Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151825 (bone pain)
 3,118 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serial histological studies in patients after successful renal transplantation indicate that with restoration of adequate renal function osteomalacia invariably improves with symptomatic relief in bone pain. Histological changes of osteitis fibrosa resolve more slowly and radiological changes may persist longer, occasionally in the absence of confirmatory histological evidence of secondary hyperparathyroidism. For accurate and sensitive follow-up a combination of biochemistry, histology and radiology is desirable.
Proc Eur Dial Transplant Assoc 1975
PMID:Assessment of renal osteodystrophy following renal transplantation. 110 59

Using radioimmunological estimation of beta 2-microglobulin (beta 2M), significantly greater serum values were found in 36 dialysis patients (44.4 +/- 20.3 mg/l) in comparison to healthy probands (1.5 +/- 0.2 mg/l). A significant relation to the duration of dialysis, diuresis and serum aluminium and ferritin was found. The used dialysers MLW 1.3/1.8 m2 (regenerated cellulose membrane) did not eliminate beta 2M from the blood. Significantly greater beta 2M concentrations were observed in patients suffering from arthralgia and bone pain, but not in radiologically verified arthropathy and destructive spondylarthropathy. Post-mortem examinations of 13 patients on haemodialysis treatment for between 10 and 90 months revealed synovial beta 2M-derived (AB-)amyloid deposits in four patients at different joints, but not in radiologically suspect areas. The results suggest that independent of serum beta 2M, beta 2M-derived amyloidosis may occur in elderly patients on dialysis for less than 5 years. Several cases were completely asymptomatic.
Nephrol Dial Transplant 1991
PMID:Beta 2-microglobulin serum concentration and associated amyloidosis in dialysis patients. 177 70

We have studied the effects of desferrioxamine (DFO) or successful renal transplantation on eight patients identified as having aluminium associated bone disease. All patients showed dramatic subjective improvement in their bone pain and/or fractures. All histological parameters studied improved, with the more normal bone being found in the transplanted patients. Bone aluminium fell by at least 50 per cent. Biochemically, increased bone activity was indicated by a rising alkaline phosphatase. This was particularly marked in the DFO treated group who tended to show the development of hyperparathyroidism.
Proc Eur Dial Transplant Assoc 1983
PMID:The efficacy of various treatment modalities on aluminium associated bone disease. 634 35

We investigated (1) the prevalence of aluminium overload among 96 patients with symptomatic bone disease haemodialysed from 1987 to 1989 in the Sao Paulo area, Brazil; (2) the effect of 6 months desferrioxamine (DFO) treatment (1-2g/week). All patients underwent a first bone biopsy. Aluminium overload (extent of stainable bone aluminium more than 20% trabecular surface) was observed in 74 of 96 patients. Forty overloaded patients were divided into patients with high bone formation rate (BFR) (group 1; n = 17) and patients with low BFR (group 2; n = 23), and had a second biopsy after DFO therapy. In both groups aluminium surface was reduced after treatment (P < 0.001), osteoblast surface (P < 0.02-P < 0.01) and plasma parathyroid hormone (iPTH) (P < 0.01) increased. In group 1 BFR remained high. In group 2 BFR remained low in 16 patients (2a) and increased in seven (P < 0.02) (2b). In group 2a plasma phosphorus was below that in group 2b patients, before (P < 0.03) and after (P < 0.01) DFO. The histological features of group 2a patients resembled hypophosphataemic osteomalacia, those of group 2b patients aluminium osteodystrophy. These data show a high prevalence of aluminium overload in Brazilian patients. Low-dose DFO therapy was safe, decreased bone pain, prevented fractures, and reduced stainable bone aluminium. Bone lesions only partially improved, suggesting that low phosphorus intake and/or plasma calcitriol concentrations may have prevented improvement of bone formation and mineralization.
Nephrol Dial Transplant 1994
PMID:Aluminium-related osteodystrophy and desferrioxamine treatment: role of phosphorus. 797 94

It is generally considered that a patient with myeloma who also has established renal impairment is unlikely to do well. While this is sometimes the case, analysis of recent data shows: (a) of 2768 patients in the MRC database for the fourth to the sixth trials, 10/163 with serum creatinine 300-600 microm/l and 20/89 with serum creatinine 600 micro/l at presentation had renal failure as a recorded presenting feature, whatever the renal function, the most common presenting feature was bone pain; (b) that many patients have persisting evidence of reduced renal function yet survive for more than the median time of 36 months which applies to myeloma generally. Patients with renal impairment, especially those whose myeloma is brought to plateau by chemotherapy, should be assessed thoroughly for evidence of other than myeloma induced renal damage as both renovascular disease and prostatic obstruction in males are common in the elderly population at risk.
Nephrol Dial Transplant 1998
PMID:Renal impairment in myeloma: time for a reappraisal? 987 Apr 34

Fibroblast growth factor 23 (FGF23) is a circulating factor that plays critical roles in phosphate and vitamin D metabolism, as evidenced by the fact that FGF23 missense mutations cause autosomal dominant hypophosphatemic rickets (ADHR). Autosomal dominant hypophosphatemic rickets is characterized by hypophosphatemia with inappropriately normal 1,25-dihydroxyvitamin D concentrations, as well as bone pain, fracture and rickets. This phenotype parallels that of patients with tumor induced osteomalacia (TIO), X-linked hypophosphatemic rickets (XLH), and fibrous dysplasia (FD), in whom elevated serum FGF23 levels are often observed. The fibroblast growth factor receptors (FGFR1-4) play key roles in skeletal development, as well as in normal metabolic processes. Several FGFR isoforms that potentially mediate the activity of FGF23 have been implicated. In the short term, these findings will lead to further understanding of FGF23 function, and potentially in the long term, to targeted therapies in disorders of hypo- and hyperphosphatemia that involve FGF23.
Ther Apher Dial 2005 Aug
PMID:Fibroblast growth factor 23 and its receptors. 1607 72

The Kidney Disease Outcomes Quality Initiative (K/ DOQI) 2006 recommended a minimum weekly Kt/V of 1.7 for peritoneal dialysis (PD) patients while emphasizing the importance of keeping the patient free of uremic symptoms. We examined a symptom score index [Pittsburgh Symptom Score (PSS)] designed to evaluate uremic symptoms to determine if the score improved in the first year of PD. The PSS is a 10-symptom (fatigue, trouble sleeping, difficulty concentrating, restless legs, change in taste, loss of appetite, nausea or vomiting, pruritus, bone pain, muscle pain or weakness) questionnaire that uses a Likert scale of 0 (none) to 5 (severe). From January 1, 2003, to December 31, 2006, incident PD patients completed the PSS at 0, 3, 6, 9, and 12 months. Patients were excluded from analysis if they had been on PD for less than 6 months or on hemodialysis 6 months or more before starting PD. Prevalences of individual symptoms at 1 year and at baseline were compared using the chi-square test. Differences in PSS at the various time intervals were compared using the sign test. The study included 45 patients [51% women; 31% African Americans; 33% with diabetes; mean age: 58.0 years (range: 30 - 89 years); mean initial Charlson Comorbidity Index: 5 (range: 2 - 11)]. Initial median total score improved to 8 from 12 (p = 0.005) by 3 months, with no further improvement. Improvements occurred in change in taste (p = 0.029 at 3 months), difficulty concentrating (p = 0.04 at 6 months), itching (p = 0.007 at 3 months), loss of appetite (p = 0.009 at 3 months), muscle pain or weakness (p = 0.002 at 3 months), sleep disturbance (p = 0.04 at 9 months), and restless legs (p = 0.026 at 9 months). Fatigue, bone pain, and nausea or vomiting scores were low at the start and did not significantly change over the first year. Significant decreases in symptom prevalence were seen in difficulty concentrating (p = 0.03), change in taste (p = 0.005), loss of appetite (p = 0.04), and muscle pain or weakness (p = 0.02) at 1 year. Initiation of PD results in improvement in the prevalence and severity of most uremic symptoms by 3 to 9 months and is maintained at 12 months. We recommend routine checklist evaluation of symptoms at regular clinical intervals.
Adv Perit Dial 2008
PMID:Improvement in Pittsburgh Symptom Score index after initiation of peritoneal dialysis. 1898

Hyperphosphatemia is a nearly universal complication of end-stage renal disease that is widely recognized as one of the most important and most challenging clinical targets to meet in the care of dialysis patients. Left untreated, it can lead to bone pain, pruritus and worsening secondary hyperparathyroidism. Data from observational studies demonstrate that an elevated serum phosphorus level is an independent risk factor for mortality, and that treatment with phosphate binders is independently associated with improved survival. Experimental studies provide support for the epidemiologic findings: phosphate excess promotes vascular calcification, induces endothelial dysfunction and may contribute to other emerging chronic kidney disease-specific mechanisms of cardiovascular toxicity. On the basis of this evidence, clinical practice guidelines recommend specific targets for serum phosphorus levels in the dialysis population. The purpose of this review is to summarize common challenges in meeting these targets and to identify potential opportunities for improvement.
Nephrol Dial Transplant 2013 Dec
PMID:Phosphate control in end-stage renal disease: barriers and opportunities. 2440 67

Erdheim-Chester disease (ECD) is a rare, non-Langerhans cell histiocytosis presenting most commonly with bone and central nervous system symptoms, including but not limited to bone pain and diabetes insipidus. We present a known case of ECD, which was referred for secondary hypertension workup and diagnosed with severe, proximal, bilateral renal artery stenosis.
Case Rep Nephrol Dial
PMID:Erdheim-Chester Disease Presenting with Secondary Hypertension as a Result of Bilateral, Proximal Renal Artery Stenosis: A Case Report. 2861 7

Mineral and bone disorder (MBD) is widely prevalent in children with chronic kidney disease (CKD) and is associated with significant morbidity. CKD may cause disturbances in bone remodelling/modelling, which are more pronounced in the growing skeleton, manifesting as short stature, bone pain and deformities, fractures, slipped epiphyses and ectopic calcifications. Although assessment of bone health is a key element in the clinical care of children with CKD, it remains a major challenge for physicians. On the one hand, bone biopsy with histomorphometry is the gold standard for assessing bone health, but it is expensive, invasive and requires expertise in the interpretation of bone histology. On the other hand, currently available non-invasive measures, including dual-energy X-ray absorptiometry and biomarkers of bone formation/resorption, are affected by growth and pubertal status and have limited sensitivity and specificity in predicting changes in bone turnover and mineralization. In the absence of high-quality evidence, there are wide variations in clinical practice in the diagnosis and management of CKD-MBD in childhood. We present clinical practice points (CPPs) on the assessment of bone disease in children with CKD Stages 2-5 and on dialysis based on the best available evidence and consensus of experts from the CKD-MBD and Dialysis working groups of the European Society for Paediatric Nephrology and the CKD-MBD working group of the European Renal Association-European Dialysis and Transplant Association. These CPPs should be carefully considered by treating physicians and adapted to individual patients' needs as appropriate. Further areas for research are suggested.
Nephrol Dial Transplant 2020 Nov 02
PMID:Bone evaluation in paediatric chronic kidney disease: Clinical practice points from the European Society for Paediatric Nephrology CKD-MBD and Dialysis working groups and CKD-MBD working group of the ERA-EDTA. 3324 31


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