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PubMed1978

Renal osteodystrophy in end-stage renal failure.

Renal osteodystrophy has many skeletal pathologic features, eg, fibroosteoclasia (osteitis fibrosa), osteomalacia, osteopenia, pseudofracture, cyst formation, and osteosclerosis. Many of these are caused by the secondary hyperparathyroidism that usually accompanies renal failure. Derangements in parathyroid hormone secretion, calcium and phosphate metabolism, and renal production of 1,25-dihydroxycholecalciferol (the most active form of vitamin D) are all interrelated and pathogenetic features of renal osteodystrophy. Types of abnormalities detected radiologically vary with patient age, type of management, and duration of hemodialysis, as well as with techniques and type of film used and interest of the radiologist. An x-ray film of the hands should always be made--it will show subperiosteal resorption in a large number of patients on dialysis. Prevention and management of renal osteodystrophy hinge on control of hyperphosphatemia and hypocalcemia.

Bone and Bones↗

PubMed1976

Advances in vitamin D metabolism as they pertain to chronic renal disease.

Many clinical similarities between renal osteodystrophy and nutritional rickets have suggested that a defect in either the metabolism or action of vitamin D exists in chronic renal failure. The discovery of the kidney as the organ that manufactures the active metabolite of vitamin D has provided direct evidence for a relationship between renal failure and altered vitamin D metabolism. Other observations suggest that an abnormality of vitamin D action could underlie both osteomalacia and osteitis fibrosa (secondary hyperparathyroidism) observed in patients with chronic renal failure. The administration of the active vitamin D analogs, 25(OH)D3, 1,25(OH)2D3, and lalpha(OH)D3, to uremic patients with symptomatic bone disease is capable of reversing many of the abnormalities of divalent ion metabolism. The widespread availability of these agents in the future may provide the clinician the means to correct or even prevent the serious bone disease that frequently complicates the course of chronic renal failure.

Calcium↗

PubMed1996

The aplastic form of renal osteodystrophy.

That bone disease accompanies renal failure has been known for over 100 years. This bone disease (renal osteodystrophy) has been variously attributed to hyperparathyroidism, vitamin D deficiency, aluminium toxicity, iron toxicity, uraemia, and a host of other aetiologies. In addition, the form the bone disease takes has been variously described as osteitis fibrosa, osteomalacia, mixed uraemic osteodystrophy and the aplastic (adynamic) lesion. In this manuscript we will focus on the aetiology, consequences, diagnosis and possible management of the aplastic form of the disease. The renal osteodystrophy study was a prospective, cross-sectional study of renal bone disease in a largely unselected population of patients receiving dialysis in three hospitals in Toronto. A variety of non-invasive data (parathyroid hormone (PTH), aluminium, etc.) and bone histology were obtained and analysed to assess pathogenesis, diagnostic criteria and management. We have defined the aplastic lesion as having low bone formation without a marked increase in unmineralized osteoid (i.e. excluding osteomalacia). We have noted that it may be associated with increased aluminium or little to no aluminium. With increased aluminium the patients have a poorer prognosis both with regards to bone disease and mortality, and they should be managed appropriately to alleviate aluminium toxicity. With lesser amounts of aluminium, morbidity and mortality are less severely impacted, but not normal. We have shown that the low bone formation, of the aplastic lesion without aluminium may be "normalized' by increasing PTH levels. It is concluded that aplastic bone disease carries adverse consequences both in terms of bone problems and survival. In the absence of aluminium toxicity the stimulation of PTH effectively corrects the bone formation abnormality. Whether this will alleviate the adverse consequences will be difficult to study. Avoiding the problem by not over-suppressing PTH seems a reasonable approach at this point.

Calcium↗

PubMed1996

Bone alkaline phosphatase isoenzyme in renal osteodystrophy.

Serum total alkaline phosphatase is the most commonly used biochemical marker of bone disease in renal patients, but alkaline phosphatase originates from different organs and sometimes lacks specificity. Bone isoenzyme measurement is considered superior to total alkaline phosphatase for the assessment of bone metabolism. We have studied the value of bone isoenzyme, determined by a new. IRMA (Tandem-R-Ostase), in haemodialysis patients with secondary hyperparathyroidism and renal osteodystrophy. Fifty-six haemodialysis patients were studied. Intact parathyroid hormone (PTH), osteocalcin, total alkaline phosphatase and bone alkaline phosphatase were determined. A transiliac bone biopsy was performed in 20 of the 56 patients after double tetracycline labelling. There was a significant correlation between bone alkaline phosphatase and PTH (r = 0.79, P < 0.001) and between bone and total alkaline phosphatase (r = 0.84, P < 0.001) in all patients. The patients who underwent a bone biopsy showed osteitis fibrosa in 17, mixed lesion in one, adynamic bone disease in one and normal bone in one. Bone alkaline phosphatase showed a significant correlation with static and dynamic histomorphometric indices similar to that obtained with PTH and better than those of total alkaline phosphatase and osteocalcin. It is concluded that bone alkaline phosphatase (ostase) seems to be a useful non-invasive marker of bone metabolism in patients on haemodialysis with high turnover bone disease. More studies are necessary to know its value in low turnover bone disease.

Adult↗

PubMed2002

Treatment of secondary hyperparathyroidism with vitamin D derivatives and calcimimetics before and after start of dialysis.

Chronic renal failure is almost always associated with secondary uraemic hyperparathyroidism. Action should be taken as early as possible to avoid it or reduce its severity in patients with chronic kidney disease (CKD). Over the last decade, the most effective way of achieving this has been defined as therapy with active vitamin D derivatives. However, the so-called 'non-hypercalcaemic' vitamin D derivatives, which are said to be superior, have not met our expectations so far. In contrast, calcimimetic agents, the new class of compounds that act specifically on the calcium-sensing receptor, are very promising for the treatment and prevention of hyperparathyroidism. CKD is associated with disturbances in calcium, phosphate, and vitamin D metabolism that occur early in the course of renal disease. In most patients, these disturbances lead to secondary hyperparathyroidism and osteitis fibrosa or associated, more complex, skeletal lesions. Here, we focus on recent advances in the prevention and treatment of secondary hyperparathyroidism by vitamin D derivatives and by calcimimetic agents.

Aniline Compounds↗

PubMed1990

Iron overload and bone disease in chronic dialysis patients.

Bone pathology was studied in 27 patients showing either iron or aluminium accumulation in bone. These patients belonged to a group of 120 unselected chronic haemodialysis patients in whom transiliac bone biopsies had been obtained. Group A consisted of 12 patients with bone iron deposits (positive Perls' staining at the calcified bone boundary, CBB) and only minimal aluminium accumulation (bone aluminium below 20 micrograms/g wet weight). Group B included 15 patients with pronounced aluminium accumulation (positive aluminium staining at the CBB and bone aluminium of 20 micrograms/g wet weight or more) and without significant bone iron deposition (negative Perls' staining at the CBB). Bone diseases were classified as early hyperparathyroidism, osteitis fibrosa, mixed disease, osteomalacia, adynamic bone disease or other bone condition using osteoid volume, relative osteoblastic activity (ROBA%), and the presence of fibrosis, as criteria. In group A, 5 of 12 patients showed adynamic bone disease, a fairly uncommon condition in the general population of non-parathyroidectomised dialysis patients. In fact, in a control group of 80 patients without iron and without aluminium overload, only five patients showed adynamic bone disease. In group B, 8 of 15 patients showed osteomalacia, and 2 of 15 presented with mixed disease, which is in agreement with the established relationship between bone aluminium accumulation and the occurrence of defective bone mineralisation. It is concluded that iron overload in dialysis patients is associated with an increased frequency of adynamic bone disease.

Aluminum↗

PubMed1991

A comparison of parathyroid-gland function in haemodialysis patients with different forms of renal osteodystrophy.

Parathyroid function was studied in three different histological forms of renal osteodystrophy: osteitis fibrosa (OF), low-turnover aluminium-associated bone disease (LTAABD), and aplastic bone disease without aluminium (ABD). Parathyroid function was determined by the evaluation of the sigmoidal parathyroid hormone-(PTH)-calcium curve, which was obtained by the performance of a reduced calcium and an increased calcium haemodialysis. Parameters of the sigmoidal PTH-calcium curve evaluated included maximally stimulated (PTHMax) and inhibited (PTHMin) PTH, the set point of calcium for PTH (ICA50), defined as the ionised calcium concentration at which PTHMax was reduced by 50%, the ratio of basal PTH to maximally stimulated PTH (PTHBase:PTHMax), the ionised calcium concentration at which basal (ICABase), maximally stimulated (ICAMax), and maximally inhibited (ICAMin) PTH values were observed, and the slope of the PTH-calcium curve. Both PTHMax and PTHMin were greater in OF than the other two groups (P less than 0.02). The ratio of basal to maximally stimulated PTH was greater (P less than 0.02) in OF (61 +/- 7%) than LTAABD (33 +/- 5%) and ABD (36 +/- 7%). The ICA50 and the ICAMax were greater (P less than 0.03) in OF than the other two groups; however, no differences were observed in the ICABase and ICAMin. The slope of the PTH-calcium curve (% maximal PTH), which should indicate the sensitivity of parathyroid cells, was greater in OF than LTAABD (P less than 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗

PubMed2005

Impact of parathyroidectomy on renal graft function, blood pressure and serum lipids in kidney transplant recipients: a single centre study.

BACKGROUND: Successful kidney transplantation is believed to reverse secondary hyperparathyroidism, but persistent disease has emerged in a significant number of allograft recipients. Parathyroid hormone (PTH) is not only involved in the aetiology of calcium/phosphate abnormalities and osteitis fibrosa, but it is also a permissive factor in the occurrence of hypertension, cardiovascular damage and dyslipidaemia. In experimental renal failure, abrogation of hyperparathyroidism by administration of a calcimimetic or parathyroidectomy (PTX) attenuates progression of renal failure. To evaluate the impact of PTX on blood pressure (BP), renal graft function and serum lipids, we performed a retrospective case-controlled study in renal graft recipients. METHODS: Charts of 1647 kidney allograft recipients, transplanted between 1989 and 2004, were reviewed. Thirty-two patients with a functioning graft and a history of a successful PTX performed at least 9 months after transplantation were identified. Biochemical and clinical data available 6 months pre- and post-PTX were registered. Changes in BP, renal function and serum lipids were assessed. The data were compared with those obtained in a similar time frame in a control group closely matched for date of transplantation. RESULTS: Systolic BP (149.9 vs 141.7 mmHg), diastolic BP (85.6 vs 81.9 mmHg), pulse pressure (64.3 vs 58.8 mmHg), total cholesterol concentration (221.4 vs 211.1 mg/dl) and low-density lipoprotein cholesterol concentration (123.9 vs 106.7 mg/dl) improved significantly after successful PTX. Serum creatinine, conversely, significantly increased after PTX (1.75 vs 2.13 mg/dl, P<0.0001). No significant changes were observed in the control group in the same time period. CONCLUSION: In patients with a functioning renal graft, BP and dyslipidaemia improve, whereas serum creatinine worsens following successful PTX. Our data are in agreement with a stimulatory effect of PTH on plasma renin activity and an inhibitory effect on lipase activity, as previously demonstrated by others. To what extent the increased serum creatinine following PTX reflects a true deterioration of the glomerular filtration rate and/or is the consequence of vitamin D-induced reduction of the renal tubular secretion of creatinine needs to be elucidated by further research.

Blood Pressure↗

PubMed1990

Parathyroidectomy in chronic renal failure: a nine-year follow-up study.

Seventy-three patients with chronic renal failure who underwent parathyroidectomy between March 1978 and April 1987 were reviewed. Thirty-four patients had undergone sub-total parathyroidectomy, and 39 patients had undergone total parathyroidectomy with parathyroid autograft into the forearm. Eight patients showed persistent hyperparathyroidism requiring a second surgical procedure. In all other patients there was highly statistical improvement in parathyroid hormone, total calcium, ionized calcium, alkaline phosphatase and a significant reduction in calcium x phosphate product. Histological evidence of osteitis fibrosa was present in 21 of 22 patients before surgery. Postoperatively, four showed complete resolution and improvement. Three patients developed histological evidence of osteomalacia during the study period. Only four of the 39 patients who underwent total parathyroidectomy with autograft had true recurrent hyperparathyroidism and only two of the 34 patients who underwent sub-total parathyroidectomy had recurrent disease, indicating that there is little to choose between the two techniques in the control of secondary hyperparathyroidism and its subsequent recurrence. In one patient with recurrence of hyperparathyroidism from a forearm parathyroid graft the histological picture was different from that of normal hyperplastic parathyroid tissue. Although it is probable that abnormal parathyroid tissue had been implanted there was no evidence of invasive growth into the forearm muscle. The most striking feature of long term follow-up was the difference in calcium x phosphate product in patients in whom vascular calcification increased compared to those patients with no change or regression of calcification. Mean calcium phosphate product in those patients with progressive vascular calcification was 4.93 for small and medium size vessels and 5.38 for large vessels compared to 4.10 for small and medium vessels and 4.09 for large vessels. In the former case the serum phosphate was 2.00 and 2.17 as compared to 1.75 or 1.73, suggesting that the aim in patients with end stage renal failure maintained by dialysis should be to control the serum phosphate concentration to 1.8 mmol or less and the calcium x phosphate product to less than 4.2.

Adult↗

PubMed2000

Normocalcemic hyperparathyroidism in Vietnamese immigrants living in southern California.

OBJECTIVE: To characterize the normocalcemic hyperparathyroidism in Vietnamese immigrants living in southern California. METHODS: Of 14 Vietnamese patients with primary hyperparathyroidism who were observed between 1991 and 1996, 50% (7 patients; 2 men and 5 women) had normal and/or fluctuating levels of serum total calcium. When the serum calcium was corrected for the albumin, the "corrected" calcium was lower than the measured serum total calcium. Their mean age was 56.4 +/- 11.4 years. All patients had normal serum levels of albumin and serum phosphate. RESULTS: Women were affected more often than men by a ratio of 5:2. The serum-ionized calcium as well as intact PTH were increased in all patients. Five patients underwent surgery with confirmation of parathyroid adenomas. Two patients refused surgery. They did not have osteitis fibrosa cystica by radiological examination. One patient had low plasma levels of 25-hydroxyvitamin D. Five of 7 normocalcemic patients (70%) were born in the month of December compared with 2 of seven hypercalcemic patients (30%). CONCLUSION: The blood ionized calcium and intact parathyroid hormone are necessary for confirmation of normocalcemic hyperparathyroidism. Most of our normocalcemic hyperparathyroid patients (70%) were born in the month of December. We postulate that a combination of exposure to solar ultraviolet light during the formation of the fetal parathyroid glands and stimulation from low vitamin D levels in the wintertime may be related to the development of hyperparathyroidism. However, it is difficult to prove a definite correlation between normocalcemic hyperparathyroidism and their month of birth (December), especially when these observations were seen in a small group of patients.

Adult↗

PubMed1981

Treatment of secondary hyperparathyroidism in patients with chronic renal failure by total parathyroidectomy and parathyroid autograft.

Sixty-one patients with chronic renal failure and secondary hyperparathyroidism underwent total parathyroidectomy and parathyroid autograft. Symptoms relieved by parathyroidectomy included bone pain, pruritus, soft tissue calcification, muscle weakness and healing of fractures. Serum parathormone levels measured before and after operation in 48 patients returned to normal in all but two patients. Serum alkaline phosphatase levels also returned toward normal after operation, except in one patient with a retained parathyroid gland. Complete radiographic studies before and after operation were available in 30 of 61 patients. Twenty-three of 24 patients with osteitis fibrosa had evidence of healing, and in one patient no change occurred. Osteosclerosis noticed in 23 patients improved slightly in eight patients, did not change in 14 and became worse in one. Pathologic examinations revealed 45 patients to have diffuse hyperplasia and 16 nodular hyperplasia. There were two early postoperative deaths, in the first 30 days, and 16 late postoperative deaths, from four months to four years afterward. In no case did the operation contribute to death. Some patients required the administration of supplemental calcium after operation, but in no instance did profound hypocalcemia occur. No patient developed recurrent hyperparathyroidism.

Adolescent↗

PubMed1992

Assessment of renal osteodystrophy in hemodialysis patients.

We performed a prospective study of 30 patients undergoing chronic hemodialysis to determine which of 6 generally available diagnostic procedures provided the most useful information for the assessment of bone disease in hemodialysis patients. The 6 procedures were: routine biochemical measurements, N-terminal parathyroid hormone (N-PTH), radiographic analysis of hands and clavicles, bone density determination by dual photon absorptiometry (DPA), deferoxamine stimulation test, and iliac crest bone biopsy. Serum N-PTH was elevated in 83% of patients but was not significantly associated with abnormalities of other biochemical parameters. No significant relationship was demonstrated between biochemical data and radiographic findings or between biochemical data and bone density by DPA. All patients with abnormal DPA had an elevation of N-PTH; therefore, DPA did not reveal any unsuspected disease. Bone biopsies were done in 20 patients and findings in each were consistent with uremic osteodystrophy, including osteitis fibrosa cystica in 11 patients and aluminum-associated bone disease in 2 patients. Six patients had mixed disease, and 1 patient had osteoporosis. Despite 11 positive deferoxamine tests, bone biopsy revealed aluminum deposition in only 7 of these patients, suggesting extraosseous aluminum accumulation in the remaining 4. Evaluation of the positive and negative predictive accuracies of DPA, x-ray analysis, N-PTH levels, and aluminum bone deposition revealed that normal DPA or x-ray findings do not exclude bone disease, that N-PTH level is a good marker for secondary hyperparathyroidism, and that a negative deferoxamine test excludes aluminum-associated bone disease. Discriminant analysis also reinforced these conclusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗

PubMed1977

Hyporegenerative anemia in primary hyperparathyroidism.

A series of patients with primary hyperparathyroidism showed a high incidence of anemia. Red cell morphology and indices, iron, folate and B12 were generally normal and reticulocyte counts inappropriately low. Focal fibrosis of the marrow space was observed in marrow biopsies from two patients, but no patient showed overt signs of a myelophthisic process. Anemia tended to occur in those with more severe hyperparathyroidism (higher serum calcium level or radiographic osteitis fibrosa cystica). Since severe hyperparathyroidism frequently compromises renal function, it is not always clear whether the anemia should be attributed to renal failure or to the metabolic disease. In nine of the 24 anemic patients, however, renal function was normal. Hyperparathyroidism may cause a hyporegenerative anemia, the mechanisms for which have not been elucidated.

Anemia↗

PubMed1984

Neurofibromatosis and primary hyperparathyroidism.

Patients who have cutaneous and osseous neurofibromatosis, especially those with pathologic fractures, bone pain, roentgenographic evidence of cystic lesions, or hypercalcemia, should be evaluated carefully for the presence of a hormonally active parathyroid adenoma. They may have a reversible cause of osteitis fibrosa cystica. Palpation of the neck, serum and urine collections for measuring calcium and phosphorus levels, PTH determinations, bone roentgenograms, and bone biopsy help to establish the diagnosis.

Adenoma↗

PubMed1998

Renal osteodystrophy.

Secondary hyperparathyroidism develops in most patients with chronic renal failure, and is associated with the histologic finding of osteitis fibrosa cystica. The disease is characterized by growth failure and severe bone deformities in children, especially the very young. The pathogenesis of renal osteodystrophy is related to phosphate retention, and its effect on calcium and calcitriol metabolism, in addition to roles played by metabolic acidosis, cytokines, and degradation of parathyroid hormone. Treatment includes restriction of dietary phosphorous intake, phosphate binders, and use of active metabolites of vitamin D.

Acidosis↗

PubMed1993

Recent advances in the management of renal osteodystrophy in children.

Secondary hyperparathyroidism remains the predominant histologic lesion in pediatric patients undergoing regular dialysis, but recent evidence indicates that the regulation of parathyroid hormone secretion by calcium does not differ substantially between patients with osteitis fibrosa and subjects with normal renal function. Growth retardation and skeletal deformities are major findings in pediatric patients with renal osteodystrophy, and alterations in vitamin D metabolism and insulin-like growth factor almost certainly contribute to these findings. Avoidance of aluminum-containing medications and the introduction of intermittent calcitriol therapy provide newer approaches to the effective management of secondary hyperparathyroidism in pediatric patients with end-stage renal disease.

Child↗

PubMed1997

The parathyroid-bone axis in uremia: new insights into old questions.

In recent years, considerable progress has been made in our understanding of the pathophysiology of secondary hyperparathyroidism in chronic renal failure and the contribution of the level of circulating parathyroid hormone to the genesis of the various types of uremic bone disease. A better insight into the cellular and molecular basis of abnormal parathyroid hormone secretion has been obtained; in particular the abnormal expression of the receptors for calcium and vitamin D in the hyperplastic parathyroid tissue, the demonstration of a direct enhancing effect of extracellular phosphate on parathyroid hormone secretion, the involvement of abnormally expressed growth factors such as transforming growth factor-alpha in parathyroid hyperplasia, and the occurrence of monoclonal parathyroid cell growth, which is probably responsible for the eventual development of autonomous hyperparathyroidism. In the pathogenesis of osteitis fibrosa, a synergistic action of parathyroid hormone with cytokines and growth factors is highly probable from a theoretical point of view, and personal preliminary observations support this hypothesis. The relative importance of metabolic acidosis is controversial. The existence of a skeletal resistance to parathyroid hormone in chronic renal failure could be partly as a result of a down-regulation of the parathyroid hormone/parathyroid hormone-related peptide receptor. In the presence of normal or only slightly elevated plasma intact parathyroid hormone levels, this may favour the development of adynamic bone disease. Finally, in terms of clinical practice the non-invasive diagnosis of the precise type of renal osteodystrophy will require the introduction of recently developed, more accurate plasma markers of bone formation and resorption, in addition to plasma intact parathyroid hormone.

Animals↗

PubMed1999

The calcium receptor and calcimimetics.

Parathyroid cells can sense small changes in plasma Ca2+ levels by virtue of a cell surface Ca2+ receptor. Calcimimetics are newly synthesized compounds that act as agonists or positive allosteric modulators at the Ca2+ receptor and can suppress parathyroid hormone secretion. The first-generation calcimimetic, NPS R-568, has undergone clinical trials in primary hyperparathyroidism and in hyperparathyroidism secondary to chronic renal insufficiency. The data accumulated so far demonstrate that calcimimetics have potential as therapeutic agents for hyperparathyroidism and related bone diseases such as osteitis fibrosa.

Aniline Compounds↗