Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died withacute kidney injury.
When used colloquially, the termkidney disease may refer tochronic kidney disease (CKD), an umbrella term for any progressive loss of kidney function over at least three months, from any cause.[2] In contrast, kidney damage over a shorter period of time is known asacute kidney injury.[1]
From a technical standpoint, the heterogenous group ofkidney diseases can be broadly divided into categories based on which anatomical structures are involved: theglomeruli, the filtering capillaries of the kidney;tubules, which carry filtered blood; the renalinterstitium, the fluid-filled space between these structures; and the renalblood vessels, which deliver blood towards and away from the kidney.[1] Glomerular disease, orglomerulonephritis, can be further divided into thenephritic andnephrotic syndromes, which are respectively characterized by blood and protein leaking into the urine.[3]
All forms of kidney disease, glomerular or otherwise, have the potential to damage all four components of the kidney, culminating inend-stage renal disease—the stage of disease at whichdialysis or a kidneytransplant are necessary.[4]
Rates for both chronic kidney disease and mortality have increased, associated with the rising prevalence of diabetes and the aging global population.[5][6] TheWorld Health Organization has reported that "kidney diseases have risen from the world's nineteenth leading cause of death to the ninth, with the number of deaths increasing by 95% between 2000 and 2021."[7] In the United States, prevalence has risen from about one in eight in 2007,[8] to one in seven in 2021.[9]
"Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic disease, affecting a half million Americans.[10] The clinical phenotype can result from at least two different gene defects. One gene that can cause ADPKD has been located on the short arm of chromosome 16."[11]
IgA nephropathy is the most commonglomerulonephritis throughout the world[12] Primary IgA nephropathy is characterized by deposition of theIgAantibody in the glomerulus. The classic presentation (in 40–50% of the cases) is episodic frankhematuria which usually starts within a day or two of a non-specificupper respiratory tract infection (hencesynpharyngitic) as opposed topost-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.
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.
Another possible cause of Kidney disease is due to decreased function ofxanthine oxidase in thepurine degradation pathway. Xanthine oxidase will degradehypoxanthine toxanthine and then touric acid. Xanthine is not very soluble in water; therefore, an increase in xanthine forms crystals (which can lead tokidney stones) and result in damage to the kidney.Xanthine oxidase inhibitors, likeallopurinol, can cause nephropathy.
Despite expensive treatments,lupus nephritis remains a major cause of morbidity and mortality in people with relapsing or refractory lupus nephritis.[14]
COVID-19 is associated with kidney disease. In patients hospitalized with COVID-19, theprevalence of acute kidney injury is estimated to be 28%, and the prevalence ofrenal replacement therapy is estimated to be 9%.[15]
One cause of nephropathy is the long term usage of pain medications known asanalgesics. The pain medicines which can cause kidney problems includeaspirin,acetaminophen, andnonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen and naproxen. 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.).
Kidney disease induced by iodinated contrast media (ICM) is calledcontrast induced nephropathy (CIN) or contrast-inducedacute kidney injury (AKI). Currently, the underlying mechanisms are unclear. But there is a body of evidence that several factors includingapoptosis-induction seem to play a role.[16]
Nephropathy can be associated with some therapies used to treat cancer. The most common form of kidney disease in cancer patients isacute 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 toonconephrology. Several chemotherapeutic agents, for examplecisplatin, are associated with acute and chronic kidney injuries.[17] Newer agents such asanti-vascular endothelial growth factor (anti-VEGF) are also associated with similar injuries, as well asproteinuria,hypertension, andthrombotic microangiopathy.[18]
Lithium, a medication commonly used to treatbipolar disorder andschizoaffective disorders, can causenephrogenic diabetes insipidus; its long-term use can lead to nephropathy.[19] Long termlithium treatment is known to cause chronic kidney disease after 10-20 years of treatment in 1-5% of people.[20][21] End-stage renal disease due to lithium occurs in 0.53% of people versus 0.2% in the general population.[22][23][24] Dosing lithium more than once per day is associated with more kidney damage.[25] Kidney harm can be mitigated by dosing lithium once per day at night and keeping the dose as low as possible.[26] Dosing lithium once per day allows for long periods where the kidney is exposed to low levels of lithium, which minimizes kidney harm.[27]
Regular and long-term use ofanabolic-androgenic steroids (AAS) can cause both acute and chronic kidney disease through several direct and indirect mechanisms.[28][29][30]Focal segmental glomerulosclerosis is the most common condition arising in such cases.[31][32] Discontinuation of AAS in the early stage of Kidney Disease can result in a reversal of the kidney damage.[33][34]
Higher dietary intake of animal protein, animal fat, and cholesterol may increase risk formicroalbuminuria, a sign of kidney function decline,[35] and generally, diets higher in fruits, vegetables, and whole grains but lower in meat andsweets may be protective against kidney function decline.[36] 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 morebase-producing.[37][38][39][40][41][42][43][44][45][46][excessive citations]
Treatment approaches for kidney disease focus on managing the symptoms, controlling the progression, and also treating co-morbidities that a person may have.[48]
Millions of people across the world have kidney disease. Of those millions, several thousand will needdialysis or akidney transplant at itsend-stage.[49] In the United States, as of 2008, 16,500 people needed a kidney transplant.[49] Of those, 5,000 died while waiting for a transplant.[49] Currently, there is a shortage of donors, and in 2007 there were only 64,606 kidney transplants in the world.[49] 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.[49] The act of buying an organ through the black market is illegal in the United States.[50] 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 andhuman leukocyte antigen factors with their donors. They must also have no reactions to theantibodies from the donor's kidneys.[51][49]
For most patients, a kidney transplant offers a significant survival advantage and improvedquality of life compared to remaining on dialysis, often adding years tolife expectancy, though early risks exist, especially with certain donor types or in the elderly, but long-term outcomes favor transplant. Studies consistently show better long-termsurvival rates for transplant recipients, with one-year survival rates often above 90-95% for transplant, while dialysis patients facehigher mortality.[52][53][54]
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 causekidney failure.
^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.Bibcode:2007JAMA..298.2038C.doi:10.1001/jama.298.17.2038.ISSN1538-3598.PMID17986697.
^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.PMID2239929.
^D'Amico, G (1987). "The commonest glomerulonephritis in the world: IgA nephropathy".Q J Med.64 (245):709–727.PMID3329736.
^Longo et al.,Harrison's Principles of Internal Medicine, 18th ed., p. 2982
^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.ISSN1873-0183.PMID22982174.
^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.
^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 (inactive 1 July 2025).ISSN1724-6059.PMID20872351.{{cite journal}}: CS1 maint: DOI inactive as of July 2025 (link)
^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.ISSN0028-4793.PMID7050706.
