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Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, 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, hyperkalaemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.
Uremia is the term for high levels of urea in the blood. Urea is one of the primary components of urine. It can be defined as an excess in the blood of amino acid and protein metabolism end products, such as urea and creatinine, which would be normally excreted in the urine. Uremic syndrome can be defined as the terminal clinical manifestation of kidney failure. It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. The former denotation will be used for the rest of the article.
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 (CKD) is a type of kidney disease in which a gradual loss of kidney function occurs over a period of months to years. Initially generally no symptoms are seen, but later symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications can relate to hormonal dysfunction of the kidneys and include high blood pressure, bone disease, and anemia. Additionally CKD patients have markedly increased cardiovascular complications with increased risks of death and hospitalization.
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 to high.
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine. Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury. Symptoms of protein toxicity include unexplained vomiting and loss of appetite. Untreated protein toxicity can lead to serious complications such as seizures, encephalopathy, further kidney damage, and even death.
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 kidney failure.
A non-communicable disease (NCD) is a disease that is not transmissible directly from one person to another. NCDs include Parkinson's disease, autoimmune diseases, strokes, heart diseases, cancers, diabetes, chronic kidney disease, osteoarthritis, osteoporosis, Alzheimer's disease, cataracts, and others. NCDs may be chronic or acute. Most are non-infectious, although there are some non-communicable infectious diseases, such as parasitic diseases in which the parasite's life cycle does not include direct host-to-host transmission.
Cystatin C or cystatin 3, a protein encoded by the CST3 gene, is mainly used as a biomarker of kidney function. Recently, it has been studied for its role in predicting new-onset or deteriorating cardiovascular disease. It also seems to play a role in brain disorders involving amyloid, such as Alzheimer's disease. In humans, all cells with a nucleus produce cystatin C as a chain of 120 amino acids. It is found in virtually all tissues and body fluids. It is a potent inhibitor of lysosomal proteinases and probably one of the most important extracellular inhibitors of cysteine proteases. Cystatin C belongs to the type 2 cystatin gene family.
Uremic frost is a colloquial description for crystallized urea deposits that can be found on the skin of those affected by chronic kidney disease (CKD). In states of prolonged kidney failure and subsequent uremia, the high level of urea in the bloodstream leads to high levels of urea secreted by eccrine sweat glands as a component of sweat. As water evaporates off the skin, it results in crystallization of the remaining urea.
Lori Hartwell is the Founder and President of the Renal Support Network, author of Chronically Happy: Joyful Living in Spite of Chronic Illness, and co-host of KidneyTalk, a biweekly webcast of issues of interest to those with Chronic Kidney Disease (CKD).
T. Alp Ikizler is a nephrologist, currently holding the Catherine McLaughlin Hakim chair in Medicine at Vanderbilt University School of Medicine, where he does clinical work and heads a research lab. Born in Istanbul, Turkey, he received his M.D. from the Istanbul University Faculty of Medicine.
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. In absence of SLE, DPGN pathology looks more like Membranoproliferative glomerulonephritis
The International Society of Renal Nutrition and Metabolism (ISRNM) is a learned society on nephrology that has the objective of advancing knowledge, education and awareness pertaining to nutrition and metabolism in kidney disease by fostering communication of the advancements of knowledge in renal nutrition. The ISRNM website states that it promotes expert patient care, advances medical research, and educates the kidney community on the role of nutrition in chronic kidney disease and acute kidney injury including the role of nutritional status, uremic malnutrition, protein-energy wasting, and dietary derangement. The site also mentions a role in informing policymakers about issues of relevant to kidney and nutrition communities and the patients.
Carmine Zoccali is an Italian nephrologist and a clinical investigator. He has contributed to research in several fields, most notably hypertension and cardiovascular complications in chronic kidney disease (CKD), CKD progression and clinical epidemiology of kidney diseases at large. He is known for his studies on cardiovascular risk in CKD and dialysis patients. He was among the earliest investigators that focused on the relevance of endothelial dysfunction and inflammation for the high risk of cardiovascular disease in these populations. In this research area, he was the first to link endogenous inhibitors of the nitric oxide system with death and cardiovascular disease. and the first to document a relationship between sympathetic over-activity and these outcomes Dr Zoccali is a practicing specialist in Nephrology, with a national qualification for the full professorship in Nephrology. He is also a specialist in hypertension, certified by the European Society of Hypertension (ESH).
Sucroferric oxyhydroxide, sold under the brand name Velphoro, is a non-calcium, iron-based phosphate binder used for the control of serum phosphorus levels in adults with chronic kidney disease (CKD) on haemodialysis (HD) or peritoneal dialysis (PD). It is used in form of chewable tablets.
Chronic kidney disease–mineral and bone disorder (CKD–MBD) is one of the many complications associated with chronic kidney disease. It represents a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following:
A renal diet is a diet aimed at keeping levels of fluids, electrolytes, and minerals balanced in the body in individuals with chronic kidney disease or who are on dialysis. Dietary changes may include the restriction of fluid intake, protein, and electrolytes including sodium, phosphorus, and potassium. Calories may also be supplemented if the individual is losing weight undesirably.
Andrew S. Levey is an American nephrologist who transformed chronic kidney disease (CKD) clinical practice, research, and public health by developing equations to estimate glomerular filtration rate (GFR), and leading the global standardization of CKD definition and staging.
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- ↑ Himmelfarb, Jonathan; Stenvinkel, Peter; Ikizler, T. Alp; Hakim, Raymond M. (November 2002). "The elephant in uremia: Oxidant stress as a unifying concept of cardiovascular disease in uremia". Kidney International. 62 (5): 1524–1538. doi: 10.1046/j.1523-1755.2002.00600.x . PMID 12371953.[ non-primary source needed ]
- ↑ Carrero, Juan Jesús; Stenvinkel, Peter (December 2009). "Persistent Inflammation as a Catalyst for Other Risk Factors in Chronic Kidney Disease: A Hypothesis Proposal". Clinical Journal of the American Society of Nephrology. 4 (Supplement_1): S49–S55. doi:10.2215/CJN.02720409. PMID 19996005.[ non-primary source needed ]
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- ↑ Locatelli, F.; Canaud, B.; Eckardt, K.-U.; Stenvinkel, P.; Wanner, C.; Zoccali, C. (July 2003). "Oxidative stress in end-stage renal disease: an emerging threat to patient outcome". Nephrology Dialysis Transplantation. 18 (7): 1272–1280. doi:10.1093/ndt/gfg074. PMID 12808161.[ non-primary source needed ]
- ↑ Stenvinkel, Peter; Ketteler, Markus; Johnson, Richard J.; Lindholm, Bengt; Pecoits-Filho, Roberto; Riella, Miguel; Heimbürger, Olof; Cederholm, Tommy; Girndt, Matthias (April 2005). "IL-10, IL-6, and TNF-α: Central factors in the altered cytokine network of uremia—The good, the bad, and the ugly". Kidney International. 67 (4): 1216–1233. doi: 10.1111/j.1523-1755.2005.00200.x . PMID 15780075.[ non-primary source needed ]
- ↑ Kato, Sawako; Chmielewski, Michal; Honda, Hirokazu; Pecoits-Filho, Roberto; Matsuo, Seiichi; Yuzawa, Yukio; Tranaeus, Anders; Stenvinkel, Peter; Lindholm, Bengt (September 2008). "Aspects of Immune Dysfunction in End-stage Renal Disease". Clinical Journal of the American Society of Nephrology. 3 (5): 1526–1533. doi:10.2215/CJN.00950208. PMC 4571158 . PMID 18701615.[ non-primary source needed ]
- ↑ Pecoits-Filho, R. (September 2002). "Interleukin-6 is an independent predictor of mortality in patients starting dialysis treatment". Nephrology Dialysis Transplantation. 17 (9): 1684–1688. doi:10.1093/ndt/17.9.1684. PMID 12198224.
- ↑ International Consortium for Blood Pressure Genome-Wide Association Studies; et al. (October 2011). "Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk". Nature. 478 (7367): 103–109. Bibcode:2011Natur.478..103T. doi:10.1038/nature10405. PMC 3340926 . PMID 21909115.
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- ↑ Stenvinkel, P. (November 2010). "Chronic kidney disease: a public health priority and harbinger of premature cardiovascular disease". Journal of Internal Medicine. 268 (5): 456–467. doi:10.1111/j.1365-2796.2010.02269.x. PMID 20809922.[ non-primary source needed ]
- ↑ Kooman, Jeroen P.; Kotanko, Peter; Schols, Annemie M. W. J.; Shiels, Paul G.; Stenvinkel, Peter (December 2014). "Chronic kidney disease and premature ageing". Nature Reviews Nephrology. 10 (12): 732–742. doi:10.1038/nrneph.2014.185. PMID 25287433. S2CID 12077662.[ non-primary source needed ]
- ↑ Hobson, S.; Arefin, S.; Witasp, A.; Hernandez, L.; Kublickiene, K.; Shiels, P.G.; Stenvinkel, P. (14 April 2023). "Accelerated Vascular Aging in Chronic Kidney Disease: The Potential for Novel Therapies" (PDF). Circulation Research. 132 (8): 950–969. doi:10.1161/CIRCRESAHA.122.321751. PMID 37053277. S2CID 258052784.[ non-primary source needed ]
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- ↑ Mafra, Denise; Borges, Natalia A.; Lindholm, Bengt; Shiels, Paul G.; Evenepoel, Pieter; Stenvinkel, Peter (March 2021). "Food as medicine: targeting the uraemic phenotype in chronic kidney disease" (PDF). Nature Reviews Nephrology. 17 (3): 153–171. doi:10.1038/s41581-020-00345-8. PMID 32963366. S2CID 221841229.[ non-primary source needed ]
- ↑ Fouque, D.; Kalantar-Zadeh, K.; Kopple, J.; Cano, N.; Chauveau, P.; Cuppari, L.; Franch, H.; Guarnieri, G.; Ikizler, T.A.; Kaysen, G.; Lindholm, B.; Massy, Z.; Mitch, W.; Pineda, E.; Stenvinkel, P.; Trevinho-Becerra, A.; Wanner, C. (February 2008). "A proposed nomenclature and diagnostic criteria for protein–energy wasting in acute and chronic kidney disease". Kidney International. 73 (4): 391–398. doi:10.1038/sj.ki.5002585. PMID 18094682.[ non-primary source needed ]
- ↑ Carrero, Juan Jesús; Stenvinkel, Peter; Cuppari, Lilian; Ikizler, T. Alp; Kalantar-Zadeh, Kamyar; Kaysen, George; Mitch, William E.; Price, S. Russ; Wanner, Christoph; Wang, Angela Y.M.; ter Wee, Pieter; Franch, Harold A. (March 2013). "Etiology of the Protein-Energy Wasting Syndrome in Chronic Kidney Disease: A Consensus Statement From the International Society of Renal Nutrition and Metabolism (ISRNM)". Journal of Renal Nutrition. 23 (2): 77–90. doi:10.1053/j.jrn.2013.01.001. PMID 23428357.[ non-primary source needed ]
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- ↑ "Interview with Peter Stenvinkel | Staff Portal". staff.ki.se.
- ↑ Stenvinkel, Peter; Avesani, Carla M.; Gordon, Line J.; Schalling, Martin; Shiels, Paul G. (2021). "Biomimetics provides lessons from nature for contemporary ways to improve human health". Journal of Clinical and Translational Science. 5 (1): e128. doi:10.1017/cts.2021.790. PMC 8327543 . PMID 34367673.[ non-primary source needed ]
- ↑ Stenvinkel, Peter; Shiels, Paul G.; Johnson, Richard J. (February 2023). "Lessons from evolution by natural selection: An unprecedented opportunity to use biomimetics to improve planetary health". Journal of Environmental Management. 328: 116981. doi: 10.1016/j.jenvman.2022.116981 . PMID 36508982.[ non-primary source needed ]
- ↑ Stenvinkel, Peter (5 January 2024). "The curious link between animal hibernation and ageing – and what humans could learn from it". The Conversation.[ non-primary source needed ]
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