Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The musculoskeletal effects of renal failure are seen in a variety of tissue, including bone, joints, and soft tissue. These effects include avascular necrosis, osseous abnormalities, ligamentous laxity, destructive arthropathies, and soft-tissue calcifications. With the advent of therapy (dialysis, transplantation), a new generation of disorders affecting these tissues has emerged. In particular, a high prevalence of destructive cervical spondyloarthropathy, which may be due to beta 2-microglobulin type amyloidosis, can be a particularly serious problem in long-term hemodialysis patients.
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PMID:Renal disease and rheumatic manifestations. 803 82

Ten patients undergoing long-term renal dialysis for end-stage renal failure developed a destructive, non-infectious spondylarthropathy. All 10 patients had biopsy-proven dialysis-associated spondylarthropathy and subsequent spinal instability secondary to beta 2-microglobulin deposition in the vertebrae, intervertebral disc spaces, and support structures of the spine. Nine patients had cervical spinal instability and one had thoracolumbar spinal instability, with resultant neural compression. In at least one patient, the spinal instability was rapidly progressive. All had received renal dialysis for 34 months or longer (mean 109 months, range 34 to 154 months). Each patient required spinal stabilization (external in seven patients, internal in three). Nine of the 10 patients underwent neural decompression and spinal stabilization and fusion procedures. One patient's neurological condition was worse following surgery due to a postoperative cervical epidural hematoma; in the other nine patients, the presenting symptoms and signs improved. Three of these chronically ill patients did not survive their hospitalization, for a perioperative mortality rate of 30%. Death was due to cardiopulmonary arrest in two patients on Day 5 and 9 postoperatively and to sepsis in the third on Day 14. Of the seven early survivors, two additional patients died: one on Day 59 due to congestive heart failure and the other on Day 273 due to a cerebrovascular accident. Four of five patients who were followed for 8 months or longer (mean 14 months, range 8 to 20 months) had successful neural decompression and spinal stabilization procedures with evidence of stable bone fusion, indicating that these chronically ill, difficult-to-manage patients can be successfully treated. Clinicians who treat patients with renal disease and neurosurgeons who treat spinal disorders should be aware of dialysis-associated spondylarthropathy as a potential cause of degenerative vertebral column instability.
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PMID:Dialysis-associated spondylarthropathy. Report of 10 cases. 815 49

The performance of a membrane in renal failure therapy is determined by its structure, its overall mass transfer properties, and its blood compatibility. In this regard, removal of beta 2-microglobulin (beta 2M) has become a major objective of dialysis therapy. In the present study, a newly developed high-flux membrane composed of a polyester-polymer alloy (PEPA) with the components of polyarylate and polyethersulfone (dialyzer FLX-12 GW; Nikkiso Co., Japan) has been evaluated with regard to both biocompatibility and elimination capacity for beta 2M during hemodialysis of 8 stable chronic uremic patients. The clearance values of low molecular weight solutes were in the same range as those reported for high-flux dialyzers of comparable surface area. There was no drop in leukocyte counts and only a minimal fall in platelet counts nearly in the same range as has been observed by other investigators using polyamide membrane. C3a Des Arg generation was low, and C5a Des Arg formation was not significantly influenced. There was a sharp drop in the serum beta 2M level (-35%) during dialysis with a clearance between 59.7 +/- 5.6 ml/min (QB 200 ml/min) and 70.1 +/- 9.7 ml/min (QB 300 ml/min), respectively. Accordingly, the sieving coefficient was calculated to be 0.2 at 30 min after start of dialysis and 0.6 1 h later. The membrane was able to remove 184.0 +/- 22.3 mg/4 h due to an apparent rate of adsorption during the first hour of treatment in combination with high transmembrane transfer in the following time.
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PMID:Clinical evaluation of a new dialyzer, FLX-12 GW, with a polyester-polymer alloy membrane. 850 69

Urinary excretion of five low molecular weight proteins (LMWP) [beta 2-microglobulin (beta 2m), cystatin C (cyst C), Clara cell protein (CC16), retinol-binding protein (RBP) and alpha 1-microglobulin (alpha 1m)], albumin and N-acetyl-beta-D-glucosaminidase (NAG) were quantified in 16 patients who followed a weight reduction program which included Chinese herbs, which have been incriminated in the genesis of Chinese herbs nephropathy (CHN). An additional group of four patients transplanted for CHN were investigated. Urinary data were obtained for comparison purpose in five groups of proteinuric patients: two groups with normal serum creatinine (SCr) and glomerular albuminura [12 patients with diabetes mellitus and microalbuminuria (DN), 10 patients with primary nephrotic syndrome (NS)]; two groups with normal SCr and toxic nephropathy [6 patients with analgesic (AN), 9 patients with cadmium nephropathy (CdN)]; and one group of seven patients with glomerular diseases and increased SCr (GN). Patients were classified according to serum level S beta 2m to take into account the possibility of overflow proteinuria at S beta 2m > or = 5 mg/liter. Three patients (CHN0) with a S beta 2m < 5 mg/liter, had a normal urinary protein pattern including NAG and a normal S beta 2m. Eight patients (CHN1) with a S beta 2m < 5 mg/liter had various abnormalities of their urinary protein pattern. In four of them (CHN1a) only beta 2m, RBP and CC16 were increased while total proteinuria and SCr were normal. In the other four (CHN1b and c) albumin, cyst C, alpha 1m and NAG were also elevated, while total proteinuria and SCr were moderately raised. Five patients (CHN2) with a S beta 2m > or = 5 mg/liter had a markedly increased excretion of all LMWP, albumin and NAG (CHN1 vs. CHN2, P < 0.05) as well as a further increase in total proteinuria and SCr. The urinary LMWP/albumin concentration ratio was strikingly higher in CHN patients than in patients with glomerular albuminuria (CHN1 vs. DN and NS, P < 0.01) or moderate renal failure with elevated S beta 2m level (CHN2 vs. GN, P < 0.01), confirming the existence of a tubular proteinuria independent of glomerular albuminuria or overflow proteinuria. A similar proteinuria pattern was present in the two toxic nephropathies (CdN and AN). This pattern was no longer recognizable after transplantation. In conclusion, CHN exhibits various profiles of tubular proteinuria which are the hallmarks of the disease. This pattern is still detectable in patients with renal failure and/or glomerular albuminuria. It is identical to that observed in cadmium and analgesic nephropathies. It does not recur after transplantation. Its most sensitive and reliable marker is a raised urinary level of CC16 or RBP.
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PMID:Low molecular weight proteinuria in Chinese herbs nephropathy. 854 16

It has been demonstrated that beta 2-microglobulin is a major constituent of amyloid fibrils in dialysis-related amyloidosis, a serious complication leading to bone and joint destruction in long-term hemodialysis patients. However, the molecular pathogenesis of this complication remains unknown. Several lines of evidence suggest that beta 2-microglobulin plays an active role in the development of dialysis-related amyloidosis. It is unlikely that intact beta 2-microglobulin per se contributes to the pathogenesis, because no difference in the plasma levels of intact beta 2-microglobulin has yet been found between hemodialysis patients with and without this complication. Some investigators, therefore, have focused on the modification of this molecule. Recent studies have revealed a new modification of beta 2-microglobulin in amyloid fibrils: advanced glycation end products (AGEs) formed by a nonenzymatic reaction between aldoses and proteins. Further studies have suggested that the interaction of AGE-modified beta 2-microglobulin with monocyte/macrophage and osteoclast/osteoblast gives a plausible, albeit partial, explanation for the mechanism of bone and joint destruction in dialysis-related amyloidosis. This article focuses on the modification of beta 2-microglobulin with AGEs, especially on their structure and pathological role in dialysis-related amyloidosis. Furthermore, the implication of renal failure in the pathophysiology of AGEs is also discussed.
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PMID:New aspects in the pathogenesis of dialysis-related amyloidosis: pathophysiology of advanced glycation end products in renal failure. 869 8

Twenty patients with end-stage renal failure on maintenance hemodialysis were studied for the effect of intravenous 1,25(OH)2 vitamin D3 on biochemical bone markers. Active vitamin D, 1,25(OH)2 vitamin D3, was given intravenously after hemodialysis, 1 microgram thrice weekly. Serum ionized calcium, phosphorus, alkaline phosphatase (AKPase), intact parathyroid hormone (PTH), osteocalcin (bone Gla protein), carboxy terminal propeptide of type I procollagen (PICP), cross-linked telopeptide of type I collagen (ICTP) and beta 2-microglobulin were measured before and after 3 and 6 months of treatment with 1,25(OH)2 vitamin D3. The serum ionized calcium and osteocalcin levels were significantly increased at 3 and 6 months after treatment. The serum beta 2-microglobulin level were also increased 6 months after treatment, whereas the serum levels of AKPase and intact PTH decreased after treatment. However, the serum levels of phosphorus, PICP and ICTP did not change significantly after treatment. The decreased levels of serum AKPase and intact PTH suggest reduced bone resorption. Increases of serum osteocalcin levels were caused by stimulation of the osteoblast by 1,25(OH)2 vitamin D3, baseline 20.6 +/- 12.5 micrograms/l, and 36.1 +/- 34.0 and 31.0 +/- 24.6 micrograms/l at 3 and 6 months, respectively (p < 0.01). The lower osteocalcin level at 6 rather than at 3 months may imply reduced bone resorption and/or increased bone mineralization. The meaning of the increase of serum beta 2-microglobulin in uremic patients after calcitriol treatment is unclear. It may indicate reduced deposition and is masked by increased bone resorption from secondary or tertiary hyperparathyroidism. This study did not validate PICP and ICTP measurements as bone markers in uremic patients.
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PMID:Changes of bone markers during long-term intravenous calcitriol therapy in maintenance dialysis patients. 880 25

The principal physiologic roles of the kidney are to maintain normal plasma volume and composition, to regulate calcium metabolism by controlling the synthesis of 1,25-dihydroxycholycalciferol (1,25-D3), to regulate hematocrit and to metabolize low molecular weight peptides. Alterations in protein metabolism result principally from losses of these functions. Metabolic acidosis causes increased skeletal muscle protein catabolism through regulated activation of the ATP-ubiquitinproteasome proteolytic pathway. Increased proteolysis is followed by oxidation of branch chain essential amino acids. Alanine and glycine released from muscle and glutamine and glutamate released from liver serve as substrate for renal ammoniagenesis, ultimately correcting acidosis. The cycle is subverted when kidneys are absent. Secretion of a variety of proteins is also perturbed. Hepatic secretion of insulin like growth factor-1 (IGF-I) in response to growth hormone is reduced. This in turn contributes to growth retardation, adding to the effects of acidosis. Muscle is also resistant to insulin in renal failure. Renal production of 1,25-D3 is reduced contributing to hyperparathyroidism, which in turn causes increased intracellular calcium in a variety of tissues contributing to decreased synthesis of immunoglobulins, mitogen-stimulated T-cell proliferation, and decreased glucose-stimulated insulin secretion. Hepatic synthesis of some proteins, such as apolipoprotein A-I and IGF-I are decreased, but synthesis of others, such as albumin, is normal. Low molecular weight peptides such as beta 2-microglobulin, normally filtered and catabolized in the proximal tubule, accumulate in plasma and may have deleterious effects.
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PMID:Derangements of protein metabolism in chronic renal failure. 889 32

To clarify the development of tubular necrosis and its healing process in ischemic renal failure observing degeneration, necrosis, cell proliferation and the involvement of apoptosis in the renal tubular epithelial cells before and after renal ischemia in rats through morphological examination. Eight week-old male rats were used for this study. The model for acute renal failure was by obstruction of bilateral renal arteries and veins for 45 minutes in several intervals (0 hr, 1 hr, 3 hr, 6 hr, 12 hr, 24hr, 48 hr, 96 hr, 1 week, 2 weeks and 4 weeks) each following reperfusion. Urinary beta 2-microglobulin (BMG) levels were measured to evaluate renal tubular function. In evaluating tubular necrosis and cell proliferation, observations of renal tubular tissue were made serially by use of light microscopy and immunological staining of proliferating cell nuclear antigen (PCNA) and bromodeoxyuridine (BrdU), respectively. The number of nuclei in the proximal tubular epithelium/circumference of the basement membrane (n/BM index) was calculated using a tissue measuring device. Transmission electron microscopy and the TdT-mediated dUTP-biotin nick end labeling (TUNEL) methods were used as indices of apoptosis. Maximal BMG values were obtained 24 hours after ischemia when injury in the proximal tubular epithelium was most prominent. The maximal number of PCNA and BrdU-positive cells were obtained 24 hours after ischemia and thereafter gradually decreased. The n/BM index in the disorder group was significantly increased 96 hours and 1 week after ischemia (p < 0.001). Electron microscopy revealed nuclear fragmentation and apoptosis in the tubular area indicating that there were significant differences. The number of positive cells for in situ nick end labelling increased 24 hours and 2 weeks after ischemia, exhibiting a two peak curve. However, the number of positive cells significantly decreased 4 weeks after ischemia. In the proximal kidney tubules damaged by reperfusion after ischemia, epithelial hyperplasia developed 3 to 6 days after the most active period of S-phase cells was noted. Thereafter, a decreasing number of epithelial cells was observed. It seemed that the decreasing number of these cells had been produced by apoptosis detected 2 weeks after ischemia.
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PMID:[A pathomorphological study on damage and repair process of tubuli after renal ischemia]. 895 3

Tumour-associated trypsin inhibitor (TATI) is a low molecular weight (MW) protein employed as a tumour marker. The blood levels of some low MW proteins increase in renal insufficiency. The aim of this study is to evaluate the relationship between serum TATI and glomerular filtration rate (GFR). Serum beta 2-microglobulin (beta 2M) and plasma creatinine were also determined. The decrease of GFR was accompanied by an increase in the other parameters. The maximum increase of TATI was from a mean basal value of 8.51 +/- 5.58 micrograms l-1 in subjects with normal renal function to 107.27 +/- 63.34 micrograms l-1 in patients with renal failure; beta 2M increased from 1.45 +/- 0.38 to 11.16 +/- 5.73 mg l-1 and creatinine from 1.05 +/- 0.17 to 5.07 +/- 1.93 mg dl-1. The increase in TATI occurs sooner and is greater than that of beta 2M and of creatinine. These results suggest that TATI is handled by the kidney. It is sensitive marker of reduction in renal function. When TATI is used as a tumour marker, renal function must be taken into account in the evaluation of the results.
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PMID:Serum tumour-associated trypsin inhibitor (TATI) and renal function. 898 62

Seventy-one fetal urine samples were taken from the bladder or renal pelvis of 33 fetuses at 13-36 weeks' gestation with a diagnosis of urinary tract anomaly. Severe isolated hydronephrosis in the absence of an enlarged bladder was the indication for sampling in 12/33 fetuses (26 samples), who were retrospectively classified into three groups: normal, intermediate, and dysplastic, based on the evaluation of postnatal renal function or histology. For all samples, urinary sodium (Na+), calcium (Ca2+), creatinine, beta 2-microglobulin, and N-acetyl-beta-D-glucosaminidase (NAG) were measured. Among the 71 fetal urine samples, both beta 2-microglobulin and NAG correlated inversely with gestational age, Na+, and Ca2+, but not with creatinine concentrations. However, the correlation of urinary beta 2-microglobulin with gestational age was dependent on the Na+ and Ca2+ concentrations, whereas urinary NAG correlated significantly with urinary Na+ and Ca2+, and also with gestational age. In fetuses with isolated hydronephrosis, only Na+, and not Ca2+, was significantly related to both beta 2-microglobulin and NAG. Only Na+ and beta 2-microglobulin were significantly, and similarly, higher in both dysplastic and intermediate kidneys when compared with fetuses with normal postnatal function. If only the last urine sampled was considered, there was overlapping of all parameters in the three groups. In isolated hydronephrosis, only the most extreme forms of renal failure might be suggested by elevated levels of Na+, Ca2+, beta 2-microglobulin, and NAG, without an obvious superiority of any of these parameters.
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PMID:In fetuses with isolated hydronephrosis, urinary beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase (NAG) have a limited role in the prediction of postnatal renal function. 899 43


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