RESUMO
Introducción: las alteraciones del metabolismo óseo-mineral, son una causa importante de morbilidad en los pacientes con trasplante renal, por lo que el manejo de las complicaciones del paciente trasplantado, a largo plazo, deben de ser seguidas. El estudio intenta demostrar cambios en el metabolismo óseo y mineral en pacientes con enfermedad renal crónica sometidos a trasplante renal en el Hospital General Plaza de la Salud durante el período comprendido entre enero 2010 agosto 2018, Santo Domingo, República Dominicana. Método: estudio observacional, descriptivo, retrospectivo y transversal de 131 trasplantes realizados en el Hospital General Plaza de la Salud, evaluando cambios de calcio (Ca), fósforo (P) y hormona paratiroidea (PTH) antes y tres meses post-trasplante. Resultados: la edad media de los pacientes incluidos fue 43.1 ±13.1 años, 72.51 % pertenecía al sexo masculino, con un tiempo medio en hemodiálisis en meses de 27.0 ± 33.6, 60 % de los trasplantes realizados fueron de donante vivo y un 63 % de los pacientes tenía HTA como comorbilidad. El nivel medio de PTH disminuyó en los primeros 3 meses posteriores al trasplante comparado con el pre-trasplante (779.6 ± 1004.0 vs. 167.9 ± 138.2 pg/ml). El fosfato disminuyó significativamente (4.9 ± 1.6 vs. 3.5 ± 0.8) y el calcio aumentó (9.0 ± 1.2 mg/dl vs. a 9.7± 0.8 mg/dl). Discusión: los cambios generales en los niveles séricos de Ca, P, PTH, BUN y creatinina desde el momento del TR a los 3 meses post TR, fueron todos significativos
Introduction: Alterations of bone-mineral metabolism are an important cause of morbidity in patients with kidney transplantation, so the management of long-term transplant patient complications should be followed. The study tries to demonstrate changes in bone and mineral metabolism in patients with chronic renal disease undergoing kidney transplant in the Hospital General Plaza de la Salud during the period January 2010 to August 2018, Santo Domingo, Dominican Republic. Method: Observational, Descriptive, Retrospective and Cross-sectional Study of 131 transplants performed at Hospital General Plaza de la Salud, evaluating changes of calcium (Ca), phosphorus (P) and parathyroid hormone (PTH) before and 3 months post-transplant. Results: The mean age of the patients included was 43.1 ± 13.1 years, 72.51% belonged to the male sex, with a mean time on hemodialysis in months of 27.0 ± 33.6, 60% of the transplants performed were from live donors and 63% from the patients had hypertension as comorbidity. The mean PTH level decreased in the first 3 months after transplantation compared to the pre-transplant (779.6 ± 1004.0 vs 167.9 ± 138.2 pg/ml). Phosphate decreased significantly (4.9 ± 1.6 vs 3.5 ± 0.8) and calcium increased (9.0 ± 1.2 mg / dl vs. 9.7 ± 0.8 mg / dl). Discussion: The general changes in serum levels of Ca, P, PTH, BUN and Creatinine from the time of TR to 3 months post TR were all significant
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Adulto Jovem , Distúrbio Mineral e Ósseo na Doença Renal Crônica/metabolismo , Transplante de Rim , Insuficiência Renal Crônica/metabolismo , Estudos Transversais , Estudos Retrospectivos , Insuficiência Renal Crônica/cirurgia , Hiperparatireoidismo Secundário/metabolismoRESUMO
Parathyroid hormone (PTH) has an important role in the maintenance of serum calcium levels. It activates renal 1α-hydroxylase and increases the synthesis of the active form of vitamin D (1,25[OH]2D3). PTH promotes calcium release from the bone and enhances tubular calcium resorption through direct action on these sites. Hallmarks of secondary hyperparathyroidism associated with chronic kidney disease (CKD) include increase in serum fibroblast growth factor 23 (FGF-23), reduction in renal 1,25[OH]2D3 production with a decline in its serum levels, decrease in intestinal calcium absorption, and, at later stages, hyperphosphatemia and high levels of PTH. In this paper, we aim to critically discuss severe CKD-related hyperparathyroidism, in which PTH, through calcium-dependent and -independent mechanisms, leads to harmful effects and manifestations of the uremic syndrome, such as bone loss, skin and soft tissue calcification, cardiomyopathy, immunodeficiency, impairment of erythropoiesis, increase of energy expenditure, and muscle weakness.
Assuntos
Hiperparatireoidismo Secundário/etiologia , Hormônio Paratireóideo/metabolismo , Insuficiência Renal Crônica/complicações , Uremia/etiologia , Remodelação Óssea , Osso e Ossos/metabolismo , Cálcio/metabolismo , Metabolismo Energético , Fator de Crescimento de Fibroblastos 23 , Fatores de Crescimento de Fibroblastos/metabolismo , Humanos , Hiperparatireoidismo Secundário/metabolismo , Fósforo/sangue , Insuficiência Renal Crônica/metabolismo , Uremia/metabolismoRESUMO
OBJECTIVE: To compare the bone metabolism of adolescents and adults with obesity before undergoing a Roux-en-Y gastric bypass (RYGB) and 6 and 12 months after the surgery. MATERIALS AND METHODS: Adolescents (G1) and adults (G2) with obesity assessed before (T0), six (T1), and 12 months after (T2) RYGB. Sun exposure, serum concentrations of 25(OH)D, calcium, phosphorous, magnesium, zinc, alkaline phosphatase, parathyroid hormone (PTH), and bone mineral density (BMD) were evaluated. RESULTS: Sixty adolescents and 60 adults were assessed. At T0, there was no significant difference between the groups' serum 25(OH)D levels (G1 21.87 + 7.52 ng/mL, G2 21.73 + 7.60 ng/mL, p = 0.94) or sun exposure (G1 17 ± 2.0 min/day, G2 13.2 ± 5.2 min/day, p = 0.85). G1 had high levels of inadequacy of calcium (66.7%), phosphorous (80.0%), and zinc (18.3%) at T0 and had a significant fall in their 25(OH)D (p < 0.01) and magnesium (p < 0.01) levels from T1 to T2. G2 saw a significant lowering of their serum zinc levels from T0 to T1 and T2 (T1 p < 0.01; T2 p < 0.01). In both groups, there was a significant rise in PTH from T1 to T2 (G1 p = 0.04, G2 p = 0.02) and from T0 to T2 (G1 and G2 p < 0.01). In G2, 40.4% of individuals with osteopenia and osteoporosis presented inadequacy of 25(OH)D. CONCLUSION: RYGB was found to worsen the inadequacy of micronutrients related to bone metabolism and was associated with secondary hyperparathyroidism and low BMD values, especially among the adolescents. The irreversible damaging effects of obesity on bone metabolism can occur in adolescence.
Assuntos
Osso e Ossos/metabolismo , Derivação Gástrica , Obesidade Mórbida/cirurgia , Obesidade Infantil/cirurgia , Adolescente , Adulto , Fatores Etários , Fosfatase Alcalina/sangue , Densidade Óssea/fisiologia , Doenças Ósseas Metabólicas/epidemiologia , Doenças Ósseas Metabólicas/etiologia , Doenças Ósseas Metabólicas/metabolismo , Cálcio/sangue , Feminino , Seguimentos , Derivação Gástrica/efeitos adversos , Derivação Gástrica/métodos , Humanos , Hiperparatireoidismo Secundário/epidemiologia , Hiperparatireoidismo Secundário/etiologia , Hiperparatireoidismo Secundário/metabolismo , Estudos Longitudinais , Masculino , Pessoa de Meia-Idade , Obesidade Mórbida/epidemiologia , Obesidade Mórbida/metabolismo , Hormônio Paratireóideo/sangue , Obesidade Infantil/epidemiologia , Obesidade Infantil/metabolismo , Adulto JovemRESUMO
Secondary hyperparathyroidism is a complication of chronic kidney disease that compromises skeletal integrity. In patients with secondary hyperparathyroidism undergoing parathyroidectomy, parathyroid hormone levels dramatically decrease. The effects of parathyroidectomy on bone tissue are poorly understood, especially regarding the proteins expressed by osteocytes, such as fibroblast growth factor 23, dentin matrix protein 1, matrix extracellular phosphoglycoprotein, sclerostin, receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin, which regulate bone turnover. The objective of this study was to characterize the bone expression of these proteins by immunohistochemistry and correlate these results with those of bone histomorphometry before and after parathyroidectomy. We studied bone biopsies that were obtained from 23 patients before and 12â¯months after parathyroidectomy. We observed an improvement in bone microarchitecture, but impaired mineralization after parathyroidectomy. We found significant increases in sclerostin and osteoprotegerin expression and a decrease in the RANKL/osteoprotegerin ratio after parathyroidectomy, suggesting that their expression is regulated by parathormone. These proteins correlated with structural and bone formation parameters. We conclude that after parathyroidectomy, significant changes occur in the bone expression of osteocyte proteins and that these proteins potentially regulate bone remodeling.
Assuntos
Osso e Ossos/metabolismo , Hiperparatireoidismo Secundário/metabolismo , Paratireoidectomia , Insuficiência Renal Crônica/metabolismo , Insuficiência Renal Crônica/cirurgia , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Humanos , Osteócitos/fisiologia , Osteoprotegerina/metabolismoRESUMO
Chronic kidney disease mineral bone disorder (CKD-MBD) is common in end-stage renal disease and is associated with an increased risk of cardiovascular morbidity and mortality. Mainstays of treatment include decreasing serum phosphorus level toward the normal range with dietary interventions and phosphate binders and treating increased parathyroid hormone levels with activated vitamin D and/or calcimimetics. There is significant variation in serum levels of mineral metabolism markers, intestinal absorption of phosphorus, and therapeutic response among individual patients and subgroups of patients with end-stage renal disease. This variation may be partly explained by polymorphisms in genes associated with calcium and phosphorus homeostasis such as the calcium-sensing receptor gene, the vitamin D-binding receptor gene, and genes associated with vascular calcification. In this review, we discuss how personalized medicine may be used for the management of CKD-MBD and how it ultimately may lead to improved clinical outcomes. Although genetic variants may seem attractive targets to tailor CKD-MBD therapy, complete understanding of how these polymorphisms function and their clinical utility and applicability to personalized medicine need to be determined.
Assuntos
Doenças Ósseas Metabólicas/terapia , Cálcio/metabolismo , Hiperparatireoidismo Secundário/terapia , Falência Renal Crônica/terapia , Fósforo/metabolismo , Doenças Ósseas Metabólicas/etiologia , Doenças Ósseas Metabólicas/genética , Doenças Ósseas Metabólicas/metabolismo , Doenças Cardiovasculares , Humanos , Hiperparatireoidismo Secundário/etiologia , Hiperparatireoidismo Secundário/metabolismo , Absorção Intestinal , Falência Renal Crônica/complicações , Falência Renal Crônica/metabolismo , Hormônio Paratireóideo/metabolismo , Polimorfismo Genético , Medicina de Precisão , Receptores de Detecção de Cálcio/genética , Calcificação Vascular/etiologia , Calcificação Vascular/metabolismo , Vitamina D/metabolismo , Proteína de Ligação a Vitamina D/genéticaRESUMO
OBJECTIVE: Chronic kidney disease is associated with several metabolic disturbances that can affect energy metabolism. As resting energy expenditure (REE) is scarcely investigated in patients on hemodialysis (HD) therapy, we aimed to evaluate the REE and its determinants in HD patients. DESIGN: Cross-sectional study. SETTING: Dialysis Unit of the Nephrology Division, Federal University of São Paulo, Brazil. SUBJECTS: The study included 55 patients (28 male, 41.4+/-12.6 years old) undergoing HD therapy thrice weekly for at least 2 months, and 55 healthy individuals pair matched for age and gender. Subjects underwent fasting blood tests, as well as nutritional assessment, and the REE was assessed by indirect calorimetry. RESULTS: REE of HD patients was similar to that of pair-matched controls (1379+/-272 and 1440+/-259 kcal/day, respectively), even when adjusted for fat-free mass (P=0.24). REE of HD patients correlated positively with fat-free mass (r=0.74; P<0.001) and body mass index (r=0.37; P<0.01), and negatively with dialysis adequacy (r=-0.46; P<0.001). No significant univariate correlation was found between REE and age, dialysis vintage, serum creatinine, urea, albumin, bicarbonate, parathyroid hormone (PTH) or high-sensitivity C-reactive protein (CRP). In the multiple linear regression analysis, using REE as dependent variable, the final model showed that besides the well-recognized determinants of REE such as fat-free mass and age, PTH and CRP were the independent determinants of REE in HD patients (R (2)=0.64). CONCLUSIONS: In this study, the REE of HD patients was similar to that of healthy individuals, even with the positive effect of secondary hyperparathyroidism and inflammation on REE of these patients.
Assuntos
Metabolismo Basal/fisiologia , Composição Corporal/fisiologia , Falência Renal Crônica/metabolismo , Falência Renal Crônica/terapia , Diálise Renal , Adulto , Fatores Etários , Idoso , Brasil , Proteína C-Reativa/metabolismo , Calorimetria Indireta , Estudos de Casos e Controles , Estudos Transversais , Metabolismo Energético/fisiologia , Feminino , Humanos , Hiperparatireoidismo Secundário/metabolismo , Hiperparatireoidismo Secundário/fisiopatologia , Falência Renal Crônica/sangue , Masculino , Pessoa de Meia-Idade , Músculo Esquelético/metabolismo , Avaliação Nutricional , Hormônio Paratireóideo/sangueRESUMO
BACKGROUND: Extracellular Ca++ concentration [Ca++] and parathormone (PTH) are related by a sigmoidal function. The set point of the control system is the [Ca++] that produces a half-maximal inhibition of PTH secretion. Whether or not this set point is abnormal in patients with chronic renal failure (CRF) and secondary hyperparathyroidism (SHP) is controversial. METHODS: We investigated whether the way [Ca++] is varied [hemodialysis (HD) or calcium gluconate/sodium citrate infusions (INF)] and the way the curve is constructed (four-parameter model or adapted four-parameter, created by Felsenfeld) could influence this set point. We performed dynamic tests of PTH secretion in 12 patients with CRF and SHP during either HD or INF. Both the four-parameter model or adapted four-parameter methods were used, creating four combinations: (a) hypocalcemia and hypercalcemia induced during HD, calculated by Brown's formula (HDB); (b) hypocalcemia and hypercalcemia induced during HD, calculated by Felsenfeld's formula (HDF); (c) hypocalcemia and hypercalcemia induced during infusion, calculated by Brown's formula (INFB); and (d) hypocalcemia and hypercalcemia induced during infusion, calculated by Felsenfeld's formula (INFF). RESULTS: The set points obtained with HDB correlated perfectly with those obtained with HDF (R2 = 0.999). A similar relationship was found between INFB and INFF (R2 = 0.9997). In contrast, there was no correlation between either HDB and INFB (R2 = 0.0157) or HDF and INFF (R2 = 0.0204). CONCLUSIONS: These findings indicate that the calculated [Ca++] set point in patients with CRF and SHP is determined by the way [Ca++] is varied, rather than by the mathematical model used to generate the curves. Further studies are needed to determine the differing physiological mechanisms triggered by HD and INF and the way they influence [Ca++] homeostasis in this setting.
Assuntos
Gluconato de Cálcio , Hipocalcemia/induzido quimicamente , Falência Renal Crônica/metabolismo , Hormônio Paratireóideo/metabolismo , Diálise Renal , Adolescente , Adulto , Cálcio/sangue , Citratos/administração & dosagem , Feminino , Humanos , Hiperparatireoidismo Secundário/etiologia , Hiperparatireoidismo Secundário/metabolismo , Falência Renal Crônica/complicações , Falência Renal Crônica/terapia , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Modelos Biológicos , Reprodutibilidade dos Testes , Citrato de SódioRESUMO
Since the introduction of irradiated ergosterol into our food supply, nutritional vitamin D-deficiency rickets has become an uncommon disease. However, skeletal disorders due to abnormalities of vitamin D function still occur. These disorders can now be classified more exactly into two groups: those in which there is a deficiency of the active metabolite of vitamin D, 1,25-dihydroxyvitamin D, and those in which there is an abnormality of renal tubular function resulting in renal hypophosphatemia despite normal vitamin D metabolism. The various entities of these two groups are described and the theoretical basis of their treatment given.