Kidney disease

Not to be confused with Neuropathy.
Nephropathy
Classification and external resources
Specialty urology
ICD-10 N00- N29
MeSH D007674

Kidney disease, also known as nephropathy or renal disease, is damage to or disease of a kidney. Nephritis is inflammatory kidney disease. Nephrosis is noninflammatory nephropathy. Kidney disease usually causes kidney failure (renal failure) to more or less degree, with the amount depending on the type of disease. In precise usage, disease denotes the structural and etiologic disease entity whereas failure denotes the dysfunction (lack of working well, that is, impaired renal function); but in common usage these meanings overlap; for example, the terms chronic kidney disease and chronic renal failure are usually considered synonymous. Acute kidney disease has often been called acute renal failure, although nephrologists now often tend to call it acute kidney injury. About 1 in 8 Americans suffer from chronic kidney disease.[1]

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 IgA 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

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 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

Main article: Diabetic nephropathy

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.[2]

Diet

Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for microalbuminuria, a sign of kidney function decline,[3] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.[4] 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.[5][6][7][8][9][10][11][12][13][14]

IgA nephropathy

Main article: IgA nephropathy

IgA nephropathy is the most common glomerulonephritis throughout the world [15] 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.[16]

Lithium

The long-term use of lithium, a medication commonly used to treat bipolar disorder and schizoaffective disorders, is known to cause nephropathy.

Lupus

Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.[17]

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 of 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

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 (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.[18] 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.[19]

Development

Kidney disease is a chronic non-communicable disease, having serious consequences if it cannot be controlled effectively. Generally, the process of kidney disease development is from light to serious. The process of most kidney diseases is renal insufficiency, renal failure, and then uremia.

Transplants

Millions of people across the world suffer from kidney disease. Of those millions, several thousand will eventually or do need kidney transplants.[20] Out of those millions in the world, 16,500 in the United States needed a kidney transplant in 2008.[21] Of those 16,500 people, 5,000 died while waiting for a transplant.[22] 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.[24] The act of buying an organ through the black market is illegal in the United States.[25] 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. [26]

See also

References

  1. ↑ 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.
  2. ↑ Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.2982
  3. ↑ 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: CJASN. 5 (5): 836–843. doi:10.2215/CJN.08001109. ISSN 1555-905X. PMC 2863979Freely accessible. PMID 20299364.
  4. ↑ 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: The Official Journal of the National Kidney Foundation. 57 (2): 245–254. doi:10.1053/j.ajkd.2010.09.027. ISSN 1523-6838. PMC 3026604Freely accessible. PMID 21251540.
  5. ↑ 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 4233646Freely accessible. PMID 24708763.
  6. ↑ 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. ISSN 0002-9165. PMID 12450898.
  7. ↑ 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. ISSN 1724-6059. PMID 20872351.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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: CJASN. 6 (7): 1526–1532. doi:10.2215/CJN.00150111. ISSN 1555-905X. PMC 3552445Freely accessible. PMID 21700817.
  11. ↑ 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.
  12. ↑ 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 4151375Freely accessible. PMID 25151260.
  13. ↑ 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: CJASN. 8 (3): 371–381. doi:10.2215/CJN.02430312. ISSN 1555-905X. PMC 3586961Freely accessible. PMID 23393104.
  14. ↑ 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.
  15. ↑ D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy.". Q J Med. 64 (245): 709–727. PMID 3329736.
  16. ↑ 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. doi:10.2174/187152306776872442.
  17. ↑ 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.
  18. ↑ 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
  19. ↑ 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 3058726Freely accessible. PMID 21146124.
  20. ↑ Tabarrok, Alex (January 8, 2010). The Meat Market. Wall Street Journal.
  21. ↑ Tabarrok, Alex (January 8, 2010). The Meat Market. Wall Street Journal.
  22. ↑ Tabarrok, Alex (January 8, 2010). The Meat Market. Wall Street Journal.
  23. ↑ Tabarrok, Alex (January 8, 2010). The Meat Market. Wall Street Journal.
  24. ↑ Tabarrok, Alex (January 8, 2010). The Meat Market. Wall Street Journal.
  25. ↑ Scheve, Tom. "How Organ Donations Work". HowStuffWorks. Retrieved 9 March 2015.
  26. ↑ Tabarrok, Alex (January 8, 2010). The Meat Market. Wall Street Journal.
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