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 development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.
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PMID:Renin-angiotensin system in stroke-prone spontaneously hypertensive rats. 42 75

In freshly collected urine from a patient with glomerulotubular proteinuria there were two bands which contained retinol-binding proteins. The cathodal band showed fluorescence in the ultraviolet. After extraction with organic solvents only the anodal non-fluorescent band remained. After addition of an excess retinol only one band remained which by mobility corresponded to the cathodal band. The anodal of the two bands was therefore probably the apo form and the cathodal the holo form of the same retinol-binding protein. Their proportions, determined by densitometric scanning were approximately 4/1 (anodal/cathodal band). More than 85% of the retinol-binding protein in the urine bound to prealbumin-Sephrose. The apo retinol-binding protein from urine had the same electrophoretic mobility on agarose gel el-ctrophoresis and the same pattern on isoelectric focusing as an retinol-binding protein prepared from serum. The carboxy-terminal amino acid sequence of the retinol-binding protein from freshly collected urine that bound to prealbumin-Sepharose, was -Arg-Leu. The amino-terminal sequence was Glu-Arg-Asp-Cys-Arg-Val-Ser-X-Phe-Arg-Val-Lys-Glu-Asn-Phe-Asp-Lys-Ala-Arg-Phe-X-Gly-Thr-Trp-Tyr-. This sequence and the amino acid composition are compatible with the view that the retinol-binding protein in urine is the same as in plasma.
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PMID:Retinol-binding protein from human urine and its interaction with retinol and prealbumin. 57 35

To determine whether or not urinary Alanine aminopeptidase (AAP) could be used as an early marker for diabetic nephropathy, urinary AAP, microalbumin and N-acetyl-beta-D-glucosaminidase (NAG) were measured in 132 diabetic patients and 59 normal subjects. Urinary AAP, microalbumin and NAG in the diabetic patients and the normal subjects were 15.5 +/- 11.7 U/g. Cr and 9.1 +/- 6.9 (P less than 0.01), 27.4 +/- 35.5 mg/g. Cr and 8.4 +/- 4.4 (P = 0.0001), 10. 3 +/- 9.5 U/g. Cr and 3.9 +/- 2.1 (P = 0.0001), respectively. AAP had a moderate correlation with NAG (r = 0.58, P = 0.0001). AAP, microalbumin and NAG showed a slight positive correlation with age (AAP: r = 0.25, P less than 0.01, microalbumin: r = 0.32, P less than 0.01, NAG: r = 0.21, P less than 0.05), although it is significant, and AAP had a positive correlation with urinary protein concentration (r = 0.45, P = 0.0001) in diabetic patients. However, AAP in diabetic patients without proteinuria was higher than that in age-matched normal subjects. Urinary AAP was correlated with the indices of renal tubular damage like NAG, alpha 1-microglobulin and beta 2-microglobulin, so it seemed to be tubular origin but in the patients with clinical proteinuria, it might be partially glomerular origin. Since urine AAP increased in some patients without microalbuminuria and was not influenced by control of blood sugar, AAP could be used as an early marker of diabetic nephropath y in addition to microalbumin and NAG, but the effect of age should be considered in its estimation as in the case of NAG.
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PMID:[Clinical evaluation of urinary alanine aminopeptidase in the patients with diabetes mellitus-comparison among AAP microalbumin and N-acetyl-beta-D-glucosaminidase]. 168 Jul 83

Effects of cadmium intoxication on renal transport systems for various amino acids were studied. Subcutaneous injections of CdCl2, at a dose of 2 mg Cd/kg.day for 2 weeks, resulted in polyuria, proteinuria, glycosuria, phosphaturia, and aminoaciduria, as observed in chronic cadmium-intoxicated humans and experimental animals. The nature of aminoaciduria was nonspecific, including iminoacid as well as almost all species of neutral, acidic, and basic amino acids. In renal cortical brush border membrane vesicles isolated from cadmium-intoxicated rats, Na(+)-dependent transport of L-proline, L-alanine, and L-lysine was markedly attenuated, whereas the amino acid transport in the basolateral membrane vesicle was not significantly affected. Similar results were obtained in the normal membrane vesicles directly exposed to inorganic cadmium. These results indicate that cadmium intoxication impairs various Na(+)-amino acid cotransport systems in the renal brush border membrane, which leads to panaminoaciduria.
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PMID:Alteration of renal amino acid transport system in cadmium-intoxicated rats. 225 75

Two patients admitted after ingestion of 80% acetic acid are described. Only the first patient developed haemolysis, slight intravascular coagulation and oliguric kidney insufficiency. They were treated with a nasogastric tube and total parenteral feeding. During the first week after admission urinary excretion of beta 2-microglobulin, alanine-aminopeptidase and N-acetyl-glucosaminidase was significantly increased. The patients remained haemodynamically stable and did not develop fever. The above-mentioned elevated excretions returned to normal levels. Both patients showed similar patterns of tubular proteinuria. The observations in the second patient suggest a direct toxic effect of acetic acid on the proximal tubule of the kidney.
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PMID:[Kidney tubule dysfunction caused by acetic acid]. 256 37

The urinary enzymes alanine amino-peptidase, alkaline phosphatase, gamma-glutamyltransferase and N-acetyl-beta-D-glucosaminidase and the two urine low-molecular mass proteins lysozyme and ribonuclease were measured in 30 healthy men and 36 insulin-dependent diabetics. 17 diabetics had "clinical proteinuria" (greater than 7.5 g/mol creatinine) and were defined as patients with manifest diabetic nephropathy. The remaining 19 diabetics were without proteinuria. The excretion rates of the two urine proteins and all enzymes except for gamma-glutamyltransferase were the highest in patients suffering from diabetic nephropathy. The excretion rates in both diabetic groups exceeded those of the control group. N-Acetyl-beta-D-glucosaminidase was more often increased than albumin in diabetics without manifest diabetic nephropathy. It is concluded that the tubular dysfunction is an early indicator of the incipient diabetic nephropathy. Thus, tubular parameters, especially the lysosomal enzyme N-acetyl-beta-D-glucosaminidase may be used in follow-up studies of diabetics.
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PMID:[Urine enzymes and low molecular weight proteins as indicators of diabetic nephropathy]. 273 55

Forty-five patients suffering from a major depression were administered zimeldine, amitriptyline or placebo (15 patients in each group) in a double-blind controlled study. In the zimeldine group, seven of the 14 patients treated for more than one week presented a toxic syndrome consisting in a severe prostration, fever, myalgias and arthralgias. In all patients presenting this syndrome, laboratory analyses revealed an elevation of alkaline phosphatase and of aspartate and alanine aminotransferases and a decrease in white blood cell and platelet counts. Three patients presented a mild proteinuria and hematuria. Although an immunological mechanism cannot be ruled out, several characteristics of this reaction suggest the formation of a metabolite of zimeldine with direct cellular toxicity. The relatively high starting dose of 200 mg/day of zimeldine administered in the present study and the increment to 300 mg/day after only seven days might have contributed to the high incidence of toxic reactions observed.
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PMID:High incidence of multisystemic reactions to zimeldine. 315 76

The activities of the lysosomal endopeptidase cathepsin B (cath B; CZB-Ala-Arg-Arg-MNA as substrate) and the lysosomal exopeptidase dipeptidylpeptidase II (DAP II; Lys-Ala-2NA as substrate) were fluorometrically determined in the renal homogenate of normal and experimental (castration followed by a 14-day treatment with estradiol and testosterone) rats of both sexes. In addition, methodological investigations of the renal homogenate were performed in order to differentiate cath B from other proteinases. These showed that cath-B activity was highest at around pH 6, was strongly inhibited by 4-hydroxymercuribenzoate and leupeptin, and was activated by dithiothreitol. Trypsin-like activities were not demonstrable under the used incubation conditions. The animal experiments showed that renal cath-B activities (1) were significantly higher in females than in males, (2) increased significantly in males and decreased significantly in females after castration (no significant difference between both sexes), (3) decreased in female and male castrates after treatment with testosterone and increased strongly after treatment with estradiol, and (4) showed an activity pattern similar to that of DAP II. The results are discussed in relation to the sex-dependent and sex-hormone-dependent proteinuria of rats. It is suggested that there is a correlation between protein catabolism in the kidney and proteinuria, i.e. high lysosomal proteinase activities correspond with low proteinuria.
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PMID:Renal cathepsin-B activities in rats after castration and treatment with sex hormones. 374 98

Succinylacetone (SA) (4,6-dioxoheptanoic acid) is an abnormal metabolite produced in patients with hereditary tyrosinemia as a consequence of an inherited deficiency of fumaryl acetoacetate hydrolase activity. Patients with this disease are associated with a number of abnormalities, including aminoaciduria, proteinuria, liver failure, commonly hepatoma, and decreased GSH concentration in the liver. In the course of our studies of tyrosinemia, we found that the urine of patients with this disorder contains material(s) that absorbs light at 315 nm. We investigated the nature of the 315 nm material in detail. SA was found to react with amino acids and protein nonenzymatically, to form stable adducts at physiological temperature and pH. All SA adducts with amino acids and/or proteins exhibited an absorption peak at 315 nm. Although all amino acids reacted with SA, the most reactive amino acid was lysine (Lys), followed, in order, by glycine, methionine, phenylalanine, serine, alanine, and glutamine. SA-adducts were unstable at pH below 6, while they were made considerably more stable after reduction with NaBH4, suggesting that SA forms an adduct via Schiff base formation. High-performance liquid chromatography (HPLC) analysis of urines from patients with tyrosinemia revealed the existence of SA-glycine, SA-methionine, SA-tyrosine, and SA-phenylalanine. After digestion of urines with proteinase K, three more HPLC peaks appeared, which all corresponded to SA-Lys adducts. TLC analysis of SA-Lys showed that SA-Lys could form as many as seven different adducts. No SA-adduct peaks were observed in HPLC in urines from normal subjects, patients with other forms of aminoaciduria, or patients with the nephrotic syndrome. In addition to amino acids and proteins, SA reacted with reduced glutathione (GSH) and formed a stable adduct. These findings suggest that SA adduct formation with amino acids, GSH, and proteins is a significant process occurring in tyrosinemia, and may account for certain of the pathologic findings in this hereditary disorder.
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PMID:Hereditary tyrosinemia. Formation of succinylacetone-amino acid adducts. 392 1

The effects of Captopril on blood pressure and renal function were evaluated in ten patients with different degrees of hypertension. In seven, blood pressure was reduced after 7 weeks of therapy; in three it remained practically unchanged. No correlation was found between the standing plasma renin activity before treatment and the hypotensive response. Plasma renin activity increased significantly from the median value of 5.4 (range 1-16.7) to 9.5 (range 2.6-19.8) ng ml-1 h-1 (P less than 0.05) and urine aldosterone significantly fell from 13 (range 2.3-52.5) to 7.4 (range 1.6-14) microgram 24 h-1 (P less than 0.01) during therapy. Renal plasma flow decreased from 534 (range 300-616) to 471 (range 333-606) ml min-1, but the difference was not significant, and glomerular filtration rate fell significantly form 122 (range 64-143) to 88 (range 71-116) ml min-1 (P less than 0.05). No urinary excretion of alpha 2-macroglobulin was observed during Captopril. 24 h proteinuria, albumin and transferrin clearance, alanine-amino transferase, gammaglutamyl transferase and alpha glucosidase excretion rate and malate-dehydrogenase clearance remained unaltered throughout the treatment. This indicates that neither glomerular permeability nor renal tubular function were affected by the drug.
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PMID:Hypotensive and renal effects of captopril. 680 Aug 13


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