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)

A 10-year-old mentally retarded girl was sent to our hospital due to generalized edema, vomiting and poor appetite for several days. Serum albumin level was low, but no proteinuria was detected. Her stool was bulky and foul. Stool examination for parasite with formalin-ether concentration method revealed negative result. Trypsin activity test of stool revealed low trypsin activity as compared with normal specimen. Daily fecal fat exceeded upper normal limit. The diagnosis of giardiasis was confirmed by duodenal juice examination. Intestinal histology revealed mild shortening of the villi with increased mononuclear cell infiltration in the lamina propria. The daily stool amount decreased markedly after treatment with metronidazole 250 mg three times a day for 7 days. The edema subsided during the treatment. Serum albumin bevel returned to normal after the treatment. Giardiasis with malabsorption syndrome has often been overlooked in Taiwan. It is advised that in case of malabsorption syndrome giardiasis should be included in the list of differential diagnosis.
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PMID:[Giardiasis with malabsorption syndrome: report of one case]. 227 67

Clinical data of 65 patients with myeloma were analyzed to identify factors associated with hypoalbuminemia. The serum albumin level was not affected by patient age and gender, type of myeloma, and the occurrence of Bence Jones protein, lytic bone lesions, or hypercalcemia, and it was not related to changes in body weight or in liver and renal function. The albumin level, lower in patients with proteinuria, was unrelated to severity of proteinuria. Albumin level correlated significantly with the monoclonal IgG levels, hemoglobin concentration, clinical stage of disease, and estimated body tumor burden. Further analysis indicated the disease stage or the tumor burden as the dominant factor in determining albumin level. An albumin level of 29.0 g/L or less identified unequivocally advanced disease. Practically all patients with stage III myeloma had a serum albumin level of 37.0 g/L or less. Thus, hypoalbuminemia is primarily related to the extent of myeloma proliferation and is therefore of diagnostic and prognostic importance.
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PMID:Hypoalbuminemia in patients with multiple myeloma. 200 Nov 48

We report the case of a 32-year-old multipara who presented preeclampsia on the fourth day after childbirth without receiving proper treatment that progressed to eclampsia 4 days later. Pregnancy and delivery had been uneventful. The patient presented proteinuria (30 mg/dl), serum total proteins 5.3 g/dl and serum albumin 3.3 g/dl. Blood pressure was controlled with methyldopa, 500 mg at six-hour intervals by intravenous route. The patient presented hypoxemia secondary to bilateral pleural effusion and aspirative pneumonia requiring mechanical ventilation and invasive hemodynamic monitoring. Treatment with cefotaxime, 1 g at six-hour intervals by intravenous route and clindamycin, 600 mg at six-hour intervals by intravenous route was initiated. Sedation was maintained with thiopental sodium, 3 mg/kg/hour in continuous infusion. At dismission, the patient was completely recovered from her clinical picture and needed no antihypertensive therapy. Physiopathologic features and the aforementioned complications are discussed with particular reference to differential diagnosis.
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PMID:[Late postpartum eclampsia. Apropos of a case]. 233 15

This study has examined glycation of serum albumin and its role in evolving diabetic proteinuria. Renal clearances of endogenous glycated and nonglycated albumin were studied in groups of normal and streptozotocin-induced diabetic Wistar-Kyoto rats over a 32 week period. Concentrations of glycated and nonglycated albumin in serum and urine were measured by rat albumin radioimmunoassay following separation on m-aminophenylboronate affinity columns. Levels of glycated serum albumin in diabetic rats were significantly higher than in normal rats (5.9 +/- 0.7% vs 4.4 +/- 0.3%, P less than 0.05). Median total urinary albumin excretion increased from 120 micrograms/24 h at baseline to 879 micrograms/24 h (P less than 0.05) 28-32 weeks after induction of diabetes. The renal clearance of glycated albumin was approximately twice as great as that of nonglycated albumin in both normal (P less than 0.01) and diabetic (P less than 0.01) rats. However, the glycated albumin/nonglycated albumin clearance ratio in diabetic rats did not correlate with duration of diabetes or with the level of albuminuria. These results indicate that glycation of albumin does not contribute disproportionately to the development of proteinuria in the diabetic rat, during which median renal albumin clearance increased 7-fold. Other factors, such as glycation of the glomerular filtration surface, may have a more important role in the pathogenesis of proteinuria in experimental diabetes.
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PMID:Longitudinal evaluation of the renal clearance of glycated albumin in the diabetic rat. 234 Jul 93

These studies examine the effect of cholesterol feeding in normal rats and in rats with streptozotocin-induced diabetes mellitus. Four groups were studied: normal rats fed either a standard rat chow or a standard rat chow supplemented with cholesterol and diabetic rats fed standard chow or standard chow plus cholesterol. Diabetic rats fed a standard diet excreted more creatinine and urea in the urine, had higher levels of blood urea nitrogen, and lower serum albumin levels than rats fed standard diet plus cholesterol. Blood glucose levels were similar in the two groups; however, diabetic rats given cholesterol had a greater body weight at the end of the study than diabetic rats eating standard chow. Urine volumes and sodium and potassium excretion in the urine were greater in diabetic rats fed a standard diet than in those fed a high cholesterol diet. Diabetic rats fed a standard diet had distinctive renal lesions characterized by swelling of tubular epithelial cells with clearing of cytoplasm. The nephron segments involved by this striking vacuolar change were the distal convoluted tubule and the thick limbs of Henle's loop. These lesions were identical to those described by Armanni-Ebstein in severely glycosuric patients. These lesions were not observed in any of the animals of the other three groups (including diabetic rats fed a high cholesterol diet). Glomeruli were normal in animals of all groups. Thus, cholesterol administration prevents the development of the Armanni-Ebstein lesions in diabetic rats despite persistent hyperglycemia. The mechanism by which cholesterol administration prevents the accumulation of glycogen in distal tubule cells has not been elucidated. It is suggested that glycogen accumulation in distal tubular segments may explain the greater urine volumes, natriuresis, kaliuresis, and proteinuria observed in diabetic animals fed a standard diet when compared with rats fed the same diet plus cholesterol.
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PMID:A high cholesterol diet ameliorates renal tubular lesions in diabetic rats. 235 86

It has been established previously that nephrotic hyperlipidemia is characterized by both an increase in lipid synthesis and a defect in removal of lipoproteins. The relationship between these defects and altered albumin metabolism is uncertain. One hypothesis is that hepatic lipogenesis increases in parallel with albumin synthesis. To test this hypothesis, albumin synthesis was increased in nephrotic rats fed an 8.5% protein diet (LPN) by increasing dietary protein to 40% (HPN). Proteinuria was modulated in half of the rats fed 40% protein by enalapril (HPE). Albumin synthesis was the same in both HPN and HPE, but proteinuria was reduced in HPE compared to HPN, and so were serum cholesterol and triglycerides (TG). To examine the effect of serum albumin on lipid clearance in the absence of proteinuria, plasma clearance of chylomicrons (CM) and VLDL was measured in Nagase analbuminemic rats (NAR) and found to be no different than in normal SD rats. When proteinuria was induced in NAR and in SD rats, a severe and identical defect in both CM and VLDL clearance was acquired in both groups and blood lipid levels were increased to a similar degree in both groups. Neither hyperlipidemia nor defective removal of lipoproteins from the circulation are linked to albumin synthesis or serum albumin concentration but result, at least in part, from proteinuria. Postheparin lipoprotein lipase (LPL) activity was reduced slightly in nephrotic animals compared to nonnephrotic controls, but the most striking finding was a highly significant decrease in postheraprin LPL activity in normal NAR compared to SD rats (P less than 0.001), suggesting that reduced LPL activity is not responsible for reduced clearance of CM and VLDL in nephrotic rats.
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PMID:Proteinuria, not altered albumin metabolism, affects hyperlipidemia in the nephrotic rat. 238 6

Injection of rats with large doses of bovine serum albumin causes proteinuria which may persist long after the period of overload has ended. In order to assess in this model of proteinuria the relative importance of podocytic epithelial changes versus alterations in anionic groups in the glomerular capillary wall a morphological study has been made of animals in which the kidneys were fixed by vascular perfusion or by in situ drip fixation. By transmission electron microscopy, podocytes showed protein droplets, cytoplasmic vacuoles, spreading of epithelial cytoplasm with loss of foot processes, and focal separation of epithelium from the glomerular basement membrane, occasionally with cytoplasmic disruption. Staining with colloidal iron showed no reduction in the density of anionic groups per unit area on epithelial cell surfaces or elsewhere in glomeruli. However, the reduced surface area of epithelial cells caused by the changes to their structure accounts adequately for the less intense glomerular colloidal iron staining evident by light microscopy. Changes in podocyte structure, particularly those leading to focal cytoplasmic defects on the outer surface of the glomerular basement membrane, appear to be more important than loss of glomerular anionic groups for the development of proteinuria in protein overload nephropathy.
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PMID:Glomerular podocytic injury in protein overload proteinuria. 241 4

Plasma fibronectin concentration was measured by means of rocket immunoelectrophoresis in 20 cases of glomerular proteinuria of various origins, and correlated with urinary protein loss, serum albumin, cholesterol and plasma alpha 1 antitrypsin and alpha 2 macroglobulin. Plasma fibronectin was significantly increased in the patient's group as compared to the controls (1.91 +/- 0.659 U/ml, 1.01 +/- 0.193 U/ml respectively, p less than 0.001) and correlated with cholesterolaemia (r = 0.662, p less than 0.001). Increased plasma fibronectin may be an additional risk factor for thrombotic tendency in NS.
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PMID:Plasma fibronectin levels in patients with glomerular proteinuria. 243 37

The role of epitope density in cationic antigen was investigated in an active model of in situ immune complex glomerulonephritis (ICGN) using the hapten-carrier system. Trinitrophenol (TNP) was conjugated with variable density to cationic human immunoglobulin (C-HIgG) to yield TNP6.2-C-HIgG (low-valency antigen) and TNP31.3-C-HIgG (high-valency antigen). In rats preimmunized with TNP17.3-bovine serum albumin (BSA), endocapillary proliferative GN with proteinuria developed in rats receiving high-valency antigen. In contrast, no significant abnormalities in renal histology or urinalysis were observed when a low-valency antigen was injected. These results indicate that glomerular injury produced by hapten-specific immune reaction is affected by the number of haptenic groups conjugated to the carrier molecule (epitope density) in active in situ ICGN.
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PMID:Active in situ immune complex glomerulonephritis using the hapten-carrier system: role of epitope density in cationic antigens. 246 47

The cause of the thrombotic tendency in nephrotic patients is unknown. Recent reports of thrombotic complications in patients with deficiencies of protein C or protein S (natural inhibitors of coagulation) have raised the possibility that decreased levels of these proteins may play a role in the hypercoagulable state of nephrotic patients. We measured the levels of protein C, total protein S, and free protein S antigens in 42 patients (21 nephrotic and 21 non-nephrotic) with one of four types of glomerular pathology: diabetic nephropathy (DM), focal glomerular sclerosis (FGS), membranous glomerulonephritis (MGN), and chronic renal failure due to hypertension (CRF). Protein C and total protein S antigen levels were significantly higher in FGS and MGN than they were in DM or CRF. Free protein S levels were lower in DM than they were in MGN. Protein C, total protein S, and free protein S levels did not significantly correlate with either serum albumin or degree of proteinuria. The mean levels of the three proteins did not differ between nephrotic and non-nephrotic patients. Free protein S and protein C were, however, significantly correlated (P less than .005 and P less than .002, respectively) with the type of glomerular pathology, independent of differences in age, sex, serum albumin, or degree of proteinuria. These data suggest that abnormalities of free protein S and protein C are related to the nature of the underlying renal disease, rather than to the degree of proteinuria.
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PMID:Protein S and C antigen levels in proteinuric patients: dependence on type of glomerular pathology. 252 34


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