Anders Grubb
Born1944 (age 79–80)
NationalitySwedish
Occupation(s)Chemist, physician, and academic
AwardsPoul Astrup´s Award for Distinguished Research in Clinical Chemistry
Eric K. Fernström's Award for Distinguished Biomedical Research
The Kone Award for Distinguished Research in Clinical Chemistry, British Association of Clinical Biochemistry
The jubilee-award for distinguished scientific work, Swedish Society of Medical Sciences
Lorentz Eldjarn´s award (2010, 2016)
Academic work
InstitutionsLund University

Anders Grubb (born 1944) is a Swedish chemist, physician, and academic. He is currently a Senior Professor of Clinical Chemistry at Lund University.[1]

Education

Grubb earned his Ph.D. degree in Clinical Chemistry in 1974 and an M.D. in 1975. Following this, he attended The New York University Medical Center as a Postdoctoral fellow in 1975, and The University Hospital Ramon y Cajal in Madrid in 1980.[1]

Career

Grubb joined the medical faculty of Lund university in 1967. In 1989 he was appointed as Professor and Senior Physician in the Department of Clinical Chemistry and Pharmacology. Since 2011, he has been serving as Senior Professor at the Department of Clinical Chemistry and Pharmacology at Lund University.[1]

Research

Grubb has published over 350 articles, has been cited over 31,000 times with an h-index of 90, and has 10 patents awarded.[2] His research spans the areas of protein chemistry, renal medicine and clinical chemistry.[3]

Structure and Function of Cystatin C

Grubb and coworkers isolated a protein previously described to be present in urine and spinal fluid, but without known structure and function, called, among other things, ɣ-trace, and developed a method for measuring it in various body fluids.[4] He also determined the amino acid sequence of the protein's single polypeptide chain and the secondary and 3D-structure of the protein as well as the nucleotide sequence of its mRNA and gene.[5][6][7] Northern blot studies showed that cystatin C was produced by all nucleated human cells.[8] The biological function of cystatin C was suggested to be inhibition of cysteine proteinases by Grubb and coworkers in 1984.[9] The role of cystatin C, and peptidyl derivatives mimicking its inhibitory site, in inhibiting the replication of viruses and bacteria was thereafter described,[10] as well as its role in the hereditary disorder Hereditary Cystatin C Amyloid Angiopathy (HCCAA).[11]

Role of Cystatin C in Estimating Glomerular Filtration Rate (GFR)

Grubb and coworkers discovered in 1979 that cystatin C was a marker of GFR[4] and could be used to estimate GFR.[12] They have used cystatin C for estimation of GFR in the clinical routine since 1994.[13] Grubb and coworkers have developed cystatin C-based GFR-estimating equations, which in several patient cohorts are superior in diagnostic efficiency to creatinine-based GFR-estimating equations, and, in contrast to creatinine-based GFR-estimating equations, do not require controversial coefficients for race or sex.[14][15] Grubb was chairman of an IFCC working group for development of an international calibrator for cystatin C and such a calibrator, designated ERM-DA471/IFCC, was produced and described in 2010.[16] In a proteomic study, Grubb and coworkers studied the plasma levels of 2893 proteins and found that cystatin C was the one with the highest correlation to measured GFR.[17]

Cystatin C, Glomerular Filtration Quality and Shrunken Pore Syndrome

Grubb and coworkers have established that the most reliable way to estimate GFR is to use both a cystatin C-based and a creatinine-based GFR-estimating equation and compare the results of the two estimations.[18] If they agree, the estimation has the same reliability as an invasive determination of GFR.[18] This comparative procedure allowed the definition of a new type of kidney disorder characterized by a greater reduction of renal clearances of larger molecules (e.g. cystatin C, 13,343Da) than of smaller ones (e.g. creatinine, 113Da) and identified by a greater reduction of the cystatin C-based GFR-estimate (eGFRcystatin C) than that based upon creatinine (eGFRcreatinine). This kidney disorder was called Shrunken Pore Syndrome to emphasize the greater reduction in renal clearance of molecules bigger than creatinine in this disorder.[19][20] Dardashti, Grubb and coworkers demonstrated that Shrunken Pore Syndrome was associated with a marked increase in mortality[21] and that the lower the eGFRcystatin C/eGFRcreatinine-ratio, the higher the mortality.[22] Grubb and coworkers have described that the pathophysiology of the syndrome might be connected to the altered proteome in the disorder with accumulation of inter alia atherosclerosis-promoting proteins.[23][24] The syndrome has been described by Grubb and coworkers to be one of the most common kidney disorders.[25][26]

Awards and honors

  • 1984 - Poul Astrup´s Award for Distinguished Research in Clinical Chemistry
  • 1987 - Eric K. Fernström's Award for Distinguished Biomedical Research
  • 1989 - The Kone Award for Distinguished Research in Clinical Chemistry, British Association of Clinical Biochemistry
  • 1991 - The jubilee-award for distinguished scientific work, Swedish Society of Medical Sciences
  • 2007 - The Falcon Order of Iceland for successful cooperation/education with/of Icelandic scientists
  • 2010, 2016 - Lorentz Eldjarn´s award

Bibliography

Books

  • Cystatin C as a multifaceted biomarker in kidney disease and its role in defining "Shrunken Pore Syndrome". (2017) In Biomarkers of kidney disease ISBN 978-0-12-803014-1. Editor: C. L. Edelstein. Elsevier. pp. 225–240.
  • Laurells Klinisk kemi i praktisk medicin (2018) ISBN 978-91-44-11974-8

References

  1. 1 2 3 "Anders Grubb". Lund University.
  2. ↑ "Anders Grubb". scholar.google.se.
  3. ↑ "ORCID". orcid.org.
  4. 1 2 Löfberg, H.; Grubb, A. O. (1979). "Quantitation of γ-trace in human biological fluids: Indications for production in the central nervous system". Scandinavian Journal of Clinical and Laboratory Investigation. 39 (7): 619–626. doi:10.3109/00365517909108866. PMID 119302.
  5. ↑ Grubb, A.; Löfberg, H. (1982). "Human gamma-trace, a basic microprotein: amino acid sequence and presence in the adenohypophysis". Proceedings of the National Academy of Sciences of the United States of America. 79 (9): 3024–3027. Bibcode:1982PNAS...79.3024G. doi:10.1073/pnas.79.9.3024. PMC 346341. PMID 6283552.
  6. ↑ Grubb, Anders; Löfberg, Helge; Barrett, Alan J. (May 21, 1984). "The disulphide bridges of human cystatin C (γ-trace) and chicken cystatin". FEBS Letters. 170 (2): 370–374. doi:10.1016/0014-5793(84)81346-0. S2CID 84217118 – via ScienceDirect.
  7. ↑ Janowski, R.; Kozak, M.; Jankowska, E.; Grzonka, Z.; Grubb, A.; Abrahamson, M.; Jaskolski, M. (2001). "Human cystatin C, an amyloidogenic protein, dimerizes through three-dimensional domain swapping". Nature Structural Biology. 8 (4): 316–320. doi:10.1038/86188. PMID 11276250. S2CID 28916747.
  8. ↑ Abrahamson, M; Olafsson, I; Palsdottir, A; Ulvsbäck, M; Lundwall, Å; Jensson, O; Grubb, A (June 1, 1990). "Structure and expression of the human cystatin C gene". Biochemical Journal. 268 (2): 287–294. doi:10.1042/bj2680287. PMC 1131430. PMID 2363674 – via Silverchair.
  9. ↑ Barrett, A. J.; Davies, M. E.; Grubb, A. (1984). "The place of human gamma-trace (cystatin C) amongst the cysteine proteinase inhibitors". Biochemical and Biophysical Research Communications. 120 (2): 631–636. doi:10.1016/0006-291x(84)91302-0. PMID 6203523.
  10. ↑ Björck, Lars; Åkesson, Per; Bohus, Martin; Trojnar, Jerzy; Abrahamson, Magnus; Olafsson, Isleifur; Grubb, Anders (January 24, 1989). "Bacterial growth blocked by a synthetic peptide based on the structure of a human proteinase inhibitor". Nature. 337 (6205): 385–386. doi:10.1038/337385a0. PMID 2643059. S2CID 4267641 – via www.nature.com.
  11. ↑ Grubb, A.; Jensson, O.; Gudmundsson, G.; Arnason, A.; Löfberg, H.; Malm, J. (1984). "Abnormal metabolism of gamma-trace alkaline microprotein. The basic defect in hereditary cerebral hemorrhage with amyloidosis". The New England Journal of Medicine. 311 (24): 1547–1549. doi:10.1056/NEJM198412133112406. PMID 6390199.
  12. ↑ Grubb, A.; Simonsen, O.; Sturfelt, G.; Truedsson, L.; Thysell, H. (1985). "Serum concentration of cystatin C, factor D and beta 2-microglobulin as a measure of glomerular filtration rate". Acta Medica Scandinavica. 218 (5): 499–503. doi:10.1111/j.0954-6820.1985.tb08880.x. PMID 3911736.
  13. ↑ Kyhse-Andersen, J.; Schmidt, C.; Nordin, G.; Andersson, B.; Nilsson-Ehle, P.; Lindström, V.; Grubb, A. (1994). "Serum cystatin C, determined by a rapid, automated particle-enhanced turbidimetric method, is a better marker than serum creatinine for glomerular filtration rate". Clinical Chemistry. 40 (10): 1921–1926. doi:10.1093/clinchem/40.10.1921. PMID 7923773.
  14. ↑ Dharnidharka, V. R.; Kwon, C.; Stevens, G. (2002). "Serum cystatin C is superior to serum creatinine as a marker of kidney function: a meta-analysis". American Journal of Kidney Diseases. 40 (2): 221–226. doi:10.1053/ajkd.2002.34487. PMID 12148093.
  15. ↑ Ottosson Frost, Carl; Gille-Johnson, Per; Blomstrand, Emanuel; St-Aubin, Viggo; Leion, Felicia; Grubb, Anders (February 2, 2022). "Cystatin C-based equations for estimating glomerular filtration rate do not require race or sex coefficients". Scandinavian Journal of Clinical and Laboratory Investigation. 82 (2): 162–166. doi:10.1080/00365513.2022.2031279. PMID 35107398. S2CID 246474625.
  16. ↑ Grubb, A.; Blirup-Jensen, S.; Lindström, V.; Schmidt, C.; Althaus, H.; Zegers, I.; IFCC Working Group on Standardisation of Cystatin C (WG-SCC) (2010). "First certified reference material for cystatin C in human serum ERM-DA471/IFCC". Clinical Chemistry and Laboratory Medicine. 48 (11): 1619–1621. doi:10.1515/CCLM.2010.318. PMID 21034257. S2CID 27001585.
  17. ↑ Christensson, A.; Ash, J. A.; Delisle, R. K.; Gaspar, F. W.; Ostroff, R.; Grubb, A.; Lindström, V.; Bruun, L.; Williams, S. A. (2018). "The Impact of the Glomerular Filtration Rate on the Human Plasma Proteome". Proteomics. Clinical Applications. 12 (3): e1700067. doi:10.1002/prca.201700067. PMID 29281176. S2CID 33866012.
  18. 1 2 Grubb, A. (2010). "Non-invasive estimation of glomerular filtration rate (GFR). The Lund model: Simultaneous use of cystatin C- and creatinine-based GFR-prediction equations, clinical data and an internal quality check". Scandinavian Journal of Clinical and Laboratory Investigation. 70 (2): 65–70. doi:10.3109/00365511003642535. PMC 4673578. PMID 20170415.
  19. ↑ Grubb, Anders; Lindström, Veronica; Jonsson, Magnus; Bäck, Sten-Erik; Åhlund, Tomas; Rippe, Bengt; Christensson, Anders (2015). "Reduction in glomerular pore size is not restricted to pregnant women. Evidence for a new syndrome: 'Shrunken pore syndrome'". Scandinavian Journal of Clinical and Laboratory Investigation. 75 (4): 333–340. doi:10.3109/00365513.2015.1025427. PMC 4487590. PMID 25919022.
  20. ↑ Zhou, H.; Yang, M.; He, X.; Xu, N. (2019). "eGFR, cystatin C and creatinine in shrunken pore syndrome". Clinica Chimica Acta; International Journal of Clinical Chemistry. 498: 1–5. doi:10.1016/j.cca.2019.08.001. PMID 31398310. S2CID 199518035.
  21. ↑ Dardashti, Alain; Nozohoor, Shahab; Grubb, Anders; Bjursten, Henrik (December 9, 2015). "Shrunken Pore Syndrome is associated with a sharp rise in mortality in patients undergoing elective coronary artery bypass grafting". Scandinavian Journal of Clinical and Laboratory Investigation. 76 (1): 74–81. doi:10.3109/00365513.2015.1099724. PMC 4720044. PMID 26647957.
  22. ↑ Herou, Erik; Dardashti, Alain; Nozohoor, Shahab; Zindovic, Igor; Ederoth, Per; Grubb, Anders; Bjursten, Henrik (2019). "The mortality increase in cardiac surgery patients associated with shrunken pore syndrome correlates with the eGFRcystatin C/eGFRcreatinine-ratio". Scandinavian Journal of Clinical and Laboratory Investigation. 79 (3): 167–173. doi:10.1080/00365513.2019.1576101. PMID 30767571. S2CID 73422769.
  23. ↑ Almén, Markus Sällman; Björk, Jonas; Nyman, Ulf; Lindström, Veronica; Jonsson, Magnus; Abrahamson, Magnus; Vestergren, AnnaLotta Schiller; Lindhe, Örjan; Franklin, Gary; Christensson, Anders; Grubb, Anders (January 1, 2019). "Shrunken Pore Syndrome Is Associated With Increased Levels of Atherosclerosis-Promoting Proteins". Kidney International Reports. 4 (1): 67–79. doi:10.1016/j.ekir.2018.09.002. PMC 6308389. PMID 30596170. S2CID 57013450 – via www.kireports.org.
  24. ↑ Xhakollari, L.; Jujic, A.; Molvin, J.; Nilsson, P.; Holm, H.; Bachus, E.; Leosdottir, M.; Grubb, A.; Christensson, A.; Magnusson, M. (2021). "Proteins linked to atherosclerosis and cell proliferation are associated with the shrunken pore syndrome in heart failure patients: Shrunken pore syndrome and proteomic associations". Proteomics. Clinical Applications. 15 (4): e2000089. doi:10.1002/prca.202000089. PMID 33682349. S2CID 232140448.
  25. ↑ Åkesson, A.; Lindström, V.; Nyman, U.; Jonsson, M.; Abrahamson, M.; Christensson, A.; Björk, J.; Grubb, A. (2020). "Shrunken pore syndrome and mortality: a cohort study of patients with measured GFR and known comorbidities". Scandinavian Journal of Clinical and Laboratory Investigation. 80 (5): 412–422. doi:10.1080/00365513.2020.1759139. PMID 32459111. S2CID 218910266.
  26. ↑ Grubb, Anders (September 24, 2020). "Shrunken pore syndrome - a common kidney disorder with high mortality. Diagnosis, prevalence, pathophysiology and treatment options". Clinical Biochemistry. 83: 12–20. doi:10.1016/j.clinbiochem.2020.06.002. PMID 32544475. S2CID 219726525.
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