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1.
Asian J Surg ; 42(1): 6-10, 2019 Jan.
Article in English | MEDLINE | ID: mdl-29908897

ABSTRACT

BACKGROUND: Secondary hyperparathyroidism (SHPT) and calcium and phosphorus metabolism disorder are important complications in haemodialysis patients. Parathyroidectomy (PTX) may prevent or delay the progress of vascular calcification in haemodialysis patients. OBJECTIVE: To investigate the impacts of PTX on calcium and phosphorus metabolism, arterial calcification and arterial stiffness in haemodialysis patients with SHPT. METHODS: Twenty-one SHPT-haemodialysis patients were selected for PTX. The preoperative and postoperative 1-year scores of coronary artery calcification were measured via multislice spiral CT, along with the brachial-ankle pulse wave velocity (baPWV), and preoperative and postoperative 1-year indexes such as calcium, phosphorus, calcium-phosphorus product concentration and parathyroid hormone (PTH) level were compared. RESULTS: Compared with the preoperative score, the postoperative 1-year coronary artery calcification score was significantly reduced; the mean baPWVs of the bilateral limbs were reduced; and the levels of serum calcium, phosphorus, calcium-phosphorus product concentration and PTH were all reduced; all differences were statistically significant (P < 0.05). CONCLUSIONS: PTX can be used to correct calcium and phosphorus metabolism disorder, reduce arterial calcification, and improve arterial stiffness.


Subject(s)
Calcium Metabolism Disorders/etiology , Calcium Metabolism Disorders/prevention & control , Hyperparathyroidism/etiology , Parathyroidectomy , Phosphorus Metabolism Disorders/etiology , Phosphorus Metabolism Disorders/prevention & control , Renal Dialysis/adverse effects , Vascular Calcification/etiology , Vascular Calcification/prevention & control , Vascular Stiffness , Adult , Ankle Brachial Index , Calcium Metabolism Disorders/therapy , Female , Humans , Male , Middle Aged , Phosphorus Metabolism Disorders/therapy , Pulse Wave Analysis
2.
J Appl Oral Sci ; 26: e20170495, 2018 Jul 23.
Article in English | MEDLINE | ID: mdl-30043933

ABSTRACT

OBJECTIVES: To analyze the association between periodontal conditions and inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis (HD) patients. MATERIAL AND METHODS: We analyzed 128 HD patients divided into two groups: dentate (n = 103) and edentulous (n=25). The following items were assessed: baseline characteristics, age at the start and duration of HD, biochemical data: C-reactive protein (CRP), serum albumin, calcium, phosphorus, alkaline phosphatase, parathormone. A single dentist performed a complete dental/periodontal examination, including parameters of oral hygiene and gingival bleeding. RESULTS: One person had healthy periodontium, 62.14% of the patients had gingivitis, and 36.9% had moderate or severe periodontitis. The age at HD onset had a positive impact on periodontal status and negatively correlated with the number of teeth. A positive correlation between age and CRP level and negative correlations between age and serum albumin and phosphorus were found. Pocket depth (PD) was negatively correlated with serum albumin. The number of teeth was negatively correlated with serum CRP. CONCLUSIONS: High prevalence and severity of periodontal disease are observed in hemodialysis patients. There is a high probability that periodontal disease may be present at the early stages of chronic kidney disease (CKD) before the hemodialysis onset.


Subject(s)
Calcium Metabolism Disorders/etiology , Gingivitis/etiology , Nutritional Status/physiology , Periodontitis/etiology , Phosphorus Metabolism Disorders/etiology , Renal Dialysis/adverse effects , Aged , Aged, 80 and over , Alkaline Phosphatase/blood , C-Reactive Protein/analysis , Calcium/blood , Calcium Metabolism Disorders/blood , Dental Plaque Index , Female , Gingivitis/blood , Humans , Male , Middle Aged , Oral Hygiene , Parathyroid Hormone/blood , Periodontal Index , Periodontitis/blood , Phosphorus/blood , Phosphorus Metabolism Disorders/blood , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/therapy , Risk Factors , Serum Albumin/analysis , Severity of Illness Index
3.
J. appl. oral sci ; 26: e20170495, 2018. tab
Article in English | LILACS, BBO - Dentistry | ID: biblio-954517

ABSTRACT

Abstract Objectives To analyze the association between periodontal conditions and inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis (HD) patients. Material and Methods We analyzed 128 HD patients divided into two groups: dentate (n = 103) and edentulous (n=25). The following items were assessed: baseline characteristics, age at the start and duration of HD, biochemical data: C-reactive protein (CRP), serum albumin, calcium, phosphorus, alkaline phosphatase, parathormone. A single dentist performed a complete dental/periodontal examination, including parameters of oral hygiene and gingival bleeding. Results One person had healthy periodontium, 62.14% of the patients had gingivitis, and 36.9% had moderate or severe periodontitis. The age at HD onset had a positive impact on periodontal status and negatively correlated with the number of teeth. A positive correlation between age and CRP level and negative correlations between age and serum albumin and phosphorus were found. Pocket depth (PD) was negatively correlated with serum albumin. The number of teeth was negatively correlated with serum CRP. Conclusions High prevalence and severity of periodontal disease are observed in hemodialysis patients. There is a high probability that periodontal disease may be present at the early stages of chronic kidney disease (CKD) before the hemodialysis onset.


Subject(s)
Humans , Male , Female , Aged , Aged, 80 and over , Periodontitis/etiology , Phosphorus Metabolism Disorders/etiology , Calcium Metabolism Disorders/etiology , Nutritional Status/physiology , Renal Dialysis/adverse effects , Gingivitis/etiology , Oral Hygiene , Parathyroid Hormone/blood , Periodontitis/blood , Phosphorus Metabolism Disorders/blood , Phosphorus/blood , Severity of Illness Index , Calcium Metabolism Disorders/blood , C-Reactive Protein/analysis , Serum Albumin/analysis , Periodontal Index , Dental Plaque Index , Calcium/blood , Risk Factors , Alkaline Phosphatase/blood , Renal Insufficiency, Chronic/complications , Renal Insufficiency, Chronic/therapy , Gingivitis/blood , Middle Aged
4.
Actual. osteol ; 12(2): 97-106, 2016. graf, tab
Article in Spanish | LILACS, UNISALUD, BINACIS | ID: biblio-1372249

ABSTRACT

Previamente hemos demostrado que la diabetes mellitus tipo 1 experimental (D.m.1) inducida por estreptozotocina (STZ) produce estrés oxidativo intestinal en las primeras etapas de la enfermedad, lo que conduce a la inhibición de la absorción intestinal de Ca+2, alterando la vía transcelular del transporte del catión. El objetivo de este trabajo fue estudiar la vía paracelular del transporte del Ca+2 y analizar si la D.m.1 induce estrés nitrosativo a nivel duodenal. Se utilizaron ratas Wistar machos a las que se inyectaron 60 mg STZ/kg de peso corporal; se sacrificaron a los 30 días postratamiento. Se determinó la expresión génica y proteica de claudina 2 y 12, proteínas involucradas en el transporte paracelular del Ca+2. En la mucosa duodenal se determinó el contenido de óxido nítrico (NO) y la expresión proteica de óxido nítrico sintasa inducible (iNOS). Los resultados revelaron que la expresión génica de claudina 2 en las ratas diabéticas fue más del doble en comparación con la de los controles, mientras que la expresión génica de claudina 12 fue similar en ambos grupos. La expresión proteica de claudina 2 y 12 aumentó en las ratas diabéticas. El contenido de NO fue similar en ambos grupos; sin embargo, la expresión proteica de iNOS fue mayor en las ratas diabéticas en comparación con la de las ratas controles. En conclusión, la D.m.1 experimental se acompaña de estrés oxidativo y de aumento en la expresión proteica de iNOS, alterándose la vía paracelular de absorción de Ca+2 como un mecanismo compensatorio. (AU)


We have previously shown that experimental type 1 diabetes mellitus (D.m.1) produced by streptozotocin (STZ) in rats causes intestinal oxidative stress in the early stages of the disease, which leads to the inhibition of intestinal Ca2+ absorption, altering the transcellular Ca2+ pathway. The aim of this work was to study the paracellular Ca2+ pathway and analyze if D.m.1 induces duodenal nitrosative stress. The animals were assigned to two groups: 1) control rats, and 2) STZ-induced diabetic rats (60 mg/kg b.w.). Rats were sacrificed 30 days after induction of diabetes. The gene and protein expression of claudin 2 and 12, proteins involved in paracellular Ca2+ pathway, was determined as well as the nitric oxide (NO) content and protein expression of iNOS in rat duodenum mucosa. The results revealed that claudin 2 expression was more that double in diabetic rats compared to control rats at 30 days, while the gene expression of claudin 12 was similar in both groups. The protein expression of claudin 2 and 12 increased in the diabetic rats. NO content was similar in both groups, but the iNOS protein expression was enhanced in diabetic rats. To conclude, the experimental type I D.m.1 is accompanied by duodenal oxidative stress, increase iNOS protein expression and alteration of the paracellular Ca2+ pathway as a compensatory mechanism. (AU)


Subject(s)
Animals , Male , Rats , Calcium Metabolism Disorders/etiology , Diabetes Mellitus, Experimental/enzymology , Nitric Oxide Synthase Type II/metabolism , Intestinal Absorption , Phosphates/blood , Blood Glucose , Gene Expression , Calcium/blood , Rats, Wistar , Oxidative Stress , Diabetes Mellitus, Experimental/complications , Disease Models, Animal , Claudins/genetics
5.
Clin Calcium ; 25(7): 1029-36, 2015 Jul.
Article in Japanese | MEDLINE | ID: mdl-26119316

ABSTRACT

Following the discovery of the calcium-sensing receptor (CaSR) in 1993, its pivotal role in disorders of calcium homeostasis was demonstrated. Compelling evidence suggests that the CaSR plays multiple roles extending well beyond not only regulating the level of extracellular Ca(2+), but also controlling diverse and crucial roles in human physiology and pathophysiology. This review covers current knowledge of the role of the CaSR in disorders of calcium homeostasis (familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism, autosomal dominant hypocalcemia, primary and secondary hyperparathyroidism, hypercalcemia of malignancy) as well as unrelated diseases such as breast and colorectal cancer, Alzheimer's disease and pancreatitis. In addition, it examines the use or potential use of CaSR agonists or antagonists in the management of disorders as diverse as hyperparathyroidism and Alzheimer's disease.


Subject(s)
Calcium Metabolism Disorders/etiology , Calcium/metabolism , Receptors, Calcium-Sensing/physiology , Alzheimer Disease/etiology , Animals , Breast Neoplasms/etiology , Colorectal Neoplasms/etiology , Female , Homeostasis , Humans , Male , Mice , Molecular Targeted Therapy , Mutation , Pancreatitis , Receptors, Calcium-Sensing/agonists , Receptors, Calcium-Sensing/antagonists & inhibitors , Receptors, Calcium-Sensing/genetics
6.
Endocrinol Metab Clin North Am ; 43(3): 743-67, 2014 Sep.
Article in English | MEDLINE | ID: mdl-25169565

ABSTRACT

The prevalence of vitamin D deficiency among HIV-infected persons is substantial and comparable to the general population. The factors associated with vitamin D deficiency are similar for both populations but additional factors (ie, use of certain antiretroviral agents) also contribute to vitamin D deficiency among HIV-infected persons. The adverse outcomes associated with vitamin D deficiency considerably overlap with non-AIDS defining illnesses (NADIs) that are increasingly becoming widespread in the aging HIV-infected population. However, there is scant evidence to support any causal inference. Further studies are warranted as efforts to identify and address modifiable risk factors contributing to NADIs continue.


Subject(s)
Calcium Metabolism Disorders/etiology , HIV Infections/complications , Vitamin D Deficiency/etiology , Animals , Calcium/blood , Calcium Metabolism Disorders/epidemiology , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/etiology , HIV Infections/epidemiology , HIV-1 , Humans , Musculoskeletal Diseases/epidemiology , Musculoskeletal Diseases/etiology , Risk Factors , Vitamin D/blood , Vitamin D Deficiency/epidemiology
9.
PLoS Med ; 10(4): e1001436, 2013.
Article in English | MEDLINE | ID: mdl-23637579

ABSTRACT

BACKGROUND: Calcimimetic agents lower serum parathyroid hormone levels in people with chronic kidney disease (CKD), but treatment effects on patient-relevant outcomes are uncertain. We conducted a systematic review and meta-analysis to summarize the benefits and harms of calcimimetic therapy in adults with CKD and used cumulative meta-analysis to identify how evidence for calcimimetic treatment has developed in this clinical setting. METHODS AND FINDINGS: Cochrane and Embase databases (through February 7, 2013) were electronically searched to identify randomized trials evaluating effects of calcimimetic therapy on mortality and adverse events in adults with CKD. Two independent reviewers identified trials, extracted data, and assessed risk of bias. Eighteen trials comprising 7,446 participants compared cinacalcet plus conventional therapy with placebo or no treatment plus conventional therapy in adults with CKD. In moderate- to high-quality evidence (based on Grading of Recommendations Assessment, Development, and Evaluation criteria) in adults with CKD stage 5D (dialysis), cinacalcet had little or no effect on all-cause mortality (relative risk, 0.97 [95% confidence interval, 0.89-1.05]), had imprecise effect on cardiovascular mortality (0.67 [0.16-2.87]), and prevented parathyroidectomy (0.49 [0.40-0.59]) and hypercalcemia (0.23 [0.05-0.97]), but increased hypocalcemia (6.98 [5.10-9.53]), nausea (2.02 [1.45-2.81]), and vomiting (1.97 [1.73-2.24]). Data for clinical outcomes were sparse in adults with CKD stages 3-5. On average, treating 1,000 people with CKD stage 5D for 1 y had no effect on survival and prevented about three patients from experiencing parathyroidectomy, whilst 60 experienced hypocalcemia and 150 experienced nausea. Analyses were limited by insufficient data in CKD stages 3-5 and kidney transplant recipients. CONCLUSIONS: Cinacalcet reduces the need for parathyroidectomy in patients with CKD stage 5D, but does not appear to improve all-cause or cardiovascular mortality. Additional trials in CKD stage 5D are unlikely to change our confidence in the treatment effects of cinacalcet in this population.


Subject(s)
Calcimimetic Agents/therapeutic use , Cardiovascular Diseases/mortality , Naphthalenes/therapeutic use , Parathyroid Hormone/blood , Renal Insufficiency, Chronic/drug therapy , Calcimimetic Agents/adverse effects , Calcium Metabolism Disorders/etiology , Calcium Metabolism Disorders/prevention & control , Cinacalcet , Humans , Hyperparathyroidism/drug therapy , Hyperparathyroidism/surgery , Naphthalenes/adverse effects , Nausea/etiology , Parathyroidectomy , Renal Insufficiency, Chronic/blood , Renal Insufficiency, Chronic/mortality , Vomiting/etiology
10.
Gynecol Endocrinol ; 29(6): 515-9, 2013 Jun.
Article in English | MEDLINE | ID: mdl-23350730

ABSTRACT

Parathyroid disorders are not common among pregnant women, but harbor a significant morbidity and mortality potential if they remain unrecognized and untreated. The symptoms caused by abnormally low or high blood free calcium level are mostly non-specific in the initial stages, thus when recognized might pose a real danger. Here we will survey the alterations in calcium metabolism induced by pregnancy, and describe the clinical manifestations, diagnosis and treatment of parathyroid and other calcium metabolism disorders during pregnancy. The current literature on the impact of calcium and vitamin D deficiency during pregnancy will also be reviewed.


Subject(s)
Calcium Metabolism Disorders/etiology , Parathyroid Diseases/etiology , Pregnancy Complications , Animals , Bone and Bones/metabolism , Calcium/metabolism , Calcium Metabolism Disorders/epidemiology , Female , Fetus/metabolism , Humans , Osteoporosis/epidemiology , Osteoporosis/etiology , Osteoporosis/metabolism , Parathyroid Diseases/epidemiology , Pregnancy , Pregnancy Complications/epidemiology , Pregnancy Complications/metabolism
11.
Clin Biochem ; 45(12): 943-53, 2012 Aug.
Article in English | MEDLINE | ID: mdl-22503956

ABSTRACT

Following the discovery of the calcium-sensing receptor (CaSR) in 1993, its pivotal role in disorders of calcium homeostasis such as Familial Hypocalciuric Hypercalcemia (FHH) was quickly demonstrated. Since then, it has become clear that the CaSR has immense functional versatility largely through its ability to activate many different signaling pathways in a ligand- and tissue-specific manner. This allows the receptor to play diverse and crucial roles in human physiology and pathophysiology, both in calcium homeostasis and in tissues and biological processes unrelated to calcium balance. This review covers current knowledge of the role of the CaSR in disorders of calcium homeostasis (FHH, neonatal severe hyperparathyroidism, autosomal dominant hypocalcemia, primary and secondary hyperparathyroidism, hypercalcemia of malignancy) as well as unrelated diseases such as breast and colorectal cancer (where the receptor appears to play a tumor suppressor role), Alzheimer's disease, pancreatitis, diabetes mellitus, hypertension and bone and gastrointestinal disorders. In addition, it examines the use or potential use of CaSR agonists or antagonists (calcimimetics and calcilytics) and other drugs mediated through the CaSR, in the management of disorders as diverse as hyperparathyroidism, osteoporosis and gastrointestinal disease.


Subject(s)
Receptors, Calcium-Sensing/physiology , Animals , Bone Diseases/drug therapy , Bone Diseases/metabolism , Brain Diseases/metabolism , Calcium Metabolism Disorders/etiology , Calcium Metabolism Disorders/metabolism , Cardiovascular Diseases/metabolism , Gastrointestinal Diseases/metabolism , Humans , Hyperparathyroidism/metabolism , Mutation , Neoplasms/complications , Neoplasms/metabolism , Receptors, Calcium-Sensing/genetics , Receptors, Calcium-Sensing/metabolism
12.
Curr Opin Pulm Med ; 17(5): 297-302, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21832916

ABSTRACT

PURPOSE OF REVIEW: Calcium metabolism impairments have long been recognized as a complication of sarcoidosis. For more than six decades physicians and investigators have been trying to elucidate this severe problem; nevertheless it seems puzzlingly new for both readers and researchers. RECENT FINDINGS: This review highlights the problems of calcium metabolism in sarcoidosis in relation to vitamin D synthesis, which is definitely altered by granulomatous inflammation. Increasing evidence suggests that vitamin D is an immunomodulating hormone that inhibits both antigen presentation by cells of the innate immune system, and the cytokine release and proliferation of Th1 cells. As calcium homeostasis is primary controlled by levels of vitamin D, parathyroid hormone (PTH) and calcitonin, this literature review emphasizes the role of general immunomodulating properties of vitamin D and the correlation with calcium metabolism impairments, with the special accent on already known interactions with sarcoidosis. SUMMARY: Granuloma formation has been related to a failure of the innate immune system. One of the possible explanations is a vitamin D deficiency. The evidence-based findings on calcium metabolism impairments and the interactions with vitamin D might help both clinicians and researchers in developing new strategies.


Subject(s)
Calcium Metabolism Disorders/diagnosis , Calcium Metabolism Disorders/drug therapy , Evidence-Based Medicine , Sarcoidosis/complications , Calcium Metabolism Disorders/etiology , Homeostasis/physiology , Humans , Immunity, Innate/physiology , Sarcoidosis/metabolism , Sarcoidosis/physiopathology , Vitamin D/physiology , Vitamin D Deficiency/metabolism
13.
Nephrology (Carlton) ; 15(1): 54-62, 2010 Feb.
Article in English | MEDLINE | ID: mdl-20377772

ABSTRACT

AIM: Chronic kidney disease (CKD) causes the dysregulation of systemic mineral metabolism. A major issue in CKD patients is the emergence of ectopic calcification in soft tissues, presumably due to increased levels of calcium (Ca) or inorganic phosphorus (Pi); however, the precise mechanisms have not been fully elucidated. Therefore, this study aims to evaluate Ca dynamics in an animal model of CKD. METHODS: Renal failure was produced in rats by feeding an adenine-containing diet for 4 weeks, and time-course changes in biochemical parameters, including Ca, Pi, creatinine (Cr), blood urea nitrogen (BUN), parathyroid hormone (PTH), 1,25-dihydroxyvitamin D(3), and N-telopeptide and cross-linked collagen type I (NTx), were monitored once a week during the feeding period. Intestinal absorption, tissue contents, and urinary excretion of Ca were monitored using radioisotope (RI) (45)Ca. RESULTS: Adenine-fed rats exhibited renal failure, ectopic calcification and altered serum parameters, including elevated levels of serum Pi, Cr, PTH and BUN. Serum Ca levels were not increased in rats with renal failure. RI-based experiments revealed that abnormal Ca dynamics including attenuated intestinal absorption, increased incorporation into soft tissues, particularly aortic tissue, in which it was increased threefold, and enhanced urinary excretion occurred in renal failure rats. CONCLUSION: Rats with renal failure induced by an adenine diet exhibited severe abnormality of Ca dynamics, including Ca shortage and ectopic accumulation of Ca. These findings would provide useful information to research CKD-related complications.


Subject(s)
Calcium Metabolism Disorders/etiology , Renal Insufficiency/complications , Renal Insufficiency/metabolism , Adenine/administration & dosage , Animals , Chronic Disease , Male , Rats , Rats, Inbred F344 , Renal Insufficiency/chemically induced
14.
Nephrol Ther ; 6(3): 151-7, 2010 Jun.
Article in French | MEDLINE | ID: mdl-20399169

ABSTRACT

The new recommendations of "Kidney disease: improving global outcomes" for the definition and classification of chronic kidney disease and mineral and bone disorders were released in August 2009. We report the most important of these recommendations and a brief comment from a clinician's point of view. The main points to be noted with regard to the new recommendations are as follows: serum calcium should be in the normal range; phosphorus concentration should be lowered toward the normal range and serum parathyroid hormone (PTH) levels should be two to nine times the upper limit of the normal range; bone remodelling can be assessed using alkaline phosphatase; the use of calcium-phosphorus (Ca x P) product as an index is not recommended anymore; at any stage of CKD, vitamin D deficiency and insufficiency must be corrected; vascular calcification should be detected in a simple way using lateral abdominal radiography and echocardiography; a bone biopsy should be performed before therapy with bisphosphonates; the prescription of dialysate calcium should be individualized within the range of 1.25-1.5 mmol/l; the phosphate binder (calcium- or non-calcium-based) and the other treatments for secondary hyperparathyroidism should be individualized based on a global strategy. A majority of these recommendations are not based on evidence and their feasibility and relevance need to be assessed.


Subject(s)
Bone Diseases/etiology , Bone Diseases/prevention & control , Calcium Metabolism Disorders/etiology , Calcium Metabolism Disorders/prevention & control , Kidney Diseases/complications , Phosphorus Metabolism Disorders/etiology , Phosphorus Metabolism Disorders/prevention & control , Chronic Disease , France , Humans , Practice Guidelines as Topic
16.
Blood Purif ; 29(2): 163-76, 2010.
Article in English | MEDLINE | ID: mdl-20093823

ABSTRACT

Calcium mass balance (Ca(MB)) is determined by the difference between Ca absorbed between dialyses (Ca(Abs)) and the Ca removed during dialysis (J(d)Ca(2+)). A mathematical model to quantify (1) Ca(Abs) as a function of Ca intake (Ca(INT)) and the doses of vitamin D analogues, and (2) J(d)Ca(2+) as a function of Ca(2+) dialysance, the mean plasma Ca(2+) ((M)C(pi)Ca(2+)) minus dialysate Ca(2+) (C(di)Ca(2+)), ultrafiltration rate (Q(f)) and treatment time is developed in this paper. The model revealed a basic design flaw in clinical studies of Ca-based as opposed to non-Ca-based binders in that C(di)Ca(2+) must be reduced with the Ca-based binders in order to avoid a positive Ca(MB) relative to the non-Ca-based binders. The model was also used to analyze Ca(MB) in 320 Renal Research Institute hemodialysis patients and showed that all patients irrespective of type of binder were in positive Ca(MB) between dialyses (mean +/- SD 160 +/- 67 mg/day) with current doses of vitamin D analogues prescribed. Calculation of the optimal C(di)Ca(2+) for the 320 Renal Research Institute patients revealed that in virtually all instances, the C(di)Ca(2+) required for neutral Ca(MB), where Ca removal during dialysis was equal to Ca accumulation between dialyses, was less than 2.50 mEq/l and averaged about 2.00 mEq/l. This sharply contradicts the recent KDIGO (Kidney Disease: Improving Global Outcomes) Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease - Mineral and Bone Disorder, that suggests a C(di)Ca(2+) of 2.5-3.0 mEq/l. Review of the KDIGO work group discussions shows that this discrepancy stems from the unwarranted work group assumption that intradialytic Ca(MB) is zero. We strongly believe that this guideline for dialysate Ca(2+) is inappropriate and should be modified to more realistically reflect the needs of dialysis patients.


Subject(s)
Algorithms , Bone Density Conservation Agents/administration & dosage , Calcium Metabolism Disorders/prevention & control , Calcium/metabolism , Dialysis Solutions/chemistry , Ergocalciferols/administration & dosage , Kidney Failure, Chronic/therapy , Models, Biological , Practice Guidelines as Topic , Reference Values , Renal Dialysis , Acetates/administration & dosage , Acetates/therapeutic use , Bone Density Conservation Agents/therapeutic use , Calcitriol/blood , Calcitriol/therapeutic use , Calcium/administration & dosage , Calcium/pharmacokinetics , Calcium Compounds/administration & dosage , Calcium Compounds/therapeutic use , Calcium Metabolism Disorders/etiology , Calcium, Dietary/pharmacokinetics , Chelating Agents/administration & dosage , Chelating Agents/therapeutic use , Chronic Kidney Disease-Mineral and Bone Disorder/etiology , Chronic Kidney Disease-Mineral and Bone Disorder/prevention & control , Dialysis Solutions/adverse effects , Dialysis Solutions/pharmacokinetics , Dialysis Solutions/therapeutic use , Ergocalciferols/therapeutic use , Homeostasis , Humans , Intestinal Absorption , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/metabolism , Phosphorus/metabolism , Renal Dialysis/adverse effects , Renal Dialysis/methods , Research Design , Ultrafiltration
17.
Soins Gerontol ; (86): 10-3, 2010.
Article in French | MEDLINE | ID: mdl-21298956

ABSTRACT

The prevalence of chronic renal insufficiency (CRI) increases with age. This growth shall result in it becoming a public health issue for the most elderly In this age group, chronic renal insufficiency primarily stems from diabetes and vascular and glomerular origins. The limiting point is the assessment of the glomerular filtration rate which remains imprecise. Care aims to limit the development of renal insufficiency and to prevent its complications, which are sources of fragility.


Subject(s)
Mass Screening/methods , Renal Insufficiency, Chronic/diagnosis , Renal Insufficiency, Chronic/therapy , Acidosis/etiology , Age Distribution , Aged , Calcium Metabolism Disorders/etiology , Causality , Diabetes Mellitus, Type 2/complications , France/epidemiology , Glomerular Filtration Rate , Humans , Hyperkalemia/etiology , Hypertension/complications , Mass Screening/nursing , Nurse's Role , Phosphorus Metabolism Disorders/etiology , Prevalence , Public Health , Renal Insufficiency, Chronic/epidemiology , Renal Insufficiency, Chronic/etiology
18.
Scand J Gastroenterol ; 45(2): 133-8, 2010.
Article in English | MEDLINE | ID: mdl-19958055

ABSTRACT

Malabsorption of dietary calcium is a cause of osteoporosis. Dissolution of calcium salts (e.g. calcium carbonate) in the stomach is one step in the proper active and passive absorption of calcium as a calcium ion (Ca(2+)) in the proximal small intestine. Stomach acid markedly increases dissolution and ionization of poorly soluble calcium salts. If acid is not properly secreted, calcium salts are minimally dissolved (ionized) and, subsequently, may not be properly and effectively absorbed. Atrophic gastritis, gastric surgery, and high-dose, long-term use of antisecretory drugs markedly reduce acid secretion and may, therefore, be risk conditions for malabsorption of dietary and supplementary calcium, and may thereby increase the risk of osteoporosis in the long term.


Subject(s)
Achlorhydria/complications , Calcium Metabolism Disorders/etiology , Calcium/metabolism , Gastric Mucosa/metabolism , Osteoporosis/etiology , Achlorhydria/metabolism , Dietary Supplements , Gastrectomy/adverse effects , Gastric Acid/metabolism , Gastritis, Atrophic/complications , Humans , Proton Pump Inhibitors/adverse effects , Risk Factors
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