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J G Heaf

Publications and source records attributed to J G Heaf.

33 records · Page 2Linked to original sources

Noninvasive diagnosis of uremic osteodystrophy: uses and limitations.

45 bone biopsies from patients with chronic uremia were reviewed to define which noninvasive investigations were of value in predicting the histological diagnosis and to quantify the spectrum of uremic bone disease at a center that has consistently used an aluminum-free dialysis bath. 17 biopsies were taken postmortem. 15 patients received conservative treatment, the rest were on maintenance dialysis. 13 patients had symptomatic bone disease. Virtually all patients with a uremia duration greater than 3 years had uremic osteodystrophy. All patients with clinical bone disease, hypercalcemia or raised alkaline phosphatase activity had osteodystrophy, but the specific histology was not indicated. Greatly raised parathyroid levels suggested secondary hyperparathyroidism, but the test was only 100% specific when 20 times normal. Total aluminum consumption was highly indicative of bone aluminum concentration (p less than 0.0001) and aluminum-related osteomalacia (5 cases), suggesting that a considerable proportion of uremic bone disease is iatrogenic. Serum aluminum was of some use in the diagnosis of aluminum-related osteomalacia, but was not wholly reliable. Bone mineral content (BMC) using both forearm measurements and total body bone mineral levels (TBBM) were assessed in 32 patients and were found to be reduced in 12, with a preponderance of secondary hyperparathyroidism. BMC and TBBM were negatively correlated to resorbing surfaces and bone formation rate, suggesting that secondary hyperparathyroidism is the uremic bone disease that represents the greatest threat to bone mass. It is concluded that while noninvasive investigations give considerable information, reliable diagnosis requires the use of histological methods.

Adolescent↗

The effect of oral aluminium salts on the bone of non-dialysed uremic patients.

12 patients with conservatively treated uremia were investigated using bone histomorphometry, bone aluminium concentration determination and total body bone mineral content (TBBM). The bone aluminum was raised in 10 patients and was significantly related to oral aluminium salt consumption (p less than 0.01). Two of four patients who had not received aluminium also had raised levels but the difference was not significant from nonuremic patients. The two patients with the highest levels had a mineralisation defect despite normal levels of 1,25-dihydroxyvitamin D. Three patients had significant bone loss of whom one had osteomalacia (OM) while two had secondary hyperparathyroidism (2HP). It is concluded that 1) aluminium salt consumption results in bone aluminium accumulation, and may contribute to the mineralisation defect; 2) uremic patients not treated ith aluminium salts may have slightly raised levels, but this seems not to be clinically important; 3) secondary hyperparathyroidism causes greater destruction of bone mass than other uremic bone diseases; 4) atomic absorption spectrometry is a more sensitive method for detecting aluminium bone deposition than histochemical methods.

Acetates↗

Metabolic bone disease and aluminium contamination in 38 uremic patients. A bone histomorphometric study.

Iliac crest biopsies from 38 uremic patients, 26 hemodialysis, and 12 chronic uremics from a nephrology department with verified aluminium free dialysis water were investigated with histomorphometric method and aluminium-specific staining. For both the uremic and the dialysed group the results showed a high incidence of both metabolic bone disease (75%, 69% respectively) and aluminium contamination (25%, 62%).

Aluminum↗

Bone aluminum deposition in maintenance dialysis patients treated with aluminium-free dialysate: role of aluminium hydroxide consumption.

Postmortem iliac crest biopsies were performed on 16 uremic patients. 3 had been treated conservatively while 13 had been entered into a maintenance dialysis program. The dialysate was treated by reverse osmosis for more than 10 years, and the aluminium concentration was consistently below the detection limit of 0.15 mol/l. 14 patients had been treated with aluminium hydroxide. Bone histomorphometry, aluminium labelling intensity, osteoid surface aluminium labelling extent (Al/OBI) and bone aluminium concentration were measured. 14 patients had significant bone aluminium deposition, including 2 who were not on dialysis of whom 1 had not received aluminium hydroxide. Bone aluminium concentration and labelling intensity were correlated to total aluminium hydroxide consumption (p less than 0.001, p less than 0.05) and present dose (p less than 0.01, p less than 0.01), while Al/OBI was not. The two patients with the highest aluminium concentrations had symptomatic osteomalacia, but 4 patients with significantly raised concentrations and mineralisation front labelling had secondary hyperparathyroidism. It is concluded that bone aluminium deposition occurs despite the use of aluminium-free dialysate and is associated with total and present aluminium hydroxide consumption; heavy aluminium deposition is associated with severe and symptomatic osteomalacia, but can also be observed in the presence of predominant hyperparathyroidism; aluminium deposition can occur in the absence of treatment with dialysis or aluminium hydroxide; bone aluminium concentration and labelling intensity are a better measure of bone deposition than Al/OBI.

Adolescent↗

Albumin-induced changes in the electrocardiographic QRS complex.

The amplitude of the QRS wave of the electrocardiogram was correlated with conventional serum electrolyte concentrations in 94 nonhypertensive and 53 hypertensive patients. There was a highly significant correlation of QRS amplitude with serum albumin level in both groups. There was also significant correlation with serum calcium level in the nonhypertensive group, but this significance disappeared after correction for albumin. Changes in the serum albumin level during the hospital admission of the nonhypertensive patients were positively correlated with changes in QRS amplitude. Albumin infusion into 13 healthy persons resulted in significantly increased QRS amplitude, which was related to changes in serum albumin concentration. These results suggest that changes in serum protein concentration cause changes in QRS amplitude, possibly as a result of increased conductivity.

Adult↗

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↗

Use of bone mineral content determination in the evaluation of osteodystrophy among hemodialysis patients.

During a period of 2 years, bone mineral content (BMC) was measured regularly in patients undergoing regular dialysis treatment (RDT). Low BMC values were found to be correlated to long duration of uremia, raised alkaline phosphatase activity, hyperaluminemia, hypermagnesemia, hypophosphatemia and clinical osteodystrophy. High levels of BMC loss were found among patients with relatively high initial BMC levels and severely calciopenic patients actually gained bone density during the investigation. Serum alkaline phosphatase activity and serum immunoreactive parathyroid hormone (PTH) levels were positively related to bone loss. It is suggested that the low BMC among RDT patients is caused by a predialytic loss that is arrested by entrance into a dialysis programme. Investigations using BMC or total body calcium as a measure of therapeutic effect must take account of this. The role of hypermagnesemia and hyperaluminemia remains undefined. Patients with BMC reduced below ca. 80% of normal may be candidates for treatment with active vitamin D metabolites.

Adult↗

Parathyroidectomy for hyperparathyroidism in maintenance dialysis patients.

Parathyroidectomy was performed during a 5-year period in 11 of 196 patients undergoing maintenance dialysis for renal failure. Characteristics of the series were relatively long periods of dialysis, severe symptomatic bone disease, hypercalcemia, increased alkaline phosphatase, greatly raised serum levels of immunoreactive parathyroid hormone and X-ray changes appearing as abnormal bone structure, metastatic calcifications and pathologic fractures. Most of the operations consisted of total parathyroidectomy alone or accompanied by autotransplantation of parathyroid tissue. Subjective and objective improvement followed the operation in most cases, and the outlined indications thus appeared to be adequate. However, only a minority of the patients became symptom-free, and current methods of treating autonomic hyperparathyroidism in patients on regular dialysis must be regarded as suboptimal. The relative indications for the 2 types of operations are discussed. Total parathyroidectomy may be an acceptable operation for patients of this category.

Adult↗

Parathyroid hormone during maintenance dialysis: influence of low calcium dialysate, plasma albumin and age.

UNLABELLED: Intact PTH measurements between 1989-96 in a 116-patient (63 HD, 53 PD) dialysis unit were reviewed to evaluate the determinants of PTH. Prophylactic treatment included calcium carbonate and maximal alphacalcidol therapy. A forward stepwise multiple regression analysis showed that duration of dialysis, phosphate, albumin and chronic glomerulonephritis were independently positively correlated with PTH, and that ionized calcium, parathyroidectomy, age, diabetic nephropathy and systemic disease were independently negatively correlated. During the first five years of dialysis PTH rose from 124 ng/L (SD range 33-462) to 160 (63-402)* in HD patients but fell from 119 ng/L (33-423) to 88 (31-251)** in PD patients despite the less intensive treatment. PTH fell with increasing age (40-50 years 173 ng/L (52-575); > 60 years 100 (31-316)**) and hypoalbuminemia (< 400 micromol/L 68 ng/L (22-209); > 550 pmol/1138 (41-457)**). PD patients were generally older and increasingly malnourished; after correcting for these factors, no influence of dialysis modality on PTH could be seen. Low-calcium dialysate (1.25 mmol/L) was introduced for both dialysis groups in 1994. Consequent to this, aluminium consumption was virtually eliminated and consumption of alphacalcidol increased. PTH fell from 161 to 128 ng/L in HD patients but rose from 119 to 135 ng/L in PD patients. The incidence of parathyroidectomy fell from 4.3%/year to 1.5%/year*. CONCLUSION: Malnourishment and increasing age reduce PTH secretion and are important determinants of hyperparathyroidism during maintenance dialysis. Adynamic bone disease is common in PD patients and associated with low PTH levels, and may be a consequence of malnourishment and involutional changes. The introduction of low-calcium dialysate reduced the incidence of parathyroidectomy. Control of hyperparathyroidism improved in HD but not PD patients.

Adult↗