Kidney disease

Kidney disease, or renal disease, also known 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 causes the gradual loss of kidney function over time. 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) suffer from chronic kidney disease.[1]

Kidney Disease


Kidney diseases world map-Deaths per million persons-WHO2012
Deaths due to kidney diseases per million persons in 2012

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.


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).


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]


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

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]


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


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

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]


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.[20]


Millions of people across the world suffer from kidney disease. Of those millions, several thousand will need dialysis or a kidney transplant at its end-stage.[21] In the United States, as of 2008, 16,500 people needed a kidney transplant.[21] Of those, 5,000 died while waiting for a transplant.[21] Currently, there is a shortage of donors, and in 2007 there were only 64,606 kidney transplants in the world.[21] 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.[21] The act of buying an organ through the black market is illegal in the United States.[22] 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.[23][21]


Kidney disease is a non-communicable disease. It 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


  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. 5 (5): 836–843. doi:10.2215/CJN.08001109. ISSN 1555-905X. PMC 2863979. 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. 57 (2): 245–254. doi:10.1053/j.ajkd.2010.09.027. ISSN 1523-6838. PMC 3026604. 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 4233646. 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. 6 (7): 1526–1532. doi:10.2215/CJN.00150111. ISSN 1555-905X. PMC 3552445. 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 4151375. 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. 8 (3): 371–381. doi:10.2215/CJN.02430312. ISSN 1555-905X. PMC 3586961. 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.
  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 3058726. PMID 21146124.
  20. ^ Content initially copied from: Hansen, Kristoffer; Nielsen, Michael; Ewertsen, Caroline (2015). "Ultrasonography of the Kidney: A Pictorial Review". Diagnostics. 6 (1): 2. doi:10.3390/diagnostics6010002. ISSN 2075-4418. PMC 4808817. (CC-BY 4.0)
  21. ^ a b c d e f Tabarrok, Alex (January 8, 2010). "The Meat Market". Wall Street Journal.
  22. ^ Scheve, Tom. "How Organ Donations Work". HowStuffWorks. Retrieved 9 March 2015.

External links

Acute kidney injury

Acute kidney injury (AKI), previously called acute renal failure (ARF), is an abrupt loss of kidney function that develops within 7 days.Its causes are numerous. Generally it occurs because of damage to the kidney tissue caused by decreased kidney blood flow (kidney ischemia) from any cause (e.g., low blood pressure), exposure to substances harmful to the kidney, an inflammatory process in the kidney, or an obstruction of the urinary tract that impedes the flow of urine. AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine.

AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects on other organ systems, including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future. Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy.

Alport syndrome

Alport syndrome is a genetic disorder affecting around 1 in 5,000-10,000 children, characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. Alport syndrome can also affect the eyes, though the changes do not usually affect sight, except when changes to the lens occur in later life. Blood in urine is universal. Proteinuria is a feature as kidney disease progresses.

The disorder was first identified in a British family by the physician Cecil A. Alport in 1927. Alport Syndrome once also had the label hereditary nephritis, but this is misleading as there are many other causes of hereditary kidney disease and 'nephritis'.

Alport syndrome is caused by an inherited defect in type IV collagen—a structural material that is needed for the normal function of different parts of the body. Since type IV collagen is found in the ears, eyes, and kidneys, this explains why Alport syndrome affects different seemingly unrelated parts of the body (ears, eyes, kidneys, etc.).

Autosomal dominant polycystic kidney disease

Autosomal dominant polycystic kidney disease (ADPKD) is the most prevalent, potentially lethal, monogenic human disorder. It is associated with large interfamilial and intrafamilial variability, which can be explained to a large extent by its genetic heterogeneity and modifier genes. It is also the most common of the inherited cystic kidney diseases — a group of disorders with related but distinct pathogenesis, characterized by the development of renal cysts and various extrarenal manifestations, which in case of ADPKD include cysts in other organs, such as the liver, seminal vesicles, pancreas, and arachnoid membrane, as well as other abnormalities, such as intracranial aneurysms and dolichoectasias, aortic root dilatation and aneurysms, mitral valve prolapse, and abdominal wall hernias. Over 50% of patients with ADPKD eventually develop end stage kidney disease and require dialysis or kidney transplantation. ADPKD is estimated to affect at least one in every 1000 individuals worldwide, making this disease the most common inherited kidney disorder with a diagnosed prevalence of 1:2000 and incidence of 1:3000-1:8000 in a global scale.

Autosomal recessive polycystic kidney disease

Autosomal recessive polycystic kidney disease (ARPKD) is the recessive form of polycystic kidney disease. It is associated with a group of congenital fibrocystic syndromes. Mutations in the PKHD1 (chromosomal locus 6p12.2) cause ARPKD.

Chronic kidney disease

Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months or years. Early on there are typically no symptoms. Later, leg swelling, feeling tired, vomiting, loss of appetite, or confusion may develop. Complications may include heart disease, high blood pressure, bone disease, or anemia.Causes of chronic kidney disease include diabetes, high blood pressure, glomerulonephritis, and polycystic kidney disease. Risk factors include a family history of the condition. Diagnosis is generally by blood tests to measure the glomerular filtration rate and urine tests to measure albumin. Further tests such as an ultrasound or kidney biopsy may be done to determine the underlying cause. A number of different classification systems exist.Screening at-risk people is recommended. Initial treatments may include medications to manage blood pressure, blood sugar, and lower cholesterol. NSAIDs should be avoided. Other recommended measures include staying active and certain dietary changes. Severe disease may require hemodialysis, peritoneal dialysis, or a kidney transplant. Treatments for anemia and bone disease may also be required.Chronic kidney disease affected 753 million people globally in 2016, including 417 million females and 336 million males. In 2015 it resulted in 1.2 million deaths, up from 409,000 in 1990. The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000.

Diabetic nephropathy

Diabetic nephropathy (DN), also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. Protein loss in the urine due to damage to the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) and result in the nephrotic syndrome. Likewise, the estimated glomerular filtration rate (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage kidney disease (ESKD). It usually is slowly progressive over years.Pathophysiologic abnormalities in DN begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the nephrons. (There are normally about 750,000–1.5 million nephrons in each adult kidney). Initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration; this gradually changes to hypofiltration over time. Concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.The status of DN may be monitored by measuring two values: the amount of protein in the urine - proteinuria; and a blood test called the serum creatinine. The amount of the proteinuria reflects the degree of damage to any still-functioning glomeruli. The value of the serum creatinine can be used to calculate the estimated glomerular filtration rate (eGFR), which reflects the percentage of glomeruli which are no longer filtering the blood. Treatment with an angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB), which dilates the arteriole exiting the glomerulus, thus reducing the blood pressure within the glomerular capillaries, which may slow (but not stop) progression of the disease. Three classes of diabetes medications – GLP-1 agonists, DPP-4 inhibitors, and SGLT2 inhibitors – are also thought to slow the progression of diabetic nephropathy.Diabetic nephropathy is the most common cause of ESKD and is a serious complication that affects approximately one quarter of adults with diabetes in the United States. Affected individuals with end-stage kidney disease often require hemodialysis and eventually kidney transplantation to replace the failed kidney function. Diabetic nephropathy is associated with an increased risk of death in general, particularly from cardiovascular disease.

Hypertensive kidney disease

Hypertensive kidney disease is a medical condition referring to damage to the kidney due to chronic high blood pressure. HN can be divided into two types: benign and malignant. Benign nephrosclerosis is common in individuals over the age of 60 while malignant nephrosclerosis is uncommon and affects 1-5% of individuals with high blood pressure, that have diastolic blood pressure passing 130 mm Hg. It should be distinguished from renovascular hypertension, which is a form of secondary hypertension. In addition, HN can be referred to as hypertensive nephrosclerosis, benign nephrosclerosis, and nephroangiosclerosis.

Jack Matheson

John "Jack" Matheson (July 25, 1924 – January 24, 2011) was a Canadian sports journalist known for his wide coverage of sports for the Winnipeg Tribune from 1946 to 1980.Matheson was born on July 25, 1924 in Winnipeg, Manitoba. He began his newspaper career in 1946 with the Winnipeg Tribune. He became the sports editor for the newspaper in 1959, a position he held until the newspaper ceased publication in 1980. Matheson covered a variety of sports, including hockey, curling and football with the Tribune, and on the radio, working with CJOB. He is most noted for his coverage of the Winnipeg Blue Bombers, and various curling events.Matheson was inducted into the Canadian Football Hall of Fame in 1986 and Manitoba Hockey Hall of Fame in 1999. The Jack Matheson Award is annually presented by the Manitoba Sportswriters and Sportscasters Association to aspiring students in sports communications.Matheson was married to his wife Peggy for 63 years until his death. Matheson's son, James Donald "Jim" is also a distinguished sports writer, working for the Edmonton Journal since 1970. Jim was inducted into the Hockey Hall of Fame as a media honoree and received the Elmer Ferguson Memorial Award in 2000.Jack Matheson died January 24, 2011 in Winnipeg at the Grace Hospital of kidney disease.


The kidneys are two bean-shaped organs found in vertebrates. They are located on the left and right in the retroperitoneal space, and in adult humans are about 11 centimetres (4.3 in) in length. They receive blood from the paired renal arteries; blood exits into the paired renal veins. Each kidney is attached to a ureter, a tube that carries excreted urine to the bladder.

The nephron is the structural and functional unit of the kidney. Each human adult kidney contains around 1 million nephrons, while a mouse kidney contains only about 12,500 nephrons. The kidney participates in the control of the volume of various body fluid compartments, fluid osmolality, acid-base balance, various electrolyte concentrations, and removal of toxins. Filtration occurs in the glomerulus: one-fifth of the blood volume that enters the kidneys is filtered. Examples of substances reabsorbed are solute-free water, sodium, bicarbonate, glucose, and amino acids. Examples of substances secreted are hydrogen, ammonium, potassium and uric acid. The kidneys also carry out functions independent of the nephron. For example, they convert a precursor of vitamin D to its active form, calcitriol; and synthesize the hormones erythropoietin and renin.

Renal physiology is the study of kidney function. Nephrology is the medical specialty which addresses diseases of kidney function: these include chronic kidney disease, nephritic and nephrotic syndromes, acute kidney injury, and pyelonephritis. Urology addresses diseases of kidney (and urinary tract) anatomy: these include cancer, renal cysts, kidney stones and ureteral stones, and urinary tract obstruction.Procedures used in the management of kidney disease include chemical and microscopic examination of the urine (urinalysis), measurement of kidney function by calculating the estimated glomerular filtration rate (eGFR) using the serum creatinine; and kidney biopsy and CT scan to evaluate for abnormal anatomy. Dialysis and kidney transplantation are used to treat kidney failure; one (or both sequentially) of these are almost always used when renal function drops below 15%. Nephrectomy is frequently used to cure renal cell carcinoma.

Kidney failure

Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys no longer function. It is divided into acute kidney failure (cases that develop rapidly) and chronic kidney failure (those that are long term). Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, or confusion. Complications of acute disease may include uremia, high blood potassium, or volume overload. Complications of chronic disease may include heart disease, high blood pressure, or anemia.Causes of acute kidney failure include low blood pressure, blockage of the urinary tract, certain medications, muscle breakdown, and hemolytic uremic syndrome. Causes of chronic kidney failure include diabetes, high blood pressure, nephrotic syndrome, and polycystic kidney disease. Diagnosis of acute disease is often based on a combination of factors such as decrease urine production or increased serum creatinine. Diagnosis of chronic disease is typically based on a glomerular filtration rate (GFR) of less than 15 or the need for renal replacement therapy. It is also equivalent to stage 5 chronic kidney disease.Treatment of acute disease typically depends on the underlying cause. Treatment of chronic disease may include hemodialysis, peritoneal dialysis, or a kidney transplant. Hemodialysis uses a machine to filter the blood outside the body. In peritoneal dialysis specific fluid is placed into the abdominal cavity and then drained, with this process being repeated multiple times per day. Kidney transplantation involves surgically placing a kidney from someone else and then taking immunosuppressant medication to prevent rejection. Other recommended measures from chronic disease include staying active and specific dietary changes.In the United States acute disease affects about 3 per 1,000 people a year. Chronic disease affects about 1 in 1,000 people with 3 per 10,000 people newly develop the condition each year. Acute disease is often reversible while chronic disease often is not. With appropriate treatment many with chronic disease can continue working.

Medullary cystic kidney disease

Medullary cystic kidney disease (MCKD) is an autosomal dominant kidney disorder characterized by tubulointerstitial sclerosis leading to end-stage renal disease. Because the presence of cysts is neither an early nor a typical diagnostic feature of the disease, and because at least 4 different gene mutations may give rise to the condition, the name autosomal dominant tubulointerstitial kidney disease (ADTKD) has been proposed, to be appended with the underlying genetic variant for a particular individual. Importantly, if cysts are found in the medullary collecting ducts they can result in a shrunken kidney, unlike that of polycystic kidney disease. There are two known forms of medullary cystic kidney disease, mucin-1 kidney disease 1 (MKD1) and mucin-2 kidney disease/uromodulin kidney disease (MKD2). A third form of the disease occurs due to mutations in the gene encoding renin (ADTKD-REN), and has formerly been known as familial juvenile hyperuricemic nephropathy type 2.


Nephrology (from Greek nephros "kidney", combined with the suffix -logy, "the study of") is a specialty of medicine and pediatrics that concerns itself with the kidneys: the study of normal kidney function and kidney disease, the preservation of kidney health, and the treatment of kidney disease, from diet and medication to renal replacement therapy (dialysis and kidney transplantation).

Nephrology also studies systemic conditions that affect the kidneys, such as diabetes and autoimmune disease; and systemic diseases that occur as a result of kidney disease, such as renal osteodystrophy and hypertension. A physician who has undertaken additional training and become certified in nephrology is called a nephrologist.

The term "nephrology" was first used in about 1960. Before then, the specialty was usually referred to as "kidney medicine."

Polycystic kidney disease

Polycystic kidney disease (PKD or PCKD, also known as polycystic kidney syndrome) is a genetic disorder in which the renal tubules become structurally abnormal, resulting in the development and growth of multiple cysts within the kidney. These cysts may begin to develop in utero, in infancy, in childhood, or in adulthood. Cysts are non-functioning tubules filled with fluid pumped into them, which range in size from microscopic to enormous, crushing adjacent normal tubules and eventually rendering them non-functional as well.

PKD is caused by abnormal genes which produce a specific abnormal protein; this protein has an adverse effect on tubule development. PKD is a general term for two types, each having their own pathology and genetic cause: autosomal dominant polycystic kidney disease (ADPKD) and autosomal recessive polycystic kidney disease (ARPKD). The abnormal gene exists in all cells in the body; as a result, cysts may occur in the liver, seminal vesicles, and pancreas. This genetic defect can also cause aortic root aneurysms, and aneurysms in the circle of Willis cerebral arteries, which if they rupture, can cause a subarachnoid hemorrhage.

Diagnosis may be suspected from one, some, or all of the following: new onset flank pain or red urine; a positive family history; palpation of enlarged kidneys on physical exam; an incidental finding on abdominal sonogram; or an incidental finding of abnormal kidney function on routine lab work (BUN, serum creatinine, or eGFR). Definitive diagnosis is made by abdominal CT exam.

Complications include hypertension due to the activation of the renin–angiotensin–aldosterone system (RAAS), frequent cyst infections, urinary bleeding, and declining renal function. Hypertension is treated with angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs). Infections are treated with antibiotics. Declining renal function is treated with renal replacement therapy (RRT): dialysis and/or transplantation. Management from the time of the suspected or definitive diagnosis is by a board-certified nephrologist.

Polycystin 1

Polycystin 1 (often abbreviated to PC1) is a protein that in humans is encoded by the PKD1 gene . Mutations of PKD1 are associated with most cases of autosomal dominant polycystic kidney disease, a severe hereditary disorder of the kidneys characterised by the development of renal cysts and severe kidney dysfunction .

Polycystin 2

Polycystin-2 is a protein that in humans is encoded by the PKD2 gene.This gene encodes a member of the polycystin protein family, called TRPP2, previously known as polycystin-2, PC2 or APKD2. TRPP2 contains multiple transmembrane domains, and cytoplasmic N- and C-termini. The protein may be an integral membrane protein involved in cell-cell/matrix interactions. TRPP2 may function in renal tubular development, morphology, and function, and may modulate intracellular calcium homeostasis and other signal transduction pathways. This protein interacts with polycystin 1 (TRPP1) to produce cation-permeable currents. It was discovered by Stefan Somlo at Yale University.

Renal function

Renal function, in nephrology, is an indication of the kidney's condition and its role in renal physiology. Glomerular filtration rate (GFR) describes the flow rate of filtered fluid through the kidney. Creatinine clearance rate (CCr or CrCl) is the volume of blood plasma that is cleared of creatinine per unit time and is a useful measure for approximating the GFR. Creatinine clearance exceeds GFR due to creatinine secretion, which can be blocked by cimetidine. In alternative fashion, overestimation by older serum creatinine methods resulted in an underestimation of creatinine clearance, which provided a less biased estimate of GFR. Both GFR and CCr may be accurately calculated by comparative measurements of substances in the blood and urine, or estimated by formulas using just a blood test result (eGFR and eCCr).

The results of these tests are used to assess the excretory function of the kidneys. Staging of chronic kidney disease is based on categories of GFR as well as albuminuria and cause of kidney disease.Dosage of drugs that are excreted primarily via urine may need to be modified based on either GFR or creatinine clearance.

Renal osteodystrophy

Renal osteodystrophy is currently defined as an alteration of bone morphology in patients with chronic kidney disease (CKD). It is one measure of the skeletal component of the systemic disorder of chronic kidney disease-mineral and bone disorder (CKD-MBD). The term "renal osteodystrophy" was coined in 1943, 60 years after an association was identified between bone disease and renal failure.The traditional types of renal osteodystrophy have been defined on the basis of turnover and mineralization as follows: 1) mild, slight increase in turnover and normal mineralization; 2) osteitis fibrosa, increased turnover and normal mineralization; 3) osteomalacia, decreased turnover and abnormal mineralization; 4) adynamic, decreased turnover and acellularity; and, 5) mixed, increased turnover with abnormal mineralization. A Kidney Disease: Improving Global Outcomes report has suggested that bone biopsies in patients with CKD should be characterized by determining bone turnover, mineralization, and volume (TMV system).On the other hand, CKD-MBD is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: 1) abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; 2) abnormalities in bone turnover, mineralization, volume, linear growth, or strength (renal osteodystrophy); and 3) vascular or other soft-tissue calcification.


TRPP (transient receptor potential polycystic) is a family of transient receptor potential ion channels which when mutated can cause polycystic kidney disease.


Tetracapsuloides bryosalmonae is a myxozoan parasite of salmonid fish. It is the only species currently recognized in the monotypic genus Tetracapsuloides. It is the cause of Proliferative Kidney Disease (PKD), one of the most serious parasitic diseases of salmonid populations in Europe and North America[1] that can result in losses of up to 90% in infected populations.

Diseases of the urinary system (N00–N39, 580–599)
Kidney disease
Urinary tract

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