Complications of renal failure - aluminum poisoning2017-06-25 08:58
Conventional dialysis treatment of end-stage renal disease patients prone to aluminum poisoning. Lead to chronic renal failure regular hemodialysis patients with aluminum poisoning for many reasons, including: dialysis solution containing too much aluminum. When the aluminum content in the dialysis solution is close to 50μg / L, the incidence of aluminum-related bone disease is high. Therefore, the authors suggest that the aluminum content of the dialysate should be at least 10 μg / L, preferably less than 5 μg / L. Kidney is the only way to row of aluminum, chronic renal failure when the absorption of aluminum in the accumulation of aluminum poisoning. End-stage renal disease patients with excretion of aluminum blocked, more heavy aluminum accumulation in the body, so that the body can be higher than the normal 20 times the amount of aluminum. Aluminum has the largest number of organs for bone, liver and spleen. Increased levels of aluminum in the bone are associated with aluminum poisoning and can lead to aluminum-related bone disease. Aluminum is mainly deposited on the edge of calcified bone, that is, mineralized bone and non-mineralized cubital interface, causing bone softening. The severity of osteomalacia histological changes is associated with the deposition of aluminum at the margin of calcified bone. While the aplastic bone disease may be caused by aluminum softening of the prelude to softening. Aplastic bone disease is the first reported in 1982, a kidney bone malnutrition. It is now considered a major bone lesion in patients with chronic renal failure for peritoneal dialysis. Some cases are caused by excessive accumulation of aluminum, but too much inhibition of parathyroid hormone may be more important reasons. Parathyroid hormone plays an important role in maintaining normal bone metabolism. Parathyroid hormone may prevent the deposition of aluminum in the mineralization frontier by increasing bone transport, whereas parathyroidectomy is a risk factor for the occurrence of aluminum-related bone disease, which reduces bone formation rate and regeneration rate , So that aluminum accumulation in the calcified bone edge, thus interfering with bone mineralization process. Clinically, in patients with secondary hyperparathyroidism to consider doing parathyroidectomy should be excluded before the aluminum-related bone disease, because the lower levels of parathyroid hormone can accelerate the coexistence of bone softening of patients in the deposition of aluminum in the bone and accelerated aluminum The occurrence of bone disease. The incidence of aluminum-related bone disease reported in the past was as high as 15% to 25%. In recent years, the incidence has been significantly reduced by noticing the use of phosphorus-containing binders and improving the treatment of dialysate. The clinical manifestations of aluminum-related bone diseases are extensive bone and joint pain that can be located on the back, buttocks and ribs. Proximal muscle weakness, recurrent fractures common in the ribs, femoral neck, spine and femoral shaft, but also for the performance of bone deformation. These symptoms reflect the content of aluminum in the synovial cavity. Although aluminum-related bone disease can be seen in patients with chronic renal failure with aluminum preparations, but the risk of diabetes in patients with a greater risk, which may be related to its bone formation rate is lower than normal. Type 1 diabetes in the presence of clinical diabetic nephropathy before the bone formation rate that is decreased, the reason is unclear, but these patients with plasma parathyroid hormone levels are often low. In the early stages of aluminum-related encephalopathy, there were intermittent linguistic disorders, dyslexia, and late symptoms of persistent language disorder, flapping-wing tremor, myoclonus, seizures, personality changes, disorder, orientation disorder, progressive dementia and aphasia The EEG changes to dominant rhythm mildly slow.
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