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September 1969

Invited Discussion

Author Affiliations

St. Louis; Denver; Washington, DC; Baltimore

From the departments of medicine, Washington University, St. Louis (Dr. Bricker), University of Colorado, Denver (Dr. Ogden), and Georgetown University Hospital, Washington, DC (Dr. Schrei-; ner); and the Department of Pharmacology and Experimental Therapeutics, Johns Hopkins University School of Medicine, Baltimore (Dr. Walser).

Arch Intern Med. 1969;124(3):292-301. doi:10.1001/archinte.1969.00300190032006

Neal S. Bricker, MD: I would like to speak briefly about the pathogenesis of secondary hyperparathyroidism and propose a schema that perhaps departs somewhat from traditional concepts. The schema is one that has been designed by Drs. Slatopolsky, Reiss, Avioli, and myself and has some data to support it.1

The essential feature of the hypothesis pothesis is that secondary hyperparathyroidism in chronic progressive renal disease begins with the destruction of the first nephron. Figure 1 depicts an idealized sketch of the natural history of uremia over a period of many years. As nephron destruction proceeds, glomerular filtration rate falls. Phosphate concentrations, however, are maintained near normal throughout most of the natural history of the disease. Only after the glomerular filtration rate is reduced to perhaps 30% of normal does hyperphosphatemia begin. Normocalcemia tends to persist during the interval of time that the phosphate concentrations remain normal, although there