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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From studies on 11 different proteins (including native albumin and albumin with reduced disulfide-bridges) treated with sulfosalicylic, 2-naphthalenesulfonic, toluenesulfonic, dichloroacetic, or trichloroacetic acids, we elucidate the interactions determining the resulting turbidities and other factors affecting turbidities, and we discuss the clinical utility of such turbidimetry. At least three interactions are important in determining turbidity: reduction of positive charges on the protein, hydrogen bonding of the non-ionized chloroacetic acids with the protein, and hydrophobic interaction of the aromatic sulfonic acids with albumin. Turbidity varies appreciably with the species of acid and protein, concentrations of acid, temperature, and standing time after acid is added. We conclude that this technique should be restricted to confirming proteinuria.
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PMID:Re-evaluation of turbidimetry of proteins by use of aromatic sulfonic acids and chloroacetic acids. 21 46

We observed idiopathic light-chain proteinuria in a patient with multiple abnormalities of proximal-tubule transport mechanisms (Fanconi syndrome), nephrogenic diabetes insipidus, and distal renal tubular acidosis. Seventeen of the 19 urinary amino acid levels measured were elevated. Uric acid and phosphate clearances were greater than 60 per cent and 50 per cent, respectively, of the simultaneous inulin clearance. When water deprivation was coupled with vasopressin administration, the maximum urinary concentration observed was 384 mOsm per kilogram of water. During ammonium-chloride loading, the level of hydrogen-ion concentration in the urine remained less than 100 times that in the blood. Kappa light-chain excretion was 149 mg per 24 hours. It appears that the concurrence of proximal tubular dysfunction, distal tubular dysfunction and light-chain proteinuria represents a distinct syndrome, which we call "combined light-chain nephropathy." Available evidence indicates that excessive light-chain production with subsequent filtration, reabsorption and catabolism, causes the complex tubular dysfunctions observed.
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PMID:Light-chain nephropathy. Renal tubular dysfunction associated with light-chain proteinuria. 81 85

Renal tubular acidosis (RTA) can be separated into three main types: distal RTA (the defect in the excretion of hydrogen ion), proximal RTA (the defect in the reabsorption of bicarbonate), and hyperkalemic RTA. Some patients present combined types of proximal and distal RTA. Most of the pediatric patients with RTA manifest failure to thrive. They have hyperchloremic metabolic acidosis and normal plasma anion gap. Fractional excretion of bicarbonate is below 5% in dRTA and over 15% in pRTA. Renal complications of dRTA are nephrocalcinosis, renal calculi, renal cysts and reversible low molecular weight proteinuria. The patient with isolated pRTA is very rare.
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PMID:[Renal tubular acidosis]. 143 12

To identify the specific in vivo renal effect of reactive oxygen species (ROS), hydrogen peroxide (H2O2) was infused directly into the left renal artery in Munich-Wistar rats. H2O2 (5 to 50 mumol over 1 h) induced a dose-dependent increase in urine protein excretion rate in infused kidneys, reaching a maximum at the dose of 35 mumol (on average, a 60-fold increase from baseline). The H2O2 (35 mumol)-induced proteinuria peaked over 1 h and completely normalized by 24 h after the infusion. Electrophoresis revealed that the urine protein is primarily of glomerular origin. Fractional clearances of graded-size neutral dextran of larger molecular radii, an index of glomerular size selectivity, were significantly and substantially elevated immediately but normalized by 24 h after the infusion. GFR and RPF rate remained unchanged throughout the entire time course examined. The H2O2-induced proteinuria was largely prevented by pretreatment with catalase (20 mg, iv) or deferoxamine (30 mg/100 g body wt, iv). Thus, iron-dependent metabolites of hydrogen peroxide appear to be involved in this proteinuria and glomerular size-selective defect. Light and electron microscopy, including determination of anionic site density at lamina rara externa of glomerular capillary wall by polyethyleneimine staining, did not reveal any appreciable abnormality throughout the study period, including at the peak of proteinuria. Thus, ROS can cause massive, reversible proteinuria by inducing a molecular size-selectivity defect of the glomerular capillary wall without apparent ultrastructural abnormalities. The results raise the possibilities: (1) that persistent proteinuria of a variety of renal diseases may reflect persistence of pathogenic ROS acting on glomeruli because the potent proteinuric effect of ROS can be transient (2) that the light and electron microscopy abnormalities in glomeruli of ROS-induced renal injuries reported thus far may have no direct causal linkage to proteinuria; and, finally, (3) ROS-induced reversible proteinuria may relate to the mechanism of clinical functional proteinuria, which involves increased oxygen and ROS metabolism, e.g., exercise-induced proteinuria.
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PMID:Reactive oxygen metabolites cause massive, reversible proteinuria and glomerular sieving defect without apparent ultrastructural abnormality. 172 53

Hydrogen peroxide (H2O2) contributes to renal cellular injury. alpha-Keto acids nonenzymatically reduce H2O2 to water while undergoing decarboxylation at the 1-carbon (1-C) position. We examined, in vitro and in vivo, the protective role of sodium pyruvate in H2O2-induced renal injury. Pyruvate effectively scavenged H2O2 in vitro, and suppressed H2O2-induced renal lipid peroxidation. Injury to LLC-PK1 cells induced by hydrogen peroxide was attenuated by pyruvate to an extent comparable to that seen with catalase. Studies utilizing [1-14C]pyruvate further demonstrated 1-C decarboxylation concurrent with cytoprotection by pyruvate from H2O2-induced injury. Pyruvate was also protective in vivo. Infusion of pyruvate before and during the intrarenal infusion of H2O2 attenuated H2O2-induced proteinuria. Systemic administration of pyruvate was also protective in the glycerol model of acute renal failure, a model also characterized by increased generation of H2O2. These findings indicate that pyruvate, a ubiquitous alpha-keto acid, scavenges H2O2 and protects renal tissue in vitro and in vivo from H2O2-mediated injury. These data suggest a potential therapeutic role for pyruvate in diseases in which increased generation of H2O2 is incriminated in renal damage.
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PMID:Hydrogen peroxide-induced renal injury. A protective role for pyruvate in vitro and in vivo. 175 50

Diethylene glycol (DEG) is a widely used substance with various risks of intoxication. In adult rats influences of DEG on functional parameters are characterized, indicating early signs of nephrotoxicity. A dose dependent proteinuria, an oliguric effect, an increased excretion of free hydrogen ions and a compensated impairment of renal tubular transport processes can be stated (0.25, 0.5 and 0.75 ml DEG/100 g b.m. i.p.). Following a single dose of 0.5 ml DEG/100 g b.m. i.p. the maximally expressed nephrotoxic effect is measurable 4 to 8 days after administration.
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PMID:Nephrotoxic effects of diethylene glycol (DEG) in rats. 187 10

We examined the effect of glucocorticoid on intrinsic glomerular antioxidant enzyme (AOE) activities. Munich-Wistar rats were treated with daily i.p. injection of vehicle or methylprednisolone [MP, 15 mg/kg body wt, (MP15)] either for three days or nine days. Glomeruli isolated from rats given MP15 had significantly higher activities of total (T-) and manganese (Mn-) superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase than vehicle-treated rats (P less than 0.05). MP15-treated rats were subjected to intrarenal arterial infusion of hydrogen peroxide (35 mumol over 1 hr). Values for urinary protein excretion rate (UprV) after hydrogen peroxide infusion were markedly lower in rats pretreated with MP15 for both three days and nine days than in untreated rats (109 +/- 18 and 55 +/- 24 vs. 416 +/- 73 micrograms/min, respectively, both P less than 0.005). To test whether the same therapeutic intervention attenuates reactive oxygen species (ROS)-mediated glomerular injury in another model, rats given a single i.v. dose of puromycin aminonucleoside (PAN) (50 mg/kg body wt) were treated with daily i.p. injection of vehicle or MP15. Two days after PAN administration, when compared to vehicle-treated controls, PAN rats given MP15 had significantly higher activities of Mn-SOD, GSH-Px and catalase. After eight days of PAN injection, T- and Mn-SOD activities were, likewise, significantly higher in MP15- than vehicle-treated PAN rats. PAN rats given MP15 also had substantially less proteinuria, compared to PAN rats given vehicle alone, UprV averaging 32.3 +/- 9.4 versus 159.0 +/- 13.8 mg/24 hr (P less than 0.05). Elevated glomerular malondialdehyde (MDA) level characteristic of PAN rats was absent in rats treated with MP15. Moreover, epithelial foot process fusion and cell vacuolization seen in vehicle-treated PAN rats were markedly attenuated in MP15-treated PAN rats. These data indicate that the mechanism for therapeutic effect of glucocorticoids on ROS-mediated renal injuries includes an enhancement of endogenous glomerular AOE activities, which attenuates lipid peroxidation of glomerular tissue.
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PMID:Glucocorticoid activates glomerular antioxidant enzymes and protects glomeruli from oxidant injuries. 194 78

In an attempt to examine the role of reactive oxygen species on bivalent hapten immune complex glomerulonephritis, superoxide dismutase (SOD) concentration in renal tissue was studied by Electron Spin Resonance (ESR) and the protective effect of radical scavengers were evaluated. Injection of immune complex (IC) induced severe glomerulonephritis, characterized by neutrophil and/or monocyte infiltration in glomeruli in an association with proteinuria. SOD concentration in renal tissue decreased when neutrophil and/or monocytes infiltration and proteinuria developed, indicating a possible role of reactive oxygen species on renal injury. SOD, superoxide scavenger, and catalase (CAT), which destroy hydrogen peroxide, apparently reduced proteinuria on 14th day (18.5 +/- 3.17 mg/day, 20.7 +/- 7.35 mg/day, respectively, in comparison with control group, 29.5 +/- 4.21 mg/day), but there was no statistical significance. On the other hand, hydroxy radical scavenger, dimethylthiourea (DMTU) significantly reduced proteinuria (15.3 +/- 4.21 mg/day) and remarkable improvement in renal histology was observed. It is concluded that reactive oxygen species, especially hydroxy radical, play a significant role on renal injury in bivalent hapten immune complex glomerulonephritis.
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PMID:[Role of reactive oxygen species (Ros) in model immune complex nephritis]. 214 98

1. The function of the kidney glomerulus, and the formation of reactive oxygen species in the glomerulus, is reviewed. 2. Experimental models of glomerular injury, resulting from immunological and non-immune reactions, are known to give rise to morphological and functional changes of the glomerulus, resulting in proteinuria. 3. From the use of oxygen radical scavengers and inhibitors, glomerular injuries have been shown to be associated with the production of hydrogen peroxide, hydroxyl radical, and superoxide anion radical.
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PMID:Reactive oxygen and glomerular dysfunction. 223 11

Gastric emptying, mouth-to-cecum transit and whole gut transit of a solid-liquid meal were measured in 43 insulin-treated diabetics and in 30 control subjects by using scintigraphic techniques, the hydrogen breath test and stool markers. In the diabetics various parameters including duration of diabetes, gastrointestinal symptoms and complications such as autonomic neuropathy, peripheral neuropathy and proteinuria were determined and related to gastrointestinal transit times. Gastric emptying was significantly prolonged in diabetics as compared to the control group (p less than 0.05) with 35% of the diabetics disclosing abnormally delayed gastric emptying, whereas no significant overall differences were observed between diabetics and controls concerning mouth-to-cecum transit and whole gut transit time. However, abnormally prolonged mouth-to-cecum transit was detected in 23% and delayed whole gut transit in 26% of the diabetics (p less than 0.02 as compared to the control group). There was a significant correlation of dyspeptic symptoms and diarrhea with prolonged gastric emptying (p less than 0.001). Gastric emptying, but not mouth-to-cecum transit or whole gut transit was significantly related to autonomic nerve dysfunction (p less than 0.001) and peripheral neuropathy (p less than 0.02). Furthermore, gastric emptying and WGT were significantly correlated to proteinuria (p less than 0.03). Using a linear regression model, autonomic neuropathy, diarrhea and dyspeptic symptoms were the major parameters in predicting delayed gastric emptying. It is concluded that in diabetics different compartments of the gut are affected by gastrointestinal motor abnormalities and that these segments are probably regulated by independent or different control mechanisms.
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PMID:Gastrointestinal transit disorders in patients with insulin-treated diabetes mellitus. 230 21


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