Evolution of Secondary Hyperparathyroidism during Oral Calcitriol Therapy in Pediatric Renal Osteodystrophy

2015 ◽  
pp. 189-195 ◽  
Author(s):  
William G. Goodman ◽  
Isidro B. Salusky
Keyword(s):  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy

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

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.

scholarly journals Sagliker Syndrome: A Case Report on a Rare Case of Severe Renal Osteodystrophy Due to Untreated Secondary Hyperparathyroidism

2020 ◽  
Vol 12 (1) ◽  
pp. 38-40
Author(s):  
Luis B Castro ◽  
Rui Mendes ◽  
Fátima B Coelho ◽  
Vanessa Capella ◽  
Andreia B Silva
Keyword(s):  
Case Report ◽  
Secondary Hyperparathyroidism ◽  
Renal Osteodystrophy ◽  
Rare Case
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