Urinary iron loss in the nephrotic syndrome—an unusual cause of iron deficiency with a note on urinary copper losses

Brown, E. A.; Sampson, B.; Muller, B; Curtis, J. Randall

doi:10.1136/pgmj.60.700.125

Cited by 33 publications

(18 citation statements)

References 10 publications

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“…Not only urinary erythropoietin excretion but also uri nary loss of trace metals such as iron, zinc and copper has been also suggested to be involved in the etiology of ane mia in NS [20][21][22], However, the possibilities arc unlikely because serum levels of these elements were within nor mal range in the present case.…”

Section: Discussioncontrasting

confidence: 47%

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Ishimitsu

Ono²,

Sugiyama³

et al. 1996

Nephron

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A 62-year-old woman presented with nephrotic syndrome and severe anemia although the renal function was not impaired. Renal biopsy revealed the histology of membranoproliferative glomerulonephritis, and the proteinuria was resistant to steroid therapy. Iron deficiency, bleeding and other causes of anemia were ruled out, however, her serum erythropoietin level was inappropriately low. The anemia was rapidly corrected by administration of recombinant human erythropoietin. It is suggested that inappropriately low erythropoietin level, in part at least, accounts for the anemia in nephrotic syndrome. It is proposed that erythropoietin therapy should be taken into consideration for severe anemia in nephrotic syndrome even when the renal function is not impaired.

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Section: Discussioncontrasting

confidence: 47%

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Ishimitsu

Ono²,

Sugiyama³

et al. 1996

Nephron

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“…It has been reported that urinary copper excretion is significantly correlated with urinary protein excretion in aminonucleoside-induced nephrotic rats (15) and patients with NS (16)(17)(18). However, except for one case of severe proteinuria (33 g/L) due to congenital NS (19), no cases of severe copper and Cp depletion causing severe anemia have been previously reported in the setting of human NS, as the rate of copper excretion via urinary nephrotic excretion [1.0 to 4.0 μmol (15,16)] is less than that of physiological absorption via the small intestine [0.5 to 1.5 mg (7.9 to 23.6 μmol) per day (4)].…”

Section: Discussionmentioning

confidence: 99%

“…However, except for one case of severe proteinuria (33 g/L) due to congenital NS (19), no cases of severe copper and Cp depletion causing severe anemia have been previously reported in the setting of human NS, as the rate of copper excretion via urinary nephrotic excretion [1.0 to 4.0 μmol (15,16)] is less than that of physiological absorption via the small intestine [0.5 to 1.5 mg (7.9 to 23.6 μmol) per day (4)]. It is likely that, in our patient, the copper deficiency-associated bicytopenia was caused primarily by the lack of copper in the long-term TPN therapy and not by the excretion of copper via urinary nephrotic excretion.…”

Section: Discussionmentioning

confidence: 99%

Nephrotic Syndrome and End-stage Kidney Disease Accompanied by Bicytopenia due to Copper Deficiency

et al. 2014

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A 69-year-old man presented with proteinuria and hematuria. He had received total parenteral nutrition for massive small bowel resection. However, due to the iatrogenic lack of trace elements for the next four years, he developed severe copper-deficiency anemia and neutropenia. In addition, his proteinuria and kidney dysfunction worsened concurrently with the development of nephrotic syndrome and end-stage kidney disease. After receiving trace elements, the patient's anemia and neutropenia improved, and the anuria dramatically resolved. Copper-containing enzymes, including ceruloplasmin have an antioxidant activity. In patients with various types of glomerular injuries, the ceruloplasmin expression is known to be increased. Copper deficiency can worsen nephrotic syndrome by decreasing the ceruloplasmin activity, which protects the glomeruli.

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“…Iron is not normally stored in the kidneys in great quantities and is only minimally excreted in urine since most circulating iron is bound to proteins such as the iron-transport protein, transferrin, and iron that does pass into the renal tubules is mostly reabsorbed 55 . Increased levels of iron have been found in the kidney tissue, associated with glomerular lesions 56,57 , and urine 53,58 of human CKD patients compared to humans without renal disease. However, we measured lower concentrations of iron in cat, compared to dog, kidneys and, in both species, in kidneys with CIN compared to those without.…”

Section: Renal Histopathology and Prevalence Of Chronic Interstitial mentioning

confidence: 99%

Renal accumulation of prooxidant mineral elements and CKD in domestic cats

Alborough

Grau‐Roma

Brot

et al. 2020

Sci Rep

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felids have a high incidence of chronic kidney disease (cKD), for which the most common renal lesion is chronic interstitial nephritis (cin). cin can be induced by tissue oxidative stress, which is determined by the cellular balance of pro-and anti-oxidant metabolites. Fish-flavoured foods are more often fed to cats than dogs, and such foods tend to have higher arsenic content. Arsenic is a pro-oxidant metallic element. We propose that renal accumulation of pro-oxidant elements such as arsenic and depletion of anti-oxidant elements such as zinc, underpin the high incidence of cin in domestic cats. total arsenic and other redox-reactive metal elements were measured in kidneys (after acid-digestion) and urine (both by inductively-coupled plasma-mass spectrometry) of domestic cats (kidneys, n = 56; urine, n = 21), domestic dogs (kidneys, n = 54; urine, n = 28) and non-domesticated Scottish Wildcats (kidneys, n = 17). Renal lesions were graded by severity of CIN. In our randomly sampled population, CIN was more prevalent in domestic cat versus domestic dog (51%, n = 32 of 62 cats; 15%, 11 of 70 dogs were positive for cin, respectively). cin was absent from all Scottish wildcats. tissue and urinary (corrected for creatinine) arsenic content was higher in domestic cats, relative to domestic dogs and wildcats. Urine arsenic was higher in domestic cats and dogs with cin. Arsenobetaine, an organic and relatively harmless species of arsenic, was the primary form of arsenic found in pet foods. in summary, the kidneys of domestic cats appear to have greater levels of pro-oxidant trace elements, as compared to dogs and wildcats. Since there was no difference in renal arsenic levels in cats with or without CIN, renal arsenic accumulation does not appear a primary driver of excess CIN in cats. Given clear differences in renal handling of pro vs. anti-oxidant minerals between cats and dogs, further in vivo balance studies are warranted. These may then inform species-specific guidelines for trace element incorporation into commercial diets.Chronic kidney disease (CKD) is commonly diagnosed in domestic cats, with a reported prevalence of 1-3% in the overall domestic cat population 1 . One study reported prevalence as high as 50% and 80% in cats of all ages and aged over 15 years, respectively 2 . This contrasts to a reported prevalence of <1% in all dogs 3 and only 10% in dogs over 15 years of age 1 . CKD is defined as the irreversible loss of structure and/or function of one or both kidneys that results from a progressive process occurring over a period of 3 months or more 1 . CKD has various aetiologies, but mononuclear cell tubulointerstitial nephritis -inflammation of the interstitial cells surrounding tubules, predominantly proximal -together with interstitial fibrosis and tubular atrophy is the common histopathological finding in most cases of CKD in cats 4,5 and dogs 6 .Renal tubular epithelial cells are highly metabolically active with high mitochondrial density in order to support oxidative phosphorylation and energy-depe...

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Urinary iron loss in the nephrotic syndrome—an unusual cause of iron deficiency with a note on urinary copper losses

Cited by 33 publications

References 10 publications

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Successful Erythropoietin Treatment for Severe Anemia in Nephrotic Syndrome without Renal Dysfunction

Nephrotic Syndrome and End-stage Kidney Disease Accompanied by Bicytopenia due to Copper Deficiency

Renal accumulation of prooxidant mineral elements and CKD in domestic cats

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