PTH stimulates renal Ca(2+) reabsorption through the coordinated expression of renal transcellular Ca(2+) transport proteins. Moreover, the PTH-induced stimulation is enhanced by the magnitude of the Ca(2+) influx through the gatekeeper TRPV5, which in turn facilitates the expression of the downstream Ca(2+) transport proteins. Therefore, the renal transcellular Ca(2+) transport proteins, including TRPV5, could contribute to the pathogenesis of PTH-related disorders.

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In vivo 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) decreased PTH and calcitonin gene transcription. A low calcium is the major signal for PTH secretion, and a high calcium for calcitonin secretion. We report here that calcium has no effect on calcitonin messenger RNA (mRNA) levels in vivo in the rat, but that a low calcium markedly stimulates PTH mRNA levels. Serum calcium was decreased by ip phosphorus and increased by calcium gluconate (ip or iv infusion) and demonstrated that a low serum calcium markedly increased PTH mRNA levels whereas a high serum calcium had no effect. There was no change in mRNAs for calcitonin or actin in the same thyroparathyroid extracts. After phosphorus ip serum calcium decreased from 10.4 to 8.5 mg/dl and PTH mRNA increased up to 3-fold at 1, 3, and 6 h. Gel blots showed that a low calcium increased PTH mRNA levels with no change in its size (833 base pairs). Calcitonin ip decreased both serum calcium and phosphorus with an up to 5-fold increase in PTH mRNA at 1 h, thus demonstrating that the effect of phosphorus on PTH mRNA was due to the low serum calcium and not the high serum phosphorus. When phosphorus and 1,25(OH)2D3 (100 pmol/100 g) were injected together, despite the low serum calcium, there was a decrease in PTH mRNA levels. These results show a linear relationship between calcium and PTH gene expression, but not calcitonin or actin, with a dominant role for 1,25(OH)2D3.

The diagnostic usefulness of bone marrow hemosiderin, serum ferritin, transferrin saturation, mean corpuscular volume (MCV) and red cell protoporphyrin (EPP) in the evaluation of iron status in patients on chronic hemodialysis was studied in 39 subjects. The correlation between serum ferritin and the number of transfusions received per month was slightly higher (r = 0.717; p < 0.001) than the correlation between bone marrow hemosiderin and transfusions (r = 0.685; p < 0.01). Serum ferritin was useful in identifying subjects with both increased or reduced iron stores. In contrast, transferrin saturation could only be used for indicating iron overload. MCV for indicating iron deficiency, and EPP was not useful in either case. The abnormal increase of EPP in chronic uremia has not been previously described. It is unrelated to iron deficiency and is most probably explained by the known reduction in red cell ferrochelatase activity associated with chronic uremia. Serum ferritin is clearly the most useful diagnostic aid for assessing iron stores in patients on chronic hemodialysis. Whether ferritin is also the best predictor of response to iron therapy, cannot be determined on the basis of the present data.

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