Renal Siderosis in Patients with Heart-Valve Prostheses: Clinical Implications

Pardo-Mindan, F. J.; Díez, Javier; Esparza, Noemí; Robledo, Celeste

doi:10.1093/ndt/5.10.847

Cited by 30 publications

(15 citation statements)

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“…In the urine of these patients with renal siderosis, hemosiderin may be found in tubular epithelial cells. Renal siderosis has been documented in patients with heart valve prostheses (12) (as in the current case). Studies show its association with prolonged intravascular hemolysis (13).…”

Section: Discussionsupporting

confidence: 65%

Renal Siderosis in Donor Allograft: Pathologic and Clinical Sequelae

Salim¹,

Asad²,

Kumar

et al. 2004

American Journal of Transplantation

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Transplantation of a cadaver kidney with marked siderosis and its outcome has not been reported. Increasing use of marginal kidneys has become common practice to expand the donor pool to meet the growing demand and will lead to increased recognition of kidney disease in cadaver donors with an unknown effect on graft outcome. This is a case report of a recipient of a cadaver kidney with marked siderosis monitored by surveillance biopsies and evaluated by clinico-pathological correlation. The recipient continued to have transplant kidney function, and a surveillance biopsy shows the natural course of the pathologic resolution of renal siderosis. Case ReportA 73-year-old woman with end stage renal disease, diabetes and hypertension presented for renal transplantation. Available organ was from a 63-year-old man with a medical history of mechanical heart valve replacement for many years (mitral and aortic) and an embolic stroke. The organ had been rejected for transplantation at other centers. Final donor BUN and creatinine values were 27 mg/dL and 1.0 mg/dL, respectively.The kidney was brown in color to the naked eye examination and flushed well with cold University of Wisconsin solution before transplantation. Pathologic evaluation of the graft was performed before transplantation, using Banff 97 (1) schema. An approximate hemosiderin quantitation was performed on Prussian blue-stained sections using the same method originally described by Scheuer et al. (1,2) for the quantitation of hemosiderin in liver biopsies, with grade 0 being negative and grades 1, 2, 3 and 4 representing increasing amounts of stainable hemosiderin. Microscopically, chronic changes of global glomerulosclerosis (10%), fibrosis and arterial sclerosis were noted [ci1, cv1, Banff 97 (1)]. The tubular epithelium showed severe iron overload (4+/4+) ( Figure 1A). The iron was distributed predominantly in the proximal tubular epithelial cells and the absolute level was quantified from paraffin-embedded tissue at 3985 lg/g of dry weight. The organ was utilized for transplantation. Cold ischemic time was 15 h and warm ischemic time was 25 min. The clinical assumption was that the kidney would function in the recipient because it was functioning well in the donor and the iron would slowly be removed from the graft in a recipient who did not have iron overload. The immunosuppression was basiliximab induction, and maintenance with cyclosporine, mycophenolate mofetil and prednisone. The kidney functioned immediately and the recipient did not require dialysis support in the post transplant period. Two months post transplant a biopsy for clinical rejection showed 1A rejection (Banff 97) and decreased iron (3+/4+). The chronic fibrosis, vascular and tubular grades were unchanged since transplantation ( Figure 1B). One-year protocol biopsy showed quantitatively decreased tubular epithelial iron (2+/4), occasional interstitial macrophages containing iron pigment and no rejection. The chronic fibrosis, vascular and tubular grades were unchanged since transplan...

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Section: Discussionsupporting

confidence: 65%

Renal Siderosis in Donor Allograft: Pathologic and Clinical Sequelae

Salim¹,

Asad²,

Kumar

et al. 2004

American Journal of Transplantation

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“…Several, but not all, studies have found an association between high iron burden or increased iron consumption with elevated risk of cardiovascular disease in subjects with or without renal disease [10, 11, 12, 13, 14]. Moreover, iron overload has been linked to the progression of renal disease [15, 16, 17, 18]. …”

Section: Introductionmentioning

confidence: 99%

Iron and Oxidative Stress in Renal Insufficiency

Lim

Vaziri

2004

Am J Nephrol

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Background/Aims: Iron (Fe) can cause tissue injury and oxidative stress by catalyzing hydroxyl radical production and lipid peroxidation. Intravenous (i.v.) Fe preparations are routinely administered to treat anemia in patients with chronic renal failure (CRF), a condition marked by oxidative stress and inflammation. In an earlier study, we showed that iron overload augments oxidative stress in the cardiovascular tissues of CRF rats. This study was designed to expand these observations to other major organs. Methods: Rats were randomized into CRF (5/6 nephrectomized) and sham-operated control (CTL) groups. Each group was subdivided into Fe-loaded (single i.v. injection of iron dextran complex, 0.5 g/kg) and placebo-treated subgroups. After 13 weeks, systolic blood pressure, blood hemoglobin (Hb), plasma Fe concentration, lipid peroxidation products, superoxide generating enzyme, NAD(P)H oxidase, and antioxidant enzymes were determined. Results: Systolic blood pressure was equally elevated and creatinine clearance was equally reduced in both CRF groups. Fe administration raised Hb, serum Fe and transferrin saturation in both CRF and CTL groups. The plasma concentration of lipid peroxidation product, malondialdehyde, was increased by Fe injection in CRF rats but not the control group. Renal tissue abundance of gp91^phox subunit of NAD(P)H oxidase was elevated in the untreated CRF group and was partially reduced in the iron dextran-treated CRF group. Tissue abundance of the antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) were decreased in both untreated and iron dextran-treated CRF groups. Conclusion: CRF resulted in marked SOD, CAT and GPX deficiencies. A single i.v. administration of iron dextran in rats with CRF induced oxidative stress as measured by increased lipid peroxidation products and decreases in antioxidant enzymes.

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“…hronic iron overload is associated with marked iron deposition in the glomeruli and proximal and distal tubules accompanied by glomerular hypercellularity, mesangial expansion, tubular atrophy, and interstitial fibrosis of the kidneys (Landing et al, 1989;Pardo-Mindan et al, 1990;Zhou, et al, 1996). It is now known that approximately 10% of the American population carry the gene for hemochromatosis, and 1% actually suffer from iron overload (Edwards et al, 1991).…”

mentioning

confidence: 99%

Association of Renal Injury with Increased Oxygen Free Radical Activity and Altered Nitric Oxide Metabolism in Chronic Experimental Hemosiderosis

Zhou

Lászik

Wang

et al. 2000

Laboratory Investigation

126

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SUMMARY:Chronic iron (Fe) overload is associated with a marked increase in renal tissue iron content and injury. It is estimated that 10% of the American population carry the gene for hemochromatosis and 1% actually suffer from iron overload. The mechanism of iron overload-associated renal damage has not been fully elucidated. Iron can accelerate lipid peroxidation leading to organelle membrane dysfunction and subsequent cell injury/death. Iron-catalyzed generation of reactive oxygen species (ROS) is responsible for initiating the peroxidatic reaction. We investigated the possible association of oxidative stress and its impact on nitric oxide (NO) metabolism in iron-overload-associated renal injury. Rats were randomized into Fe-loaded (given 0.5 g elemental iron/kg body weight as iron dextran; IV), Fe-depleted (given an iron-free diet for 20 weeks), and control groups. Renal histology, tissue expression of endothelial and inducible nitric oxide synthases (eNOS and iNOS), renal tissue expression of nitrotyrosine, plasma, and renal tissue lipid peroxidation product, malondialdehyde (MDA), and plasma and urinary NO metabolites (NOx) were examined. Iron overload was associated with mild proteinuria, tissue iron deposition together with significant glomerulosclerosis, tubular atrophy, and interstitial fibrosis. Rare focal glomerulosclerosis and tubulointerstitial changes were noted in normal controls. No renal lesions were observed in Fe-depleted rats. Iron deposits were seen in glomeruli, proximal tubules, and interstitium. The iron staining in the distal tubules was negligible. Both plasma and renal tissue MDA and renal tissue nitrotyrosine were increased significantly in Fe-loaded rats compared with control rats. In contrast, Fe-depleted animals showed a marked reduction in plasma and renal tissue MDA and nitrotyrosine together with significant elevation of urinary NOx excretion. In addition, iron-overload was associated with up-regulation of renal eNOS and iNOS expressions when compared with the control and Fe-depleted rats that showed comparable values. In conclusion, chronic iron overload resulted in iron deposition in the glomeruli and proximal tubules with various renal lesions and evidence of increased ROS activity, enhanced ROS-mediated inactivation, and sequestration of NO and compensatory up-regulation of renal eNOS and iNOS expressions. However, iron depletion was associated with reduced MDA and tissue nitrotyrosine abundance, increased urinary NOx excretion, normal nitric oxide synthase (NOS) expression, and absence of renal injury. These findings point to the possible role of ROS in chronic iron overload-induced renal injury. (Lab Invest 2000, 80:1905-1914.

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Renal Siderosis in Patients with Heart-Valve Prostheses: Clinical Implications

Cited by 30 publications

References 0 publications

Renal Siderosis in Donor Allograft: Pathologic and Clinical Sequelae

Renal Siderosis in Donor Allograft: Pathologic and Clinical Sequelae

Iron and Oxidative Stress in Renal Insufficiency

Association of Renal Injury with Increased Oxygen Free Radical Activity and Altered Nitric Oxide Metabolism in Chronic Experimental Hemosiderosis

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