Secondary hyperparathyroidism (2 degree HPT) develops as a result of renal failure. Hypocalcemia, phosphorus retention, calcitriol deficiency and skeletal resistance to the calcemic action of parathyroid hormone (PTH) are closely interrelated pathogenic factors important for the development of 2 degrees HPT in renal failure. Since previous studies have mainly focused on advanced renal failure, only limited data are available in early renal failure. The goal of the present study was to evaluate how alterations in the dietary calcium and phosphorus composition affect the factors known to contribute to the genesis of 2 degrees HPT in early and more advanced renal failure. To achieve this goal, graded differences in renal function were surgically induced in 453 rats while the dietary content of calcium and phosphorus was varied. Three different diets were used: (1) a high phosphorus diet (HPD), to induce phosphorus retention and stimulate 2 degrees HPT; (2) a high calcium diet (HCaD), to inhibit calcitriol synthesis; and (3) a moderate calcium-moderate phosphorus diet (MCaPD), to separate the effects of high dietary phosphorus and calcium. Based on the serum creatinine (SCr) concentration rats were assigned to one of four different groups: (1) normal renal function (SCr < or = 0.3 mg/dl); (2) mild renal failure (SCr 0.4 to 0.6 mg/dl); (3) moderate renal failure (SCr 0.7 to 0.8 mg/dl); or (4) advanced renal failure (SCr > or = 0.9 mg/dl). As the severity of renal failure increased, progressive 2 degrees HPT developed in each of the dietary groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Secondary hyperparathyroidism (2 degrees HPT) is a consistent finding in renal failure. A decreased calcemic response (CR) to parathyroid hormone (PTH) contributes to the development of 2 degrees HPT. Since parathyroidectomy (PTX) corrects the decreased CR to PTH in azotemic animals, down-regulation of PTH receptors induced by an elevation of PTH has been advanced as an important factor in the development of 2 degrees HPT. The goal of the study was to determine in azotemic rats whether a progressive reduction of PTH improves the CR to PTH and whether the maintenance of normal PTH levels corrects the CR to PTH. Seven groups of pair-fed rats were studied. Three groups of rats had normal renal function (NRF groups) and received either a high phosphorus (HPD-NRF), a moderate phosphorus (MPD-NRF), or a low phosphorus (LPD-NRF) diet. Three azotemic (NX) groups received similar diets (HPD-NX, MPD-NX and LPD-NX groups) in order to vary the magnitude of 2 degrees HPT. A PTX was performed in a fourth azotemic group (PTX-NX) to induce the complete absence of PTH. After 14 to 16 days on the maintenance diets, the CR to PTH was determined with a 48 hour infusion of 1-34 rat PTH.(ABSTRACT TRUNCATED AT 250 WORDS)

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