Peter Stenvinkel | |
---|---|
Born | |
Nationality | Swedish |
Occupation(s) | Nephrologist and academic |
Academic background | |
Education | M.D. Medicine Ph.D. Nephrology |
Alma mater | Karolinska Institutet |
Academic work | |
Institutions | Karolinska University Hospital Karolinska Institutet |
Peter Stenvinkel (born 1957) is a Swedish nephrologist and academic. He is a senior lecturer at Karolinska University Hospital and a professor of nephrology at Karolinska Institutet. [1]
Stenvinkel has conducted translational research aimed at identifying risk factors for metabolic,cardiovascular,and nutritional complications in chronic kidney disease (CKD). His work has delved into various aspects of inflammation,wasting,and metabolism in CKD patients. For his contributions to the field of renal medicine,he has won the Karolina Price,Vizenca Price, [2] Addis Gold Medal and the ERA-EDTA prize for outstanding educational activities. [3]
Stenvinkel is an Honorary member of the Polish Society of Nephrology, [4] as well as the Australian and New Zealand Society of Nephrology. He served as an Editor-in-chief for NDT-E and has served as Editor for the Journal of Internal Medicine since 2022. [5]
Stenvinkel earned his Doctor of Medicine degree from Karolinska Institute in 1982. While working as a Specialist in Nephrology,he graduated with a doctoral degree in Renal Medicine in 1994. [6]
Stenvinkel began his academic career as an associate professor at Karolinska Institutet in 1997. Since 2009,he has been serving as a professor of nephrology at Karolinska Institutet and Senior lecturer at Karolinska University Hospital and where he engages in clinical duties,research,and administration. [7]
Stenvinkel was a member of the KDOQI working group on risk factors for CVD in CKD from 2001 to 2004 and also on multiple advisory boards,including the Gambro Advisory Board,the Scientific Advisory Board of ERA-EDTA,and the Baxter Medical Advisory Board until 2013. [8]
Stenvinkel has conducted translational research,emphasizing risk factors for metabolic,cardiovascular,and nutritional complications in chronic kidney disease (CKD).
Stenvinkel's research has focused on the need for effective interventions addressing cardiovascular and nutritional complications in chronic kidney disease (CKD). In one of his highly cited studies,he explored the correlation between malnutrition,inflammation,and atherosclerosis to delve into their collective impact on cardiovascular disease (CVD) development in CKD patients,suggesting a synergistic effect in promoting atherosclerosis. [9] Discussing chronic inflammation in CKD patients,he proposed a classification system for two types of malnutrition in CKD, [10] and expanded on the relationship between inflammation and malnutrition by presenting the hypothesis that increased oxidative stress significantly influences CVD development in uremic patients. [11] He showed that inflammation acts as a catalyst and changes the risk factor profile [12] and also contributed to a technical note emphasizing the complexity of uremic retention,highlighting the need for comprehensive analytical methods beyond traditional markers like urea and creatinine. [13]
Among other highly cited works,Stenvinkel's collaborative research explored the role of oxidative stress in CKD,focusing on its impact on CVD morbidity and mechanisms leading to enhanced oxidative stress in CKD. [14] Additionally,he investigated how dysregulated cytokine networks contributed to accelerated atherosclerosis,resulting in increased inflammation risk in CKD patients, [15] as well as demonstrated a link between immune dysfunction,CVD,and infections,leading to mortality in ESRD patients. [16] In 2002,he show that IL-6 is a predictor of mortality in CKD which was evidenced by his study on end-stage renal disease (ESRD) patients at the outset of dialysis treatment. [17]
Stenvinkel was part of the consortium,which identified sixteen novel genetic loci associated with blood pressure regulation,offering insights and potential therapeutic pathways for cardiovascular disease prevention. [18] He has examined the bidirectional association between CKD and CVD,emphasizing the challenges in identifying cardiovascular culprits due to paradoxical associations and suggesting the potential role of proteomics and epigenetics in understanding vascular risk factors. [19] He also addressed the overlooked epidemic of CKD and its association with CVD to emphasize early diagnosis through proteinuria. [20] In recent years his research highlighted the premature aging, [21] and accelerated vascular aging in the toxic uremic milieu, [22] as well as advocated for interdisciplinary collaboration for innovative CKD treatments using insights from diverse species. [23] In related research,he advocated for the concept of "food as medicine" in metabolic diseases like CKD,emphasizing dietary interventions,as bioactive nutrients have shown promise in mitigating CKD-related features. [24]
Stenvinkel was part of the group that standardized the terminology for muscle wasting,malnutrition,and inflammation in CKD and AKI,and introduced "protein-energy wasting (PEW)" to describe loss of body protein mass and fuel reserves. [25] He researched PEW in CKD patients,outlining its multifactorial etiology,including insufficient food intake,uremia-induced alterations,inflammation,acidosis,comorbidities [26] and addressed interventions for PEW underscoring the effectiveness of nutritional supplementation and emerging therapies like anabolic agents. [27]
Stenvinkel's research in planetary health has examined how environmental and climate threats have triggered processes like inflammation,oxidative stress,and mitochondrial dysfunction,reshaping disease patterns and increasing the risk of chronic conditions such as dementia,obesity,and diabetes. [28] His work has also endorsed more sustainable healthcare practices,including reconsidering food production and consumption, [29] and has suggested the use of interdisciplinary collaboration,biomimetic organizational models,and nature-inspired solutions in mitigating climate change as strategies to address environmental degradation and biodiversity loss. [30] In 2024,he published a Swedish science book on Nature´s Intelligence and has published science texts on the link between animal hibernation and aging. [31]
Nephrology is a specialty for both adult internal medicine and pediatric medicine that concerns the study of the kidneys, specifically 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. The word "renal" is an adjective meaning "relating to the kidneys", and its roots are French or late Latin. Whereas according to some opinions, "renal" and "nephro" should be replaced with "kidney" in scientific writings such as "kidney medicine" or "kidney replacement therapy", other experts have advocated preserving the use of renal and nephro as appropriate including in "nephrology" and "renal replacement therapy", respectively.
Kidney failure, also known as renal failure or end-stage renal disease (ESRD), 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, hyperkalemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.
Uremia is the condition of having 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 normally be 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 long-term kidney disease, in which either there is a gradual loss of kidney function which occurs over a period of months to years, or an abnormal kidney structure. 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. CKD can lead to kidney failure requiring kidney dialysis or kidney transplantation.
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.
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.
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.
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.
Phenylacetylglutamine is a product formed by the conjugation of phenylacetate and glutamine. It is a common metabolite that occurs naturally in human urine.
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). Uremic frost was first described in 1865 by Harald Hirschsprung (1830-1916), a Danish pediatrician. He was also the first to describe Hirschsprung's disease in 1886. The disease now carries his name. Uremic frost has become increasingly uncommon with the advent of dialysis in the 1950s. Uremic frost is a classical pre-dialysis era description of crystallized urea deposits over the skin of patients with prolonged kidney failure and severe uremia. High blood urea level leads to high secretion of urea by sweat glands as a component of sweat. As water evaporates off the skin, it results in crystallization of the remaining urea which appear as white salts over the skin. This condition is more common in severe, untreated uremia and is associated with serum BUN levels >200. It is becoming rare in people with chronic kidney disease managed on long-term hemodialysis, with estimated prevalence between 0.8 and 3%.
Malnutrition–inflammation complex (syndrome) (MICS), also known as malnutrition–inflammation–cachexia syndrome, is a common condition in chronic disease states such as chronic kidney disease and chronic heart failure.
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.
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).
Onconephrology is a specialty in nephrology that deals with the study of kidney diseases in cancer patients. A nephrologist who takes care of patients with cancer and kidney disease is called an onconephrologist. This branch of nephrology encompasses nephrotoxicity associated with existing and novel chemotherapeutics, kidney disease as it pertains to stem cell transplant, paraneoplastic kidney disorders, paraproteinemias, electrolyte disorders associated with cancer, and more as discussed below.
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.