Chronic renal failure will lead to what disease ?

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Often complicated by high blood pressure , anemia , heart failure, pericarditis , cardiomyopathy , utilities and acid-base balance disorders , renal osteodystrophy , fractures, infections. In addition to the above complications , the long-term dialysis chronic renal failure who also have the following complications:
1 aluminum toxicity of conventional dialysis patients with ESRD complicated aluminum poisoning. Many causes of chronic renal failure in hemodialysis patients regularity aluminum poisoning , including: excessive dialysate aluminum content . When the aluminum content of the dialysate close to 50μg / L, a high incidence of aluminum-related bone disease . Therefore, the authors recommend at least dialysate aluminum content should be less than 10μg / L, preferably less than 5μg / L. The kidney is the only way to rows of aluminum , chronic renal failure, when the absorption of aluminum accumulation in the body caused the aluminum poisoning.
End-stage renal disease patients excretion of aluminum is blocked, more heavy accumulation of aluminum in the body , so that the aluminum content of the body can be 20 times higher than normal . Most organs of aluminum accumulation as bone, liver , and spleen . Increased bone content of aluminum and aluminum poisoning , can cause the aluminum -related bone disease.
Aluminum deposited mainly in calcified bone edges that are not mineralized bone and bone mineralization of young interface , causing osteomalacia . Osteomalacia histological changes in the severity and extent of deposition of aluminum edge -related bone calcification . And aplastic bone disease osteomalacia may be a prelude to aluminum caused . Aplastic bone disease was first reported in 1982, a renal osteodystrophy . Now that this is peritoneal dialysis patients with chronic renal failure , a major bone lesions. Some cases are caused by the excessive accumulation of aluminum , but the excessive suppression of parathyroid hormone may be a more important reason. PTH has an important role in maintaining normal bone metabolism . Parathyroid hormone may be transported by increasing bone mineralization and prevent the deposition of aluminum on the front edge , and parathyroidectomy on the occurrence of aluminum-related bone disease is a risk factor that can reduce bone formation rate and update rate so that the edge of the aluminum accumulation in bone calcification , thus interfering with the process of bone mineralization . Clinically, in patients with secondary hyperparathyroidism consider doing before parathyroidectomy aluminum-related bone disease should be excluded because of lower parathyroid hormone levels in patients with osteomalacia deposited aluminum can accelerate coexist in the bone and accelerates the aluminum -related bone disease occurs.
Last reported incidence of aluminum-related bone disease was as high as 15% to 25 %. In recent years , due to the restrictions on the use of aluminum-containing noticed phosphorus binders and improved dialysis treatment , the incidence rate has decreased significantly.
Clinical manifestations of aluminum-related bone disease is extensive bone and joint pain , can be positioned at the back, hips and ribs. Proximal muscle weakness , recurrent fracture is common in the ribs, neck , spine and femoral shaft , can be manifested as bone deformation . These symptoms reflect the content of aluminum in the synovial cavity .
Although aluminum-related bone disease in patients taking aluminum-containing formulations in patients with chronic renal failure , but the incidence of diabetes greater risk , which may be related to bone formation rate than normal about . Type 1 diabetes occurs before clinical diabetic nephropathy decreased bone formation rate that is , the reason is unclear, but the plasma parathyroid hormone levels in these patients is often low.
Aluminum-related encephalopathy early manifestation of intermittent language barriers , dyspraxia , late manifested as persistent language barriers , flapping wing tremor , myoclonus , seizures, personality changes, disordered thinking , disorientation, progressive dementia and aphasia . EEG dominant rhythm mild bradycardia .
Laboratory examination revealed anemia and other clinical manifestations of secondary aluminum poisoning caused by reversible small cell hypochromic anemia , iron supplementation does not improve , one of the reasons is too much aluminum can interfere with the absorption of iron . Treatment with recombinant human erythropoietin response has been poor , after correcting aluminum toxicity with deferoxamine can restore the efficacy of recombinant human erythropoietin for anemia .
Radiographic features of loose belt or pseudo fractures. True ribs and hip fractures and vertebral compression fracture is more common in patients on dialysis osteomalacia and less seen osteitis . There osteomalacia chronic uremic patients may also suffer from secondary hyperparathyroidism , therefore , may coexist with changes in bone erosion osteomalacia .
Bone histology osteomalacia is not excessive osteoid mineralization is characterized , this change is due to bone disorder caused by a protein matrix mineralization . The main change is not mineralized osteoid widened. Osteoid mineralization delay due to a certain extent, can also occur when the change osteitis . Therefore, the need to identify the damaged tetracycline mark mineralization rate. Maloney staining with aluminum can be found in most of osteomalacia in dialysis patients have a lot of aluminum deposition in bone . Most aplastic ( or lack of sexual power ) bone disease caused by aluminum poisoning, similar performance and osteomalacia , the main difference is that it does not have a big bone osteoid seam .
Bone biopsy is the gold standard for the diagnosis of aluminum poisoning , but not as a common means of diagnosis. By atomic absorption spectroscopy of plasma aluminum content can be accurately measured , but only the plasma levels reflect recent aluminum aluminum load , whether or not reflect toxicity of aluminum , because the aluminum concentration in plasma is not closely related to the storage tissue of aluminum. However , plasma levels of most aluminum aluminum-related bone disease patients was significantly higher ( i.e. > 75 ~ 100μg / L, normal <10μg / L). If the patient long-term contact with aluminum , aluminum levels in plasma and increased significantly (more than 150 ~ 200μg / L or more ) is very likely to occur aluminum-related bone disease , or encephalopathy.
Has been recognized , the test deferoxamine (DFO) is a diagnostic aluminum toxicity related diseases reliable indicator . Commonly used method is deferoxamine 40mg/kg, within half an hour after dialysis intravenous infusion, measured the pre-dialysis ( not given before deferoxamine ) and before the next dialysis ( 44h post- dose ) serum aluminum levels , difference between the two > 150μg / L or > 200μg / L as positive .
2 dialysis-related amyloidosis dialysis-related amyloidosis (DRA) is a long-term dialysis patients seen in bone and joint disease. The incidence of clinical symptoms and closely related to the length of time of dialysis . When dialysis is 0,12 5 years of 50% to 100% at 20 years . Amyloid deposition in the organization considerably earlier than clinical symptoms and radiological manifestations . It is reported that a group of prospective hemodialysis shorter than 2 years, the joint amyloid deposition rate of 21 %, 7 to 50 percent of those 13 years were 90% , more than 13 years by 100% .
( 1 ) in the pathogenesis :
① β2- globulin (β2-microglobulin, β2-M) deposition and other forms of amyloidosis as amyloid disease in bone cysts, and synovial tissue found in the Congo red staining , visible under a polarizing microscope apple green double refraction body . However, with primary amyloidosis , and fragments of immunoglobulin light chain amyloidosis secondary sediment serum A (amyloid A) is not the same , this disease amyloid protein mainly composed of β2-M , it is believed that β2 -M has a great affinity with collagen , is sufficient to explain the onset of the main sites of the joints and bones.
β2-M is a biocompatible type I antigen having a molecular weight of 11,800 . Available by glomerular filtration and is proximal tubular reabsorption and metabolism. Even at very low glomerular filtration rate of dialysis patients lacking this metabolic pathway by the very serious damage , resulting in a positive balance of β2-M while it increased plasma levels . β2-M 3mg/kg daily production was at or near 1500mg / week , standard fiber membrane can only remove a few β2-M, that the use of high permeability dialysis membrane can only be cleared <400 ~ 600mg / week β2-M. Peritoneal dialysis can remove 300mg / week β2-M.
Since DRA 8 rarely occurs before dialysis , dialysis and not all patients develop DRA, therefore , in addition to elevated plasma levels , there may be other factors involved in , for example, residual renal function , hemodialysis membranes , and the reaction inflammation , β2-M and other modified proteins while deposition.
② residual renal function : As long as there is a small amount of residual renal function , it is possible to maintain a certain amount of β2-M clearance and metabolism. Therefore , before the loss of renal function is not fully , it is possible to prevent the occurrence of DRA .
③ fiber membrane dialyzer properties : fiber membrane made ​​using standard hemodialysis porous fiber membrane than do dialysis plasma β2-M levels higher. Convection rate of high permeability membranes larger , and can be combined directly with β2-M, the lower the clinical use of high permeability dialysis membrane made ​​of bone disease and amyloidosis incidence of carpal tunnel syndrome . Type of dialysis membrane are also important factors . With cuprophane hemodialysis , in addition to low permeability , the patient 's peripheral blood mononuclear cells also increased β2-M . Poly (methyl methacrylate) film without activating complement not.
④ inflammatory response : studies show that with the expression of activated macrophages influx IL-I and TNF-β , along with severe amyloidosis lesions appear. These macrophage phagocytosis can not be sufficiently deposited in β2-M. Thus , the occurrence of destructive spondyloarthropathy may partly by the amyloid deposition and inflammation mediated reactions .
⑤ glycosylated β2-M: recently found that the presence of glycosylation β2-M in the wan amyloid deposits . This is a from 3 - deoxy- glucose (3-deoxyglucose) the modification of the activity of micro- globulin. By 3 - deoxy- glucose levels increased in serum of patients with uremia and dialysis , the patient may be more prone to renal failure β2-M modified . Amyloid deposits occur in the glycosylation by β2-M might stimulate the secretion of cytokines and as derived mononuclear cells was further promote these lesions. Pathogenic role of glycosylation β2-M can be prevented through the use of aminoguanidine , this preparation can inhibit advanced glycation end products .
While other proteins can promote the deposition of amyloid deposition material .
( 2 ) Clinical manifestations : The main clinical manifestations of DRA as carpal tunnel syndrome, bone cysts, spondyloarthropathy , pathologic fractures and joint swelling and pain , especially around the shoulder humeral joint inflammation seen . DRA is also a systemic disease , amyloid deposits are also found in skin, subcutaneous tissue , rectal mucosa , liver , spleen, and blood vessels.
① carpal tunnel syndrome (CTS): the most common symptoms. Common in hemodialysis after 8 to 10 years, more than nine years of dialysis by about 30% have this symptom .
② humeral joint inflammation around the shoulder : the shoulder is a common site to produce symptoms , leading to chronic back pain . DRA amyloid deposits seen in the subacromial bursa and synovial tissue.
③ exudative joint disease : more than 8 years of dialysis patients often exudative joint disease , which can occur with carpal tunnel syndrome. Exudate bilateral, especially seen in the knee and shoulder .
④ spondyloarthropathy : 10% to 20% of dialysis patients first symptom is pain in the neck . Damage seen in the cervical area, leading to the radial bone disease ; disc and spinal stenosis edge corrosion common ; may also occur under the notochord sclerosis , severe cases can lead to paralysis or infiltration through the epidural space leading to cauda equina compression. MRI can accurately find the extent of lesions.
⑤ bone disease : Typical performance for the end of a long bone bone cyst formation . Cystic lesions containing amyloid , which increases with time , may be associated with carpal , pathologic fractures of fingers , femoral and humeral head and acetabulum , tibial plateau and distal radius .
3 changes of trace elements renal failure and dialysis great impact on trace element metabolism , they accumulate in various parts of the body can cause toxicity.
( 1 ) Aluminum : See aluminum poisoning.
( 2 ) Copper: dialysis patients with chronic renal failure without making plasma copper levels are often normal , but can also be slightly lower. With cuprophane hemodialysis patients might accumulate copper , it is not observed the accumulation of any clinical impact . Copper may cause acute poisoning with a high copper content dialysate do hemodialysis . Clinical manifestations of high fever and severe hemolytic anemia. An increase in neutrophils may also occur , metabolic acidosis , pancreatitis , diarrhea and vomiting. In vitro , the red blood cells can lead to loss of contact with copper reduction glutamine , Heinz body formation increased their increased hemolysis , inhibition of glutathione reductase and glucose-6 - phosphate dehydrogenase reduce . Copper can also directly damage red blood cell membrane. When the pH of water is less than 6.5 , brass and copper parts inside can be filtered out , and therefore not suitable for use as dialysis water .
( 3 ) Zinc: eating a low -protein diet in chronic renal failure, nephrotic syndrome and massive loss of protein in urine is often very low plasma zinc content . It was reported that the zinc content of plasma and red blood cell levels in hemodialysis patients with certain zinc significantly increased , this may be because the zinc content in the dialysate than in plasma levels due to the filtrate . Now dialysate are used deionized water or reverse osmosis water content of plasma and tissue of patients with normal or low in zinc . Many patients taking ferrous sulfate can lead to poor absorption of zinc . Together with zinc in the dialysate may cause loss of zinc deficiency . If oral zinc supplements , preferably ferrous sulfate suspended in order to promote the absorption of zinc .

Zinc deficiency in hemodialysis patients can cause taste and smell diminish or disappear . Impotence and low plasma testosterone levels associated with high plasma levels of gonadotropins and progesterone have been attributed to the emergence of zinc deficiency, but the lack of definitive evidence. Preferably every six months on dialysis patients by atomic absorption spectroscopy of a plasma zinc levels . However , determination of plasma levels of zinc is just a rough indicator of zinc deficiency judgment , granulocytes and platelets in the determination of zinc is more sensitive than the plasma content. Children receiving regular hemodialysis growth retardation occurs should consider whether caused by zinc deficiency.