Background. Chronic renal failure in women is frequently associated with en
docrine disturbances leading to menstrual disorders. However, most studies
on renal osteodystrophy have not taken into account the possible role of th
ese hormonal disturbances on the pathogenesis of bone alterations seen in t
hese patients. In the present study, we evaluated bone mineral metabolism i
n a group of young hemodialyzed women with persistent amenorrhea and compar
ed them with similar women with regular menstruation.
Methods. We studied 74 women who were further subdivided into 43 women with
regular menstrual periods and 31 women with persistent amenorrhea, defined
as the absence of menstrual bleeding for more than six months. In all pati
ents, we performed a bone mineral density (BMD) analysis and simultaneously
evaluated different biochemical parameters, intact parathyroid hormone (iP
TH), sexual hormone determinations that included total estradiol, follicle-
stimulating (FSH), and luteinizing hormone and markers of bone resorption s
uch as the procollagen type 1 cross-linked carboxy-terminal telopeptide (IC
TP).
Results. Serum calcium, phosphorus, and iPTH were similar in both groups. S
erum alkaline phosphatase was higher in amenorrheic women. Although the tot
al serum estradiol concentration was normal in the amenorrheic women when c
ompared with nonuremic women, the values were significantly lower than thos
e in regularly menstruating women. Serum FSH and ICTP values were significa
ntly higher in the amenorrheic women. Trabecular BMD in the lumbar spine wa
s also significantly lower in the amenorrheic women compared with regularly
menstruating dialysis patients. Lumbar spine BMD and total estradiol level
s correlated significantly in the amenorrheic group.
Conclusions. These studies show that persistent amenorrheic young women on
dialysis have lower trabecular BMD and evidence of increased bone resorptio
n when compared with normal menstruating women on dialysis. The possible im
pact of these results in the natural history of the uremic osteodystrophy r
emains to be determined.