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)

Nephrosis was induced in Sprague-Dawley rats in two separate studies by injections of aminonucleoside with sacrifice of animals on days 20 and 54, respectively. Experimental animals in both studies showed the typical findings of nephrosis, i.e., hypoalbuminemia, hypercholesterolemia, and proteinuria. Biochemical findings included hypozincemia and hyperzincuria. A significant correlation between hypozincemia and hypoalbuminemia was noted in the short-term study. Proteinuria occurred on the 10th day in the short-term study and the 15th day in the long-term study and increased quantitatively over the remaining days. The hyperzincuria and proteinuria correlated significantly in the long-term study. Measurements of tissue zinc revealed no change in testes and kidney in the short-term study. Kidney and muscle zinc were increased, testicular zinc was unchanged and femur zinc was decreased in the long-term study. Our conclusions are that in the aminonucleoside induced nephrosis of the rat: 1) hypozincemia occurs probably as a result of hypoalbuminemia, 2) the hyperzincuria is likely due to proteinuria and 3) zinc deficiency is not observed in nephrotic rats who receive ample zinc in their diet and who are observed up to 6 weeks.
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PMID:Zinc metabolism in aminonucleoside-induced nephrosis. 114 20

The critical levels for monitoring cadmium health effects in 358 workers engaged in ore crushing/roasting (cadmium concentration in the workplace air 2.5-6.5 mg/m3), dry smelting (10.8-23.3 mg/m3), cadmium melting (0.01-0.16 mg/m3), and ingot making (2.8-4.7 mg/m3), were investigated. Exposure parameters such as blood and urinary cadmium were determined, together with biological parameters such as proteinuria, amino acids, glucose, beta 2-microglobulin, retinol-binding protein, albumin, plasma beta 2-microglobulin, creatinine clearance, tubular reabsorption of beta 2-microglobulin and phosphate, and blood and urinary levels of zinc, copper and lead. Factor analysis and stepwise regression analysis were then applied to the data to classify parameters and to find the main contributing parameter. Blood and urinary cadmium, urinary beta 2-microglobulin, retinol-binding protein and the ratio of urinary beta 2-microglobulin to albumin were also subjected to multiple correlation analysis, multiple regression analysis and the Chi-square test was applied to contingency tables. It is concluded, based on the data, that cadmium health effects may be assessed by using the following critical levels: blood cadmium: 10 micrograms/l, urinary cadmium: 10 micrograms/g creatinine; urinary beta 2-microglobulin: 2000 micrograms/g creatinine, urinary retinol-binding protein: 200 micrograms/g creatinine and a ratio of urinary beta 2-microglobulin to albumin of 0.001.
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PMID:Critical levels of blood and urinary cadmium, urinary beta 2-microglobulin and retinol-binding protein for monitoring cadmium health effects. 130 59

Serum copper, magnesium, zinc, calcium and ionized calcium (Ca++) concentrations were compared in 6 rabbits infected with Trypanosoma brucei brucei and 5 uninfected rabbits. There was a significant depletion of Mg and Zn and a significant increase in Cu from about day 10 of infection to the end. There was no change in plasma total calcium or free diffusible calcium. There was a development of kidney damage as shown clinically by proteinuria and urinary loss of magnesium and zinc, and histologically by the observation of hypercellularity in the glomeruli and tubular degeneration. Our findings thus indicate that trypanosomiasis causes kidney damage which may be responsible for the depletion of the cations seen in the study. Some of the clinical manifestations associated with African trypanosomiasis such as convulsions, anaemia, electrocardiographic changes and splenomegaly may therefore be related to these cation changes.
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PMID:Cations in body fluids of Trypanosoma brucei in infected rabbits. 208 64

The objective of the work was to evaluate the basic parameters of zinc metabolism, i.e. serum levels and urinary excretion of zinc (Zn) in insulin dependent diabetes. The authors investigated a group of diabetics with normal renal function (DM) and with chronic renal insufficiency as a result of diabetic nephropathy (RIDM). Two control groups were formed by healthy volunteers (C) and non-diabetic subjects with chronic renal insufficiency (RI). In diabetics without impaired renal functions (DM) the Zn serum levels did not differ significantly from controls, urinary excretion was significantly raised. The authors did not reveal a correlation of serum Zn levels with parameters of compensation of diabetes nor with the insulin dose. Urinary Zn output correlated positively with proteinuria and the average blood sugar level during the collection of urine. The authors did not find a correlation with diuresis, fractional water excretion, glycosuria or urea excretion. The fractional Zn clearance in diabetic subjects was significantly raised and correlated with the mean blood sugar level. This finding suggests a decline of the tubular Zn absorption in hyperglycaemia. In diabetics with renal failure (RIDM) the results did not differ from non-diabetics with the same degree of renal insufficiency: serum Zn levels were, as compared with healthy controls, in both groups significantly reduced, the urinary excretion being normal. Thus insulin dependent diabetes nor its metabolic compensation do not influence in a marked way serum Zn levels but lead to higher urinary Zn losses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum levels and urinary excretion of zinc in patients with insulin-dependent diabetes]. 220 24

The effect of proteinuria on urinary zinc and copper excretion was studied in children with nephrotic syndrome (NS). Clearance, fractional excretion, and urinary excretion of zinc and copper were significantly higher in children with relapse of NS than in the same children with remission of NS or in healthy children. A linear correlation was found between proteinuria and urinary zinc and copper excretion in relapse of NS. The results of this study suggest that zinc and copper deficiency in NS may be related also to increased urinary zinc and copper losses.
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PMID:Zinc and copper metabolism in nephrotic syndrome. 224 74

Acute zinc toxicosis from the ingestion of pennies was diagnosed in a dog with Heinz body hemolytic anemia (PCV = 14%), leukocytosis (51,000 cells/ml) with a left shift (3,060 band neutrophils; 37,740 segmented neutrophils) and monocytosis (4,080 cells/ml), azotemia (BUN = 60 mg/dl), bilirubinemia (total bilirubin = 5.3 mg/dl), hypokalemia (3.0 mEq/L), high serum alkaline phosphatase activity (691 U/L), high total plasma solids (8.1 g/dl), hemoglobinuria, and proteinuria. Despite aggressive medical treatment, renal failure ensued, and the dog died of cardiac arrest. The clinical signs, clinical course, and laboratory findings in this dog were similar to what has been reported in other cases of acute zinc toxicosis in dogs, with the exception of a history of generalized seizures and the findings of Heinz bodies. Although a causative relationship between plasma zinc values and Heinz body formation cannot be proven, their association suggests that oxidative damage to erythrocyte hemoglobin and cell membrane proteins may be involved in the pathogenesis of zinc-induced hemolysis.
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PMID:Heinz body hemolytic anemia associated with high plasma zinc concentration in a dog. 226 50

In this study, plasma levels of magnesium, calcium, zinc and copper were simultaneously determined in pregnancies complicated by either abortion, intrauterine growth retardation (IUGR), diabetes or EPH (edema, proteinuria, hypertension) gestosis. The levels of the four cations in non-pregnant women and in healthy, pregnant women were also determined. Compared with controls, a significant decrease in magnesium, with increase of the Ca/Mg ratio, was found in spontaneous abortions, but not when patients had a successful continuation of pregnancy. In EPH gestosis, total calcium was reduced, with a significant decrease of the plasma Ca/Mg ratio. A slight, but significant, increase in plasma zinc was observed in women affected by either diabetes or IUGR, probably as a result of reduced zinc uptake by the fetus. In addition, higher copper levels were found in the pathologies studied, with the exception of missed abortions. The possible role of an altered Ca/Mg ratio homeostasis in relation to gestational pathologies is discussed.
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PMID:Maternal plasma concentrations of magnesium, calcium, zinc and copper in normal and pathological pregnancies. 227 Apr 73

Zinc content of serum, hair and erythrocytes, urinary zinc excretion, zinc clearance (CZn) and the ratio of CZn to creatinine clearance (CCr) (CZn/CCr) were measured in 32 children aged between 2.1 and 14.4 years suffering from idiopathic nephrotic syndrome (INS) without renal failure (CCr greater than 70 ml/min 1.73 m2 body surface area). Nineteen subjects had proteinuria and the remaining 13 were in remission. All children received calcium and vitamin D supplementation while on steroid therapy. There was high dietary zinc and protein intake. The results were compared with those obtained from 19 healthy subjects (aged 2-14 years). Zinc concentration in serum, erythrocytes and urine were measured by a colourimetric method. Proton induced X-ray emission was used to determine zinc content in hair. In patients both with and without proteinuria, the mean contents of serum, hair and erythrocytes were significantly lower than in the control group. The urinary zinc excretion, CZn and CZn/CCr in INS children were significantly higher than in the control group. A positive correlation was found between urinary zinc and protein excretion. In spite of high dietary zinc intake and normal intestinal absorption, children with INS had a zinc deficiency. This was probably caused by an increased urinary zinc loss.
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PMID:Impaired zinc metabolic status in children affected by idiopathic nephrotic syndrome. 233 16

The authors investigated the renal zinc excretion in 33 children with chronic glomerulonephritis, in 30 children with tubulo-interstitial nephritis, 12 children with nephrotic syndrome and 31 children with isolated haematuria. In all groups the Zn clearance was slightly raised, as compared with the control group. The Zn clearance was highly significantly elevated in nephrotic syndrome. The authors correlated the urinary finding (proteinuria, haematuria, leucocyturia) with Zn clearance. Children with a positive urinary finding had a higher Zn clearance than those with a negative finding. There was a close correlation between selective proteinuria and Zn clearance in children with nephrotic syndrome.
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PMID:[Renal excretion of zinc in children with kidney diseases]. 263 52

Prolonged cadmium exposure has been associated with proteinuria, calcuria and loss of calcium from bones in humans. Previous studies have shown that kidney uptake of cadmium in vivo results from proximal tubule absorption of the circulating cadmium metallothionein complex (CdMT), and intracellular release of the Cd2+ ion prior to induction of renal metallothionein. Parenteral administration of CdMT has been found to selectively damage the proximal tubule cell lysosome system with development of a tubular proteinuria pattern similar to that observed under chronic exposure conditions. The present studies also demonstrate a concomitant calcuria but no changes in the excretion of other electrolytes or glucose using this model. These marked changes in renal calcium metabolism occurred in the absence of mitochondrial damage, changes in total, Na/K or Mg-stimulated ATPase activities, renal ATP levels, membrane 45Ca2+ transport or overt tubule cell necrosis during an 8 hour period following CdMT injection. Proteinuria and calcuria were prevented by prior zinc induction of the renal MT pool. Data from these studies indicate that renal proximal tubule cell uptake and degradation of the circulating CdMT complex produces both a marked proteinuria and calcuria. The calcuria does not appear to stem from changes in renal energy metabolism or membrane transport of this element but is probably a secondary result of calcium binding to excreted proteins which are increased in urine to a similar extent. The studies also suggest that zinc status and maintenance of the renal ZnMT pool may play an important role in regulating cadmium-induced renal proteinuria and calcuria by preventing Cd2+ perturbation of the proximal tubule cell lysosome system.
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PMID:Mechanism of cadmium-metallothionein-induced nephrotoxicity: relationship to altered renal calcium metabolism. 282 68


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