Cell-free Fetal DNA in Maternal Circulation after Am-

the exception of one patient), albumin, and 1M. 1M dominated in comparison with albumin, so that the renal function of these patients was rated as restricted tubulointerstitial reabsorption (one patient with glomerulopathy and restricted tubulo-interstitial reabsorption). The restricted tubular reabsorption may lead to the appearance of cTnT and cTnI in urine. Restricted tubular reabsorption may occur as a result of tubulus ischemic damage or an overload of the tubular reabsorption capacity. A decrease in the glomerular filtration rate to 70 mL/min will cause an overload of the tubular reabsorption capacity for 1M (10 ), and the 1M concentration in the plasma will increase with increasingly restricted filtration. Group C patients presented with massive, combined glomerular and tubular renal damage (albumin 638 mg/g of creatinine and 1M 895 mg/g of creatinine). We found cTnT in the plasma and urine of all eight of the patients, but we found cTnI, at very low concentrations, in the plasma of only two cases, and no cTnI in the urine of any of the cases. The calculated protein ratios in urine and plasma (Fig. 1D) considered the initial plasma concentration of the proteins, and a direct comparison between the troponin ratios with 1M and albumin ratios was possible. The 1M and albumin ratios suggested a dependence of the molecular weight and the degree of renal impairment. In group A, troponins were not detectable. In group B, the troponin ratios were in the order of magnitude of 1M and albumin, and the cTnT ratios were higher in group C than in group B. The cTnI ratios for group C could not be calculated because cTnI was not detectable in this group, as is frequently seen in these patients. Although increased cTnT values are an important prognostic factor for cardiovascular disease in hemodialysis patients, the frequently observed differences in the values between cTnT and cTnI are not clear. The lack of cTnI in these patients could be the result of changes in the molecular structure of antigenic regions caused by degradation, oxidation, phosphorylation, or nonenzymatic glycation. On the basis of the demonstrated parallels between the troponin and the 1M and albumin results, we can not exclude an influence of the kidney on troponin kinetics. Usually, a complex of troponin I and troponin C (cTnI-C complex) is the dominant form in blood, but under uremic conditions, the portion of free cTnI could increase and produce alterations in the glomerular filtration compared with cTnT. Other studies could not confirm an influence of kidney function on plasma troponin concentrations (11, 12 ). Hannemann-Pohl et al. (13 ), however, found differences in the plasma concentration of myoglobin in patients with renal failure depending on the degree of renal impairment. On the basis of our data, kidney function seems to contribute to the elimination of troponins.

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