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Care of patients with disorders affecting the kidneys and the urinary tract, particularly genetic disorders leading to an abnormal regulation of mineral ion homeostasis and bone health.
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MassGeneral Hospital for Children
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1976-1982 Medizinische Hochschule Hannover, Germany, Arzt
1980-1981 Tufts University, Medical School, Boston, MA, Third-Year Medical Student
1983-1989 Dept. of Pediatrics, Medizinische Hochschule Hannover, Hannover, Germany
1986-1988 Research Fellow in Medicine, Harvard Medical School, Mass General Hospital, Boston, MA
1989-1993 Assistant Professor of Pediatrics, Harvard Medical School, Boston, MA
1993-2006 Associate Professor of Pediatrics, Harvard Medical School, Boston, MA
2003-2007 Associate Pediatrician, Massachusetts General Hospital, Boston, MA
2003- Chief, Pediatric Nephrology Unit, Massachusetts General Hospital, Boston, MA
2006- Professor of Pediatrics, Harvard Medical School, Boston, MA
Dr. Jueppner has been studying the regulation of calcium and phosphate homeostasis. After joining the Endocrine Unit in 1986, he worked initially on the characterization and then the molecular cloning of the PTH/PTHrP receptor (PTHR1) through an expression cloning approach. Besides characterizing this G protein-coupled receptor extensively, additional investigations focused on defining inherited human disorders associated with an abnormal regulation of mineral ion homeostasis and bone metabolism. In addition to determining the molecular cause of Jansen’s metaphyseal chondrodysplasia, infantile cortical hyperostosis, and different forms of hypo- and hyperphosphatemia, his efforts led to the discovery of microdeletions within or up-stream of the GNAS locus as the cause of autosomal dominant pseudohypoparathyroidism type Ib (PHP-Ib) and to the discovery of homozygous or compound heterozygous mutations in NPT2c (also referred to as NaPi-IIc) as the cause of hereditary hypophoshatemic rickets with hypercalciuria (HHRH). He developed the first murine model of PHP-Ib and tested in vivo the effect of different PTH analogs on phosphate homeostasis and Npt2a/c expression. For example, he showed that the acute phosphaturic actions of PTH are mediated through the cAMP/PKA pathway, while the long-term regulation of renal phosphate handling requires the IP3/PKC signaling pathway. In addition, Dr. Jueppner developed one of the first assays for the measurement of FGF23, which was used for evaluating the role of this phosphaturic hormone in different disorders, particularly in patients with chronic kidney disease (CKD). He furthermore has expertise in the measurement of PTH through different immunoassays and using these measurements for predicting bone disease in CKD patients.
MGH Hotline 1.7.11 Michael Linshaw, MD, a pediatric nephrologist for MassGeneral Hospital for Children (MGHfC), died Dec. 31 at his home in Newton. Linshaw, who worked at MGHfC for more than a decade, was 70 years old.
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