RT Journal
A1 Bricker NS, Ogden DA, Schreiner GE, Walser M
T1 INvited discussion
JF Archives of Internal Medicine
JO Archives of Internal Medicine
YR 1969
FD September 1
VO 124
IS 3
SP 292
OP 301
DO 10.1001/archinte.1969.00300190032006
UL http://dx.doi.org/10.1001/archinte.1969.00300190032006
AB 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.1The 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