Iron in urine

Iron in urine has been determined by Zettner and Mansback 6S) by direct aspiration, and by Devoto 66) following digestion with sulfuric acid and extraction of the iron with a 3.3 % solution of thenoyltrifluoroacetone in MIBK. 

Iron is not normally excreted in urine. But following therapy of iron toxicity with specific chelators, such as desferrioximine, atomic absorption spectrometry [34] and spectrophotometry [56] can be utilized to measure iron in urine. 

Dithiocarbamates are chemically characterized by the presence of metals in the molecule (iron, manganese, zinc, etc.) therefore, the measurement of these metals in urine has been proposed as an alternative approach to monitor exposure. For instance, increased urinary excretion of manganese has been reported in workers exposed to mancozeb (Canossa et al., 1993). Available data are at present insufficient to confirm the possibility of using metals as biomarkers of human exposure to DTC. 

Excretion - The daily loss of iron from urine, sweat, and sloughing of intestinal mucosal cells amounts to approximately 0.5 to 1 mg in healthy men. In menstruating women, approximately 1 to 2 mg is the normal daily loss. 

Mechanism of Action An enzymatic mineral that is an essential component in the formation of Hgb, myoglobin, and enzymes. Promotes effective erythropoiesis and transport and utilization of oxygen (Oj). Therapeutic Effect Prevents iron deficiency. Pharmacokinetics Absorbed in the duodenum and upper jejunum. Ten percent absorbed in patients with normal iron stores increased to 20%-30%in those with inadequate iron stores. Primarily bound to serum transferrin. Excreted in urine, sweat, and sloughing of intestinal mucosa. Half-life 6 hr. 

Iron is transported via transferrin. When body stores of iron are high, ferric iron combines with apoferritin to form ferritin. Ferritin is the protein of iron storage. About 80 percent iron in plasma goes to erythroid marrow. The excretion of iron is minimal. Only little amount of iron is lost by exfoliation of intestinal mucosal cells and trace amount is excreted in urine, sweat and bile. 

There is no mechanism for excretion of iron. Small amounts are lost in the feces by exfoliation of intestinal mucosal cells, and trace amounts are excreted in bile, urine, and sweat. These losses account for no more than 1 mg of iron per day. Because the body s ability to excrete iron is so limited, regulation of iron balance must be achieved by changing intestinal absorption and storage of iron, in response to the body s needs. As noted below, impaired regulation of iron absorption leads to serious pathology. 

Deferoxamine is isolated from Streptomycespilosus. It binds iron avidly but essential trace metals poorly. Furthermore, while competing for loosely bound iron in iron-carrying proteins (hemosiderin and ferritin), it fails to compete for biologically chelated iron, as in microsomal and mitochondrial cytochromes and hemoproteins. Consequently, it is the chelator of choice for iron poisoning (Chapters 33 and 59). Deferoxamine plus hemodialysis may also be useful in the treatment of aluminum toxicity in renal failure. Deferoxamine is poorly absorbed when administered orally and may increase iron absorption when given by this route. It should therefore be administered intramuscularly or, preferably, intravenously. It is believed to be metabolized, but the pathways are unknown. The iron-chelator complex is excreted in the urine, often turning the urine an orange-red color. 

Metal chelate complexes should be excreted rapidly in the faeces or urine with no redistribution of iron from relatively non-toxic sites such as the liver, to more harmful ones such as the heart. Complexes formed intracellularly should not accumulate within cells, but should leave cells freely. In the case of liver cells this should result in significant excretion of iron in the bile. Clearly this biliary iron-chelator complex should not then be reabsorbed from the gut. 

ORIENS — A Solution of Iron in Muriatic Acid. The Ascent, Red Olitet, the Father, Red Vitriol, the Ruby, Husband, Salt of Urine, Sun, Gold and Sulphur, Summer, Tartar, Ashes, Ore, Wine. 

This new fluorometric technique makes the determination of kynurenic acid simpler and that of xanthurenic acid more specific if the ferrous or ferric iron technique is used for the latter, higher results are obtained, probably due to the presence in urine of chelating substances which combine with iron (P8). 3-Hydroxykynurenine is determined by an analogous method (B23). 

Dastych M, Jezek P, Richtrova M. Der Einfluss einer PenidUamintherapie auf die Konzentration von Zink, Kupfer, Eisen, Kalzium und Magnesium in Serum und auf deren Ausscheidung in Urin. [Effect of penicillamine therapy on the concentration of zinc, copper, iron, calcium and magnesium in the serum and their excretion in urine.] Z Gastroenterol 1986 24(3) 157-60. 

Transferrin, fhe iron-transporting protein, occurs in urine at concentrations that are about 15 times lower fhan that of albumin. The protein has a shghtly larger effective molecular radius (around 4.0 run) than albumin (3.6 run). Its detection in fhe urine allows a more sensitive indicator of early glomerular involvement in some nephropathies such as cadmium nephropathy. A strong association has been found between the presence of albumin and transferrin in fhe urine of patients with fhe nephrotic syndrome. In these patients, increased transferrin synthesis is insufficient to compensate for urinary losses and plasma levels are reduced [94]. 

Figure 6, Analytical calibration curves for iron in 1% NaCl reference solutions (O) and in the dilute (D), normal (N)y and concentrated (C) urine samples. See Table IV, The analysis wavelength was 261,2 nm.

Intestinal absorption of is low, ranging from 0.4% to 2.5%, so fecal output is mainly unabsorbed dietary chromium. Absorption is increased marginally by ascorbic acid, amino adds, oxalate, and other dietary factors. After absorption, chromium binds to plasma transferrin with an affinity similar to that of iron. It then concentrates in human liver, spleen, other soft tissue, and bone. Urine chromium output is around 0.2 to 0.3 U,g/day, the amount excreted being to some extent dependent upon intake. Paradoxically, urine output appears to be relatively increased at low dietary levels. Thus 2% is lost in urine at an intake of lOpg/day, but only 0.5% at an intake of 40pg/day. Both running and resistive exercise increases urine chromium excretion. 

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