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)

Mice undergoing prolonged (5 to 8 weeks) immunization with cadium-free feeritin were studied 1 to 32 days following the last ferritin injection. Urine protein was measured and renal tissue examined by light, immunofluorescence, and electron microscopy. Immunized animals developed significant proteinuria and circulating antibody to ferritin.by light microscopy, proetinuric animals had a proliferative glomerular lesion with mesangial hypercellularity and martrix increase, focal and segmental necrosis, fibrin deposits, and occasional crescents. Iron stains revealed prominent mesangial iron deposition. In immunized animals, IgG and C3 deposits were localized mainly in the mesanglium. Electron microscopic studies revealed marked deposition of ferratin complexesexpanded mesangial matrix and mesangial interposition. Ferratin immune complexes were also visualized in epithelial spaces. In the latter location ferritin immune complexes occasionally formed characteristic electron-dense subepithelial deposits. In this model, mesangial and subepithelial localization of autologous ferritin immune complexes is associated with development of glomerulonephritis and characteristic mesangial lesions resembling those seen in some types of human glomerulonephritis.
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PMID:Experimental glomerulonephritis in the mouse associated with mesangial deposition ofautologous ferritin immune complexes. 12 61

Female wistar rats, 170--190 g, were exposed for 90 days to cadmium oxide aerosols containing 25 and 50 microgram Cd/m3 and for 63 days to 100 microgram Cd/m3. Simultaneously female wistar rats, 170--190 g, were fed 25, 50, and 100 ppm cadmium in drinking water for 90 days. After inhalation and ingestion of the metal, there were comparable kidney cadmium levels, but higher liver and blood levels after oral uptake. Coincident with the higher blood cadmium concentrations, proteinuria was observed only after oral administration. Likewise, there was a significant decrease of serum iron after ingestion and no lowering of the serum iron after inhalation of the metal. The inhalation led to a marked dose dependent weight increase of the lungs, which was followed by an impairment of gas exchange. Obviously, after inhalative cadmium uptake of 90 days pulmonary changes precede renal damage.
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PMID:Early signs of oral and inhalative cadmium uptake in rats. 20 65

Acute pulmonary silicoproteinosis, massive proteinuria and fatal renal failure developed in a 23 year old male sandblaster. Examination of the kidney by immunofluorescence revealed granular deposits of immunoglobulin M (IgM) and the third component of complement (C3) along the glomerular basement membrane. Light microscopy disclosed mild proliferative glomerulonephritis with loss of colloidal iron staining for sialoprotein, and electron microscopy disclosed an increased density of epithelial cytoplasm, altered lysosomes and endothelial cell microtubular structures. The silicon content of the kidney was 264 parts per million (ppm), but particles of silicon were not demonstrated by electron microscopy. No primary or systemic causes of renal diseases were elucidated. The renal dysfunction apparently resulted from acute renal silicon toxicity, a new complication of acute pulmonary silicoproteinosis.
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PMID:Massive proteinuria and acute renal failure in a patient with acute silicoproteinosis. 34 91

In order to study the effects of the protein moiety independent of the protein-iron complex in the development of ferritin-induced glomerulonephritis, we compared the effects of ferritin, equimolar amounts of apoferritin, and equimolar amounts of iron dextran in Swiss albino mice. The results were compared to both saline-injected and non-injected controls. Ferritin resulted in a glomerulonephritis associated with predominantly mesangial deposition of immune complexes. Tubulo-interstitial changes occurred as well. Iron dextran resulted in similar but less severe tubulo-interstitial changes and evoked no glomerular alterations. Apoferritin resulted in an immune complex glomerulonephritis usually associated with membranous deposits. No tubular or interstitial changes occurred. Proteinuria developed in animals receiving apoferritin. Since the protein-iron complex caused tubular and interstitial damage, apoferritin may provide a more suitable model of immune-complex-mediated glomerulonephritis.
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PMID:Ferritin- and apoferritin-induced immune complex glomerulonephritis in mice. 49 22

The susceptibility of the heme biosynthetic pathway to lead, as reflected by increased free erythrocyte porphyrin (FEP) concentration, is in humans as well as in rats in the order of young greater than or equal to female greater than male. The difference between adult male and female rats can be explained at least partially by the interaction of estradiol and progesterone with the FEP response to lead; the hormonal influence on FEP does not seem to be mediated through changes in plasma iron. The classical "tubular type" proteinuria in workers chronically exposed to cadmium has two not necessarily concomitant components, namely, a tubular type and a glomerular type component characterized by increased excretion of low and high molecular weight proteins, respectivley. No synergistic effect of cadmium and lead on the proteinuria of workers simultaneously exposed to both metals was observed. Mercury (most likely methylmercury) is freely transferred from the mother to the fetus; there is only a slight placental barrier for lead and a rather strong one for cadmium. Compared to maternal blood, placenta does not accumulate lead or mercury but concentrates cadmium about 10-fold.
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PMID:Investigations of factors influencing exposure and response to lead, mercury, and cadmium in man and in animals. 72 Mar 8

Human infection with Schistosome hematobium is common in the Subsahel region of Ghana. Between January 1987 and July 1988, a study was conducted of all pregnant women attending Bawku District Hospital Antenatal-Clinic (ANC), Bawku/Upper East Region (Subsahel-Savanna), Ghana, with complaints and S. hematobium detected in their urine. Pregnant women received iron and folic acid tablets and tetanus-immunization. The partograms of 500 consecutive deliveries in Bawku Hospital (1600 deliveries/year) in the same period were used to collect data for the control group. To estimate the prevalence of S. hematobium infection in pregnancy in Bawku District, 200 pregnant women with a healthy pregnancy were screened. In 9 cases (4.5%) S. hematobium eggs were found in the urine. In 197 cases, the urine test revealed that 51 had proteinuria, 38 had blood in the urine, and 19 women had proteinuria and hematuria. The values were 22-40% with an average of 30%. The hospital delivery analysis of 500 consecutive partograms of the control group showed an average gestation at delivery of 38 weeks, birth weight of 2.917 kg, birth length of 48 cm, and gravidity of 3.6. 41 pregnant women were infected with S. hematobium. One of them had a double-infection of S. hematobium an S. mansoni. Because of 18 drop-outs, the outcome of the pregnancy in 23 women was followed up to delivery. Preterm (37 weeks) deliveries were 34.8% in this group vs. 23.8% in the control group. The births weights in term deliveries (37 weeks) were not significantly different (3012 g vs. 3103 g). In the preterm deliveries, the birth weight was significantly lower in the infected group (1768 g vs. 2457 g, p0.005). The complaints leading to subsequent diagnosis of infection were in 28 cases dysuria, 17 hematuria, 8 waistpain, and 10 lower abdominal pain. In the hospital deliveries, there was one neonatal death in which case the diagnosis of S. hematobium infection was made at the time of the premature delivery.
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PMID:Schistosoma haematobium infection in pregnancy. 135 2

This study was carried out in rats with nephrotoxic serum nephritis after autologous phase proteinuria was well established to determine the effect of tubule fluid iron chelation on the course of this disease. Deferoxamine administration caused a reduction in urinary iron potentially capable of catalyzing hydroxyl radical (.OH) formation and kidney iron uptake (224 +/- 60 vs. 398 +/- 152 mg/kg). This was associated with a decrease rate of progression of renal failure over the 21-day study period (creatinine clearance -0. 199 +/- 0.152 vs. -0.509 +/- 0.336 ml/min, P < 0.05) and improved survival (8/8 vs. 4/8, P < 0.05). In addition deferoxamine caused a reduction in urinary transferrin excretion (32 +/- 15 vs. 74 +/- 16 mg/day) and fractional excretion of transferrin (2.01 +/- 1 vs. 5.9 +/- 3.7%) and an increase in serum transferrin levels (229 +/- 36 vs. 139 +/- 45 mg/dl, all P < 0.05). It is suggested that iron presented to the tubule fluid as a result of the glomerular leak for transferrin is dissociated from transferrin. In turn the iron is available in a form capable of catalyzing .OH formation, resulting in lipid peroxidation of tubule cell membranes. Deferoxamine chelation of tubule fluid iron retards the development of both tubulointerstitial injury and superimposed glomerular sclerosis in this model of membranous nephropathy.
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PMID:Toxicity of tubule fluid iron in the nephrotic syndrome. 138 59

Iron, which has been shown to accumulate within proximal tubule lysosomes in proteinuric models of renal disease, may play a role in the progression of chronic renal disease by the generation of reactive oxygen species. Therefore, renal biopsies from humans with proteinuria and/or chronic renal failure were examined at an ultrastructural level for iron by energy dispersive analysis and compared with normal biopsies. Iron accumulated in proximal tubular lysosomes in renal disease (P < 0.05 v normals), accompanied in some cases by phosphorus and silicon. Both the number of iron-containing lysosomes per tubular cross-section (1.86 +/- 0.41 v 0.66 +/- 0.22, P < 0.05) and the mean concentration of lysosomal iron (254.5 +/- 73.4 mg/dL v 81.2 +/- 23.8, P < 0.001) was greater in patients with nephrotic syndrome (n = 12) than in those without (n = 8). Iron accumulation (number of iron-containing lysosomes/tubule) correlated with protein excretion (r = 0.68, P = 0.003, n = 20), but not with glomerular filtration rate. Damaged tubules contained greater amounts of iron than tubules with less damage (288.5 +/- 68.5 mg/dL v 80.4 +/- 13.9, P < 0.01). Further studies are needed to define the possible role of iron in causing tubular damage and progression of renal disease.
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PMID:Iron accumulation in human chronic renal disease. 146 86

The relationship between iron status and degree of infection by Schistosoma haematobium was examined in 174 schoolchildren from Niger in an area endemic for urinary schistosomiasis. Iron deficiency was defined by a combination of 3 reliable indicators: a low serum ferritin level combined with a low transferrin saturation, a high erythrocyte protoporphyrin level, or both. Hematuria and proteinuria were seen in 76.4% and 79.9% of the children, respectively, while 95.4% excreted eggs (geometric mean egg count of 31.5 eggs/10 ml of urine). Anemia was seen in 59.7% of the subjects. The prevalence of iron deficiency was 47.1%. Anemia was associated with iron deficiency in 57.7% of the cases. Hemoglobin level and transferrin saturation decreased significantly when the degree of hematuria increased, while prevalence of anemia and iron deficiency increased significantly. The hemoglobin level and hematocrit were negatively correlated with egg count, while anemia prevalence increased with increasing egg count. This inverse relationship between degree of infection by s. haematobium and iron status shows a deleterious consequence of urinary schistosomiasis on nutrition and hematopoietic status, which should be considered in the design of nutrition intervention programs.
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PMID:Consequences of Schistosoma haematobium infection on the iron status of schoolchildren in Niger. 152 42

A single intravenous injection of adriamycin (5 mg/kg) into rats induced nephrotic syndrome. In the various stages of the model, alterations of glomerular fixed anionic charge sites stained with colloidal iron were analyzed quantitatively by image analyzer, which is reported here for the first time. The results showed that there was a significant decrease in glomerular fixed anionic charge sites at 3 hours after administration of adriamycin as compared with the control animals (P less than 0.01). Marked loss of the anionic charge sites preceded the onset of proteinuria and steadily increased along with the progress of the disease. The results suggest that the loss of glomerular fixed anionic charge sites may play an important role in the development of proteinuria in nephrotic syndrome.
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PMID:Changes of glomerular fixed anionic charge sites in adriamycin nephrosis in rats. 171 5


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