Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In pharmacologic doses E series prostaglandins attenuate the development of immune complex nephritis. We studied the effect of the dietary prostaglandin precursor linoleic acid on murine apoferritin-induced immune complex glomerulonephritis. High, normal, or low linoleic acid diets were fed to mice for 4 weeks prior to and during the intraperitoneal apoferritin administration. A high linoleic acid diet feeding was associated with less proteinuria, less renal histologic damage, and prevented a rise in serum creatinine. We conclude that linoleic acid has a protective effect on the development of murine apoferritin-induced immune complex nephritis.
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PMID:Effects of dietary linoleic acid enrichment on induction of immune complex nephritis in mice. 315 80

The relationship between hypertension, ferritin-antiferritin mesangial immune injury (FIC), and progressive glomerular damage was studied in hypertensive (8% NaCl chow) Dahl salt-sensitive rats (DS) and in spontaneously hypertensive rats (SHR). The glomeruli of SHR are protected from the increased perfusion pressure that accompanies systemic hypertension by preglomerular vasoconstriction, while the glomeruli of hypertensive DS are not. Blood pressure, serum creatinine levels, urinary protein excretion, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined in 20-week-old SHR and DS with FIC. In addition, half of a group of 20-week-old SHR with FIC were uninephrectomized and progression of glomerular injury was assessed 12 weeks later. Control rats for each of the groups did not receive FIC. Our studies showed that more extensive mesangial expansion and glomerulosclerosis developed in hypertensive DS with FIC than in rats without FIC. Glomerular injury in DS with FIC affected cortical and deep glomeruli. Similarly, hypertensive SHR with FIC had minimal damage in cortical glomeruli. In deep glomeruli of SHR, mesangial expansion was similar to that of DS, but glomerulosclerosis was absent. In SHR, a 50% reduction in renal mass, a maneuver known to decrease preglomerular vasoconstriction, resulted in mesangial expansion similar to that in DS in cortical glomeruli while deep glomeruli developed mesangial expansion as well as glomerulosclerosis. Our results suggest that when hypertension and mesangial immune injury coexist with renal vasodilatation (as occurs in DS with 2 kidneys and in SHR after uninephrectomy), they act synergistically to induce progressive glomerular damage. Similar mechanisms may be operative in hypertensive humans with glomerulonephritis and may condition the rate of progression to renal insufficiency.
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PMID:Role of hypertension in progressive glomerular immune injury. 315 4

One hundred nine 19-year-old female students were surveyed as to academic test marks; salt detection and recognition thresholds; serum cholesterol, serum uric acid, serum cortisol, and other biochemical indices in serum; urinary sodium/creatinine and potassium/creatinine, as well as number of complaints based on the Cornell Medical Index (CMI) and personality based on the Yatabe-Guilford (Y-G) test. The salt recognition threshold showed a high negative correlation with serum uric acid concentration and a slight correlation with CMI complaint number, academic test marks, blood pressure, obesity, and serum cholesterol. The subjects with high salt thresholds had relatively passive personalities. Cholesterol, uric acid, hemoglobin, ferritin, and glucose levels in the serum were higher in the group with higher academic marks. These students also had fewer complaints and more of them were type B individuals based on the Y-G test. They also seemed to be under greater stress. In regression analysis, the partial regression coefficient between academic test marks and serum cholesterol was 60 percent higher than that between academic test marks and serum uric acid. Students who lived on campus had 24.8 milligrams per deciliter (15.7 percent) more serum cholesterol and 3.8 micrograms per deciliter (37.7 percent) more serum cortisol than those who commuted from home.
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PMID:An epidemiologic study on the correlation between salt threshold, academic test marks, biochemical data, number of complaints, and personality in women college students. 345 2

Ninety-four per cent of 169 patients with cerebral malaria developed anaemia (haematocrit less than 35 per cent) and 30 per cent required blood transfusion to maintain the haematocrit at more than 21 per cent. Anaemia was at its worst on admission in 58 patients (34 per cent); in the rest the haematocrit fell further, reaching its nadir one to 17 days later (mean 2.3 days). The mean lowest haematocrit was 24.3 +/- 7.2 per cent (+/- 1 SD) and the mean maximum fall was 7.9 +/- 5.6 per cent. Anaemia was more severe in patients with bacterial infection, retinal haemorrhages, schizontaemia and in pregnancy. The lowest haematocrit correlated with admission parasitaemia (r = -0.33, p less than 0.001), total serum bilirubin (r = -0.25, p less than 0.01) and serum creatinine (r = -0.22, p less than 0.01). In 23 patients with uncomplicated falciparum malaria the mean serum iron on admission was 53 micrograms/dl (range 16-157) and the mean serum ferritin 1773 ng/ml (range 170-10 000). There was a significant (p less than 0.001) rise in serum iron 96 h after starting antimalarial treatment; the serum ferritin declined slowly over several weeks. Stainable iron was present in all marrows examined and in eight patients the characteristic pattern of the anaemia of chronic disorders was seen. Seventy-three per cent of patients had dyserythropoiesis which was moderate to gross in 36 per cent. Dyserythropoiesis and erythrophagocytosis were often present on admission but sometimes appeared after the parasitaemia had cleared and persisted for at least three weeks into convalescence. These disturbances in iron metabolism and haemopoiesis are not completely explicable by red blood cell parasitisation. They may contribute more to the anaemia than has previously been recognised.
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PMID:The importance of anaemia in cerebral and uncomplicated falciparum malaria: role of complications, dyserythropoiesis and iron sequestration. 352 85

To study the nephropathy associated with sickle-cell disease (SCD), spin-echo magnetic resonance (MR) imaging of the kidneys was performed in 19 SCD patients, six with beta-thalassemia major (BTM), and ten healthy individuals as controls. Eleven SCD patients had decreased relative cortical signal, most evident on T2-weighted images. No correlation with serum ferritin, urine-concentrating ability, serum blood urea nitrogen, or creatinine levels was established. Iron deposition in the renal cortices of sickle-cell nephropathy patients may, at least in part, be responsible for the relatively diminished cortical signal intensity. No BTM patients, all of whom were clinically and biochemically in iron overload from frequent transfusions, demonstrated diminished renal cortical signal intensity. This suggests that renal changes in SCD seen on MR images are not due simply to systemic iron overload per se but perhaps reflect abnormalities of iron metabolism in the renal cortex peculiar to SCD nephropathy.
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PMID:Sickle-cell nephropathy: MR imaging. 394 63

In 76 patients with clinically well defined multiple myeloma (median age at diagnosis: 68.5 years) serum-ferritin (SF) and beta 2-microglobulin (beta 2M) were measured by RIA-methods. 70 sex and age-matched healthy individuals served as controls. Both serum-ferritin (median: 343 micrograms/l vs. 193 micrograms/l; p less than 10(-7)) and beta 2M (median: 4.25 mg/l vs. 3.5 mg/l; p less than 0.01) showed a significant increase in myeloma patients compared to controls. Intercorrelation analysis revealed significant correlations between SF and tumour mass, serum-creatinine and beta 2M and between beta 2M and tumour mass, percentage of plasma cell infiltration in bone marrow, agglutinin titer, serum-creatinine, hemoglobin and age of the patients. Both tumour proteins might gain clinical importance particularly in those patients in which precise monitoring of disease is impossible either due to lack of paraprotein production or due to the particular paraprotein type. This seems to account for patients with light chain paraproteins, and furthermore for those patients with biclonal gammopathies or with IgE- and/or IgD-paraproteins.
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PMID:[Serum ferritin and beta-2-microglobulin in multiple myeloma]. 618 72

In 76 patients with clinically well-defined multiple myeloma (median age at diagnosis: 68.5 years), serum ferritin (SF) and beta 2-microglobulin (beta 2M) were measured by RIA methods. Seventy sex- and age-matched healthy individuals served as controls. Both serum ferritin (median: 343 vs 193 micrograms/liter; P less than 10(-7] and beta 2M (median: 4.25 vs 3.5 mg/liter) showed a significant increase (P less than 0.05) in myeloma patients compared to controls. Intercorrelation analysis revealed significant correlations between SF and tumor mass, serum creatinine, and beta 2M, and between beta 2M and tumor mass, percentage of plasma cell infiltration in bone marrow, agglutinine titers, serum creatinine, hemoglobin, and age of the patients. Both tumor proteins might gain clinical importance particularly in those patients in which precise monitoring of disease is impossible either due to lack of paraprotein production or due to the particular paraprotein type. This seems to account for patients with light chain paraproteins, and for those patients with biclonal gammopathies or with IgE and/or IgD paraproteins.
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PMID:Serum ferritin and beta 2-microglobulin in patients with multiple myeloma. 619 21

Hypertension frequently accompanies chronic glomerulonephritis. Mesangial injury and glomerulosclerosis are common in glomerulonephritis and are often harbingers of progressive glomerular destruction. Thus, in a model of mesangial immune injury we studied the relationship between hypertension, mesangial injury, and glomerulosclerosis. We induced mesangial ferritin-antiferritin immune complex disease (FIC) in Dahl salt-sensitive (S) and salt-resistant (R) rats. S and R rats with FIC were fed chow containing 0.3% NaCl until 14 weeks of age and then switched to 8.0% NaCl chow until 28 weeks of age. Groups of control S and R rats (no FIC) were either fed 0.3% NaCl for 28 weeks or switched to 8.0% NaCl chow at 14 weeks of age. Blood pressure, serum creatinine, urinary protein, and glomerular injury (assessed by semiquantitative morphometric analysis) were determined at 14 and 28 weeks of age. R rats with or without FIC did not develop hypertension; mesangial injury was minimal. At 14 weeks of age, only S FIC rats developed hypertension, proteinuria, significant mesangial expansion and early glomerulosclerosis. At 28 weeks of age, proteinuria, mesangial expansion, and glomerulosclerosis were significantly more severe in hypertensive S rats with FIC than in those without FIC. These studies show that despite a normal salt intake, mesangial injury hastened the onset of hypertension, but only in rats genetically predisposed to hypertension (S FIC at 14 weeks). High dietary salt further aggravated hypertension, which, in turn, magnified both mesangial injury and glomerulosclerosis. Clinically, the different rates of progression of human glomerulonephritis associated with hypertension may be in part dependent on similar mechanisms.
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PMID:Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats. 623 58

Forty-three spinal cord injured patients with endstage renal disease (ESRD) maintained on hemodialysis were studied. The most prevalent renal lesions consisted of chronic pyelonephritis and amyloidosis while the main renal functional features included nephrotic range proteinuria, high urine output and relatively low serum creatinine for the degree of renal insufficiency. Normocytic, normochromic anemia with low reticulocyte response, low serum iron and iron binding capacity and high transfusion requirement and serum ferritin were noted. Various cardiovascular, pulmonary and gastrointestinal abnormalities were found with considerable frequencies. The incidence of amyloidosis was much higher than that reported previously. This is thought to be due to continued progression of amyloidosis occasioned by longer survival in the present series.
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PMID:Clinicopathological characteristics of dialysis patients with spinal cord injury. 688 88

The mesangial egress, but not the uptake of radiolabeled aggregated human immunoglobulin G (AHIgG125I) (macromolecular proteins biologically akin to immune complexes), deviated markedly from normal in rats with preexisting ferritin-antiferritin immune complexes in the mesangium. Sprague-Dawley rats, given daily intraperitoneal ferritin, 8 mg. per 100 gm. of body weight, for 6 weeks (Ferritin rats), uniformly developed intense mesangial staining for IgG and C3 by immunofluorescence microscopy but minimal glomerular proliferation by light microscopy. With electron microscopy, ferritin was seen in mesangial channels and also in mesangial cells. These rats had normal serum creatinine, no hematuria or proteinuria. AHIgG125I, 50 mg. per 100 gm of body weight, was given intravenously to control and to Ferritin rats; groups of five control and five Ferritin rats were sacrificed at 2, 4, 8, 16, and 24 hours after injection. AHIgG125I was measured in preparations of isolated glomeruli and compared with simultaneous spleen, liver, and blood levels. At all time intervals, blood levels of > 7 S AHIgG125I were similar in control and Ferritin rats. Initial, 2-hour mesangial uptake of AHIgG125I was similar in control and Ferritin rats. During the 2- to 16-hour interval, the disappearance of AHIgG125I from glomeruli of Ferritin rats was delayed; glomerular AHIgG125I concentration decreased 85 per cent in control but only 38 per cent in Ferritin rats. After the administration of AHIgG125I, hematuria (2 to 3+) developed in 60 per cent of Ferritin rats but not in control rats. These studies suggest that immune complexes of different antigen-antibody systems may influence the kinetics of each other locally, at the glomerular level. This impaired mesangial clearance of immune complexes may favor the development of glomerular injury. The experimental model described may be relevant to some forms of human glomerulonephritis in which mesangial pathology and immunopathology are characteristic, and may explain some of the pathogenetic mechanisms operative in these diseases in man.
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PMID:Impaired mesangial clearance of macromolecules in rats with chronic mesangial ferritin-antiferritin immune complex deposition. 744 26


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