Chronic Renal Failure
Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George in The Scientific Basis of Urology, 2010
Renal bone disease is a complex entity that starts to develop early in the course of progressive renal disease. It is characterized by a spectrum of metabolic bone disorders, all of which have the effect of reducing bone strength and hence predisposing to fractures. The main pathologies are as follows: Osteitis fibrosa cystica (“high turnover bone disease’’): This occurs because of secondary hyperparathyroidism (SHPT) with increased osteoblast and osteoclast activity, leading to rapid bone formation and resorption. The outcome is weakened bone structure.Adynamic bone disease (“low turnover bone disease’’): This is characterized by reduced bone formation and resorption. Parathyroid hormone (PTH) levels are suppressed in this case, either as a consequence of excessive use of vitamin D analogues, or because the patient has undergone parathyroidectomy.Osteomalacia: This normally arises as a result of low 1,25-dihydroxycholecalciferol levels, as well as metabolic acidosis. Both lead to impaired bone mineralization. Osteomalacia commonly coexists with adynamic bone disease.Mixed renal osteodystrophy: This has features of osteitis fibrosa, adynamic bone disease, and osteomalacia.
Metabolic bone disease
Philip E. Harris, Pierre-Marc G. Bouloux in Endocrinology in Clinical Practice, 2014
Chronic and end stage renal disease can lead to bone disease known as renal osteodystrophy that is most commonly caused by the decrease in the synthesis of 1,25(OH)2D3, as well as phosphate retention, which further reduces calcium resorption from the gut. This results in secondary hyperparathyroidism that is sometimes sufficiently severe as to cause osteitis fibrosa cystica. In chronic kidney disease, hyperphosphatemia will stimulate production of the phosphatonin FGF23, further compromising the ability of the kidney to manufacture 1,25(OH)2D3. A high bone turnover state occurs in osteitis fibrosa cystica, frequently associated with very high PTH levels. Adynamic bone disease, with a low bone turnover state can also occur, usually associated with lower PTH levels. In the high-turnover situation, very wide osteoid seams are typically observed, with particularly severe mineralization defects.74
Management of Hyperparathyroidism
John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie in Basic Sciences Endocrine Surgery Rhinology, 2018
PHPT was previously considered a relatively rare disorder, with clinical manifestations dominated by renal and/or bone disease. However, in modern times the diagnosis is most frequently recognized coincidentally on biochemical testing in patients evaluated for unrelated complaints. The annual incidence of PHPT is around 20 cases per 100 000, although the prevalence does vary depending on the populations studied and detection methods used.2, 3 Classical skeletal complications (osteitis fibrosa cystica) are present in less than 5% of newly presenting patients and the incidence of renal stones has fallen to around 15–20%.4 The latter, however, is still the most common complication of PHPT. More diffuse calcification may also be seen in the renal parenchyma (nephrocalcinosis) in association with hypercalciuria and a decline in renal function may be seen with long-standing PHPT.
Bone health in patients undergoing surgery for primary hyperparathyroidism at Tygerberg Hospital, Cape Town, South Africa
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2021
M Budge, W Conradie, K Beviss-Challinor, L Martin, M Conradie, A Coetzee
The once common and pathognomonic mode of presentation of PHPT, osteitis fibrosa cystica, is considered a rarity in high-income nations today.1,6,53 Developing countries such as Brazil, India and Thailand, however, still report rates of OFC between 6.7% and 47%.10 In South Africa, a 1976 study30 reported three cases of PHPT with gross bone disease, which the authors ascribed to a severe variant as opposed to delayed presentation and management. Paruk et al. reported a 47.6% (n = 10/21) prevalence of hyperparathyroidism-related bone disease on plain radiographs (a combined value given for subperiosteal resorption, bone cysts, loss of skull lamina dura, bone sclerosis and brown tumours).23 Despite very few dedicated skeletal surveys in our study, OFC was seen in five patients (9.6%). These were likely patients who were suspected of having more severe PHPT or were symptomatic from skeletal disease. This figure may well have been higher had all patients undergone screening radiographs.
Occult urolithiasis in asymptomatic primary hyperparathyroidism
Published in Endocrine Research, 2018
Yu-Kwang Donovan Tay, Minghao Liu, Leonardo Bandeira, Mariana Bucovsky, James A. Lee, Shonni J. Silverberg, Marcella D. Walker
As shown in Table 1, participants were predominantly Caucasian (81.3%) and postmenopausal women (71.9%). They had evidence of mild PHPT: mean serum calcium 10.5 ± 0.5 mg/dL (range: 9.9–11.8 mg/dl); PTH 86.9 ± 42 pg/mL (range: 26–290 pg/ml); 25OHD 31.1 ± 12 ng/dL. In the cohort, 34.4% had osteoporosis by DXA criteria, 20.8% had a history of fracture, 8.3% had an estimated glomerular filtration rate <60 ml/min (all 8 with stage 3 CKD), 10.4% were <50 years old, 12.4% had 24-hour urinary calcium excretion >400 mg/day (but no clinical stones) and 92.7% met ≥ 1 criterion for parathyroidectomy based on 2014 guidelines. No one had osteitis fibrosa cystica or nephrocalcinosis. Mean T-scores were in the osteopenic range at the femoral neck and distal 1/3- radius while they were normal at the spine and total hip (Table 1). Twenty-three percent of participants were taking calcium supplements while 61.5% were taking vitamin D supplements. The average doses are shown in Table 1.
The pathophysiology and management of vascular calcification in chronic kidney disease patients
Published in Expert Review of Cardiovascular Therapy, 2023
Mehmet Kanbay, Sidar Copur, Cem Tanriover, Furkan Yavuz, Andrea Galassi, Paola Ciceri, Mario Cozzolino
Although there are several potential therapeutic alternatives for VC in CKD patients identified on multiple clinical trials, targeted therapies are yet to be developed. The main therapeutic goals include the suppression or minimalization of inflammatory response, avoidance of high and low turnover bone mineral disorders including osteitis fibrosa cystica and adynamic bone disease, avoidance of positive calcium or phosphate balance and correction of vitamin D and vitamin K deficiencies [102] (Figure 3).
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