IRON ACCUMULATION IN HUMAN CHRONIC RENAL-DISEASE
IRON ACCUMULATION IN HUMAN CHRONIC RENAL-DISEASE
复制标题
DOI:
10.1016/s0272-6386(12)70222-6
复制
发表时间:
1992-12-01
影响因子:
13.2
通讯作者:
HARRIS, DCH
中科院分区:
文献类型:
--
作者:
NANKIVELL, BJ;BOADLE, RA;HARRIS, DCH
Iron, which has been shown to accumulate within proximal tubule lysosomes in proteinuric models of renal disease, may play a role in the progression of chronic renal disease by the generation of reactive oxygen species. Therefore, renal biopsies from humans with proteinuria and/or chronic renal failure were examined at an ultrastructural level for iron by energy dispersive analysis and compared with normal biopsies. Iron accumulated in proximal tubular lysosomes in renal disease (P< 0.05vnormals), accompanied in some cases by phosphorus and silicon. Both the number of iron-containing lysosomes per tubular cross-section (1.86 ± 0.41v0.66 ± 0.22,P< 0.05) and the mean concentration of lysosomal iron (254.5 ± 73.4 mg/dLv81.2 ± 23.8,P< 0.001) was greater in patients with nephrotic syndrome (n = 12) than in those without (n = 8). Iron accumulation (number of iron-containing lysosomes/tubule) correlated with protein excretion (r= 0.68,P= 0.003, n = 20), but not with glomerular filtration rate. Damaged tubules contained greater amounts of iron than tubules with less damage (288.5 ± 68.5 mg/dLv80.4 ± 13.9,P< 0.01). Further studies are needed to define the possible role of iron in causing tubular damage and progression of renal disease.