Parathyroid function in relation to intestinal function and renal calcium reabsorption in patients with nephrolithiasis.
Recently a technique to measure intact parathyroid hormone (PTH), i.e. the biologically active hormone, has been available. The aim of the present study was to apply this method to evaluate the parathyroid function in a material of recurrent renal stone formers (n = 324). Intact PTH was found to be inversely related to both urinary calcium (r = -0.15; p less than 0.01) and serum calcium (p less than 0.02) indicating that in the majority of the patients with hypercalciuria this was accounted for by intestinal hyperabsorption and not by high serum PTH. Hyperabsorption was also the likely explanation for the finding of a positive relationship between the urinary calcium and oxalate excretions (r = 0.22; p less than 0.001) in medication-free patients without intestinal disorders, i.e. without enteric hyperoxaluria. Altogether 25 patients (7%) had elevated serum PTH concentrations. They were followed up with fasting serum and urinary electrolytes and an oral calcium loading test (1 g of calcium) in order to evaluate the importance of renal and intestinal factors responsible for the elevated serum PTH concentrations. The investigation was carried out on a free diet and on low and high calcium intakes, respectively. The incidence of intestinal malfunction, which was sometimes present without clinical symptoms, was found to be approximately the same as that of impaired renal conservation of calcium. The findings in the patients with intestinal malfunction were a reduced intestinal absorption of calcium and an enhanced tubular reabsorption of calcium (TRCa), with greater reabsorption of calcium for higher PTH values. In patients with impaired renal conservation of calcium despite the raised PTH there was no correlation between PTH and TRCa. When PTH was suppressed during the oral calcium load the TRCa was found to be inappropriately low and the renal defect obvious. The intestinal calcium absorption was secondarily increased to compensate for the renal losses.
Lindsjö
M
M
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
Danielson
B G
BG
Fellström
B
B
Norheim
I
I
Wide
L
L
Ljunghall
S
S
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002118:Calcium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D005260:Female; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D007669:Kidney Calculi / Q000097:blood / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010070:Oxalates / Q000652:urine; D010280:Parathyroid Glands / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000097:blood* / Q000378:metabolism
D010070:Oxalates; D010281:Parathyroid Hormone; D002118:Calcium