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Lysosomal iron accumulation in diabetic nephropathy
B J Nankivell1, Y C Tay, R A Boadle
1Department of Renal Medicine, Westmead Hospital, Sydney, Australia.
Renal Failure
|January 1, 1994
Summary
Iron accumulates in kidney proximal tubules, contributing to diabetic nephropathy progression. This study found increased iron in lysosomes of diabetic rats and humans, linking it to kidney damage and protein loss.
Area of Science:
- Nephrology
- Cell Biology
- Diabetology
Background:
- Iron accumulation in proximal tubular lysosomes is implicated in renal disease progression.
- Reactive oxygen species generated by iron may exacerbate proteinuric chronic kidney disease.
Purpose of the Study:
- To investigate tubular iron accumulation at an ultrastructural level in diabetic nephropathy models.
- To compare iron levels in proximal tubules of diabetic and nondiabetic rats and humans.
Main Methods:
- Energy dispersive X-ray spectrometry was used to examine tubular iron in streptozotocin (STZ) and BB diabetic rats and humans with diabetic nephropathy.
- Samples were compared to respective nondiabetic controls.
Main Results:
- STZ diabetic rats showed significant iron accumulation in proximal tubular lysosomes compared to controls (p < 0.001).
- Tubular iron correlated with urinary protein and transferrin excretion, and tubular damage (r = 0.55, p < 0.001).
- Humans with diabetic nephropathy exhibited increased lysosomal iron concentration and numbers, correlating with elevated serum creatinine (r = 0.94, p = 0.016).
Conclusions:
- Filtered iron enters proximal tubular lysosomes via the brush-border membrane.
- Iron accumulation plays a role in the tubular damage observed in diabetic nephropathy.