Elkeless Prize (2003) Hershel Rich–Technion Innovation Award (2005) Joshua Weissgarten Nephrology Life Achievement Award (2019) Russell Berrie Award (2025)
Karl Leon Skorecki is a Canadian-Israeli nephrologist and population geneticist. He is professor emeritus at the Ruth and Bruce Rappaport Faculty of Medicine of the Technion – Israel Institute of Technology and at the Azrieli Faculty of Medicine of Bar-Ilan University. He is known for work on APOL1 genetic variants associated with chronic kidney disease in people of African ancestry, and for a 1997 study he co-authored that identified a Y-chromosome haplotype common among Jewish men who identify as Kohanim (members of the Jewish priesthood), later termed the Cohen modal haplotype. He is also an adjunct full professor at the Weizmann Institute of Science, where he heads Professional Identity Formation of the Physician Scientist.
Skorecki joined the faculty of the University of Toronto in 1984 as an assistant professor of medicine, and by 1994 was a full professor and associate chair of the Department of Medicine. He was director of the nephrology division at the Hospital for Sick Children and a senior staff physician at Toronto General Hospital.
In 1995 he moved to Israel, where he became the Annie Chutick Professor and Chair in Medicine at the Technion, a position he held until 2021. He directed the Rappaport Research Institute from 2000 to 2015 and held leadership roles at the Rambam Health Care Campus in Haifa, including director of nephrology (1995–2005) and director of medical and research development (2005–2018). He also established a technology transfer company for the Rappaport Research Institute.
From 2018 to 2023 Skorecki was dean of the Azrieli Faculty of Medicine at Bar-Ilan University in Safed. As dean he initiated the Galilee Diabetes SPHERE, a ten-year diabetes programme for northern Israel run with the Russell Berrie Foundation. Since 2025 he has held an adjunct appointment at the Weizmann Institute of Science.
Skorecki's research spans clinical nephrology and population and evolutionary genetics. His work includes genetic risk factors for chronic kidney disease, the phylogeography of Jewish and Near Eastern populations, and stem-cell-based models of disease.
APOL1 and chronic kidney disease
In 2010, a group including Skorecki reported that variants in the APOL1 gene, rather than the adjacent MYH9 locus, were associated with an increased risk of non-diabetic end-stage kidney disease in people of Sub-Saharan African descent. A team led by Martin Pollak at Harvard independently reported the same association and proposed that the risk alleles became common through natural selection conferring protection against Trypanosoma infection. That study reported that the risk variants occur on more than 30 percent of African-American chromosomes and that inheriting two copies raises the risk of kidney disease about tenfold. The six-nucleotide APOL1 deletion designated G2 was described in the Pollak group's study. In 2018, Skorecki's group reported, in collaboration with Pollak and others, an association between a null variant in the neighbouring APOL3 gene and non-diabetic nephropathy. A review by Skorecki's group discusses the population genetics of the MYH9–APOL1 locus.
Later studies, including some co-authored by Skorecki, examined the cellular mechanisms of APOL1-mediated kidney injury, including effects on lysosomal membrane permeability and protein trafficking. Skorecki is a named inventor on a patent application for compositions to treat APOL1-associated disease.
Population genetics and Jewish ancestry
In 1997, Skorecki and colleagues reported in Nature a Y-chromosome haplotype that was common among Jewish men who identified as Kohanim, including men from geographically dispersed diaspora communities. The haplotype became known as the Cohen modal haplotype; the term and an extended version of it were used in later publications by Thomas et al. (1998) and Hammer et al. (2009). The study has been followed by further research on the haplotype and related Y-chromosome lineages.
Further studies involving Skorecki examined mitochondrial DNA lineages in Jewish diaspora populations and the genome-wide structure of Jewish populations. A further study involving Skorecki examined the genetic history of the Druze.
Other scientific contributions
Reported a loss-of-function mutation in SLC34A1 (encoding NaPi-IIa) causing renal Fanconi syndrome, in collaboration with Jean-Yves Lapointe.
Reported a novel missense mutation in SLC5A2 (SGLT2) associated with autosomal recessive renal glucosuria.
Developed human embryonic stem-cell-derived models for studying the growth and invasiveness of tumour cells, in collaboration with Maty Tzukerman.
Contributed to early signal-transduction research, including a 1990 paper in Science on PLC-γ and PDGF signalling.
Awards and honours
Cody Gold Medal for First Standing in Class, University of Toronto (1977)
George Thorn Teaching Award, Brigham and Women's Hospital (1982)
Rosset S, Tzur S, Behar DM, Wasser WG, Skorecki K (2011). "The population genetics of chronic kidney disease: insights from the MYH9–APOL1 locus". Nature Reviews Nephrology. 7 (6): 313–326. doi:10.1038/nrneph.2011.52. PMID21537348.
Kruzel-Davila E, Wasser WG, Skorecki K (2017). "APOL1 nephropathy: a population genetics and evolutionary medicine detective story". Seminars in Nephrology. 37 (6): 490–507. doi:10.1016/j.semnephrol.2017.07.002. PMID29110756.
Calderon-Margalit R, Golan E, Twig G, etal. (2018). "History of childhood kidney disease and risk of adult end-stage renal disease". The New England Journal of Medicine. 378 (5): 428–438. doi:10.1056/NEJMoa1700993. PMID29385364.
↑Rosset S, Tzur S, Behar DM, Wasser WG, Skorecki K (2011). "The population genetics of chronic kidney disease: insights from the MYH9–APOL1 locus". Nature Reviews Nephrology. 7 (6): 313–326. doi:10.1038/nrneph.2011.52. PMID21537348.
↑Magen D, etal. (2010). "A loss-of-function mutation in NaPi-IIa and renal Fanconi's syndrome". The New England Journal of Medicine. 362 (12): 1102–1109. doi:10.1056/NEJMoa0905647. PMID20335586.
↑Magen D, etal. (2005). "A novel missense mutation in SLC5A2 encoding SGLT2 underlies autosomal recessive renal glucosuria and aminoaciduria". Kidney International. 67 (1): 34–41. doi:10.1111/j.1523-1755.2005.00053.x. PMID15610225.