Urinary albumin, transferrin and iron excretion in diabetic patients

Abstract

The present study was undertaken to determine urinary and serum iron, transferrin and albumin levels in diabetic patients with varying amounts of proteinuria. A highly significant correlation was found between urinary albumin and transferrin excretion over a wide range of urinary albumin excretion (0.005 to 18 g/g creatinine) (r = 0.972). The urine/serum ratio of transferrin and albumin were identical, documenting a similar glomerular leak and tubule handling for these two proteins. In contrast to the above correlation between transferrin and albumin, there was no correlation between iron and either of these proteins until nephrotic range proteinuria had occurred, and even at that time the correlation was much weaker than that found between the proteins (r = 0.680). Urinary iron excretion increased early in the course of diabetic renal disease, being increased in 3 of 11 patients without proteinuria and in 8 of 10 patients with mild proteinuria. All patients with nephrotic range proteinuria had markedly increased urinary iron excretion (150 +/- 166 micrograms/g creatinine vs. 6.4 +/- 0.7 micrograms/g creatinine in controls) and decreased serum iron levels (592 +/- 189 micrograms/liter vs. 979 +/- 394 micrograms/liter in the control group). The iron/transferrin ratio in urine was consistently greater than the iron/transferrin ratio in plasma at all stages of proteinuria. In patients with both subnephrotic and nephrotic range proteinuria, approximately 35 to 40 micrograms Fe/g creatinine was present in the urine with an excess of transferrin. In conclusion, urinary iron excretion is increased early in the course of diabetic renal disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Siderophore vaccine conjugates protect against uropathogenicEscherichia coliurinary tract infection

“…The mammalian host limits intracellular and freely circulating iron by sequestering iron in proteins such as lactoferrin, transferrin, ferritin, and hemoglobin (31). Notably, the primary site of UPEC infection, the bladder, has lower iron levels than serum (32). Thus, it is not surprising that over 14 gene clusters implicated in iron acquisition have been identified as important virulence factors in UPEC strains (33)(34)(35)(36)(37); these gene clusters encode up to four siderophore biosynthesis and uptake systems as well as receptors for the acquisition of heme, ferric citrate, and ferrous iron.…”

The Role of Iron in Diabetes and Its Complications

“…Oxidative stress from factors such as hyperglycemia, advanced glycation end products, and hyperlipidemia further contribute to the availability of intracellular iron that can generate and viciously worsen oxidative stress and renal damage. Iron content in the kidney has been shown to be increased in an animal model of diabetes (84), and urinary iron excretion is increased early in the course of diabetic renal disease in humans (83,85). There is considerable evidence that, once renal insufficiency develops, regardless of etiology, it tends to progress over time.…”

Protein Overload Activates Proximal Tubular Cells to Release Vasoactive and Inflammatory Mediators

“…Hence, in nephrotoxic serum nephritis the extent of tubulointerstitial injury correlates with iron excretion in the urine [38]. In human proteinuric conditions, such as diabetic nephropathy, iron excretion in the urine is elevated as well, and the activity of lysosomal enzymes in the proximal tubule is enhanced [39]. …”