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Renal bone disease

Consequences of metabolic acidosis include renal bone disease, reduced cardiac contractility, predisposition to arrhythmias, and protein catabolism. [Pg.883]

Salusky IB Are new vitamin D analogues in renal bone disease superior to calcitriol Pediatr Nephrol 2005 20 393. [PMID 15690188]... [Pg.978]

D Haese PC, Spasovski GB, Sikole A, Hutchison A, FreemontTJ, Sulkova S, Swanepoel C, Pejanovic S, Djukanovic L, Balducci A, Coen G, Sulowicz W, Ferreira A, Torres A, Curie S, Popovic M, Dimkovic N, De Broe ME. A multicenter study on the effects of lanthanum carbonate (Fosrenol) and calcium carbonate on renal bone disease in dialysis patients. Kidney Int 2003 85 (Suppi) ... [Pg.891]

Renal osteodystrophy includes all of the disorders of bone and mineral metabolism associated with chronic renal failure. The renal bone diseases include both... [Pg.1934]

Jones RG, Dyson EH, Cook JA, Forbes MA, Cooper EH. The use of a two-site immunoradiometric assay for bone alkaline phosphatase in the investigation of renal bone disease. Clin Chem 1991 37 1067. [Pg.1953]

The prevention and treatment of severe metabolic acidosis in patients with kidney disease is also important to prevent the development of renal bone disease, fatigue, decreased exercise tolerance, reduced cardiac contractility, and increased ventricular irritability. Metabolic acidosis also appears to stimulate protein catabolism, which can contribute to a negative nitrogen balance and lower albumin concentrations, as well as cause growth retardation in children. Lower serum bicarbonate levels in peritoneal dialysis patients have also been associated with a higher hospitalization rate and longer hospital stays. Severe acidemia (blood pH <7.1 to 7.2) suppresses myocardial contractility, predisposes patients to cardiac arrhythmias, and may lead to a decrease in total peripheral vascular resistance and blood pressure, reduced hepatic blood flow, and impaired oxygen delivery. ... [Pg.841]

Spasovski GB, et al. Spectrum of renal bone disease in end-stage renal failure patients not yet on dialysis. Nephrol Dial Transplant 2003 18 1159-1166. [Pg.849]

D Haese PC, Spasovski GB, Sikole A, et al. A multicenter study on the effects of lanthanum carbonate (Fosrenol) and calcium carbonate on renal bone disease in dialysis patients. Kidney Int 2003 85 873 78. [Pg.966]

Chronic renal failure. Normal kidney function is needed for the la-hydroxylation reaction that produces 1,25-DHCC. In chronic renal failure a cascade of events is triggered, leading to secondary hyperparathyroidism, which can progress to tertiary hyperparathyroidism and renal bone disease. [Pg.111]

The most common toxic metals in industrial use are cadmium, chromium, lead, silver, and mercury less commonly used are arsenic, selenium (both metalloids), and barium. Cadmium, a metal commonly used in alloys and myriads of other industrial uses, is fairly mobile in the environment and is responsible for many maladies including renal failure and a degenerative bone disease called "ITA ITA" disease. Chromium, most often found in plating wastes, is also environmentally mobile and is most toxic in the Cr valence state. Lead has been historically used as a component of an antiknock compound in gasoline and, along with chromium (as lead chromate), in paint and pigments. [Pg.177]

Osteopetrosis (marble bone disease), characterized by increased bone density, is due to inability to resorb bone. One form occurs along with renal tubular acidosis and cerebral calcification. It is due to mutations in the gene (located on chromosome 8q22) encoding carbonic anhydrase II (CAII), one of four isozymes of carbonic anhydrase present in human tissues. The reaction catalyzed by carbonic anhydrase is shown below ... [Pg.552]

Declining renal function disrupts the homeostasis of the systems regulated by the kidney, leading to fluid and electrolyte imbalances, anemia, and metabolic bone disease. [Pg.373]

Secondary hyperparathyroidism Increased secretion of parathyroid hormone from the parathyroid glands caused by hyperphosphatemia, hypocalcemia, and vitamin D deficiency that result from decreased kidney function. It can lead to bone disease (renal osteodystrophy). [Pg.1576]

Calcium and phosphorus metabolism Calcium and phosphorus metabolism is influenced by estrogens use caution in patients with metabolic bone diseases associated with hypercalcemia or in renal insufficiency. [Pg.180]

Renal osteodystrophy is a complex disorder with several pathogenic factors. Histological evidence of bone disease is common in early renal failure and deficits in calcitriol synthesis seems to be an important factor in the pathogenesis of secondary hyperparathyroidism in early CRF. The most common component is osteitis fibrosa manifested as subperiosteal resorption of bone. This is due to decreased excretion as well as increased secretion of parathyroid hormone. In CRF small increments of serum phosphorus cause small decreases in serum calcium. [Pg.612]

Patients with chronic renal failure develop hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, and severe metabolic bone disease. The secondary hyperparathyroidism is thought to be due to hyperphosphatemia and decreased 1, 25-(OH)2 formation. Oral or intravenous l,25-(OH)2D3 (calcitriol) therapy along with oral phosphate-binding agents and calcium supplementation is effective in reducing the effects of renal osteodystrophy. [Pg.759]

Contraindications Primary or secondary hyperparathyroidism, including hypercalci-uria (renal calcium leak), hypomagnesemic states (serum magnesium less than 1.5 mg/dl), bone disease (osteoporosis, osteomalacia, osteitis), hypocalcemic states (e.g., hypoparathyroidism, intestinal malabsorption), normal or low intestinal absorption and renal excretion of calcium, enteric hyperoxaluria, and patients with high fasting urinary calcium or hypophosphatemia. [Pg.234]

It is a cyclic polypeptide with 11 amino acids. It selectively inhibits T-lymphocytes proliferation, IL-2 and other cytokine production. It is the most effective drug for prevention and treatment of graft rejection reaction. It is used in cardiac, hepatic, renal, bone marrow transplantation and as second line drug in rheumatoid arthritis, inflammatory bowel disease, dermato-myositis, bronchial asthma and certain other autoimmune diseases. [Pg.379]

It is indicated in osteoporosis, hypoparathyroidism, hyperparathyroidism (with bone disease), renal osteodystrophy, nutritional and malabsorptive rickets, hypophosphataemic vitamin D resistant rickets and osteomalacia. [Pg.386]

In mild forms of malabsorption, vitamin D (25,000-50,000 units three times per week) should suffice to raise serum levels of 25(OH)D into the normal range. Many patients with severe disease do not respond to vitamin D. Clinical experience with the other metabolites is limited, but both calcitriol and calcifediol have been used successfully in doses similar to those recommended for treatment of renal osteodystrophy. Theoretically, calcifediol should be the drug of choice under these conditions, because no impairment of the renal metabolism of 25(OH)D to l,25(OH)2D and 24,25(OH)2D exists in these patients. Both calcitriol and 24,25(OH)2D may be of importance in reversing the bone disease. However, calcifediol is no longer available. [Pg.970]

The choice of vitamin D preparation to be used in the setting of chronic renal failure in the dialysis patient depends on the type and extent of bone disease and hyperparathyroidism. No consensus has been reached regarding the advisability of using any vitamin D metabolite in the predialysis patient. l,25(OH)2D3 (calcitriol) will rapidly correct hypocalcemia and at least partially reverse the secondary hyperparathyroidism and osteitis fibrosa. Many patients with muscle weakness and bone pain gain an improved sense of well-being. [Pg.1027]

Dihydrotachysterol, an analog of l,25(OH)2D, is also available for clinical use, though it is used much less frequently than calcitriol. Dihydrotachysterol appears to be as effective as calcitriol, differing principally in its time course of action calcitriol increases serum calcium in 1-2 days, whereas dihydrotachysterol requires 1-2 weeks. For an equipotent dose (0.2 mg dihydrotachy-sterol versus 0.5 ug calcitriol), dihydrotachysterol costs about one fourth as much as calcitriol. A disadvantage of dihydrotachysterol is the inability to measure it in serum. Neither dihydrotachysterol nor calcitriol corrects the osteomalacic component of renal osteodystrophy in the majority of patients, and neither should be used in patients with hypercalcemia, especially if the bone disease is primarily osteomalacic. [Pg.1027]

A number of gastrointestinal and hepatic diseases result in disordered calcium and phosphate homeostasis that ultimately leads to bone disease. The bones in such patients show a combination of osteoporosis and osteomalacia. Osteitis fibrosa does not occur (as it does in renal osteodystrophy). The common features that appear to be important in this group of diseases are malabsorption of calcium and vitamin D. Liver disease may, in addition, reduce the production of 25(OH)D from vitamin D, though the importance of this in all but patients with terminal liver failure remains in dispute. The malabsorption of vitamin D is probably not limited to exogenous vitamin D. The liver secretes into bile a substantial number of vitamin D metabolites and conjugates that are reabsorbed in (presumably) the distal jejunum and ileum. Interference with this process could deplete the body of endogenous vitamin D metabolites as well as limit absorption of dietary vitamin D. [Pg.1028]

Developmental Effects. Studies in human infants indicate that only certain children are affected by aluminum. Excessive aluminum accumulation and encephalopathy may occur in premature infants with reduced renal function given dialysis with aluminum-containing intravenous fluid (Polinsky and Gruskin 1984 Sedman et al. 1985). Bone disease has also been reported in infants with renal failure who were treated orally with aluminum hydroxide (Andreoli et al. 1984). [Pg.143]

David-Neto E, Jorgetti V, Soeiro NMR, et al. 1993. Reversal of aluminum-related bone disease after renal transplantation. Am J Nephrol 13 12-17. [Pg.304]

Vitamin D-binding protein and its associated vitamin are lost in nephrotic urine. Biochemical abnormalities in nephrotic patients (children and adults) include hypocalcemia, both total (protein-bound) and ionized hypocalciuria, reduced intestinal calcium absorption and negative calcium balance reduced plasma 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol and, surprisingly, also 1,25-dihydroxycholecalciferol and blunted response to parathormon (PTH) administration and increased PTH levels. Clinically, both osteomalacia and hyperparathyroidism have been described in nephrotic patients, more commonly in children than in adults, but bone biopsies are commonly normal, and clinically significant bone disease is very rare in nephrotic subjects. There is, however, evidence that patients with renal failure accompanied by nephrotic range proteinuria may be particularly prone to develop renal osteodystrophy. [Pg.203]

Care should be taken when administering aluminium salts such as aluminium hydroxide in patients with renal dysfunction and bone diseases. Patients with renal... [Pg.355]

Although Al bone disease can occur in any patient intoxicated by Al, the risk is greater in diabetics. This may be related to a lower than normal bone formation rate, an abnormality that has be demonstrated in type 1 diabetics prior to the onset of clinical renal disease [109, 110]. The risk for developing acute Al encephalopathy also seems to be increased in diabetic patients this might be related to a decreased storage capacity of the bones [17]. [Pg.22]


See other pages where Renal bone disease is mentioned: [Pg.1699]    [Pg.1935]    [Pg.1935]    [Pg.1948]    [Pg.113]    [Pg.111]    [Pg.403]    [Pg.411]    [Pg.15]    [Pg.1699]    [Pg.1935]    [Pg.1935]    [Pg.1948]    [Pg.113]    [Pg.111]    [Pg.403]    [Pg.411]    [Pg.15]    [Pg.196]    [Pg.387]    [Pg.344]    [Pg.215]    [Pg.965]    [Pg.968]    [Pg.1000]    [Pg.158]    [Pg.1025]    [Pg.18]   
See also in sourсe #XX -- [ Pg.111 ]




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