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Kidney disease

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(Redirected from Renal hypertrophy)
Not to be confused with neuropathy.
Kidney disease
Other namesRenal 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.
SpecialtyNephrology, urology Edit this on Wikidata
ComplicationsUremia, 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.

Rates for both chronic kidney disease and mortality have increased, associated with the rising prevalence of diabetes and the ageing global population.[2][3] 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."[4] In the United States, prevalence has risen from about one in eight in 2007,[5] to one in seven in 2021.[6]

Causes

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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, diabetes mellitus and high blood pressure (hypertension), which lead to diabetic nephropathy and hypertensive nephropathy, respectively.

Analgesics

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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 ed.).

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

Diabetes

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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.[7]

Autosomal dominant polycystic kidney disease

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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."[8] The same article also goes on to say that millions of Americans are effected by this disease and is very common.

COVID-19

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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%.[9]

Diet

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Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for microalbuminuria, a sign of kidney function decline,[10] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline.[11] 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.[12][13][14][15][16][17][18][19][20][21]

IgA nephropathy

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Main article: IgA nephropathy

IgA nephropathy is the most common glomerulonephritis throughout the world [22] 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

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Main article: 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.[23]

Lithium

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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]

Lupus

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Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.[25]

Xanthine oxidase deficiency

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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 stones) and result in damage to the kidney. Xanthine oxidase inhibitors, like allopurinol, can cause nephropathy.

Polycystic disease of the kidneys

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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

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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.[26] 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.[27]

Diagnosis

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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.[28]

Treatment

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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

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Main article: Kidney dialysis

Transplantation

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Main article: 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.[29] In the United States, as of 2008, 16,500 people needed a kidney transplant.[29] Of those, 5,000 died while waiting for a transplant.[29] Currently, there is a shortage of donors, and in 2007 there were only 64,606 kidney transplants in the world.[29] 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.[29] The act of buying an organ through the black market is illegal in the United States.[30] 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.[31][29]

Prognosis

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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

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References

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  1. ^ a b 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. 2016 (6): CD009440. doi:10.1002/14651858.CD009440.pub2. ISSN 1469-493X. PMC 8406453. PMID 27349639.
  2. ^ Imai, Enyu; Matsuo, Seiichi (2008-06-28). "Chronic kidney disease in Asia". The Lancet. 371 (9631): 2147–2148. doi:10.1016/S0140-6736(08)60928-9. PMID 18586155. Retrieved 2024-08-12.
  3. ^ James, Matthew T; Hemmelgarn, Brenda R; Tonelli, Marcello (2010-04-10). "Early recognition and prevention of chronic kidney disease". The Lancet. 375 (9722): 1296–1309. doi:10.1016/S0140-6736(09)62004-3. PMID 20382326. Retrieved 2024-08-12.
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  6. ^ "Chronic Kidney Disease in the United States, 2023". www.cdc.gov. 2024-05-15. Retrieved 2024-08-12.
  7. ^ Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p. 2982
  8. ^ 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.
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  17. ^ 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.
  18. ^ 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.
  19. ^ 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.
  20. ^ 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.
  21. ^ 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.
  22. ^ D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy". Q J Med. 64 (245): 709–727. PMID 3329736.
  23. ^ 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.
  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. S2CID 36253297.
  25. ^ 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.
  26. ^ 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
  27. ^ 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.
  28. ^ 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.
  29. ^ a b c d e f Tabarrok, Alex (January 8, 2010). "The Meat Market". Wall Street Journal.
  30. ^ Scheve, Tom (7 May 2008). "How Organ Donations Work". HowStuffWorks. Retrieved 9 March 2015.
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