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)

Within three patient groups (1. advanced renal failure, 2. patients under chronic hemodialysis, 3. patients with renal transplants) 16 serum proteins were determined immunochemically employing MANCINIS method. The group mean values for each protein were compared, and the statistical significance of intergroup differences was examined. The most noteworthy results were the following: a distinct increase in prealbumin in all groups, least marked in the dialyzed patients; frequent elevation of alpha2-macroglobulin in the patients with transplanted kidney, but not in the other two groups; a significant increase in beta2-glycoprotein in all groups. Other changes affected several components of the acute phase reactants which were, in part, markedly elevated. On the other hand, alpha1-antitrypsin and transferrin remained largely within the normal range. Possible mechanisms accounting for some of these changes are discussed.
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PMID:[Serum protein values in uremic patients, dialysis-patients and patients with transplanted kidneys]. 33 71

Different types of urinary protein excretion may be recognized by determination of the proteins molecular weight. Beside chromatography different electrophoretic procedures have been applied to urinary proteins to study the underlying renal disease. The various zone electrophoreses separate merely by surface charge, proteins however covered by sodium dodecyl sulfate (SDS) migrate according to their molecular radius. So by SDS-polyacrylamide electrophoresis (SDS-PAe) macromolecular proteinurias (Mr 60,000- greater than 300,000 daltons) due to glomerular damage may be distinguished from micromolecular forms (Mr 10,000-70,000 d) due to tubular dysfunction. By densitometric quantitation of the separated Ig and transferrin an index of the glomerular selectivity is obtained, i.e. the capacity of the glomerular system, to retain serum proteins of a Mr above 150,000 d. By this procedure proliferative and degenerative glomerulopathies may be distinguished from minimal change disease, focal glomerular sclerosis and early membranous nephropathy; serial determinations of this selectivity index in the latter two disease entities show a gradual deterioration of glomerular protein handling with time. A glomerular proteinuria of even "physiological" quantity has been proved as early sign of renal involvment in systemic diseases; it may be detected earlier as for example the retinopathy in juvenile diabetics. Micromolecular proteinurias also occur at least in two forms: the typical tubular proteinuria (MW 10,000-70,000 d) is associated with acute or chronic severe tubular dysfunction as in interstitial nephritis and acute kidney failure; rejection episodes of kidney transplants lead to transient tubular proteinurias, too. The second form of micromolecular proteinuria (Mr 40,000-70,000 d) has been found frequently in association with a glomerular in diabetic and hypertensive glomerulosclerosis. By measuring clearances of the microproteins, the proteinuria with this pattern could be established as form independant from glomerular and tubular proteinurias. The constancy of the two micromolecular proteinurias led to the hypothesis of at least two selective mechanism of tubular protein resorption. SDS-PAe additionally allows the differentiation of extrarenal proteinurias, as caused by overflow, paraproteins, postrenal Ig-secretion or bleeding etc. In comparing clinical and in part histological data of about 2,000 patients suffering from kidney diseases the analysis of urinary proteins by this method has been proved as valuable non-invasive tool for diagnosis and follow-up.
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PMID:Diagnostic significance of SDS-PAA-electrophoresis of urinary proteins: different forms of proteinuria and their correlation to renal diseases. 44 75

The percentage of fat-cell areas in bone marrow particles from 22 patients with untreated myelomatosis was estimated. In only 1 patient was the mean fat cell area below 25% of the bone marrow area measured. A negative correlation was found between the area of fat cells and plasma cells, indicating a displacement of the fat cell area by the plasma cells. 28% of the patients had empty bone marrow deposits of iron. However, based on a normal iron saturation of S-transferrin and a normal sideroblast count in the bone marrow, the supply of iron to the erythropoiesis was considered sufficient. All patients but one had normoblastic bone marrows. Using a deoxyuridine suppression test in 10 patients, no biochemical defect could be demonstrated. To judge from the correlation coefficient a minor degree (9-14%) of the variation in Hb values could be predicted from the cellularity in the bone marrow while a major degree (70%) could be predicted from the renal glomerular filtration rate. The results do not support a displacement of blood-forming elements, iron deficiency, vitamin B12 or folic acid deficiency to be of general significance in the pathogenesis of anaemia, but agrees with a causal relationship between anaemia and renal failure.
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PMID:Bone marrow studies in myelomatosis. 71 78

Erythropoietin activity in serum was measured using 59Fe incorporation into erythrocytes in protein-starved, hypoxic mice. The activity in serum from 20 patients with untreated myelomatosis was not significantly different from that in 31 saline controls. Only three patients had detectable erythropoietin levels in serum: 0.24 IU/ml, 0.27 IU/ml and 0.50 IU/ml (standard B), respectively. The venous haematocrit was correlated positively with the glomerular filtration rate as measured by 51Cr EDTA-clearance. No correlation could be established between venous haematocrit and serum albumin or serum transferrin. The results are in agreement with the assumption of a defective erythropoietin activity due to renal failure in myelomatosis.
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PMID:Serum erythropoietin in myelomatosis. 88 35

The practice of dietetic therapy is unusual today for patients suffering from renal failure without hypertension and reduction of glomerular filtration rate. Specific treatment is needed, however, for arterial hypertension, uremia, calculus and uralith disease. Experiments in rats showed, that a lot of uremic symptoms following poorly functioning kidneys are partly at least caused by disturbances in amino acid metabolism. Uremia patients with dysfunctioning plasma protein metabolism (transferrin, complement, cholinesterase, prealbumin and retinolbinding protein) need oral, respectively parenteral substitution of essential amino acids. This substitution is very important under catabolic stress conditions in uremic syndrome with and without vividialysis treatment.
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PMID:[Nutrition problems in kidney diseases]. 96 82

Complementuria is a common finding in patients with heavy proteinuria from a variety of causes, and was detected in 23 out of 34 nephrotic subjects. Mean excretion of C3 and C4 in these patients was 49 +/- 22 and 14 +/- 3 mg/24h, respectively. The renal handling of complement appears to be largely molecular weight (MW) dependent, an inverse relationship between the sieving coefficient and MW of transferrin, IgG, C3, and C4 obtaining, in nephrotic patients irrespective of the nature of their glomerulopathy or degree of renal function. Furthermore, glomerular sieving of C3 and C4 was not significantly different in patients with immune glomerular injury associated with extensive glomerular complement deposition, from that in patients with non-immune glomerulopathy, suggesting that no unique mechanism exists for the transglomerular passage of complement from serum into the urine of the former group. The finding of a large increase of sieving of C3 and C4 in nephrotic patients with end-stage renal failure may indicate a failure by atrophic tubules to reabsorb and catabolize filtered complement.
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PMID:Renal handling of the third (C3) and fourth (C4) components of the complement system in the nephrotic syndrome. 126 8

This study was carried out in rats with nephrotoxic serum nephritis after autologous phase proteinuria was well established to determine the effect of tubule fluid iron chelation on the course of this disease. Deferoxamine administration caused a reduction in urinary iron potentially capable of catalyzing hydroxyl radical (.OH) formation and kidney iron uptake (224 +/- 60 vs. 398 +/- 152 mg/kg). This was associated with a decrease rate of progression of renal failure over the 21-day study period (creatinine clearance -0. 199 +/- 0.152 vs. -0.509 +/- 0.336 ml/min, P < 0.05) and improved survival (8/8 vs. 4/8, P < 0.05). In addition deferoxamine caused a reduction in urinary transferrin excretion (32 +/- 15 vs. 74 +/- 16 mg/day) and fractional excretion of transferrin (2.01 +/- 1 vs. 5.9 +/- 3.7%) and an increase in serum transferrin levels (229 +/- 36 vs. 139 +/- 45 mg/dl, all P < 0.05). It is suggested that iron presented to the tubule fluid as a result of the glomerular leak for transferrin is dissociated from transferrin. In turn the iron is available in a form capable of catalyzing .OH formation, resulting in lipid peroxidation of tubule cell membranes. Deferoxamine chelation of tubule fluid iron retards the development of both tubulointerstitial injury and superimposed glomerular sclerosis in this model of membranous nephropathy.
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PMID:Toxicity of tubule fluid iron in the nephrotic syndrome. 138 59

The acute effect of amino acid based dialysis solution on peritoneal kinetics of amino acids and plasma proteins in comparison to conventional glucose-based dialysate was studied in 9 patients with end-stage renal failure on continuous ambulatory peritoneal dialysis. Instillation of 2.6% amino acid solution resulted in raised plasma concentrations of all essential amino acids included in the dialysis fluid (p less than 0.005). The amino acid solution induced an augmented leakage of plasma proteins into the dialysate at all dwell times investigated (1-8 h). After a dwell time at 8 h, the dialysate total protein increased from 2.62 +/- 0.45 g with glucose dialysate to 3.85 +/- 0.42 g with amino acid solution (p less than 0.05). Corresponding results were obtained for beta 2-microglobulin, albumin, transferrin, IgG, and for the non-essential amino acids alanine, citrulline, and glutamine (p less than 0.025) not included in the initial amino acid composition of the dialysis fluid. During the use of amino acid based dialysis fluid, the effluent prostaglandin E2 concentration increased by more than 80% in comparison to glucose dialysate (p less than 0.025). The augmented loss of proteins induced by the amino acid solution was positively correlated with increased dialysate prostaglandin E2 (r = 0.8894; p less than 0.001). Peritoneal ultrafiltration was not affected by the use of amino acid based dialysate fluid. The present results indicate that amino acid based dialysis fluid enhances the peritoneal permeability for plasma proteins and amino acids, probably mediated by locally generated prostanoids.
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PMID:Effect of amino acid based dialysis solution on peritoneal permeability and prostanoid generation in patients undergoing continuous ambulatory peritoneal dialysis. 141 67

Deposition of beta-amyloid and the formation of neurofibrillary tangles (NFTs) are central to the aetiopathogenesis of Alzheimer's disease (AD). The possible effects of aluminium on these processes have been investigated in patients with renal failure who are exposed chronically to high blood levels of aluminium. Focal accumulation of aluminium was observed in neurons with high densities of transferrin receptors, indicating transferrin-mediated uptake, in regions such as cortex and hippocampus which are selectively vulnerable in AD. Increased staining for the beta-amyloid precursor protein (APP) in cortical pyramidal neurons was evident in the majority of renal patients and immature senile plaques were present in 30% of cases, suggesting that aluminium may induce or accelerate beta-amyloid deposition. The absence of neurofibrillary changes in this group of renal patients indicates that aluminium does not directly cause the formation of NFTs. The brain aluminium content was not raised in neuropathologically assessed cases of AD and we have been unable to confirm claims of defective transferrin binding in this disorder. If aluminium contributes to the development of sporadic AD, it must do so indirectly, perhaps via effects on the synthesis or metabolism of APP, or by contributing generally to the age-related attrition of neurons and thus reducing the threshold for deficits produced by more specific disease-related processes.
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PMID:Aluminium accumulation, beta-amyloid deposition and neurofibrillary changes in the central nervous system. 149 Apr 21

In 24 patients with terminal renal failure the concentrations were determined of beta 2-microglobulin, prealbumin, alpha 1-antitrypsin, ceruloplasmin, alpha 2-macroglobulin, antithrombin III, plasminogen, transferrin, C3c and Cr complement components in the serum before and after haemodialysis. A statistically significant rise of concentrations of these proteins was found. It is thought that this rise was due mainly to haemoconcentration, while the contact with dialysing membranes is less important.
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PMID:[Effect of hemodialysis on the concentration of beta 2-microglobulin and acute phase proteins in the serum of patients with chronic renal failure]. 169 43


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