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Chronic kidney disease-mineral and bone disorder (CKD-MBD) has a direct impact on patients' quality of life, hospitalization rates and fracture risk. In recent years, osteoblasts and osteoclasts have become central to the pathophysiology of CKD-MBD. Osteoblasts interact with other organs by synthesizing fibroblast growth factor-23 (FGF-23) and sclerostin (SOST), making the skeleton an endocrine organ. Therefore, dysregulation of osteoblast differentiation is an important early event in the pathogenesis of CKD. In this paper, we systematically discuss the metabolic pathways of osteoblasts and the mechanisms related to the altered metabolic reprogramming of osteoblasts in the early CKD-MBD pathology. This paper shows that abnormalities in signaling pathways and metabolites such as Wnt/β-catenin, FGF-23, uremic toxins, metabolic acidosis, can alter the metabolic activity of osteoblasts, causing impaired maturation of the osteogenic spectrum, which in turn affects bone remodeling, which will provide a new way of thinking for explaining the pathological changes in renal bone disease and developing clinical treatment options.

Copyright of Basrah Journal of Science / Magallat Al-Barat Li-L-ulum is the property of Republic of Iraq Ministry of Higher Education & Scientific Research (MOHESR) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Renal bone disease increases morbidity and mortality in patients with chronic kidney disease by increasing the risk for fractures, osteoporosis and other bone problems and its association with cardiovascular disease, including calcification and arterial stiffness. Treatment of renal bone disease is through a combination of three main methods to reduce phosphate levels: dietary restriction of high-phosphate foods; dialysis clearance; and the use of phosphate binders to prevent its absorption. [ABSTRACT FROM AUTHOR]

Bone turnover marker (BTMs) concentrations in blood and urine reflect bone-remodelling activity, and may be useful adjuncts in the diagnosis and management of metabolic bone diseases. Newer biomarkers, mainly bone regulatory proteins, are currently being investigated to elucidate their role in bone metabolism and disease and may in future be useful in clinical diagnosis and management of metabolic bone disease. BTM concentrations increase around menopause in women, and at a population level the degree of increase in BTMs reflect bone loss. However, lack of adequate data precludes their use in individual patients for fracture risk assessment in clinical practice. The rapid and large changes in BTMs following anti-resorptive and anabolic therapies for osteoporosis treatment indicate they may be useful for monitoring therapy in clinical practice. The offset of drug effect on BTMs could be helpful for adjudicating the duration of bisphosphonate drug holidays. BTMs may offer useful additional data in skeletal diseases that are typically characterised by increased bone remodelling: chronic kidney disease (CKD), primary hyperparathyroidism (PHPT) and Paget's disease. In CKD, bone specific alkaline phosphatase (bAP) is currently endorsed for use for the assessment of mineral bone disease. The role of BTMsin predicting the bone mineral density response to successful parathyroidectomy in PHPT shows some utility but the data are not consistent and studies are limited in size and/or duration. In Paget's disease of bone, BTMs are used to confirm diagnosis, evaluate extent of disease or degree of activity and for monitoring the response to bisphosphonate treatment. Whilst BTMs are currently used in specific clinical practice instances when investigating or managing metabolic bone disease, further data are needed to consolidate their clinical use where evidence of utility is limited. [ABSTRACT FROM AUTHOR]

Secondary hyperparathyroidism (SHPT) occurs in patients with chronic renal failure complicated with renal bone disease and soft tissue/vascular calcification. In dialysis patients with severe SHPT, medical treatment may fail and parathyroidectomy (PTX) is indicated for definitive treatment. Severe hypocalcemia from hungry bone disease or postoperative hypoparathyroidism may occur during the postoperative period. We report here a case of severe SHPT in a hemodialysis patient treated with phosphate binders, calcitriol, and calcimimetics but who still required PTX. Severe hypocalcemia with muscle cramps occurred postoperatively. Around 1 year after PTX, anemia and features of SHPT have improved but the patient still has intermittent hypocalcemia with suspected postoperative hypoparathyroidism. Regular comprehensive assessment of calcium and phosphorus levels throughout all stages of chronic kidney disease is vital. The postoperative period of PTX in SHPT patients is critical, requiring monitoring to improve management. [ABSTRACT FROM AUTHOR]

Introduction:Bone disorders in chronic kidney disease (CKD) are associated with heightened risks of fractures, vascular calcification, poor quality of life and mortality compared to the general population. However, diagnosis and management of these disorders in CKD are complex and appreciably limited by current diagnostic modalities. Areas covered:Bone histomorphometry remains the gold standard for diagnosis but is not widely utilised and lacks feasibility as a monitoring tool. In practice, non-invasive imaging and biochemical markers are preferred to guide therapeutic decisions. Expertcommentary:This review aims to summarize the risk factors for, and spectrum of bone disease in CKD, as well as appraise the clinical utility of dual energy X-ray densitometry, peripheral quantitative computed tomography, high-resolution peripheral quantitative computed tomography, and bone turnover markers. [ABSTRACT FROM PUBLISHER]

In the current issue of Blood Purification, Palomares et al. [Blood Purif 2013;36:122-131] bemoan the poor level of compliance in dialysis units in achieving compliance with KDOQI and KDIGO bone and mineral guideline targets. These targets are based almost completely on observational data and rely on an obsolete assay for PTH. The so-called intact PTH assay measures both 1-84 PTH and 7-84 PTH; the latter has been demonstrated to possess biological activity that is antagonistic to that of 1-84 PTH. The assay cannot reliably distinguish high from low bone turnover in the target ranges suggested by the guideline panels. Targeting these ranges leads to an increased incidence of adynamic bone disease, higher calcium and phosphorus, and likely poor patient outcomes. © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article presents a study on chronic kidney disease (CKD) which is associated with changes in bone structure. Serum parathyroid hormone (PTH) level, an indicator of bone disease begins to increase in CKD. It also informs that there is an association between abnormal mineral metabolism and adverse cardiovascular outcomes in CKD. It further informs that 15.1 percent of the U.S. adult population has CKD which is associated with high morbidity and mortality.

Bone growth occurs in the growth-plate cartilage located at the ends of long bones. Changes in the architecture, abnormalities in matrix organization, reduction in protein staining and RNA expression of factors involved in cell signaling have been described in the growth-plate cartilage of nephrectomized animals. These changes can lead to a smaller growth plate associated with decrease in chondrocyte proliferation, delayed hypertrophy, and prolonged initiation of mineralization and vascular invasion. As a result, chronic renal failure can result in stunted body growth and skeletal deformities. Multiple etiologic factors can contribute to impaired bone growth in renal failure, including suboptimal nutrition, metabolic acidosis, and secondary hyperparathyroidism. Recent findings have also shown the tight connection between chondro/osteogenesis, hematopoiesis, and immunogenesis. [ABSTRACT FROM AUTHOR]

Copyright of West African Journal of Medicine is the property of West African Journal of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Growth failure is a common and significant clinical problem for children on dialysis and often remains a major impediment to their rehabilitation. Early referral to a paediatric nephrology centre and appropriate management before the initiation of dialysis may significantly prevent growth deterioration. Growth in children on dialysis can be affected by nutritional, metabolic, and hormonal changes. Early diagnosis of malnutrition and aggressive management should be a priority. Gastrostomy feeding should be used when adequate oral intake to maintain normal height and weight velocity cannot be achieved. Active vitamin D metabolites should be used carefully, to prevent low-turnover bone disease. All children should have an adequate regimen of dialysis and an appropriate management of malnutrition, renal osteodystrophy, metabolic acidosis, salt wasting and anaemia, before recombinant human growth hormone (rhGH) administration is considered. The current challenge of reversing growth impairment in children on dialysis can only be achieved by optimization of their care. [ABSTRACT FROM AUTHOR]

The cardiovascular risk of patients undergoing dialysis is 20-30 times higher than that of individuals of the same age, without abnormal renal function, from the general population. Observational studies of patients with normal and abnormal renal function have shown that there is an association between bone disease, vascular calcification and cardiovascular outcome and that worsening of these conditions happens in parallel. Basic science studies are elucidating several mechanisms that could explain the interaction between bone disease, vascular calcification and cardiovascular outcome. For example, the expression of osteoprotegerin--a protein that regulates bone resorption by binding receptor activator of nuclear factor KB (RANK) ligand (RANKL), thus preventing interaction with the receptor RANK and the stimulation of osteoclast maturation--is regulated by several cytokines. Additionally, osteoprotegerin seems involved in the genesis of atherosclerosis. Imbalances of bone mineral metabolism, bone matrix secretion and vascular smooth-muscle-cell apoptosis seem involved in the ossification of the arterial wall in chronic kidney disease, and could explain some of the complex interactions between bone and vascular disease in renal failure. In this article we present a brief review of some of the basic mechanisms involved in vascular calcification and the clinical evidence of an association of vascular and bone disease. [ABSTRACT FROM AUTHOR]

Background: Renal bone pathology involves a spectrum from ‘high-turnover’ to ‘low-turnover bone disease’ (adynamic bone disease, classical osteomalacia). The diagnosis of the latter usually requires bone biopsy. Inhibitory parathyroid hormone (PTH) fragments may be useful for its noninvasive diagnosis. Methods: A cross-sectional study was performed in 54 patients on chronic hemodialysis which involved measurements of intact PTH (iPTH; Nichols assay), total PTH (tPTH; Scantibodies assay), and the cyclase-activating PTH fragment (CAP). The level of cyclase-inactive PTH fragment (CIP) was calculated. At the same time, serum calcium, phosphorus, and alkaline phosphatase levels as well as the current therapy for secondary hyperparathyroidism were recorded. In selected patients, bone radiographs were evaluated for osteitis fibrosa. Results: A high correlation (r = 0.94) was found between iPTH and tPTH, with the tPTH levels being lower by 30–40%. A similar association was also found for CAP (r = 0.988) and for CIP (r = 0.93). 3 out of the 54 patients had a CAP/CIP ratio of ≤1 which has been associated with adynamic bone disease. A higher CIP ratio was significantly associated with the use of aluminum-hydroxide- and calcium-containing phosphate binders. Conclusions: iPTH and tPTH assays are highly correlated. In a general hemodialysis patient population, low-turnover bone disease appears to be rare, when the CAP/CIP ratio is used as a marker. A high CIP value was associated with therapy using aluminum hydroxide, a drug known to carry a risk of adynamic bone disease. Copyright © 2006 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Histomorphometric analysis of iliac bone samples is a key tool for studying bone metabolism and, to a lesser extent, bone mass and structure. Two types of bone metabolic activity can be distinguished: modeling and remodeling. Both processes are performed by the same effector cells, osteoblasts and osteoclasts, but differ in the way these cells are arranged. The main effect of remodeling is to renew bone, whereas modeling can lead to rapid changes in bone shape, size and mass. Standard histomorphometric analysis focuses on trabecular bone and therefore mainly provides information on remodeling. Remodeling activity changes markedly with age during development. This must be taken into account when histomorphometry is used in the pediatric setting. Remodeling disorders encountered in the context of pediatric renal bone disease include mineralization defects, as well as abnormally high remodeling activity due to secondary hyperparathyroidism or suppressed remodeling activity as a consequence of over-treatment. Children and adolescents with severe bone fragility should have a bone biopsy unless the diagnosis is obvious from noninvasive examinations. Histomorphometric analysis of transiliac bone biopsy samples is especially valuable in clinical studies, as this method provides safety and efficacy data that cannot be obtained in any other way. [ABSTRACT FROM AUTHOR]

Skeletal involvement in chronic kidney disease manifests long before the initiation of dialysis. This study aimed at identifying the extent of renal bone disease among predialysis and on maintenance dialysis patients. Thirty-two patients (Group 1) on maintenance hemodialysis (MHD) for a variable period of time were compared with 20 newly detected irregularly treated advanced renal failure (immediately predialysis), patients (Group 2) for their clinical, biochemical and imaging features. The mean age of Group 1 and Group 2 patients was 45±14 vs. 34±15 years (p<0.05). Comparison of blood biochemistries between Groups 1 and 2 showed serum creatinine 9.9±2.9 vs. 13.4±4.4 mg/dL (p<0.01); calcium 10.1±1.8 vs. 7.8±1.2 mg/dL (p<0.001); phosphate 4.4±1.2 vs. 7.9±2.1 mg/dL (p<0.001); alkaline phosphatase 116.4±31.7 vs. 85.7±30.6 IU/L (p<0.05); and parathormone 71.7±48.2 vs. 146.9±92.1 pg/mL (p<0.05). Radiological changes present in the 2 groups were as follows: osteopenia 63% vs. 65% (ns); trabecular resorption 53% vs. 20% (p<0.05); soft tissue calcification 31% vs. 10% (p<0.05); bone cysts 16% vs. 26% (ns); and subperiosteal bone resorption 16% vs. 20% (ns). Technetium 99 methylene diphosphonate (Tc-99 MDP) bone scans in both groups of patients showed similar increased uptake in wrist joint, tibia–fibula, costochondral junction, vertebral column, sternum, radius–ulna and mandible. X-ray findings were positive for bone involvement in 59% of cases, and Tc-99 scan was positive in 80% (p<0.05). It is concluded that newly detected, irregularly treated patients with advanced renal failure who are predialysis may present with deranged calcium homeostasis and a high prevalence of bone involvement similar to MHD patients. [ABSTRACT FROM AUTHOR]

Reports on chronic kidney disease (CKD) which is a significant risk factor for vitamin D deficiency, an issue which needs attention since abnormalities in vitamin D metabolism are important in the generation of hyperparathyroidism. Assessment of the effects of correcting the deficiency in early CKD; Proposed strict guidelines for the management of bone and mineral metabolism in patients with CKD stage V on dialysis; Treatment options for patients on dialysis.

Background: The carboxy-terminal cross-linking telopeptide of type I collagen (β-CrossLaps, β-CTX) is released into the circulation during degradation of type I collagen and serves as a marker of bone resorption. β-CTX is known to undergo a diurnal rhythm in normal individuals and to accumulate in chronic renal failure. β-CTX has a potential role in noninvasive diagnosis of renal bone disease. Methods: Serum β-CTX was compared to parathyroid hormone (PTH) and other biochemical bone markers in 90 unselected hemodialysis patients. Results: Mean β-CTX was elevated above the normal range (1.72 ± 0.93 μg/l); there were large individual variations. Serum β-CTX was significantly correlated with various PTH assays (r >0.56) and with tartrate-resistant acid phosphatase 5b (TRACP 5b, r = 0.629), bone-specific alkaline phosphatase (r = 0.404) and osteocalcin (r = 0.534, all correlations p < 0.001). The correlation between β-CTX and PTH was significantly higher than the correlation between TRACP 5b and PTH. Several factors which could confound interpretation of serum β-CTX were assessed in further studies: (i) There was no recognizable influence of the time of blood sampling (morning dialysis shift versus afternoon dialysis shift) on serum β-CTX. (ii) Serum β-CTX was not significantly related to residual diuresis of patients. Conclusions: We found a high association between β-CTX and other established markers of bone and calcium metabolism demonstrating the potential utility of β-CTX as marker of bone resorption in renal bone disease. However, further studies employing bone histology are still warranted to exactly define the influence of glomerular retention on serum β-CTX in end-stage renal disease. Copyright © 2004 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The histomorphometric diagnosis of osteomalacia depends on the conjunction of two or three independent criteria but for several reasons, both clinical and pathophysiologic, it would be useful to have a single index of severity. Accordingly, using an extensive library of normal values in 143 healthy women, we constructed the mineralization index (MI), defined as [osteoid thickness (O.Th) (μm) + osteoid volume/bone volume (OV/BV) (%)] × 1.15 - osteoid mineralization rate (%/day) - [bone formation rate/bone surface (BFR/BS) (μm3/μm2/year) × 0.15]. MI was normally distributed with mean 8.0, SD 3.3, and range 0–15 (arbitrary units); it was unaffected by race, menopausal status, age or bone turnover, and was slightly lower in osteoporotic patients with nontraumatic vertebral fracture than in healthy white postmenopausal women (6.83 vs. 7.95). In hypovitaminosis D osteopathy (HVO) stage I, MI was normal in 18/26 cases (70%; HVOia), demonstrating more rigorously than before that osteoid accumulation is initially due entirely to secondary hyperparathyroidism and increased bone turnover. In the remaining 30% (HVOib), MI was increased, indicating the onset of impaired mineralization while bone formation was still increased and before the appearance of osteomalacia. In secondary hyperparathyroidism due to renal bone disease, 10/20 cases (50%) had normal MI and higher BFR than in HVOia (93 vs. 32), and there was a significant inverse correlation between MI and BFR. In patients with osteomalacia according to current criteria, MI ranged from 29.2 to 166.5; an MI of 30 had high sensitivity and specificity for the diagnosis of osteomalacia. Including all patients with HVO, there was a significant (P < 0.001) inverse correlation between MI and calcium × phosphate product, but the unexplained variance of >70% suggests that vitamin D deficiency impairs mineralization by multiple mechanisms. We conclude that the MI clarifies the early effects of vitamin D deficiency on bone and the relationship between different components of renal bone disease simplifies the histologic diagnosis of osteomalacia and may contribute to its management, and explicates the mechanisms of mineralization. [Copyright &y& Elsevier]

Parathyroid hormone (PTH), PTH-derived peptides, and new PTH assays in renal osteodystrophy. Reliable measurements of parathyroid hormone (PTH) concentrations in serum or plasma are critical for the appropriate diagnosis and management of patients with renal osteodystrophy. With the introduction of second generation immunometric assays for PTH, it is now possible to measure exclusively full-length, biologically active PTH(1-84). In contrast, first generation immunometric assays that have been used widely for many years detect not only PTH(1-84), but also other large amino-terminally-truncated, PTH-derived peptides. This development will require a careful re-evaluation of PTH measurements, as determined by either first or second generation immunometric assays, and their relationship to bone histology and bone remodeling rates in patients with end-stage renal disease (ESRD). Such information is essential for proper clinical management, but only limited bone biopsy data are available to guide the interpretation of PTH results using second generation PTH assays. The different performance characteristics of first and second generation immunometric PTH assays also makes it possible to quantify the plasma levels of amino-terminally-truncated, PTH-derived peptides, which may accumulate disproportionately in patients with ESRD. Recent experimental evidence indicates that one or more of these peptides can modify bone cell activity and skeletal remodeling, possibly by interacting with a PTH receptor distinct from the type I PTH receptor that binds to the amino-terminal portion of PTH and mediates the classical biological actions of the hormone. The putative C-PTH receptor interacts with mid- and/or carboxyterminal regions of PTH and other amino-terminally-truncated PTH-derived peptides; signaling through it may contribute to the skeletal resistance to PTH that characterizes ESRD. The current review discusses certain aspects of the molecular structure of PTH and its interaction with various receptors, briefly comments about selected components of PTH secretion, highlights recent technical advances in PTH assays, and summarizes the effects of various PTH-derived peptides on bone cells and on skeletal metabolism. [ABSTRACT FROM AUTHOR]

A historical look at research in hyperphosphataemia of chronic kidney disease over the last 40 years shows remarkable advances in our understanding of this abnormality and in the technology used to manage it. Phosphate binders, which have become a mainstay in the management of hyperphosphataemia, have evolved from the early use of aluminium gels to calcium salts, to novel, non‐absorbed, aluminium‐free, calcium‐free agents such as sevelamer hydrochloride, and to magnesium‐, iron‐, and lanthanum‐based compounds. With recent advances, clinical management of this complication of chronic renal disease is evolving from adequate care to optimal care, such that new standards in phosphorous management are being set, and various parameters of patient care are being integrated to optimize outcomes and minimize side effects. This paper provides a historical view of the clinical management of hyperphosphataemia, and looks to advances in treatment that are changing the course of renal bone disease management. [ABSTRACT FROM PUBLISHER]

Photon absorptiometry provides an accurate measurement of bone mineral content. In acromegaly, the bone mineral content is normal, whereas the bone mineral content is reduced by acidosis. Decreased bone mineral content occurs in alcoholics due to osteomalacia and also in anticonvulsant therapy for the same reason. In hyperparathyroidism, there is decreased bone mineral content. Corticosteroids reduce bone mineral content especially in the central skeleton similar to Cushing's disease. Glutethimide causes osteomalacia with decreased bone mineral content. Long-term heparin therapy causes bone resorption. Immobilization causes decreased bone mineral content. Bedrest and space flight reduce lower limb bone mineral content with recovery on ambulation. Conversely, activity increases bone mineral content even in the elderly and bone mineral content is greater in athletes than non-athletes. Osteoporosis is a normal process occurring from age 45 years in females and 65 in males. Bone loss is related to menopause and lactation in females and may be arrested by estrogens, fluoride (with calcium and vitamin D), and possibly calcium carbonate. Decreased bone mineral content occurs at all stages of renal failure with rapid bone mineral content loss in azotemia and during dialysis and slower loss after transplant. Parathyroidectomy does not affect bone mineral content in renal osteodystrophy. The bone mineral content is normal in compact bone but decreased in trabecular bone in patients with spinal cord injury, as well as in leprosy and diabetes. In hemiplegia, there is decreased bone mineral content on the paralyzed side. In thyrotoxicosis, there is increased formation and resorption of bone. [ABSTRACT FROM AUTHOR]

In patients with renal bone disease skeletal and extra-skeletal abnormalities can be visualised using conventional bone scintigraphy. Some of these abnormalities are associated with characteristic scintigraphic appearances, which are reviewed in detail, and the possible mechanisms involved are discussed. Specific imaging with iodine 123 serum amyloid P component and iodine 131 β-microglobulin is also discussed in the diagnosis of β-microglobulin amyloidosis specific to patients on dialysis. In the light of available evidence, it appears that bone scintigraphy plays, so far, a limited role in the clinical evaluation of skeletal and extra-skeletal abnormalities in chronic renal failure. The potential role of bone scintigraphy in identifying patients with aluminium-related bone disease needs to be investigated further, and in this respect special attention must be given to the problem of high soft-tissue activity associated with impaired renal function. Timing haemodialysis sessions before scintigraphic imaging deserves wider recognition as it reduces high soft-tissue activity, thereby allowing bone uptake to be assessed more accurately. Specific imaging of amyloidosis resulting from β-microglobulin deposition is a promising technique, but the relative value of the two proposed radiopharmaceuticals needs further clarification. [ABSTRACT FROM AUTHOR]

The number of the patients with chronic kidney disease is now increasing in the world. The pathophysiology of renal hyperparathyroidism is closely associated with Klotho-FGF-endocrine axes, which must be solved definitively as early as possible. It was revealed that the expression of fgf23 is activated by calciprotein particles, which induces vascular ossification. And it is well known that phosphorus overload directly increases parathyroid hormone and hyperparathyroid bone disease develops in those subjects. On the other hand, low turnover bone disease is often recently. Both the patients with chronic kidney disease suffering from hyperparathyroid bone disease or low turnover bone disease are associated with increased fracture risk. Micropetrosis may be one of the causes of increased fracture risk in the subjects with low turnover bone disease. In this chapter, we now describe the diagnosis, pathophysiology and treatments of renal hyperparathyroidism., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Metabolic bone disease in chronic kidney disease and end-stage renal failure represents one of the most severe clinical complication in kidney patients, namely those on maintenance dialysis. Traditionally, bone changes are induced by secondary hyperparathyroidism. The CKD-MBD concept reflects the link between bone and cardiovascular disease in these patients. Studies documented also other bone pathological pathways in renal patients, such as osteoporosis, as in kidney and dialysis patients its risk factors are present as well as in general population. Resulting bone disease in renal disease and failure is far more complex than previously seen. However, the secondary hyperparathyroidism still represents the main pathological pathway.

The article discusses the most common complications associated with long-term haemodialysis (HD) which includes renal bone disease, cardiovascular disease, gastro-intestinal disturbance, neurological issues, immune dysfunction, eye problems and psychosocial issues. It highlights the prevention and management of these complications and mentions that educating patients about them may help in improving the quality of life. Also discussed is the role of renal nurses in taking care of patients with chronic kidney disease (CKD), which includes being aware of the complications and being familiar with the signs, symptoms, effect and management of HD.

Hyperparathyroidism is a desease caused by increase of parathormone secretion, leading to a misfunction of calcium metabolism. Although not very common among population in general, it is frequently observed in patients with cronic renal disease. It can involve a slight syntomatic form, but as a whole, its main repercurssions occur in skeletic muscles, urinary and intestinal systems. The authors conduct a broad revision of the literature, focusing on the methods of diagnosis and spot checking before and during the operations of parathyroid glands. Surgical recommendations, tatic aspects and types of surgery to be implemented are discussed. A systematization for adequate surgical technics performed at the General Surgery Service of Clementino Fraga Filho Hospital of Federal University of Rio de Janeiro is fully discribed and recommended.