The influence of age and sex on bone resorption of secondary hyperparathyroidism in renal osteodystrophy

1984 ◽  
Vol 36 (1) ◽  
pp. 25-30 ◽  
Author(s):  
H. Erik Meema ◽  
Dimitrios G. Oreopoulos ◽  
P. Robert Uldall
Keyword(s):  
Bone Resorption ◽  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy ◽  
Age And Sex

SECONDARY HYPERPARATHYROIDISM BY RENAL OSTEODYSTROPHY: OROFACIAL MANIFESTATIONS

2020 ◽  
Vol 130 (3) ◽  
pp. e204
Author(s):  
LILIANA APARECIDA PIMENTA DE BARROS ◽  
AMY BRIAN COSTA E SILVA ◽  
BIANCA SCOPEL COSTA ◽  
EDUARDO FILIPE DA PAZ SCARDUA ◽  
DANIELLE RESENDE CAMISASCA ◽  
...  
Keyword(s):  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy

Role of Estrogen Deficiency in Pathogenesis of Secondary Hyperparathyroidism and Increased Bone Resorption in Elderly Women

1997 ◽  
Vol 52 (7) ◽  
pp. 429-431 ◽  
Author(s):  
W. Roland McKane ◽  
Sundeep Khosla ◽  
Juha Ristela ◽  
Simon P. Robins ◽  
Joan M. Muhs ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Secondary Hyperparathyroidism ◽  
Elderly Women ◽  
Estrogen Deficiency

scholarly journals Effects of calcium supplementation on bone loss and fractures in congestive heart failure

2007 ◽  
Vol 156 (3) ◽  
pp. 309-314 ◽  
Author(s):  
Robert J A Frost ◽  
Carolin Sonne ◽  
Uli Wehr ◽  
Hans-Ulrich Stempfle
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Renal Function ◽  
Bone Resorption ◽  
Bone Loss ◽  
Secondary Hyperparathyroidism ◽  
Impaired Renal Function ◽  
Calcium Supplementation ◽  
Fracture Incidence ◽  
Prospective Longitudinal

Background: Cross-sectional studies have shown that more than 50% of patients with congestive heart failure (CHF) have decreased bone mineral density (BMD). There is limited knowledge about the longitudinal changes of BMD and how to treat bone loss in patients with CHF. Methods: The present study was a prospective, longitudinal trial in which 33 male patients with CHF (ejection fraction (EF): 30±11%) were assigned to 1000 mg calcium supplementation or no supplementation. BMD was measured at the lumbar spine (LS) and the femoral neck (FN) by dual-energy X-ray absorptiometry at baseline and after 12 months. Results: Osteopenia (LS 33% and FN 36%) and osteoporosis (LS 15% and FN 6%) were frequently seen in these patients; 70% showed impaired renal function, 42% secondary hyperparathyroidism, and 33% hypogonadism. Bone resorption markers were strongly elevated and correlated negatively with the EF. Patients without calcium supplementation revealed a reduction of BMD (LS 1.7% and FN 1.9%) within 12 months. The fracture incidence was 6%. Patients with calcium supplementation also demonstrated a 6% fracture incidence and a decrease in BMD (LS 1.2% and FN 1.6%), which was not significantly different from the untreated group. Loss of BMD at FN was only seen in patients with impaired renal function. Conclusions: Patients with CHF demonstrate a progressive decrease in BMD when compared with age-matched healthy individuals. Increased bone resorption due to renal insufficiency with consecutive secondary hyperparathyroidism is a main reason for BMD loss in CHF. Calcium supplementation alone cannot sufficiently prevent the decrease in BMD.

scholarly journals Renal osteodystrophy and secondary hyperparathyroidism

2002 ◽  
Vol 17 (suppl 10) ◽  
pp. 2-5 ◽  
Author(s):  
M. Fukagawa ◽  
J. J. Kazama ◽  
K. Kurokawa
Keyword(s):  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy

A Radiological Approach to the Systemic and Neurologic Features of Hyperparathyroidism

1997 ◽  
Vol 10 (3) ◽  
pp. 341-356
Author(s):  
A. Meneghello ◽  
M. Bertoli
Keyword(s):  
Nervous System ◽  
Primary Hyperparathyroidism ◽  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy ◽  
Severe Disease ◽  
Hormone Secretion ◽  
Blood Levels ◽  
Physiological Level ◽  
Blood Calcium ◽  
Pathologic Features

Parathyroid hormone (PTH) affects the nervous system directly and indirectly. The induced pathology may present typical imaging findings in neuroradiology. The hormone controls the physiological level of blood calcium. Increased serum PTH causes pathological features in the kidneys and especially in the skeleton where most calcium is situated. Primary hyperparathyroidism is due to hyperplasia or to adenomatous or carcinomatous degeneration of glandular tissue. It causes relapsing nephrolithiasis and, more seldon, nephrocalcinosis. Bone shows increased osteoclastic activity with various aspects of diffuse demineralization. In severe cases pathological fractures and sub-periosteal, sub-chondral reabsorptions appear, especially at the tendon and capsuloligamentous insertions. In even more severe disease fibrous osseous cysts and brown tumours may be found in bone. In the central nervous system, clinical symptoms, such as mental confusion, lethargy and exceptionally coma may appear. Radiologically, bone resorption can be observed in the skull as microlacunar confluent osteolysis (salt and pepper skull). Body fractures may develop in the spine. Secondary hyperparathyroidism is due principally to renal failure. Both hypocalcaemia and hyperphosphoraemia cause the hormone secretion increase. In this case, other pathologic features are associated with the typical manifestations of primary hyperparathyroidism. The uraemic kidney is inable to synthetize active vitamin D, leading to rickets in the young and osteomalacia in adults. Hyperphosphoraemia causes ectopic periarticular calcifications. Furthermore, the lack of degradation of an endogenous protein (beta 2 microglobulin) by the kidney and its poor elimination by dialytic treatment, cause chronic retention and consequent systemic amyloidosis which induces intraosseous cystic lesions and severe destructive arthropathy. All these aspects, together, are known as renal osteodystrophy. The radiological features of secondary hyperparathyroidism are the same as those observed in the primary form. In addition, all the lesions of renal osteodystrophy may be associated, further worsening the disease. In the secondary form, mild hypocalcaemia, if present, rarely leads to the neurological manifestations of the primary disease. Frequently carpal tunnel syndrome arises due to local amyloid infarction. Chronic aluminium retention may produce neurological aspects of dementia. Finally, the decrease of PTH hormone blood levels, as in hypoparathyroidism and the consequent hypocalcaemia may determine neurologic symptoms such as paresthaesias, and in severe disease, tetanic contractions. Radiologically, typical micronodular calcifications can be observed in the brain basal ganglia.

Bimaxillary Full Arch Fixed Dental Implant Supported Treatment for a Patient With Renal Failure and Secondary Hyperparathyroidism and Osteodystrophy

2015 ◽  
Vol 41 (2) ◽  
pp. e36-e43 ◽  
Author(s):  
Dennis Flanagan ◽  
Mark Mancini
Keyword(s):  
Secondary Hyperparathyroidism ◽  
Dental Implant ◽  
Renal Osteodystrophy ◽  
Phosphate Binders ◽  
Wide Diameter ◽  
Dental Prostheses ◽  
Anterior Guidance ◽  
Successful Control ◽  
Stage Renal Disease ◽  
End Stage

A long-term dialysis patient with end-stage renal disease (ESRD) also referred to as chronic kidney disease (CKD) due to IgA nephropathy complicated by severe secondary hyperparathyroidism and renal osteodystrophy was successfully treated with dental implant-supported fixed prostheses. Phosphate binders, vitamin D, calcium cinacalcet calcimimetic therapy, and dialysis 3 times weekly had been instituted with standard divalent ion serum assessments. Successful control of the patient's secondary hyperparathyroidism was achieved. Long and wide diameter implants were used with an anterior guidance occlusion scheme to reduce the per-square-millimeter off-axial implant force delivered to the bone. Patients with ESRD and renal osteodystrophy may be successfully surgically and prosthetically treated with long wide dental implants supporting fixed full arch splinted dental prostheses with an appropriate occlusal scheme.

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