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PubMed1986

Bone and mineral metabolism and chronic alcohol abuse.

Studies of bone and mineral metabolism were made in 22 patients with chronic alcohol abuse and varying degrees of liver damage. None of the patients had clinical evidence of metabolic bone disease, but quantitative bone histology showed that six had osteoporosis, three osteomalacia, and two osteoporosis and osteomalacia combined. Trabecular bone volume (TBV) tended to be reduced in relation to age, and there was histological evidence of reduced bone formation particularly among the patients with osteoporosis. Multivariate analysis of the relevant variables showed that the major determinants of age-adjusted trabecular bone volume were the serum concentration of albumin and the dietary calcium. The presence of osteoporosis was related to the state of liver function and the type of alcohol habitually consumed, and was a particular feature of patients with severe liver disease and those who only drank spirits. Six patients (five with osteoporosis) had biochemical evidence of hyperparathyroidism, but none showed histological evidence of increased bone resorption or of osteitis fibrosa. In four patients the development of hyperparathyroidism was probably related to underlying magnesium deficiency. Serum calcidiol tended to be reduced and was directly related to the state of liver function; four patients had reduced or low normal serum concentrations of calcitriol. In only three patients could the development of osteomalacia be related to vitamin D deficiency; in two patients the cause of the osteomalacia was obscure. Significant changes in bone structure and mass appear to be common among heavy drinkers even in the absence of clinical metabolic bone disease. These skeletal abnormalities are likely to be relevant to the increased fracture risk associated with heavy drinking.

Adult↗

PubMed1987

Severe renal osteodystrophy without elevated serum immunoreactive parathyroid hormone concentrations in hypomagnesemia due to renal magnesium wasting.

An 8 1/2-year-old girl presented with a long history of seizures, growth retardation, muscle weakness, gait disturbance, and hearing loss. Her evaluation revealed chronic moderate renal failure (serum creatinine 2.2 mg/dL), severe hypocalcemia (5 mg/dL), hyperphosphatemia (8.1 mg/dL), hypomagnesemia (1.5 mg/dL), increased urinary magnesium excretion (2 mg/kg/d), high fractional excretion of magnesium (21.7%), hypokalemia (3.2 mEq/L), and hyperkaliuria (26 mEq/L). Low circulating immunoreactive parathyroid hormone levels for the degree of the hypocalcemia (serum N-parathyroid hormone 212 pg/mL) and severe rickets without evidence of osteitis fibrosa cystica were found. The patient probably has primary renal leak hypomagnesemia (magnesuric hypomagnesemia) which caused impaired secretion of immunoreactive parathyroid hormone leading to severe hypocalcemia and calcium deficiency rickets. Treatment with magnesium and calcium supplements, calcitriol, and aluminum hydroxide resulted in marked clinical, biochemical, and radiologic improvement. Calcium deficiency rickets due to primary or secondary renal magnesium wasting in conjunction with moderate renal failure represents a largely unrecognized metabolic bone disease.

Aluminum Hydroxide↗

PubMed1985

The efficacy and adequacy of continuous ambulatory peritoneal dialysis.

Since it was introduced in 1976, continuous ambulatory peritoneal dialysis (CAPD) has won acceptance in many centres and it is now regarded as an important alternative to haemodialysis. CAPD patients have comparable and, in some circumstances, better survival than those on chronic haemodialysis. It is indicated particularly in patients with diabetes mellitus, cardiovascular instability and at the extremes of life. The success of kidney transplantation is similar in those maintained on CAPD and on haemodialysis. CAPD also achieves satisfactory physical and psychological rehabilitation, and the quality of life, including the level of sexual function, is similar during CAPD and haemodialysis. Women on CAPD menstruate more often than those on haemodialysis. CAPD provides adequate clearance of metabolic wastes, maintains fluid balance and ameliorates neurotoxic cognitive dysfunction. CAPD gives control of hypertension and anaemia which is superior to that on haemodialysis. Neuropathy remains stable but osteitis fibrosa seems to progress. CAPD is the most economical of the various forms of dialysis. We conclude that CAPD is an adequate form of replacement and should be made available in every nephrology centre providing treatment for patients with end-stage renal disease.

Adolescent↗

PubMed1985

Dialysis osteomalacia: clinical aspects and physiopathological mechanisms.

Dialysis osteomalacia is characterized by distinctive, although not pathognomonic, clinical and biochemical features. Symptoms and signs may include musculoskeletal pain, arthralgias, proximal muscle weakness, and spontaneous fractures. Biochemical characteristics may be hypercalcemia and normal serum alkaline phosphatase activities. Vitamin D administration may induce early severe hypercalcemia. Plasma phosphate and immunoreactive parathyroid hormone concentrations may be at any level. Only bone histology allows to establish the diagnosis of dialysis osteomalacia with certainty. Diphosphonate bone scan, however, enables to distinguish between severe osteitis fibrosa and dialysis osteomalacia. The diagnostic value of desferrioxamine administration with subsequent measurement of plasma aluminium remains to be determined. The complex interactions existing between parathyroid hormone and aluminium are not yet fully understood.

Aluminum↗

PubMed1974

Bone disease in hemodialysis patients with particular reference to the effect of fluoride.

Forty-one patients on our chronic hemodialysis program were assessed for the degree of progression of bone disease over an average period of 46 months. Seven patients were using a fluoridated dialysate. Four of these seven patients developed a marked increase in osteoid as judged by bone biopsy, while in the nonfluoridated group the amount of osteoid remained within normal limits.In the absence of fluoride, although osteitis fibrosa occurred, it was reversible in 10 out of 12 cases by dihydrotachysterol treatment, and overall there was no evidence of progression of bone disease at the end of the study period.

Adult↗

PubMed1979

25-hydroxycholecalciferol in the treatment of renal osteodystrophy in haemodialysed patients.

The effects of 25-OHD3 on renal osteodystrophy have been studied in 6 patients on maintenance haemodialysis. Administration of 25-OHD3, 50 microgram/day, did not improve biochemical data and intestinal absorption of calcium. With a dose of 100 microgram/day in all patients an increase in blood calcium levels eventually reaching hypercalcemic values was observed. In two cases a fall in alkaline phosphatase toward normal values was noted. In the same cases the treatment-induced hyperphosphatemia, uncontrolled by AI(OH)3 supplementation and similarly high iPTH levels were observed. In two cases repeated bone biopsy following 8 months treatment and not show substantial improvement of bone lesions. In one case addition of 1,25-(OH)2D3 to the treatment with 25-OHD3 led to a more rapid improvement in biochemical parameters and iPTH serum levels. Doses of 25-OHD3 capable to correct blood calcium levels and intestinal absorption of calcium, may have minimal benefit on the osteitis fibrosa component of the bone lesion.

Adolescent↗

PubMed1980

Familial pseudohypoparathyroidism without somatic anomalies.

A family is described in which affected individuals showed pseudohypoparathyroidism, with hypocalcemia, hyperphosphatemia and increased serum levels of parathyroid hormone, but none of the somatic anomalies frequently associated with this disorder. The untreated individuals showed radiologic evidence of osteitis fibrosa. The administration of parathyroid hormone evoked only a slight increase in the excretion of cyclic adenosine monophosphate but no change in the renal tubular reabsorption of phosphate and no rise in the serum calcium level. The infusion of ethylenediamine tetra-acetic acid caused an appropriate increase in the serum level of parathyroid hormone, but again there was no apparent renal or skeletal response to the hormone. There were no associated abnormalities in calcitonin, thyrotropin or prolactin levels and no thyroid dysfunction. Therapy with vitamin D corrected the hypocalcemia but did not improve the renal and skeletal responsiveness to parathyroid hormone. The inheritance of the disorder in this family was compatible with an autosomal dominant mode with variable penetrance, but other modes could not be excluded.

Adolescent↗

PubMedDate not supplied

Secondary hyperparathyroidism in chronic renal failure.

The metabolic bone disease associated with chronic renal failure has been described collectively by the terms "renal osteodystrophy" or "renal-glomerular-osteodystrophy" and consists of osteomalacia, osteitis fibrosa, and osteosclerosis. The skeletal abnormalities may occur either alone or in combination with one another. An increased concentration of circulating immunoreactive-parathyroid hormone (i-PTH) is a recognized feature of patients with chronic renal failure, and the values are usually much higher than those found in patients with primary hyperparathyroidism associated with a parathyroid adenoma. It must, however, be recognized that the high circulatory concentrations of parathyroid hormone found in patients with chronic renal failure are of immunoassayable material which may or may not be of biological significance in respect of activity. A disturbance in the homeostatic control mechanism governing parathyroid hormone, the secretion rate, its metabolism, and target organ resistance to its action are of major importance in the pathogenesis of some aspects of the metabolic bone disease in patients with chronic renal failure. The pathogenesis of the secondary hyperparathyroidism of chronic renal failure, however, also involves disturbances in cholecalciferol metabolism, phosphate retention, and the uremic state per se.

Calcium↗

PubMed1984

Serum aluminium in haemodialysis patients: relation to osteodystrophy, encephalopathy and aluminium hydroxide consumption.

The serum aluminium concentration of 82 patients undergoing regular dialysis treatment in a large dialysis department was measured. Duration of known uraemia, total cumulative aluminium hydroxide consumption, present level of aluminium hydroxide consumption and chronic interstitial nephropathy as primary kidney pathology were all positively correlated to serum aluminium concentration. Serum aluminium concentration was positively correlated to the incidence of clinical osteodystrophy and negatively correlated to bone mineral content. There was, however, no correlation to parathyroid hormone concentration or parathyroidectomy. The highest serum aluminium concentration was accompanied by clinical dialysis encephalopathy. The centre uses reverse osmosis for water purification, and there has never been measurable aluminium contamination. On the basis of these findings it is concluded that: the source of aluminium in our patients is aluminium hydroxide consumption and not the dialysis water; aluminium plays no role in the development of osteitis fibrosa; the findings are consistent with the theory that hyperaluminaemia plays a role in the development of osteomalacia, and serum aluminium measurement may be useful in the diagnosis of dialysis encephalopathy.

Adolescent↗

PubMedDate not supplied

[The hand of the patient under periodic hemodialysis treatment. Comparative radiographic and xeroradiographic aspects].

Renal osteodystrophy is the skeletal response to long-standing chronic renal disease. The radiographic features include hyperparathyroidism (osteitis fibrosa cystica), rickets or osteomalacia, osteoporosis, osteosclerosis and soft tissue and vascular calcifications. Many investigators have verified that changes in the phalanges of the hand are the most sensitive indicator of renal osteodystrophy, especially subperiosteal bone resorption. The hands of 50 chronic dialysis patients were evaluated for at least one year for tuftal resorption (acro-osteolysis), subperiosteal and intracortical bone resorption, and periosteal new bone formation (periosteal neostosis), using fine detail radiography and optical magnification. At last control, only in a group of 17 subjects (34%), xeroradiography of the hand was also performed. Results indicate the importance of the use of fine detail radiography in the early diagnosis of renal osteodystrophy and that serial radiography of the hand is a proper method of evaluating progressive bone resorption. In addition, a significant difference (p less than 0.05) is demonstrated between xeroradiography and radiography to evaluate periosteal neostosis.

Adult↗

PubMed1983

Osteomalacia in chronic renal failure before dialysis.

Bone biopsies taken from 327 patients before the start of dialysis have been correlated with clinical and biochemical findings to test various theories about the aetiology of osteomalacia. Two groups of patients, 100 with osteomalacia and 100 with pure osteitis fibrosa, have been compared in detail. Osteomalacia is associated with chronic pyelonephritis or obstruction as primary renal disease, and with acidosis, hypocalcaemia and normophosphataemia (as opposed to hyperphosphataemia). We have found no association between osteomalacia and known duration or severity of uraemia and in a small series of observations we have not confirmed previous reports of a close association between osteomalacia and depressed plasma 25(OH) cholecalciferol values.

Acidosis↗

PubMed1983

Treatment of fracturing renal osteodystrophy by desferrioxamine.

Aluminium removal by desferrioxamine chelation has been demonstrated in three long-term haemodialysis patients with dialysis encephalopathy and fracturing renal osteodystrophy. Aluminium concentrations in serum and in both bone marrow and bone trabeculae, determined separately in transiliac biopsy specimens, fell significantly over the treatment period. Bone aluminium removal was confirmed by specific histochemical staining. In two patients osteomalacia disappeared, and in two patients osteitis fibrosa emerged but improved in one following vitamin D therapy. We conclude that desferrioxamine is capable of mobilising aluminium from bone and that the calcification defect in fracturing renal osteodystrophy may be overcome.

Adult↗

PubMed1983

Renal osteodystrophy in end-stage renal failure patients in Israel.

Renal osteodystrophy is one of the major complications in patients on long-term hemodialysis. A group of 42 patients on hemodialysis (mean age 42 yr) were investigated in order to assess the prevalence of renal osteodystrophy in Israeli patients. The patients were examined by X-ray, and 66.7% were found to have signs of osteodystrophy. Of 14 patients without signs of bone involvement, 10 had been on treatment less than 1 yr. A bone biopsy, performed in 28 patients (mean age 43 yr), showed signs of renal osteodystrophy in all. Two of these patients were diagnosed as having mainly osteitis fibrosa, four as having osteomalacia and the rest as having the symptoms of both.

Adult↗

PubMed1981

Treatment of renal osteodystrophy with 1,25-dihydroxycholecalciferol.

Nine patients with renal osteodystrophy were tested for 6.5 to 35 months with 1,25-dihydroxycholecalciferol (1,25-DHCC). A close biochemical follow-up was performed during the first 6 months of treatment, including biweekly determinations of serum calcium, phosphorus, magnesium, alkaline phosphatase and creatinine levels. A bone biopsy, radiologic investigations and determinations of plasma levels of immunoreactive parathyroid hormone (IPTH) and intestinal absorption of calcium 47 were performed before and after the 6 months. Although the five patients with osteitis fibrosa showed a significant improvement, the four with predominantly osteomalacic lesions showed no response to treatment. These four had a normal initial plasma iPTH level, higher serum calcium levels than the other five patients, extreme sensitivity to 1,25-DHCC, with frequent episodes of hypercalcemia, and only a slightly increased serum alkaline phosphatase level, which remained unchanged during treatment. All but one of the patients, irrespective of the histologic abnormality, showed a decrease in the uptake of radionuclide by bone after treatment. The renal function of one patient, a man with long-standing stable renal failure who had not undergone dialysis, deteriorated during treatment.

Calcitriol↗

PubMed1982

Bone metabolism in chronic renal failure.

Quantitative bone histology was carried out on 37 haemodialysis patients. Hyperparathyroid bone disease (HPT) was diagnosed by an elevated osteoclast count, and high counts were associated with classic osteitis fibrosa. Osteomalacia (OM) was found in two distinct though frequently overlapping forms, both with increased osteoid surface. In classic OM (type 1), present in 19% of patients the osteoid seams were wide and the mineral apposition rate low, with the tetracycline bands wide and merging together. In the more common form of OM (type 2), present in 81%, the mineralising surface, as shown by tetracycline uptake, was reduced, but the mineral apposition rate was normal. Tetracycline surface was highly correlated with osteoblast surface, suggesting that osteoblasts play a role in mineralisation, and that type 2 OM is caused by a reduction in osteoblast surface. The osteoblast surface also correlated with serum parathyroid hormone, and so secondary hyperparathyroidism may obscure the diagnosis of type 2 OM, which may be almost universally present in haemodialysis patients. Type 1 OM is not obscured by secondary hyperparathyroidism. Of the 37 patients 5 had HPT, 9 OM and 22 HPT + OM. Only one had normal bone. Biochemical parameters had limited predictive value. The study also did not support the suggestion that endogenous calcitonin protects against HPT disease.

Adult↗

PubMed1980

Azotemic osteodystrophy - indications for intervention.

Because the pathogenetic mechanisms leading to azotemic osteodystrophy are incompletely understood, prophylactic and therapeutic intervention must necessarily be less than satisfactory. There is no proof that prophylactic measures, e.g. phosphate binders and vitamin D (metabolites) are beneficial in incipient renal failure but measures to prevent secondary hyperparathyroidism appear reasonable. In advanced renal failure, oral phosphate binders, administration of calcium salts and vitamin D (metabolites) are effective in returning serum chemistry towards normal, but considerably less effective in restoring normal bone histology. Hemodialysis, using adequate calcium concentrations in the dialysate, permits one to normalize predialytic calcium and phosphorus levels, and maintain calcium balance in the majority of patients. Hemodialysis does not, however, prevent hyperparathyroidism and the various types of metabolic bone disease. Symptomatic azotemic osteodystrophy increases in frequency and severity with increasing duration of dialysis. While osteitis fibrosa responds favorably to vitamin D and several vitamin D metabolites, osteomalacia is considerably less responsive. It remains unknown whether this is due to low bone turnover, absence of some crucial unknown vitamin D metabolite, or involvement of non-vitamin D-related factors. Parathyroidectomy for uncontrollable hyperparathyroidism is required only in a minority of patients.

Bone Diseases↗

PubMed1995

[Bone histomorphometric analysis in primary hyperparathyroidism].

In primary hyperparathyroidism, bone remodeling is increased due to an enhanced activation frequency which is caused by excessive PTH. In mild cases, eroded, osteoid and labeled surfaces are increased. But as bone balance per remodeling cycle in cancellous bone is zero or even slightly positive, bone volume and structure are relatively maintained. In advanced cases, bone resorption is predominant in the endosteal surface of cortical bone, resulting in progressive thinning and increased porosity, cancellisation. As far cancellous bone resorption depth is deepened to occur trabecular perforation associated with fibrous tissue replacement, osteitis fibrosa.

Bone Remodeling↗

PubMed1994

[Studies on the pathogenesis and pathophysiology of renal osteodystrophy. II. Bone histology of chronic renal failure patients at the time of starting hemodialysis].

We studied the relationship between the histomorphometric parameters of bone structure in biopsied iliac crest bone specimens and the serum biochemical parameters in 62 chronic renal failure (CRF) patients at the time of starting hemodialysis. These patients were classified into 4 groups according to Coburn's definition: 4 patients with osteomalacia, 1 with osteitis fibrosa, and 57 with mild type. Serum corrected Ca levels were significantly lower in cases with osteomalacia than those of mild type, which suggested that hypocalcemia was related to Calcification disturbance in end-stage renal failure. The bone histomorphometry revealed that in CRF patients, osteoid and bone resorption parameters were significantly higher and calcification parameters were significantly lower than those of normal controls. Osteoclast and osteoblast surfaces were significantly correlated with osteoid and bone formation parameters. In diabetic nephropathy patients, serum C-PTH levels were significantly lower than those of patients with non-diabetic nephropathies. Bone mass, osteoid and bone formation parameters were also significantly lower in diabetic nephropathy patients, which showed that low turnover bone mass decrement has already appeared at the time of starting hemodialysis. There was a significant negative correlation between serum corrected Ca levels and osteoid parameters. A significant relationship was also found between serum alkaline phosphatase levels and both osteoid and bone formation parameters. Serum C-PTH levels were significantly related to osteoid, bone resorption and bone formation parameters, demonstrating the presence of high turnover bone in secondary hyperparathyroidism. This study clarifies that morphological changes of bone structure are present at the time of starting hemodialysis in CRF patients.

Adult↗