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

The present report describes a rare case of hematophagic histiocytosis associated with acute renal failure. A 32-year-old woman was referred to us from a local hospital because of progressive deterioration of renal function, jaundice and a bleeding tendency. The physical findings at admission revealed hyperemic conjunctivae, gingival bleeding, hepatomegaly, and generalized myalgia. Laboratory data indicated a decrease in platelet count, azotemia and hyperbilirubinemia. Marked elevation of serum triglycerides and ferritin was also noted. Histiocyte proliferation with phagocytosis of erythrocytes and platelets was observed in a bone marrow aspirate. A renal biopsy specimen exhibited lesions generally observed in acute tubular necrosis: degeneration and necrosis of tubular epithelial cells; round cell infiltration and edema in the interstitium; and unremarkable glomeruli. The serum titer to coxsackievirus B1 rose from < 4x at admission to 16x after recovery from the illness, suggesting that this virus may have been the causal organism of the accompanying infection. The patient's symptoms improved rapidly with supportive therapy, and complete restoration of renal function was achieved in 20 days. The morphological characteristics of the bone marrow aspirate and the clinical course were compatible with hematophagic histiocytosis.
 ...
PMID:A case of hematophagic histiocytosis associated with acute renal failure. 833 3

Cellular content of heme is regulated by heme oxygenase, the rate limiting enzyme in the degradation of heme. Induction of heme oxygenase is a protective response in an in vivo model of heme protein mediated renal injury, the glycerol model of acute renal failure. In addition to heme, heme oxygenase is induced by diverse forms of oxidative stress, the functional significance of which is currently unknown. We examined whether heme oxygenase is induced, and the functional significance of such induction, in two in vivo models of oxidant-induced toxic nephropathy, namely, cisplatin and gentamicin nephropathies; nephrotoxicity in these models is not dependent on the delivery of a burden of heme proteins to the kidney as occurs in the glycerol model. We demonstrate induction of heme oxygenase mRNA and protein in the kidney as early as 6 and 12 hours after a single dose of cisplatin (6 mg/kg i.v.). Pretreatment with tin protoporphyrin, a competitive inhibitor of heme oxygenase, led to higher serum creatinine values on days 3 through 5 and lower inulin clearances on day 5; tin protoporphyrin also exacerbated renal injury in this model. Renal hemodynamics studied at day 2 after cisplatin demonstrate reduced renal blood flow rates, increased renal vascular resistance and increased fractional excretion of sodium in rats treated with tin protoporphyrin. Tin protoporphyrin alone had no significant effect on serum creatinine and renal hemodynamics in rats with intact, disease-free kidneys. We confirmed that tin protoporphyrin prevented the increase in heme oxygenase activity induced by cisplatin. Induction of heme oxygenase by cisplatin was associated with increased kidney heme content and ferritin content.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Induction of heme oxygenase in toxic renal injury: a protective role in cisplatin nephrotoxicity in the rat. 856 92

Considerable attention is directed to a surprising biologic phenomenon wherein tissues exposed to one insult acquire resistance to another. We identify a novel example of acquired resistance to acute renal failure and a mechanism that contributes to such resistance. Nephrotoxic serum, administered to rats 24 h before the induction of glycerol-induced acute renal failure, reduces functional and structural injury that occurs in this model. Since heme oxygenase, the rate-limiting enzyme in heme degradation, protects against heme protein-induced renal injury, we questioned whether induction of heme oxygenase underlies the protection afforded by nephrotoxic serum. Kidney heme oxygenase (HO-1) mRNA was induced 6 h after nephrotoxic serum and renal tubules were identified as the site of expression of heme oxygenase protein. Induction of heme oxygenase was accompanied by increased renal content of ferritin but not by induction of other antioxidant enzymes. Inhibition of heme oxygenase prevented the protection afforded by nephrotoxic serum. Nephrotoxic serum did not protect against ischemic acute renal failure, a model in which heme oxygenase is not induced. Thus, nephrotoxic serum protects against glycerol-induced acute renal failure by inducing heme oxygenase in tubules. This study provides the first demonstration of resistance to tubular injury acquired from glomerular inflammation, uncovers a mechanism for such resistance, and exposes the dialogue that occurs between glomeruli and tubules.
 ...
PMID:Glomerular inflammation induces resistance to tubular injury in the rat. A novel form of acquired, heme oxygenase-dependent resistance to renal injury. 890 34

The mechanisms involved and the potentially useful therapeutic strategies in the prevention of acute renal failure (ARF) are briefly reviewed. Factors mentioned are the role of calcium channel blockers, the antioxidant agents, heme oxygenase induction, and ferritin synthesis; and of substances with hemodynamic actions in ARF; such as endothelin, atrial natriuretic peptide, urodilatin, PAF antagonist, prostaglandins, diuretics, and dopamine. The loss of tubular epithelium polarity, the mechanisms involved in this process, and the usefulness of arginine-glycine-aspartic acid peptide and anti-ICAM antibodies in the prevention of tubular obstruction are also reviewed.
 ...
PMID:Therapeutic strategies in the prevention of acute renal failure. 910 98

Erythropoietin (Epo) is a glycoprotein hormone produced in the kidney in response to hypoxia or anaemia. In acute renal failure (ARF) anaemia also occurs and current opinion is that Epo production is depressed with inappropriately low plasma levels throughout the uraemic phase. Our study was designed to determine the excretion of Epo in patients with ARF. Fifty-nine ventilated patients were studied, 39 with ARF and continuous veno-venous haemofiltration therapy (group 1) and 13 patients with normal renal function who served as a control group (group 2). All patients with ARF were anaemic and needed a mean transfusion of 0.6 units/day. Values for vitamin B12, folic acid, serum iron and ferritin were normal. While patients with normal renal function had Epo values within the normal range, patients with ARF had significantly higher values at the onset of haemofiltration therapy. Mean Epo (mean +/- SEM) values on days 0-2 were 92.6 +/- 11.7 mU/ml in group 1 and 16.5 +/- 6.4 mU/ml in group 2 (p < 0.0002). Epo levels declined in group 1 to 49 +/- 10.5 mU/ml on days 9 and 10 compared to 23 +/- 9.1 mU/ml in group 2 (ns). These values were maintained until the end of the observation period. No differences were seen between oliguric and non-oliguric patients. Our data show that patients with ARF have increased Epo levels at the beginning of the disease with a strong tendency to decrease, suggesting that there might be inadequate Epo levels during the course of acute renal failure.
 ...
PMID:Erythropoietin in patients with acute renal failure and continuous veno-venous haemofiltration. 924 56

After having observed high serum ferritin concentrations in some patients with acute renal failure (ARF) we decided to evaluate serum ferritin and iron levels in patients with acute and chronic renal failure (CRF). The concentrations of BUN, serum creatinine, Hct, Hb, serum iron and serum ferritin were measured in 47 patients with renal failure who were divided into two groups (A and B). Group A included 24 patients with ARF (19 M, 5 F) and group B 23 patients with CRF (12 M, 11 F). The diagnosis of ARF or CRF was based on patients' history and clinical examination and confirmed by the standard laboratory findings and the subsequent clinical outcome. None of the patients had received iron, blood transfusions or erythropoietin during the last six months and none had malignancy or primary liver diseases. As controls were used 20 normal volunteers (group C) and 10 patients with acute infections (group D). Comparing groups A and B we did not found any difference in BUN, creatinine and serum iron levels. However patients in group A had significantly higher serum ferritin levels (1000 +/- 752 vs 90 +/- 56 ng/dl, p = 0.0001), higher Hct (31.8 +/- 4.4 vs 25.3 +/- 4.1%, p = 0.0001) and higher Hb concentrations (10.5 +/- 1.7 vs 8.1 +/- 1.4 g/dl, p = 0.0001). Ferritin levels in patients with ARF were also higher than the corresponding levels of normal controls (group C) (p = 0.0001), but did not differ significantly from those measured in patients with acute infection (group D). We conclude that in patients with acute renal failure serum ferritin levels are increased and do not reflect serum iron levels.
 ...
PMID:Serum ferritin levels are increased in patients with acute renal failure. 984 Mar 26

Acute renal failure (ARF) requiring dialysis occurs in up to 4% of patients after cardiopulmonary bypass (CPB). CPB leads to the generation of intravascular free hemoglobin, resulting in increased endothelial and renal tubular cell free iron, which is associated with renal injury. Conversely, renoprotection is conferred by processes that upregulate heme and iron sequestration pathways, such as ferritin. This study evaluates the influence of free hemoglobin generation during CPB and the capacity to sequester free iron on the occurrence of post-CPB renal insufficiency. Thirty consecutive patients undergoing CPB were enrolled in the study. Serum creatinine, free hemoglobin, and ferritin were measured preoperatively, at the end of bypass, and 24 and 48 h after surgery. Renal injury, as determined by an increase in the serum creatinine of > or =25% (ARF) by 48 h after surgery, occurred in 40% (12 of 30) of patients, and dialysis was necessary in 6.6% (2 of 30). Free hemoglobin levels increased in all patients but did not correlate with postoperative ARF. However, patients with preoperative serum ferritin levels < or =130 microg/L, the median value for the group, had a sixfold greater likelihood of developing ARF compared to patients with levels above this value (P = 0.03). Lower serum ferritin levels appear to be associated with the development of ARF. Serum ferritin levels may signify intravascular as well as endothelial and renal epithelial cell ability to bind free iron generated during CPB-induced hemolysis, and thus may help provide information regarding the risk for ARF.
 ...
PMID:Acute renal failure after cardiopulmonary bypass in related to decreased serum ferritin levels. 1054

Sepsis is often associated with a downward spiral through a spectrum of systemic inflammatory response syndrome (SIRS) culminating in organ failure and death. Here we present a 3-year-old girl with Hemophilus influenzae septic meningitis who developed SIRS and acute renal failure. In the initial stage, the patient showed uremia, cytopenia, disseminated intravascular coagulation, elevation of tissue enzyme and ferritin values, hemophagocytosis and overproduction of nitric oxide. The serum cytokine profile revealed increased levels of soluble interleukin (IL)-2 receptor, IL-6, IL-10 and tumor necrosis factor alpha. The patient responded positively to early and intensive interventions including antibiotics, repeated exchange transfusions, dexamethasone and high-dose gamma-globulin. The above laboratory abnormalities almost normalized with clinical improvement. We consider that SIRS was probably responsible for the sequence of events resulting in renal failure in this case, and suggest that renal failure should be included among the serious complications of SIRS associated with Hemophilus influenzae septic meningitis.
 ...
PMID:Systemic inflammatory response syndrome and acute renal failure associated with Hemophilus influenzae septic meningitis. 1087 2

Study results on acute phase reactants of renal failure patients are controversial. In this study, we enrolled 39 patients and divided them into 2 groups: acute renal failure (ARF), and chronic renal failure (CRF) patients. As opposed to CRF patients, the patients with ARF had higher serum ferritin levels that were independent of anemia parameters and other acute phase reactants.
 ...
PMID:Importance of serum ferritin levels in patients with renal failure. 1218 11

Heme oxygenase (HO) is a cytoprotective enzyme that degrades heme (a potent oxidant) to generate carbon monoxide (a vasodilatory gas that has anti-inflammatory properties), bilirubin (an antioxidant derived from biliverdin), and iron (sequestered by ferritin). Because of the properties of inducible HO (HO-1) and its products, we hypothesized that HO-1 would play an important role in the regulation of cardiovascular function. In this article, we will review the role of HO-1 in the regulation of blood pressure and cardiac function and highlight previous studies from our laboratory using gene deletion and gene overexpression transgenic approaches in mice. These studies will include the investigation of HO-1 in the setting of hypertension (renovascular), hypotension (endotoxemia), and ischemia/reperfusion injury (heart). In a chronic renovascular hypertension model, hypertension, cardiac hypertrophy, acute renal failure, and acute mortality induced by one kidney-one clip surgery were more severe in HO-1-null mice. In addition, HO-1-null mice with endotoxemia had earlier resolution of hypotension, yet the mortality and the incidence of end-organ damage were higher in the absence of HO-1. In contrast, mice with cardiac-specific overexpression of HO-1 had an improvement in cardiac function, smaller myocardial infarctions, and reduced inflammatory and oxidative damage after coronary artery ligation and reperfusion. Taken together, these studies suggest that an absence of HO-1 has detrimental consequences, whereas overexpression of HO-1 plays a protective role in hypoperfusion and ischemia/reperfusion injury.
 ...
PMID:Role of heme oxygenase-1 in the regulation of blood pressure and cardiac function. 1270 67


1 2 3 Next >>