Urinary iron speciation in nephrotic syndrome

Cooper, M.; Buddington, Bruce; Miller, Norman F.; Alfrey, Allen C.

doi:10.1016/0272-6386(95)90014-4

Cited by 24 publications

(11 citation statements)

References 22 publications

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“…To avoid the toxicity by the oxygen species, iron is usually presented in a nonreactive form as transferrin-bound iron in the blood, or ferritin and hemosiderin in the tissues. In patients with nephrotic syndrome, excess protein excretion, including transferrin excretion into urea, is a serious problem [4]. Transferrin leaked into tubule fluid dissociates iron below at pH 6.0 as in acidic urine [4], and the reactive formed ferric iron consequently induces free radical formation.…”

Section: Discussionmentioning

confidence: 99%

“…In patients with nephrotic syndrome, excess protein excretion, including transferrin excretion into urea, is a serious problem [4]. Transferrin leaked into tubule fluid dissociates iron below at pH 6.0 as in acidic urine [4], and the reactive formed ferric iron consequently induces free radical formation. ICGN mice at the progressing and terminal stages exhibit acidic urine (below pH 6.0; data not shown).…”

Section: Discussionmentioning

confidence: 99%

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Anemia with Chronic Renal Disorder and Disrupted Metabolism of Erythropoietin in ICR-derived Glomerulonephritis (ICGN) Mice

Yamaguchi-Yamada

Manabe

Uchio‐Yamada

et al. 2004

The Journal of Veterinary Medical Science

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ABSTRACT. The ICR-derived glomerulonephritis (ICGN) mouse, a new inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome and notably exhibits proteinuria and hypoproteinemia from the neonatal stage. In chronic renal disorder (CRD), anemia is a major subsequent symptom (renal anemia). The precise cause of renal anemia remains unclear, primarily owing to the lack of appropriate spontaneous animal models for CRD. To establish adequate animal models for anemia with CRD, we examined the hematological-biochemical properties and histopathological characteristics. With the deterioration of renal function, ICGN mice developed a normochromic and normocytic anemia, and exhibited normochromic and microcytic at the terminal stage. The expression of erythropoietin (EPO) mRNA both in the kidneys and liver and the EPO leak into the urine were observed in ICGN mice, indicating a disrupted metabolism of EPO in ICGN mice. In addition, a lack of iron induced by the hemolysis in the spleen and the leak of transferrin into urine as proteinuria aggravated the anemic condition. In conclusion, the ICGN mouse is a good model for anemia with CRD. The ICR-derived glomerulonephritis (ICGN) mouse established in the National Institute of Infectious Diseases (NIID; Tokyo, Japan) is a novel inbred mouse strain with a hereditary nephrotic syndrome of unknown etiology, and considered to be a good model of human idiopathic nephrotic syndrome [13][14][15][16]. Homozygous ICGN mice show proteinuria at a young age, later develop hypoproteinemia, hyperlipidemia, severe anemia and systemic edema, and eventually die as a result of chronic renal disorder (CRD) [15]. Our previous studies [20][21][22][23]25] showed that most of the renal tubules expanded and many kinds of extracellular matrix (ECM) components, both interstitial and basement membrane components, abnormally accumulated in glomeruli and tubulointerstitium of ICGN mouse kidneys. The progress of fibrotic degeneration in ICGN mouse kidneys may be caused by overproduction of ECM components, inhibition of ECM breakdown, and decreased activities of matrix metalloproteinases [22]. Apoptotic cells or proliferating cells were detected only in the kidneys of ICGN mice but not those of normal ICR mice [25]. In the kidneys of ICGN mice, apoptotic cells with large round nuclei were observed only in the tubulointerstitium, and proliferating cells were detected in epithelial cells of distal renal tubules. Age-dependent increases in apoptotic cell and proliferating cell densities were also noted. Such irregular cellular kinetics may cause renal dysfunction in ICGN mice.Anemia with CRD (renal anemia) is a major subsequent symptom in patients with CRD. The hematocrit levels are less than 30% in CRD patients and the condition of renal anemia directly affects their quality of life [8,18]. The lack of appropriate animal models for CRD means that the precise cause of renal anemia is unknown, however, it has been established that the lack of ...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Anemia with Chronic Renal Disorder and Disrupted Metabolism of Erythropoietin in ICR-derived Glomerulonephritis (ICGN) Mice

Yamaguchi-Yamada

Manabe

Uchio‐Yamada

et al. 2004

The Journal of Veterinary Medical Science

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“…Similarly, it has been shown that there is a substantial iron accumulation associated with increased cortical malondialdehyde in proximal tubular cells in the remnant kidney, suggesting ROS generation. The sources of increased iron in the kidney have not been well delineated, but Alfrey and colleagues (83,84) suggested that urinary transferrin provides a potential source of iron.…”

Section: Role Of Oxidants and Iron In Progressive Kidney Diseasementioning

confidence: 99%

Oxidants in Chronic Kidney Disease

Shah

Baliga

Rajapurkar

et al. 2007

Journal of the American Society of Nephrology

239

189

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Chronic kidney disease is a worldwide public health problem that affects approximately 10% of the US adult population and is associated with a high prevalence of cardiovascular disease and high economic cost. Chronic renal insufficiency, once established, tends to progress to end-stage kidney disease, suggesting some common mechanisms for ultimately causing scarring and further nephron loss. This review defines the term reactive oxygen metabolites (ROM), or oxidants, and presents the available experimental evidence in support of the role of oxidants in diabetic and nondiabetic glomerular disease and their role in tubulointerstitial damage that accompanies progression. It concludes by reviewing the limited human data that provide some proof of concept that the observations in experimental models may be relevant to human disease.

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“…Proteinuria, a highly selective urinary loss of proteins other than albumin, including vitamin D-binding protein [1] and transferrin, has been documented [2,3]. In addition to transferrin, free iron is also lost in the active state as seen in experimental nephrotic syndrome [4]. Anemia is a feature of chronic nephrotic syndrome in adults and children, which can be partially explained by a deficiency of erythropoietin.…”

Section: Introductionmentioning

confidence: 99%

Serum erythropoietin and transferrin in children with idiopathic nephrotic syndrome

Wang

Fan

et al. 2008

Front. Med. China

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Idiopathic nephrotic syndrome (INS) is characterized by marked urinary excretion of albumin and other intermediate-sized plasma proteins, such as transferrin and vitamin D-binding protein. Some cases even develop anemia. The aim of this study was to investigate the changes in serum iron, transferrin, and erythropoietin, and the relationships between serum and urine transferrin and erythropoietin. Thirty-seven children with INS and 35 age-and sex-matched healthy children were investigated. The indexes related to iron metabolism, including serum iron, ferritin, transferrin, total iron-binding capacity (TIBC), transferrin saturation, and hematological parameters [hemoglobin (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH)], and urinary transferrin and erythropoietin were measured in 37 children with INS before treatment and at the remission stage. Thirty-five age-and sex-matched healthy children served as controls. Serum iron levels (18.8 ¡ 3.8) mmol/L in INS patients before treatment were significantly lower than those of the healthy controls (22.2 ¡ 3.8) mmol/L and those measured at the remission stage (21.0 ¡ 3.5) mmol/L (all P , 001). Serum transferrin levels in INS patients before therapy (1.9 ¡ 0.3) g/L also decreased compared with the healthy controls (3.1 ¡ 0.5) g/L and the measures at the remission stage (2.9 ¡ 0.6) g/L (all P , 0.01). In contrast, serum TIBC and transferrin saturation were significantly higher in INS patients before treatment than in the healthy controls [TIBC (56.4 ¡ 9.2) mmol/L vs (50.7 ¡ 6.8) mmol/L, P , 0.01; transferrin saturation (55.7¡9.2)% vs (46.4 ¡ 8.2)%, P , 0.01] and they were also higher than the measures at remission stage [(51.9 ¡ 7.7) mmol/L and (47.4 ¡ 13.3) mmol/L] (all P , 0.01). Serum transferrin was positively correlated with serum albumin (r 5 0.609, P , 0.01) and negatively correlated with urinary transferrin (r 5 20.550, P , 0.01) in INS patients before treatment. We conclude that serum iron, transferrin and erythropoietin levels are markedly decreased in INS patients, which may be partially related to the urinary loss of these indexes.

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Urinary iron speciation in nephrotic syndrome

Cited by 24 publications

References 22 publications

Anemia with Chronic Renal Disorder and Disrupted Metabolism of Erythropoietin in ICR-derived Glomerulonephritis (ICGN) Mice

Anemia with Chronic Renal Disorder and Disrupted Metabolism of Erythropoietin in ICR-derived Glomerulonephritis (ICGN) Mice

Oxidants in Chronic Kidney Disease

Serum erythropoietin and transferrin in children with idiopathic nephrotic syndrome

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