Abstract:The idiom renal osteodystrophy (ROD) represents a heterogeneous pattern of bone disturbances caused by chronic renal insufficiency and concomitant diseases. For the clinical decision of therapy it is most important to differentiate between high and low or adynamic turnover ROD because the therapeutically consequences of these two ends of the ROD spectrum are fundamentally different. Bone histology remains the gold standard for the exact classification of ROD. Serological markers of bone metabolism are not suit… Show more
“…Since 1943, when the term ''ROD'' was introduced [8], the diagnosis was based mostly on radiographic findings. Although numerous new diagnosis modalities such as PTH levels, bone mass density, and bone biopsy have been introduced in clinical practice [9][10][11], plain film radiography, especially fine quality hand radiography, still plays a role [12]. The main radiographic findings are induced by HPTH and are located especially in hands, clavicles, sacrum-iliac and pubic bones.…”
There seems to be a pathogenetic link between bone and artery diseases in chronic HD patients. Both VCs and ROD have a high prevalence. ROD, male gender and treatment with calcium salts are risk factors for VCs.
“…Since 1943, when the term ''ROD'' was introduced [8], the diagnosis was based mostly on radiographic findings. Although numerous new diagnosis modalities such as PTH levels, bone mass density, and bone biopsy have been introduced in clinical practice [9][10][11], plain film radiography, especially fine quality hand radiography, still plays a role [12]. The main radiographic findings are induced by HPTH and are located especially in hands, clavicles, sacrum-iliac and pubic bones.…”
There seems to be a pathogenetic link between bone and artery diseases in chronic HD patients. Both VCs and ROD have a high prevalence. ROD, male gender and treatment with calcium salts are risk factors for VCs.
“…Bone histomorphometry, dynamic parameters fracture risk through changes in bone quality as well as quantity. Diagnosis of osteoporosis in CKD patients requires exclusion of osteodystrophy with bone biopsy, preferably with double tetracycline labeling [23,24] . The decision to treat CKD patients for DEXA-diagnosed osteoporosis presumes that 'areal' BMD is a true reflection of bone quantity, and that quantity is the principal determinant of bone strength and fracture risk.…”
Dual X-ray absorptiometry is the standard diagnostic modality for identification of low bone mineral density, a finding which is in the general population usually indicative of osteopenia or osteoporosis. However, chronic kidney disease (CKD) patients diagnosed with osteopenia or osteoporosis may in actual fact have renal osteodystrophy with high or low bone turnover. While bisphosphonates are currently prescribed for the prevention of fractures in osteoporosis and high-risk osteopenic patients, the clinical utility of bisphosphonate therapy in CKD has not been established. Furthermore, bisphosphonates accumulate in bone, inhibit osteoclasts, and may cause or exacerbate low-turnover (adynamic) bone disease – particularly in patients presenting with low parathyroid hormone (PTH) levels or receiving treatment for secondary hyperparathyroidism. Bone biopsy with non-decalcified histopathology remains the gold standard for the identification and evaluation of bone disorders, including osteoporosis and renal osteodystrophy. Thirteen CKD patients (stage II–IV), referred to our clinic over a 12-month period, were identified as having taken bisphosphonates from 4 to >60 months after a diagnosis of osteopenia or osteoporosis. All patients underwent biopsies of trabecular bone from the iliac crest following oral administration of time-separated doses of doxycycline and tetracycline. Bone pathology was assessed after processing for mineralized histology. For all patients, clinical data collection included assessment of likely causes of kidney disease, MDRD glomerular filtration rate, calcium-phosphate product, intact PTH level, alkaline phosphatase, and bisphosphonate exposure. All 13 patients were diagnosed with adynamic bone on biopsy evaluation. Eleven biopsies revealed decreased cancellous bone mass; 8 showed decreased osteoid surface; 8 disclosed decreased osteoid thickness, and all 13 demonstrated low or low-normal osteoclast/osteoblast interface. Assessment of dynamic bone formation demonstrated decreased or absent single- or double-labeled osteoid in all 13 bone specimens. Based on these observations, the use of bisphosphonates in CKD cannot be recommended.
“…Although bone biopsy with double tetracycline labeling to quantify bone formation rate is the criterion for diagnosis, noninvasive strategies such as the desferrioxamine (DFO) test [10,11] or markers of bone formation and resorption could be effectively used to evaluate Al intoxication and Al-induced bone disease [12][13][14][15][16][17][18][19][20]. The present study was conducted to explore the incidence and risk factors for Al intoxication and to assess a possible correlation between the bone markers and Al-induced bone diseases in chronic HD patients.…”
Background:The prevalence of aluminum (Al)-related toxicity in hemodialysis (HD) patients has declined. However, some HD patients continue to receive Al-based phosphate binders, in part because of the expense of Al-free binders. Objective: To explore the effect of Al-based binders and their discontinuation on iron status, and markers of bone formation resorption in HD patients. Methods: Following an initial screen of serum Al levels in 37 HD patients, a second screening was performed after discontinuation of Al-based binders in a 2-year follow-up. A desferrioxamine (DFO; 5 mg/kg) test, and assessment of iron status and bone markers were conducted in the second screening. Results: Mean serum Al level was initially 27.8 ± 10.3 μg/L. Thirteen patients had a serum Al >30 μg/L, a level considered possibly toxic. There was a positive correlation between serum Al levels, HD duration, and cumulative dose of Al-based binder. At the second screening, the mean serum Al level decreased to 12.5 ± 7.4 μg/L. The mean serum Al level increased to 26.0 ± 14.7 μg/L post-DFO, but in none of the patients did the change in serum Al exceed the 50 μg/L threshold associated with Al-induced bone disease. The decrease in serum Al level was associated with a significant increase in intact parathyroid hormone (iPTH) whereas total alkaline phosphatase did not change.
Conclusions:We recommend that if Al-based phosphate binders are used in HD patients, serum Al level, iron, and markers of bone formation resorption be closely monitored to ensure safe use of these drugs.
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