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 tubulo- interstitial reabsorption (one patient with glomerulopathy and restricted tubulo-interstitial reabsorption). The re- stricted 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 prog- nostic 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 degra- dation, oxidation, phosphorylation, or nonenzymatic gly- cation. 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. References 1. Dierkes J, Domro ¨se U, Westphal S, Ambrosch A, Bosselmann HP. Cardiac troponin T predicts mortality in patients with end-stage renal disease. Circulation 2000;102:1964 –9. 2. Ooi DS, Zimmermann D, Graham J, Wells GA. Cardiac troponin T predicts long-term outcomes in hemodialysis patients. Clin Chem 2001;47:412–7. 3. Wu AHB, Feng YJ, Moore R, Apple FS, McPherson PH, Buechler KF, et al. Characterization of cardiac troponin subunit release into serum after acute myocardial infarction and comparison of assays for troponin T and I. American Association for Clinical Chemistry Subcommittee on cTnI Stan- dardization. Clin Chem 1998;44:1198 –208. 4. Gerhardt W, Jjungdahl L. Troponin T: a sensitive and specific diagnostic and prognostic marker of myocardia damage. Clin Chim Acta 1998;272:47–57. 5. Richiutti V, Voss EM, Ney A, Odland M, Anderson PAW, Apple FS. Cardiac troponin T isoforms expressed in renal diseased skeletal muscle will not cause false-positive results by the second generation cardiac troponin T assay by Boehringer Mannheim. Clin Chem 1998;44:1919 –24. 6. Hofmann W, Guder WG. A diagnostic programme for quantitative analysis of proteinuria. J Clin Chem Clin Biochem 1989;27:589 – 600. 7. Apple FS, Wu AHB. Myocardial infarction redefined: role of cardiac troponin testing. Clin Chem 2001;47:377–9. 8. Thygesen K, Alpert JS, Antman E, Bassand JP. Myocardial infarction rede- fined—a consensus document of the Joint European Society of Cardiology/ American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959 – 69. 9. Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976;16:31– 41. 10. Weber MH, Scholz P, Stibbe W, Scheler F. -1-Mikroglobulin in urin und serum bei proteinurie und niereninsuffizienz. Klin Wochenschr 1991;63: 711–7. 11. Aviles RJ, Askari AT, Lindahl B, Wallentin L, Jia G, Ohman EM, et al. Troponin T levels in patients with acute coronary syndrome, with or without renal dysfunction. N Engl J Med 2002;27:2047–52. 12. Ellis K, Dreisbach AW, Lertora JJL. Plasma elimination of cardiac troponin I In end-stage renal disease. South Med J 2001;94:993– 6. 13. Hannemann-Pohl K, Glo ¨er G, Kampf SG. Myoglobin: diagnosis of acute myocardial infarction and check of successful reopening during lysis ther- apy. J Lab Med 1996;20:16 –28. Cell-free Fetal DNA in Maternal Circulation after Am- niocentesis, Osamu Samura, * Norio Miharu, Maki Hyodo, Hiroshi Honda, Yoko Ohashi, Nao Honda, Tetsuaki Hara, and Koso Ohama (Department of Obstetrics and Gynecology, Hiroshima University Faculty of Medicine, 1-2-3 Kasumi Minami-ku, Hiroshima 734-8551, Japan; * author for cor- respondence: fax 81-82-257-5264, e-mail osamura@ hiroshima-u.ac.jp) After amniocentesis, 5–20% of patients have evidence of fetal-maternal hemorrhage as indicated by increases in maternal serum -fetoprotein (1–5 ) or by the Betke– Kleihauer test (6–8). The Betke–Kleihauer test can differ- entiate fetal from maternal erythrocytes by the relative resistance of hemoglobin F-containing cells to acid elu- tion, and it is the most popular method of diagnosing and assessing the severity of fetal-maternal hemorrhage (9). The reliability of this test has been questioned, however, because numerous sources of error are associated with it (10 ). These sources of error possibly contribute to the wide variation in the reported incidence of fetal-maternal hemorrhage; a more accurate method of assessing fetal- maternal hemorrhage is therefore required in the clinical setting of rhesus D-negative pregnant women. The discovery of cell-free fetal DNA in maternal serum and plasma has opened a new avenue for noninvasive prenatal diagnosis and has provided a useful marker of complicated pregnancies (11–16 ). The analysis of fetal DNA in maternal serum or plasma has afforded diag- noses of fetal rhesus D status (12 ) and single-gene disor- Clinical Chemistry 49, No. 7, 2003 1193