1,721,032 research outputs found
Iperparatiroidismo secondario persistente dopo trapianto di rene: fattori eziopatogenici e possibili correzioni
No full textPost-transplantation osteoporosis is influenced by multiple factors. An important risk factor for bone morbidity is rappresented by persistent secondary hyperparathyroidism (PTH >65 pg/ml). From a large cohort of patients who had undergone kidney transplantation, we selected 125 caucasian patients (87 males and 38 females), who had undergone
kidney transplantation 0 to 10 year before, aged 25-65 years, with serum creatinine < 228 ?mol/L. All patients underwent an evaluation of the main biochemical parameters of bone metabolism as well as bone densitometry. In 87 patients we also studied three polymorphism of the Calcium-sensing receptor (A986S, R990G, Q1011E). PTH levels higher than 65 pg/ml were found in 68 % of the patients.
Surprisingly, 40 % of the patients presented 25-OHvitaminD values ? 30 nmol/L (deficiency), 56,8 % values between 30 and 80 nmol/L (insufficiency) and only 3,2 % values >80 nmol/L (normal range). The proportion of patients with osteoporosis was 25,6 % at the spine, 7,2 % at total femur and 16,8 % at femoral neck. Bone density resulted lower in patients who had been treated with dose of glucocorticoid higher than 6,7 mg/day. As regard to vertebral fractures, we observed
that 57 % of the patients had one or more vertebral fracture. In a logistic regression model only PTH levels were predictors of vertebral fracture. Multiple linear regression demostrated that 25-OH vitamin D levels, cumulative glucocorticoid intake, time on dialysis, age and time since transplantation were significantly predictive of persistent hyperparathyroidism.
As regard to CaSR polymorphism, A986S, R990G, Q1011E were
observed in 35,6 %, 11,5 % and 1,1 % of the patients, respectively.
The study did not demonstrate a significant influence of any of the three genetic variants on PTH levels, bone mass or fractures.
We conclude that osteoporosis and persistent secondary
hyperparathyroidism are common in renal transplant patients.
Low 25-OH vitamin D concentrations may exacerbate secondary
hyperparathyroidism. Treatment with vitamin D could be effective for the prevention of post-transplantation bone loss
Osteoporosi:la sfida della gestione della cronicità alla luce dei recenti progressi terapeutici
No full textAspetti clinici della terapia dell'osteoporosi con ibandronato. L'ibandronato: dall'efficacia alla pratica clinica.
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Bone metabolism in primary hypercalciuria
Full text linkPrimary Hypercalciuria (PH) is very frequently accompanied by some degrees of bone demineralization. The most frequent clin- ical condition in which this association has been studied is cal- cium nephrolithiasis. In these patients bone density has been reported to be very frequently low and increased susceptibility to fragility fractures has been described. One of the most im- portant aspects is the very poor definition of this bone disease from aic point of view. At present, the mostcommon findings seem to range from those of a low bone turnover condition to an osteomalacic trait. Many factors are in- volved in the complex relationships between bone loss and PH. Since bone loss has been mainly reported in patients with fast- ing hypercalciuria, a primary alteration in bone metabolism has
been proposed as a cause of both hypercalciuria and bone
demineralization. This hypothesis has been strengthened by
the observation that some bone resorbing-cytokines, such as
IL-1, IL-6, and TNF- are elevated in hypercalciuric patients. The effect of an excessive response to the acid load induced by di- etary protein intake seems an additional factor explaining a primitive alteration of bone. The intestine plays a major role in the clinical course of bone disease in PH. Patients with absorp-tive hypercalciuria less frequently show bone disease and a re-
duction in dietary calcium greatly increases the probability of bone loss in PH subjects. It has recently been reported that greater bone loss is associated with a larger increase in intesti- nal calcium absorption in PH patients. Considering the absence of PTH alterations, it has been proposed that this is not a com- pensatory phenomenon, but probably the marker of disturbed
cell calcium transport, involving both intestinal and bone tis- sue. While renal hypercalciuria is rather uncommon, the kidney still seems to play a role in the pathogenesis of bone loss of PH patients, possibly via the effect of mild to moderate urinary phosphate loss, with secondary hypophosphatemia. In conclu- sion, bone loss is very common among PH patients. Even if most of the factors involved in this process have been identi- fied, many aspects of this intriguing clinical condition remain to be elucidate
Bone disease in primary hypercalciuria
Full text linkPrimary Hypercalciuria (PH) is very often accompanied with some degrees of bone demineralization. The most frequent clinical condition in which this association has been observed is calcium nephrolithiasis. In patients affected by this disorder bone density is very frequently low and increased susceptibility to fragility fractures is reported. The very poor definition of this bone disease from a histomorphometric point of view is a crucial aspect. At present, the most common finding seems to be a low bone turnover condition. Many factors are involved in the complex relationships between bone loss and PH. Since bone loss was mainly reported in patients with fasting hypercalciuria, a primary alteration in bone metabolism was proposed as a cause of both hypercalciuria and bone demineralization.
This hypothesis was strengthened by the observation that some bone resorbing-cytokines, such as IL-1, IL-6, and TNF-a are high in hypercalciuric patients. The effect of an excessive response to the acid load induced by dietary protein intake seems an additional factor explaining a primitive alteration of bone. The intestine plays a major role in the clinical course of bone disease in PH. Patients with absorptive hypercalciuria less frequently show bone disease and a reduction in dietary calcium greatly increases the probability of bone loss in PH subjects. It has recently been reported that greater bone loss is associated with a larger increase in intestinal calcium absorption in PH patients. Considering the absence of PTH alterations, it was proposed that this is not a compensatory phenomenon, but probably the marker of disturbed cell calcium transport, involving both intestinal and bone tissues.
While renal hypercalciuria is rather uncommon, the kidney still seems to play a role in the pathogenesis of bone loss of PH patients, possibly via the effect of mild to moderate urinary phosphate loss with secondary hypophosphatemia. In conclusion, bone loss is very common in PH patients. Even if most of the factors involved in this process have been identified, many aspects of this intriguing clinical condition remain to be elucidate
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