Kidney disease

Last updated
Kidney disease
Other namesRenal disease, nephropathy
Kidney - acute cortical necrosis.jpg
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.
Specialty Nephrology, urology   OOjs UI icon edit-ltr-progressive.svg
Complications Uremia, death

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 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. About one in eight Americans (as of 2007) have chronic kidney disease, [2] a rate that is increasing over time. [1]


Deaths due to kidney diseases per million persons in 2012
.mw-parser-output .refbegin{font-size:90%;margin-bottom:0.5em}.mw-parser-output .refbegin-hanging-indents>ul{margin-left:0}.mw-parser-output .refbegin-hanging-indents>ul>li{margin-left:0;padding-left:3.2em;text-indent:-3.2em}.mw-parser-output .refbegin-hanging-indents ul,.mw-parser-output .refbegin-hanging-indents ul li{list-style:none}@media(max-width:720px){.mw-parser-output .refbegin-hanging-indents>ul>li{padding-left:1.6em;text-indent:-1.6em}}.mw-parser-output .refbegin-100{font-size:100%}.mw-parser-output .refbegin-columns{margin-top:0.3em}.mw-parser-output .refbegin-columns ul{margin-top:0}.mw-parser-output .refbegin-columns li{page-break-inside:avoid;break-inside:avoid-column}
.mw-parser-output .legend{page-break-inside:avoid;break-inside:avoid-column}.mw-parser-output .legend-color{display:inline-block;min-width:1.25em;height:1.25em;line-height:1.25;margin:1px 0;text-align:center;border:1px solid black;background-color:transparent;color:black}.mw-parser-output .legend-text{}
187-343 Kidney diseases world map-Deaths per million persons-WHO2012.svg
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. [3]


Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk for microalbuminuria, a sign of kidney function decline, [4] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat and sweets may be protective against kidney function decline. [5] 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. [6] [7] [8] [9] [10] [11] [12] [13] [14] [15]

IgA nephropathy

IgA nephropathy is the most common glomerulonephritis throughout the world [16] 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. [17]


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. [18]


Despite expensive treatments, lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis. [19]

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

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. [20] 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. [21]


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. [22]


Treatment approaches for kidney disease focus on managing the symptoms, controlling the progression, and also treating co-morbidities that a person may have. [1]



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. [23] In the United States, as of 2008, 16,500 people needed a kidney transplant. [23] Of those, 5,000 died while waiting for a transplant. [23] 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. [23] The act of buying an organ through the black market is illegal in the United States. [24] 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. [25] [23]


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

Related Research Articles

Kidney failure Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys are functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, high blood potassium, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anemia.

Chronic kidney disease Progressive loss in kidney function over a period of months or years

Chronic kidney disease (CKD) is a type of kidney disease in which there is gradual loss of kidney function over a period of months to years. Initially there are generally no symptoms; later, symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications include an increased risk of heart disease, high blood pressure, bone disease, and anemia.

IgA nephropathy Disease of the kidney

IgA nephropathy (IgAN), also known as Berger's disease, or synpharyngitic glomerulonephritis, is a disease of the kidney and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney. Aggressive Berger's disease can attack other major organs, such as the liver, skin and heart.

Henoch–Schönlein purpura Medical condition

Henoch–Schönlein purpura (HSP), also known as IgA vasculitis, is a disease of the skin, mucous membranes, and sometimes other organs that most commonly affects children. In the skin, the disease causes palpable purpura, often with joint pain and abdominal pain. With kidney involvement, there may be a loss of small amounts of blood and protein in the urine, but this usually goes unnoticed; in a small proportion of cases, the kidney involvement proceeds to chronic kidney disease. HSP is often preceded by an infection, such as a throat infection.

Glomerulonephritis Medical condition

Glomerulonephritis (GN) is a term used to refer to several kidney diseases. Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component.

Metabolic acidosis Medical condition

Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low, normal, to high.

Diabetic nephropathy Chronic loss of kidney function

Diabetic nephropathy, also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. Diabetic nephropathy is one of the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. 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 renal disease. It usually is slowly progressive over years.

Lupus nephritis Inflammation of the kidneys

Lupus nephritis is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. It is a type of glomerulonephritis in which the glomeruli become inflamed. As the result of SLE, the cause of glomerulonephritis is said to be secondary and has a different pattern and outcome from conditions with a primary cause originating in the kidney.

Membranous glomerulonephritis Medical condition

Membranous glomerulonephritis (MGN) is a slowly progressive disease of the kidney affecting mostly people between ages of 30 and 50 years, usually Caucasian.

Nephritic syndrome Medical condition

Nephritic syndrome is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation. It often occurs in the glomerulus, where it is called glomerulonephritis. Glomerulonephritis is characterized by inflammation and thinning of the glomerular basement membrane and the occurrence of small pores in the podocytes of the glomerulus. These pores become large enough to permit both proteins and red blood cells to pass into the urine. By contrast, nephrotic syndrome is characterized by proteinuria and a constellation of other symptoms that specifically do not include hematuria. Nephritic syndrome, like nephrotic syndrome, may involve low level of albumin in the blood due to the protein albumin moving from the blood to the urine.

Microalbuminuria is a term to describe a moderate increase in the level of urine albumin. It occurs when the kidney leaks small amounts of albumin into the urine, in other words, when an abnormally high permeability for albumin in the glomerulus of the kidney occurs. Normally, the kidneys filter albumin, so if albumin is found in the urine, then it is a marker of kidney disease. The term microalbuminuria is now discouraged by Kidney Disease Improving Global Outcomes and has been replaced by moderately increased albuminuria.

Interstitial nephritis Medical condition

Interstitial nephritis, also known as tubulointerstitial nephritis, is inflammation of the area of the kidney known as the renal interstitium, which consists of a collection of cells, extracellular matrix, and fluid surrounding the renal tubules. In addition to providing a scaffolding support for the tubular architecture, the interstitium has been shown to participate in the fluid and electrolyte exchange as well as endocrine functions of the kidney.

Phosphate nephropathy or nephrocalcinosis is an adverse renal condition that arises with a formation of phosphate crystals within the kidney's tubules. This renal insufficiency is associated with the use of oral sodium phosphate (OSP) such as C.B. Fleet's Phospho soda and Salix's Visocol, for bowel cleansing prior to a colonoscopy.   

Analgesic nephropathy Medical condition

Analgesic nephropathy is injury to the kidneys caused by analgesic medications such as aspirin, bucetin, phenacetin, and paracetamol. The term usually refers to damage induced by excessive use of combinations of these medications, especially combinations that include phenacetin. It may also be used to describe kidney injury from any single analgesic medication.

Balkan endemic nephropathy Medical condition

Balkan endemic nephropathy (BEN) is a form of interstitial nephritis causing kidney failure. It was first identified in the 1920s among several small, discrete communities along the Danube River and its major tributaries, in the modern countries of Croatia, Bosnia and Herzegovina, Serbia, Romania, and Bulgaria. It is caused by small long-term doses of aristolochic acid in the diet. The disease primarily affects people 30 to 60 years of age. Doses of the toxin are usually low and people moving to endemic areas typically develop the condition only when they have lived there for 10-20 years. People taking higher doses of aristolochic acid have developed kidney failure after shorter durations of exposure.

Urologic diseases or conditions include urinary tract infections, kidney stones, bladder control problems, and prostate problems, among others. Some urologic conditions do not affect a person for that long and some are lifetime conditions. Kidney diseases are normally investigated and treated by nephrologists, while the specialty of urology deals with problems in the other organs. Gynecologists may deal with problems of incontinence in women.

Glomerulonephrosis is a non-inflammatory disease of the kidney (nephrosis) presenting primarily in the glomerulus as Nephrotic Syndrome. The nephron is the functional unit of the kidney and it contains the glomerulus, which acts as a filter for blood to retain proteins and blood lipids. Damage to these filtration units results in important blood contents being released as waste in urine. This disease can be characterized by symptoms such as fatigue, swelling, and foamy urine, and can lead to chronic kidney disease and ultimately end-stage renal disease, as well as cardiovascular diseases. Glomerulonephrosis can present as either primary glomerulonephrosis or secondary glomerulonephrosis.

Diffuse proliferative glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions in SLE and is also the most common, occurring in 35% to 60% of patients. Most of the glomeruli show endothelial and mesangial proliferation, affecting the entire glomerulus, leading to diffuse hypercellularity of the glomeruli, producing in some cases epithelial crescents that fill Bowman's space. When extensive, immune complexes create an overall thickening of the capillary wall, resembling rigid "wire loops" on routine light microscopy. Electron microscopy reveals electron-dense subendothelial immune complexes. Immune complexes can be visualized by staining with fluorescent antibodies directed against immunoglobulins or complement, resulting in a granular fluorescent staining pattern. In due course, glomerular injury gives rise to scarring (glomerulosclerosis). Most of these patients have hematuria with moderate to severe proteinuria, hypertension, and renal insufficiency.

Epstein syndrome Medical condition

Epstein syndrome is a rare genetic disease characterized by a mutation in the MYH9 gene in nonmuscle myosin. This disease affects the patient's renal system and can result in kidney failure. Epstein Syndrome was first discovered in 1972 when two families had similar symptoms to Alport syndrome. Epstein syndrome and other Alport-like disorders were seen to be caused by mutations in the MYH9 gene, however, Epstein syndrome differs as it was more specifically linked to a mutation on the R702 codon on the MYH9 gene. Diseases with mutations on the MYH9 gene also include May–Hegglin anomaly, Sebastian syndrome and Fechtner syndrome.

Chronic Kidney Disease of unknown etiology (CKDu) is an increasing health concern in Sri Lanka. CKDu is recognized as chronic kidney disease without the usual associated causative factors. The first cases of CKDu were reported in Sri Lanka's North Central Province (NCP). Chronic kidney disease, was identified as the 8th leading cause of in-hospital mortality in Sri Lanka, and the leading cause of death in Anuradhapura and Polonnaruwa in 2016. This rise in mortality coincided with the increasing cases of CKDu seen across the country. Studies have shown an estimated 70,000 CKDu patients in high risk areas. Various possible causes for CKDu in Sri Lankans have been investigated, including poisoning from metals, cyanobacteria toxins, agrochemicals, and heat stress, but no definite causes have been identified.


  1. 1 2 3 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 (6): CD009440. doi:10.1002/14651858.CD009440.pub2. ISSN   1469-493X. PMID   27349639.
  2. 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.
  3. Longo et al., Harrison's Principles of Internal Medicine, 18th ed., p.2982
  4. 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.
  5. 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.
  6. 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.
  7. 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. doi: 10.1093/ajcn/76.6.1308 . ISSN   0002-9165. PMID   12450898.
  8. 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. doi:10.5301/jn.2010.5711. ISSN   1724-6059. PMID   20872351.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. 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.
  14. 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.
  15. 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.
  16. D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy". Q J Med. 64 (245): 709–727. PMID   3329736.
  17. 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.
  18. Grünfeld, JP; Rossier, BC (May 2009). "Lithium nephrotoxicity revisited". Nat Rev Nephrol. 5 (5): 270–6. doi:10.1038/nrneph.2009.43. PMID   19384328. S2CID   36253297.
  19. 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.
  20. Portilla D, Safar AM, Shannon ML, Penson RT. Cisplatin nephrotoxicity. In: UpToDate, Palevsky PM (Ed), UpToDate, Waltham, MA, 2013.
  21. 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.
  22. 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.
  23. 1 2 3 4 5 6 Tabarrok, Alex (January 8, 2010). "The Meat Market". Wall Street Journal.
  24. Scheve, Tom (7 May 2008). "How Organ Donations Work". HowStuffWorks. Retrieved 9 March 2015.