Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The health condition and course of fermentation processes in the rumen were studied in four cows of the Red Spotted breed at the age of four to nine years. The clinico-biochemical indices in the rumen liquor and urine were used. The experimental animals were exposed to a mixture of aflatoxins applied in the dose of 200 mg B1 and 80 mg B2. The toxic action of aflatoxins manifested itself as inappetence, increased temperature, changes in the pulse and respiration rate and reduced activity of the proventriculi. Diarrhoea was observed in two animals. The pH value, total acidity and ammonia level in rumen liquor ranged within the limits of reference values. The significant drop of the production of volatile fatty acids with changes in their proportions and a reduction of the acetic acid level with a simultaneous increase of the percentage of butyric acid testity to a disorder in the activity of rumen microflora. The reduction of the number of infusorians as a biological indicator of fermentation processes proves the correctness of this assumption. During the elimination of aflatoxins through the kidneys the function of the kidneys is impaired, showed proteinuria, ketonuria, glycosuria and haematuria.
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PMID:[Changes of the clinico-biochemical indices in the rumirid juice and urine in experimental aflatoxicosis of dairy cows]. 40 95

Increased renal ammoniagenesis is pathogenic in animals. Thus, tubular degradation of filtered proteins to ammonia might link proteinuria to disease progression. The tubular uptake, metabolism and fractional degradation of aprotinin 99mTc (Trasylol), were measured in 26 glomerulonephritic patients with normal renal function, 10 with proteinuria > 5 g/24 h. In addition, urinary ammonia pH, and titratable acidity were measured. Patients with heavy proteinuria had a higher tubular metabolism, a lower uptake and a higher fractional degradation of aprotinin. Urinary ammonia and titratable acidity were also increased. Fractional degradation and urinary ammonia were strongly correlated as were urinary ammonia and proteinuria.
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PMID:Tubular metabolism of aprotinin 99mTc and urinary ammonia: effects of proteinuria. 128 13

Chronic diseases of the kidney are characterized by progression once a certain portion of renal function is lost. End-stage kidneys, the result of progressive chronic renal disease, are characterized by sclerosis, tubulointerstitial scarring, and collapse of glomerular capillary tufts. The mechanisms and risk factors responsible for the progression of renal disease have been studied intensively in the past decade, and it now appears that multiple nonimmunologic factors are responsible. These factors include systemic hypertension, hyperlipidemia, proteinuria, excessive intake of protein, and adaptive changes in nephron function as a consequence of nephron loss. The latter adaptations, increased intraglomerular pressure, increased excretion of ammonia, "hypermetabolism," decreased afferent arteriolar tone, and renal hypertrophy, may also be responsible for the progression of renal disease. A complete understanding of the factors responsible for the progression of renal disease should permit rational development of appropriate therapeutic interventions.
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PMID:Progression of chronic renal disease. 213 99

This paper reviews experimental findings which support the concept that vasopressin (VP) and the process of urine concentration may be involved in the progression of chronic renal failure (CRF). The influence of dietary protein intake on the progression of CRF may also involve VP and the operation of the concentrating process. VP receptors have been identified in glomeruli and VP is able to constrict mesangial cells as does angiotensin II. Acute VP infusion increases the glomerular transcapillary hydraulic pressure difference, and chronic VP infusion increases GFR. In rats with CRF (induced by 5/6 nephrectomy), VP levels were found elevated. In rats with 5/6 nephrectomy, we increased experimentally water intake in order to decrease circulating VP levels, urine concentration, and free water reabsorption. Several indices of progression of CRF, including proteinuria, hypertension and glomerulosclerosis, were significantly reduced, thus suggesting a contribution of VP in progression. Lowering protein intake in CRF could be beneficial because proteins, but not carbohydrates or lipids, produce metabolic end products (mainly urea, ammonia, protons, etc.) that are excreted by the kidney, and concentrated in the urine. In healthy subjects (man or rat), high protein (HP) intake favors urine concentration and causes changes in kidney function and morphology very similar to those induced by chronic VP infusion or water restriction. These changes involve an increase in transport activity of the thick ascending limb (where the initial active step of the concentrating process takes place) and may affect filtration rate and/or glomerular hemodynamics secondarily, by decreasing salt concentration at the macula densa and depressing tubuloglomerular feedback.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible involvement of vasopressin and urine concentrating process in the progression of chronic renal failure. 270

Chronic potassium deficiency results in progressive tubulointerstitial injury, associated with augmented renal ammoniagenesis. We investigated the role of elevated renal ammonia levels and the interaction of ammonia with the complement system in this injury. Potassium deficiency was induced in rats by feeding a low potassium diet. Experimental animals received 150 mM NaHCO3 or equimolar NaCl, as drinking water. After 3 wk, NaHCO3 supplemented rats demonstrated decreased ammonia production, less renal hypertrophy, less histologic evidence of injury, and less proteinuria. In in vitro studies on normal cortical tubular fragments, the addition of ammonia to serum in concentrations comparable to renal cortical levels in potassium-deficient animals significantly increased tubular deposition of C3 as quantitated by a radiolabeled antibody binding technique. Thus, alkali supplementation reduced chronic tubulointerstitial disease in a rat model of hypokalemic nephropathy. We propose that increased cortical ammonia levels contribute to hypokalemic nephropathy through ammonia-mediated activation of the alternative complement pathway.
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PMID:Hypokalemic nephropathy in the rat. Role of ammonia in chronic tubular injury. 355 40

A 20-year-old female was comatose for several days after intoxication with 75 g sodium valproate (VPA). She was successfully treated with hemodialysis, hemoperfusion, i.v. infusion of glucose, and given intensive care. Although a peak serum VPA of 2120 micrograms/ml (14720 microM) was registered 8 1/2 h after drug intake, no definite drug-related hepatotoxic or thrombocytopenic effects were seen. The only signs of organotoxicity were slight increases in serum amylase and a transient proteinuria. Further acute biochemical alterations were a decrease in serum calcium, an increase in plasma ammonia as well as in serum propionate, and elevated urinary excretions of adipic and suberic acid. Analysis of amino acids in serum revealed a stable increased level of glycine.
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PMID:Acute valproate intoxication: biochemical investigations and hemodialysis treatment. 640 45

The cause of the morphological changes and functional defects in the renal tubule seen in patients with severe potassium depletion is unknown. In man and animals potassium status is a major factor regulating ammonia synthesis in the kidney and urinary ammonium excretion. A primary effect of potassium depletion is to cause an increase in ammoniagenesis by the renal tubular cells. It is proposed that the vacuolation of the renal tubular cells and the functional defects of tubular proteinuria, polyuria, resistance to arginine vasopressin, renal resistance to the action of parathyroid hormone, and increased urinary excretion of N-acetyl-beta-glucosaminidase found in potassium depletion are secondary effects caused by high concentrations of ammonia in the renal tubular cells.
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PMID:Increased ammoniagenesis and the renal tubular effects of potassium depletion. 651 81

The effects of chitosan-coated dialdehyde cellulose (Chitosan DAC), a newly developed oral adsorbent of urea and ammonia, were examined in rats with progressive chronic renal failure (CRF) induced by adriamycin. CRF rats induced by repeated injections of adriamycin were fed a diet containing chitosan DAC (5% content) or Kremezin (5% content), an oral charcoal adsorbent (AST-120) under strict paired-feeding for four months. CRF rats that received both a normal diet and Kremezin showed progressive azotemia, hyperphosphatemia, hyperlipidemia, proteinuria, and anemia, and began to die from 9 weeks after feeding started. In contrast, chitosan DAC-treatment showed marked prolongation of the survival period and decreases in blood urea nitrogen, serum creatinine, and serum phosphate. In addition, chitosan DAC-treatment ameliorated anemia in CRF rats, although hyperlipidemia and proteinuria were not improved. Furthermore, fecal weight, fecal water content, fecal nitrogen and fecal sodium were markedly increased, and the apparent protein ratio was decreased in CRF rats fed a diet containing chitosan DAC for 9 weeks. In contrast, none of these effects were observed in CRF rats receiving Kremezin. These observations suggest the further possibility of using oral adsorbent therapy for CRF patients.
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PMID:[Pharmacological properties of chitosan-coated dialdehyde cellulose (chitosan DAC), a newly developed oral adsorbent (II). Effect of chitosan DAC on rats with chronic renal failure induced by adriamycin]. 755 38

Tubulointerstitial disease is an invariant finding in proteinuric renal disease regardless of the underlying disease or the compartment in which the disease originates. Such histologic changes are functionally significant in that scores of such injury rather than glomerular histologic injury correlate with decrements in GFR. Proteinuria, the consequence of a loss of glomerular permselectivity incurred by glomerular diseases, also provides an index of renal functional decline. This review provides evidence that proteins leaked into the urinary space may directly or indirectly provoke tubulointerstitial injury, a linkage that may underlie the functional significance of proteinuria and tubulointerstitial disease. This review also highlights two products of nitrogen metabolism, ammonia and nitric oxide, in the pathogenesis of tubulointerstitial disease.
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PMID:Effect of proteinuria on renal interstitium: effect of products of nitrogen metabolism. 811 90

The cause of the relentless progression of chronic renal failure of diverse origins remains unknown and is likely to be multifactorial. Numerous studies have now demonstrated a correlation between the degree of proteinuria and the rate progression of renal failure, which has led to the hypothesis that proteinuria may be an independent mediator of progression rather than simply being a marker of glomerular dysfunction. This article reviews the evidence underlying this hypothesis and the mechanisms by which particular proteins may cause renal pathology. The abnormal filtration of proteins across the glomerular basement membrane will bring them into contact with the mesangium and with the tubular cells. There is evidence to support a role of lipoproteins on mesangial cell function, which ultimately could contribute to glomerular sclerosis. The proximal tubular cells reabsorb proteins from the tubular fluid, which leaves them particularly vulnerable to any adverse effects proteins may have. It has been postulated that the sheer amount of protein to be metabolized by these cells may overwhelm the lysosomes and result in leakage of cytotoxic enzymes into the cells. In addition, the increased metabolism of proteins may result in production of ammonia, which can mediate inflammation through activation of complement. Specific proteins that have been shown to be cytotoxic are transferrin/iron, low-density lipoprotein, and complement components, all of which appear in the urine in proteinuric states. Other specific proteins have been shown to stimulate production of cytokines, chemoattractants, and matrix proteins by tubular cells and thus may stimulate interstitial inflammation and scarring. The mechanisms by which the presence of proteins in the tubular fluid alters tubular cell biology is yet to be determined.
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PMID:The role of proteinuria in the progression of chronic renal failure. 865 Dec 39


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