Andrew S. Levey

Last updated
Andrew S. Levey
Levey Andrew 2021 (5x5).jpg
Andrew S. Levey, MD at Tufts Medical Center in 2021
Born (1950-09-16) September 16, 1950 (age 73)
Parkersburg, West Virginia
Alma mater
Known forDeveloping estimates of Renal function to define and stage Chronic Kidney Disease and apply them in clinical practice, research and public health.
Scientific career
Fields Nephrology, Epidemiology
Institutions Tufts University School of Medicine, Tufts Medical Center

Andrew S. Levey (born September 16, 1950) 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) (renal function), and leading the global standardization of CKD definition and staging.

Contents

Education and career

Levey graduated from the University of Chicago in 1972 with a Bachelor of Arts in Biological Sciences and graduated as a Doctor of Medicine (MD) in 1976 at the Boston University School of Medicine. He became a Professor of Medicine in the Tufts University School of Medicine in 1994, and was Chief of the Division of Nephrology from 1999 to 2017.

Contributions

Levey is known for developing the most widely used equations to estimate GFR (renal function) globally. He pioneered work with the MDRD Study Equation, [1] led the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI), which pooled measured kidney function CKD data from studies all over the world to develop equations to estimate kidney function from serum creatinine, cystatin C, and panels of metabolites and low-molecular-weight proteins. [2] [3] [4] The 2009 creatinine equation with race and the 2021 creatinine equation without race to replace the 2009 equation are shown below:

For both equations, α is -0.241 for females and -0.302 for males; min indicates minimum of Scr/k or 1, and max indicates maximum of Scr/k or 1

Levey is an authority on clinical practice guidelines in kidney disease. He chaired the U.S. National Kidney Foundation Kidney Disease Outcome Quality Initiative (KDOQI) Clinical Practice Guideline Workgroup on “Chronic Kidney Disease: Evaluation, Classification and Risk Stratification” [5] . The recommendations from this workgroup transformed the way Kidney Disease was defined and staged globally. The guideline has been cited over 10,000 [6] times in subsequent research publications. He led multiple KDOQI and Kidney Disease Improving Global Outcomes (KDIGO) [7] guidelines which advanced the global recognition and care for CKD, [8] [9] [10] [11] hypertension, [12] acute kidney injury, [7] living kidney donor evaluation, [13] and nomenclature. [14]

Levey was a founding member of the Chronic Kidney Disease Prognosis Consortium (CKDPC), [15] which includes over 80 cohorts and 10 million [16] participants and has informed multiple clinical practice guidelines and regulatory policies.

Levey led the U.S. National Kidney Foundation task force on cardiovascular disease in chronic kidney disease, which led to the recognition by the American Heart Association of CKD as a risk factor for cardiovascular disease. [17] [18]

Levey co-chaired the U.S. Centers for Disease Control and Prevention expert panel to develop comprehensive public health strategies for preventing the development, progression, and complications of CKD. [19]

Levey led scientific workshops sponsored by the U.S. National Kidney Foundation in collaboration with the U.S. Food and Drug Administration and European Medicines Association for the evaluation of Renal function as surrogate endpoints for clinical trials of kidney disease progression. [20] [21] [22]

Levey was editor-in-chief for American Journal of Kidney Diseases, the official journal of the U.S. National Kidney Foundation, from 2007-2016.

Awards

Personal

Levey is married to Roberta Falke, MD. In 2009 he donated a kidney to her via a 3-pair transplant [23] .

Related Research Articles

<span class="mw-page-title-main">Creatinine</span> Breakdown product of creatine phosphate

Creatinine is a breakdown product of creatine phosphate from muscle and protein metabolism. It is released at a constant rate by the body.

<span class="mw-page-title-main">Kidney failure</span> 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 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.

<span class="mw-page-title-main">Glomerular filtration rate</span> Renal function test

Renal functions include maintaining an acid–base balance; regulating fluid balance; regulating sodium, potassium, and other electrolytes; clearing toxins; absorption of glucose, amino acids, and other small molecules; regulation of blood pressure; production of various hormones, such as erythropoietin; and activation of vitamin D.

<span class="mw-page-title-main">Assessment of kidney function</span> Ways of assessing the function of the kidneys

Assessment of kidney function occurs in different ways, using the presence of symptoms and signs, as well as measurements using urine tests, blood tests, and medical imaging.

<span class="mw-page-title-main">Acute kidney injury</span> Medical condition

Acute kidney injury (AKI), previously called acute renal failure (ARF), is a sudden decrease in kidney function that develops within 7 days, as shown by an increase in serum creatinine or a decrease in urine output, or both.

<span class="mw-page-title-main">Chronic kidney disease</span> Medical condition

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.

<span class="mw-page-title-main">Loop diuretic</span> Diuretics that act along the loop of Henle in the kidneys

Loop diuretics are diuretics that act on the Na-K-Cl cotransporter along the thick ascending limb of the loop of Henle in nephrons of the kidneys. They are primarily used in medicine to treat hypertension and edema often due to congestive heart failure or chronic kidney disease. While thiazide diuretics are more effective in patients with normal kidney function, loop diuretics are more effective in patients with impaired kidney function.

<span class="mw-page-title-main">Metabolic acidosis</span> 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 to high.

<span class="mw-page-title-main">Diabetic nephropathy</span> 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 the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. The triad of protein leaking into the urine, rising blood pressure with hypertension and then falling renal function is common to many forms of CKD. Protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called 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.

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.

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.

Contrast-induced nephropathy (CIN) is a purported form of kidney damage in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury.

<span class="mw-page-title-main">Cystatin C</span>

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.

Sickle cell nephropathy is a type of nephropathy associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors sickling of red blood cells, with resultant local infarction. Functional tubule defects in patients with sickle cell disease are likely the result of partial ischemic injury to the renal tubules.

Mesoamerican nephropathy (MeN) is an endemic, non-diabetic, non-hypertensive chronic kidney disease (CKD) characterized by reduced glomerular filtration rate (GFR) with mild or no proteinuria and no features of known primary glomerular diseases. MeN is prevalent in agricultural communities along the Pacific Ocean coastal lowlands Mesoamerica, including southern Mexico, Guatemala, El Salvador, Nicaragua, Honduras and Costa Rica. Although most cases have been described among agricultural workers, MeN has also been described in other occupations, including miners, brick manufacturers, and fishermen. A common denominator among these occupations is that they are outdoor workers who reside in rural areas in hot and humid climates.

Renal angina is a clinical methodology to risk stratify patients for the development of persistent and severe acute kidney injury (AKI). The composite of risk factors and early signs of injury for AKI, renal angina is used as a clinical adjunct to help optimize the use of novel AKI biomarker testing. The term angina from Latin and from the Greek ankhone ("strangling") are utilized in the context of AKI to denote the development of injury and the choking off of kidney function. Unlike angina pectoris, commonly caused due to ischemia of the heart muscle secondary to coronary artery occlusion or vasospasm, renal angina carries no obvious physical symptomatology. Renal angina was derived as a conceptual framework to identify evolving AKI. Like acute coronary syndrome which precedes or is a sign of a heart attack, renal angina is used as a herald sign for a kidney attack. Detection of renal angina is performed by calculating the renal angina index.

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.

<span class="mw-page-title-main">Shrunken pore syndrome</span> Type of kidney disorder

Shrunken pore syndrome (SPS) is a kidney disorder described in 2015 in which the pores in the glomerular filtration barrier are hypothesized to have shrunken so that the glomerular filtration rate (GFR) of 5–30 kDa proteins, for example cystatin C, is selectively reduced compared to that of small molecules such as water and creatinine. The syndrome is associated with premature death. SPS has been identified in children.

Anders Grubb is a Swedish chemist, physician, and academic. He is currently a Senior Professor of Clinical Chemistry at Lund University.

References

  1. ↑ Levey, Andrew (1999). "A More Accurate Method to Estimate Glomerular Filtration Rate From Serum Creatinine: A New Prediction Equation. Modification of Diet in Renal Disease Study Group". Ann Intern Med. 130 (6): 461–70. doi:10.7326/0003-4819-130-6-199903160-00002. PMID   10075613. S2CID   1902375.
  2. ↑ Levey, Andrew (2009). "A new equation to estimate glomerular filtration rate". Ann Intern Med. 150 (9): 604–12. doi:10.7326/0003-4819-150-9-200905050-00006. PMC   2763564 . PMID   19414839.
  3. ↑ Inker, Lesley (2012). "Estimating Glomerular Filtration Rate from Serum Creatinine and Cystatin C". New England Journal of Medicine. 367 (367): 20–29. doi:10.1056/NEJMoa1114248. PMC   4398023 . PMID   22762315.
  4. ↑ Inker, Lesley (2021). "New Creatinine- and Cystatin C–Based Equations to Estimate GFR without Race". New England Journal of Medicine. 385 (19): 1737–1749. doi:10.1056/NEJMoa2102953. PMC   8822996 . PMID   34554658. S2CID   237608965.
  5. ↑ Levey, Andrew (2003). "National Kidney Foundation Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification". Ann Intern Med. 139 (2): 137–47. doi:10.7326/0003-4819-139-2-200307150-00013. PMID   12859163. S2CID   11973331.
  6. ↑ Levey, Andrew (2002), "K/DOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification", American Journal of Kidney Diseases, University of Minnesota, 39 (2 SUPPL. 1): i–ii+S1–S266, PMID   11904577
  7. 1 2 Levey, Andrew (2012). "KDIGO Clinical Practice Guideline for Acute Kidney Injury" (PDF). Ann Intern Med. 2 (1). doi: 10.1038/kisup.2012.1 .
  8. ↑ Levey, Andrew (2002). "Clinical Practice Guidelines For Chronic Kidney Disease: Evaluation, Classification and Stratification" (PDF). Ann Intern Med. 39 (1): S1–S266.
  9. ↑ Levey, Andrew (2005). "Definition and Classification of Chronic Kidney Disease:A Position Statement From Kidney Disease:Improving Global Outcomes(KDIGO)". Kidney International. 67 (6): 2089–2100. doi: 10.1111/j.1523-1755.2005.00365.x . PMID   15882252.
  10. ↑ Levey, Andrew (2011). "The Definition, Classification, and Prognosis of Chronic Kidney Disease: A KDIGO Controversies Conference Report". Ann Intern Med. 80 (1): 17–28. doi: 10.1038/ki.2010.483 . PMID   21150873.
  11. ↑ Levey, Andrew (2007). "Chronic Kidney Disease as a Global Public Health Problem: Approaches and Initiatives - A Position Statement From Kidney Disease Improving Global Outcomes". Ann Intern Med. 72 (3): 247–59. doi: 10.1038/sj.ki.5002343 . PMID   17568785.
  12. ↑ Levey, Andrew (2004). "K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease". American Journal of Kidney Diseases. 5 (1): S1-290. PMID   15114537.
  13. ↑ Levey, Andrew (2017). "KDIGO Clinical Practice Guideline on the Evaluation and Care of Living Kidney Donors". Transplantation. 101 (8S): S1–S109. doi:10.1097/TP.0000000000001769. PMC   5540357 . PMID   28742762.
  14. ↑ Levey, Andrew (2020). "Nomenclature for Kidney Function and Disease: Report of a Kidney Disease: Improving Global Outcomes (KDIGO) Consensus Conference". Kidney International. 97 (6): 1117–1129. doi: 10.1016/j.kint.2020.02.010 . hdl: 1765/128502 . PMID   32409237.
  15. ↑ "Chronic Kidney Disease Prognosis Consortium (CKD-PC)". CKD Prognosis Consortium. Retrieved May 5, 2020.
  16. ↑ "Participating Cohorts". CKD Prognosis Consortium. Retrieved May 24, 2020.
  17. ↑ Levey, Andrew (1998). "Controlling the Epidemic of Cardiovascular Disease in Chronic Renal Disease: What Do We Know? What Do We Need to Learn? Where Do We Go From Here? National Kidney Foundation Task Force on Cardiovascular Disease". American Journal of Kidney Diseases. 32 (5): 853–906. doi:10.1016/s0272-6386(98)70145-3. PMID   9820460.
  18. ↑ Levey, Andrew (2003). "Kidney Disease as a Risk Factor for Development of Cardiovascular Disease: A Statement From the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention". Circulation. 108 (17): 2154–69. doi:10.1161/01.CIR.0000095676.90936.80. PMID   14581387. S2CID   2530900.
  19. ↑ Levey, Andrew (2009). "Comprehensive Public Health Strategies for Preventing the Development,Progression, and Complications of CKD: Report of an Expert Panel Convened by the Centers for Disease Control and Prevention". American Journal of Kidney Diseases. 53 (3): 522–535. doi: 10.1053/j.ajkd.2008.11.019 . PMID   19231739.
  20. ↑ Levey, Andrew (2009). "Proteinuria as a Surrogate Outcome in CKD: Report of a Scientific Workshop Sponsored by the National Kidney Foundation and the US Food and Drug Administration". American Journal of Kidney Diseases. 54 (2): 205–26. doi:10.1053/j.ajkd.2009.04.029. PMID   19577347.
  21. ↑ Levey, Andrew (2014). "GFR Decline as an End Point for Clinical Trials in CKD: A Scientific Workshop Sponsored by the National Kidney Foundation and the US Food and Drug Administration". American Journal of Kidney Diseases. 64 (6): 821–35. doi:10.1053/j.ajkd.2014.07.030. PMID   25441437.
  22. ↑ Levey, Andrew (2020). "Change in Albuminuria and GFR as End Points for Clinical Trials in Early Stages of CKD: A Scientific Workshop Sponsored by the National Kidney Foundation in Collaboration With the US Food and Drug Administration and European Medicines Agency". American Journal of Kidney Diseases. 75 (1): 84–104. doi: 10.1053/j.ajkd.2019.06.009 . PMID   31473020.
  23. ↑ English, Bella (March 28, 2010). "Harvesting hope from a giving tree". Archived from the original on April 1, 2022. Retrieved May 24, 2020.{{cite news}}: CS1 maint: bot: original URL status unknown (link)
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