker, Peter; Aerenhouts, Dirk; Hebbelinck, Marcel; Clarys, Peter (1 March 2010). "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. Bibcode: 2010PFHN...65...77D.
52. ↑ Hansen, Kristoffer Lindskov; Nielsen, Michael Bachmann; Ewertsen, Caroline (23 December 2015). "Ultrasonography of the Kidney: A Pictorial Review". Diagnostics 6 (1): 2. doi:10.3390/diagnostics6010002. ISSN 2075-4418. PMID 26838799.
53. ↑ Kim, Kun Hyung; Lee, Myeong Soo; Kim, Tae-Hun; Kang, Jung Won; Choi, Tae-Young; Lee, Jae Dong (28 June 2016). "Acupuncture and related interventions for symptoms of chronic kidney disease". The Cochrane Database of Systematic Reviews 2016 (6). doi:10.1002/14651858.CD009440.pub2. ISSN 1469-493X. PMID 27349639.
54. ↑ 54.0 54.1 54.2 54.3 54.4 54.5 Tabarrok, Alex (8 January 2010). "The Meat Market". Wall Street Journal. https://www.wsj.com/articles/SB10001424052748703481004574646233272990474.
55. ↑ Scheve, Tom (7 May 2008). "How Organ Donations Work". http://health.howstuffworks.com/medicine/modern-treatments/organ-donation7.htm.
56. ↑ "The Waiting List". http://www.kidneylink.org/TheWaitingList.aspx.
57. ↑ "Top 5 reasons to refer a patient early for kidney transplant". https://www.mayoclinic.org/medical-professionals/transplant-medicine/news/top-5-reasons-to-refer-a-patient-early-for-kidney-transplant/mac-20575082.
58. ↑ "Statistics". https://pharm.ucsf.edu/kidney/need/statistics.
59. ↑ Shi, Bree; Ying, Tracey; Chadban, Steven J. (October 2023). "Survival after kidney transplantation compared with ongoing dialysis for people over 70 years of age: A matched-pair analysis" (in en). American Journal of Transplantation 23 (10): 1551–1560. doi:10.1016/j.ajt.2023.07.006. PMID 37460010. https://linkinghub.elsevier.com/retrieve/pii/S1600613523005786.

Classification|

* ICD-10: N00\- N29
* MeSH: D007674

|

* v
* t
* e

Diseases of the urinary system (N00–N39, 580–599)

Kidney disease|

| Glomerules|

| Primarily
nephrotic|

| Non-proliferative|

* Minimal change
* Focal segmental
* Membranous

|

Proliferative|

* Mesangial proliferative
* Endocapillary proliferative
* Membranoproliferative/mesangiocapillary

By condition|

* Diabetic
* Amyloidosis

Primarily
nephritic,
RPG|

| Type I RPG/Type II hypersensitivity|

* Goodpasture's syndrome

|

Type II RPG/Type III hypersensitivity|

* Post-streptococcal
* Lupus
* DPGN
* IgA/Berger's

Type III RPG/Pauci-immune|

* Granulomatosis with polyangiitis
* Microscopic polyangiitis
* Eosinophilic granulomatosis with polyangiitis

General|

* glomerulonephritis
* glomerulonephrosis

Tubules|

* Renal tubular acidosis
* proximal
* distal
* Acute tubular necrosis
* Genetic
* Fanconi syndrome
* Bartter syndrome
* Gitelman syndrome
* Liddle's syndrome

Interstitium|

* Interstitial nephritis
* Pyelonephritis
* Balkan endemic nephropathy

General|

| General syndromes|

* Nephritis
* Nephrosis
* Renal failure
* Acute renal failure
* Chronic kidney disease
* Uremic pericarditis
* Uremia
* Diabetes insipidus
* Nephrogenic
* Renal papilla
* Renal papillary necrosis
* Major calyx/pelvis
* Hydronephrosis
* Pyonephrosis
* Reflux nephropathy

|

Vascular|

* Renal artery stenosis
* Renal ischemia
* Hypertensive nephropathy
* Renovascular hypertension
* Renal cortical necrosis

Other|

* Analgesic nephropathy
* Renal osteodystrophy
* Nephroptosis
* Abderhalden–Kaufmann–Lignac syndrome

Urinary tract|

| Ureter|

* Ureteritis
* Ureterocele
* Megaureter

|

Bladder|

* Cystitis
* Interstitial cystitis
* Hunner's ulcer
* Trigonitis
* Hemorrhagic cystitis
* Neurogenic bladder dysfunction
* Bladder sphincter dyssynergia
* Vesicointestinal fistula
* Vesicoureteral reflux

Urethra|

* Urethritis
* Non-gonococcal urethritis
* Urethral syndrome
* Urethral stricture/Meatal stenosis
* Urethral caruncle

Any/all|

* Obstructive uropathy
* Urinary tract infection
* Retroperitoneal fibrosis
* Urolithiasis
* Bladder stone
* Kidney stone
* Renal colic
* Malakoplakia
* Urinary incontinence
* Stress
* Urge
* Overflow

Template:Glomerular disease

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