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The Prognostic Value of Troponin T for
Ischemic Events in Chronic Renal
Insufficiency: Implications of the
Diabetes Nephropathy and Dialysis

Bono, Julio O; Aguiar Muñoz, Sebastián;
Novoa, Pablo; De Elías, Rafael; Kiener, Oscar

Nephrology Department of Allende Clinic and Córdoba Hospital;
Coronary Unit and Central Laboratory of Allende Clinic.
Córdoba. Argentina

Introduction: It is still controverter the prognosis value of Troponin T (TNT) in patients with chronic renal insufficiency in dialysis (CRID).
Objective: To analyze the prognosis value of TNT in stable patients with CRID, in general and discriminate between patients with diabetic nephropathy (D) and non diabetic (ND).
Material and Method: it is a prospective study of 76 asymptomatic patients with CRID in our center, 20 D and 56 ND. The basal TNT was determined and the patients were classified in two groups: positive TNT (PT) to values > 0,05 ng/ml and negative TNT (NT) to smaller values. They were controlled 1, 6 and 12 months for Ischemic Events (IE): Mortality, acute MI, refractory angina and heart failure. The TNT values are shown in medium and intercualitic rank (IR).
Results: PT 69.7% and NT 30.3%. 55% of the D patients versus 21.4% ND had PT (P<0.005). The accumulative incidence of IE was 6.6%, 7.9% and 11.8% to 1, 6 and 12 months. After a year, this incidence was 13% and 11.3% in PT and NT respectively (P=0.83); also, it was 20% versus 8.9% in D and ND (P=0.19). There was no difference of IE between PT and NT in D (18% versus 22%), and neither in ND (8% versus 9%). The D patients showed a medium TNT 0.06 ng/ml (RI 0.03-0.14) and the ND 0.01ng/ml (0.01-0.03) (P<0.001)
Conclusion: The basal TNT in CRID patients didn't allow us detect high risk for the development of IE to 1, 6 and 12 months, as well as with D or ND, emphasizing a higher rate of IE among the first group.


   Troponin T (TnT) and troponin I, are proteins that are part of the complex contractile muscle and they are freed to circulation after the myocardial damage. The development of markers based in monoclonals antibodies for the serum detection of TnT at the beginning of the 90's (1-5), was the beginning of a new chapter in the history of the use of xeric markers in the diagnosis of the AMI and the risks stratification in the Acute Coronary Syndrome (ACS) (2,5,7-23).

   To many authors the prognosis benefit would also include patients with chronic renal insufficiency undergoing dialysis (CRID) (24-36), but for other authors, patients CRI show an unspecific elevation of TnT without relation to symptomatic ischemic events during follow-up (37-43). Thus, the incidence and the prognostic value in the elevation of TnT in CRID, independent of the history of the coronary disease, it is still a subject of discussion.

   There is neither consensus about the reasons by which the serum levels of cardiac TnT are found abnormally elevated in these renal patients nor agreement on what phenomenon produces the presence of the false positives. The results of some investigations suggest that dialysis would probably be one of the many reasons in the unspecific elevation of TnT in patients with CRI (26,28,35,44,45).

   On the other hand, CRID patients with diabetes and /or diabetes nephropathy show more frequently values of TnT abnormally elevated than the rest of patients with dialysis, generally related to an effective medium and long term prognosis value (24,28,46-48).

   The objective of this study is to analyze the frequency of the elevated values and the prognostic of TnT in CRID patients - diabetic and non diabetic- and in a group control of diabetic patients with renal failure but without dialysis. Our aim is to make a contribution on the implications of the diabetes nephropathy with and without dialysis and on the usefulness prognosis of cardiac TroponinT.

   In this prospective study we followed 76 patients with chronic renal insufficiency undergoing permanent treatment of dialysis (CRID) at the Nephrology, Dialysis and Renal Transplant Departments of Allende Clinic. 20 patients had diabetes nephropathy (CRID-D) and 56 were non diabetic. (CRID-ND). On the other hand, we formed another group of 25 diabetic patients with CRI without dialysis treatment (CRI-wD-D). All the patients with CRID-D, CRID-ND and CRID-wD-D included were stable and asyntomatic of cardiovascular disease at the moment of recruitment. In dialysis, only those with adequate Kt/V were included.

   All the patients CRID were recruited and evaluated in its baseline in the same month.

   The control group patients with CRI-wD-D belong to a consecutive series of progressive recruitment 3 months after the beginning of the study and all of them were followed for 6 months.

   The determinations of TnT, CK, CK_MB the rest of the routine biochemical's determinations and the oxygen saturations were done before the dialysis session (pre-dialysis).

   The baseline also included the follow up of demographic data, dialysis time, coronary disease and comorbidity backgrounds.

   The quantitative determination of TnT was done by Immunoassays of Electroquimio-luminiscencia (ECLIA, "sandwich technique") for autoanalizer Elecsys 1010/2010 (Boehringer Mannheim). The analytic sensibility was 0.01ng/ml with and analytic interval of 0.01 to 25 ng/ml and dynamic up to 50ng/ml. In this study we use by defect a cutoff >0.05ng/ml in order to consider a positive result ( PR), and a cutoff >0.10ng/ml only for comparatives studies with the bibliography. We used third generation Troponin T STAT (Roche), that is a standardized test with cardiac human TnT.

   We'd like to point out that third generation Troponin T (Troponin T STAT Elecsys) has an excellent correspondence with the second generation and with Enzymun-Test troponin T (CARDIAC T) in the diagnosis of myocardial damage (49). Both generations use the same cardiac monoclonals antibodies, the difference lays in the standard that they have been calibrated. The second generation with isolated TnT of bovine heart (37) and those of third generation with recombinant human TnT.

   Among the End Point and fatal or non fatal Ischemic Events were considered: cardiovascular mortality and sudden death, AMI, unstable angina, recurrent and refractory angina. It does not include as End Point the mortality for other reasons, the stroke or the peripheral vascular disease. In all these cases, the cause of death and the rests IE were followed by cardiologists and clinic professionals who did not have any relation to this study and were disguised so as they would not know the results of TnT.

   The follow up was of a year in patients with CRID and 6 months in patients with CRI-wD-D, with determination of IE in three transversal cuts of time (30 days, 6 months and a year). Among the professionals involved in this study, those involved in the clinical follow up of patients were blind in the TnT value.

   According to the symmetric distribution, the quantitative variables were expressed as mean ± standard deviation or median and IR (intercualitic rank: P 25%-P75%), showing their contrast with Test T or Mann-Whitney test respectively. The distributions of TnT between CRID-D versus CRID-ND versus CRI-wD-D was done with Kruskal-Wallis non parametric Test. The contrast of the proportions was done by Chi square Test with continue correction or Fisher Exact test . All the tests went to two end-lines and an alfa value 5% (P<0.05) was established for statistic significance.

   Among the 76 evaluated patients with CRID, 53 showed TnT <0.05ng/ml (69.7%) and 23 with TnT > 0.05 (30.2%); or 62 with TnT < 0.10 ng/ml (81.6%) and 14 with TnT > 0.10 (18.4%). Table 1 shows the baseline in different attributes according to the TnT category for cut value > 0.05 ng/ml.

   Out of 25 patients CRI-wD-D, 5 patients ( 20%) had a value of TnT >0.05 ng/ml; but this frequency was reduced to 16% if we took a cut of TnT>0.10 ng/ml.

   In 47.8% of those with Positive TnT (PT) and 17% of Negative TnT (NT) the etiology of CRID was diabetes nephropathy (P < 0.005). The PT patients were significantly older (P<0.05), with less triglyceric blood level (P<0.05), less oxygen saturation (P<0.05) and higher CK-mb median (2.6% versus 1.3% in NT; P <0.001). No relation was found among TNT >0.05 ng/ml and sex, dialysis time, cholesterol, blood urea nitrogen, creatinine, hemoglobin rate %, Hypertension, prevalence of previous coronary disease, or average of CK.

   In general, the 20 CRID-D patients were an average of 54.2 ± 15.5 years old ( range 22-80), 51.3% men and 48.7 % women. As far as the 56 patients CRID-ND, the men group turned out to be significantly older (62 ± 11 versus 51.5 ± 16 years old; P < 0.01), with less median time in dialysis (1 versus 3 years; P <0.05), a significant median of basal glycemia (168 versus 81 mg/dl; P <0.001) and a significant medium CK-mb (2.6% versus 1.3%; P <0.001). On the other hand, the CRID-D patients do not differ in the baseline with the control group of CRI-wD-D (Table II), except in TnT values.

   The 55% CRID-D patients against 21.4% of the CRID-ND showed TnT >0.05ng/ml (P<0.005); meanwhile these percentages were 40% and 10.7% respectively to a cut of TnT >0.10 ng/ml (P<0.01). On the other hand, the CRI-wD-D was 20% positive to a TnT >0.05 ng/ml, a significant lower frequency compared to those patients receiving dialysis (versus 55%, P<0.05; Table 2), and 16% to a cut > 0.10ng/ml.

   Patients with CRID-D showed a median TnT of 0.06%ng/ml (IR 0.03-0.14) against 0.01ng/ml (IR 0.01-0.03) in patients with CRID-ND and 0.01 ng/ml (IR 0.01-0.04) in patients with CRI-wD-D. (Kruskal-Wallis P<0.001, Figure 1)

   The accumulated rate of Ischemic Events (IE) was 6.6 % to 30 days, 7.9% to 6 months and 11.8% to a year (n=9) in patients with CRID. Within the first year IE was observed in 6 out of 53 patients NT (11.3%) and in 3 out of 23 PT (13.0%) (P=0.83). This incidence in 30 days was 5.7% and 8.7% (P=1.0) and in six months it was 5.7% and 13% (P=0.36) for NT and PT respectively.

   In CRID-D and CRID-ND, the incidence of IE to 30 days, 6 and 12 months was similar between those who had a TnT <0.05 or TnT >0.05 (Table 3); that is to say that the IE rate was independent of the TnT result in patients undergoing dialysis. In CRID-D patients with PT this rate was 18.2% in 30 days (versus 11.1% in NT, P =1.00) and it was kept without changes along the year, but it went up to a 22.2% in NT. There were no events in patients CRID-ND with PT during the first 30 days (versus 4.5% in NT; P=1.00) , meanwhile it was 8.3% in a year and also without any difference in patients NT (versus 9.1%; P=1.00).

   It is important to emphasize that the rate of IE in patients with dialysis was always higher in CRID-D than in CRID-ND patients although without any significant statistics (15% versus 3.6% in a month P= 0.11; 15% versus 5.4% in 6 months P= 0.18; and 20% versus 8.9 % a year, P= 0,19), probably because of the limited amount of patients.

   On the other side, in the control group CRI-wD-D and comparing with CRID patients, 2 patients out of 5 PT (40%) against 0 patients out of 20 NT (0%) showed some Ischemic Event during 6 months of follow up (P<0.05); and the accumulated rate of IE was 8% (n=2) in 6 months. In diabetic, pre-dialytic patients with CRI and cardiovascularly stable, TnT showed a sensibility of 100% and a specificity of 87% in a limited series and within 6 months of follow up.

   We found a prevalence of 30.2% stable patients with chronic renal insufficiency undergoing dialysis with xeric values >0.05ng/ml of TnT or 18.4% with >0.10 ng/ml. This last prevalence seems to be in the lowest rank mentioned in the bibliography for these patients with third generation of TnT (17%-42%) (45,47,50-53), in a conventional cut point of >0.10 ng/ml (54).

   In diabetic patients with CRI but without dialysis treatment, the prevalence was 20% and 16% in TnT >0.05ng/ml and >0.10 ng/ml respectively, a frequency much lower than the diabetic patients undergoing dialysis (55% and 40% respectively). This particular observation was not found in the bibliography mentioned; however, in general terms, some studies suggest that patients with CRI but without dialysis show TnT elevations less frequently (26, 28, 35, 44, 45), and then we could infer that the dialysis process might be an important reason of that abnormality or interference.

   We point out that the selected patients in our control group were all patients with diabetes nephropathy and a severe CRI and in a pre-dialysis condition ( glomerular filtration below 30ml/minute) ready to be admitted to transplant therapy. On the other hand, the diabetic patients with dialysis after an average of a year (80% with 3 years or less) could be compared in age, coronary disease background, hypertension, basal glycemia values and sex.

   If we assume the similarity between CRID-D and CRI-wD-D groups, then there's no relation with the difference found in the prevalence of elevated values of TnT and even more in the prognostic value of that elevation. In that sense, in patients receiving dialysis (diabetic or not) we could not prove relation between elevated TnT and ischemic events during a long -term follow up (29,44,57-59), meanwhile in those patients without dialysis, TnT showed a high sensibility and specificity at the same cut point to 6 months, similar to the one described in patients without renal failure.

   All this suggests that the dialysis influenced in an objective way the quantitative value and the usefulness prognosis of TnT in our patients, at least, in those ones with diabetes nephropathy.

   The degree in which the dialysis may affect the quantitative value of TnT, it can be estimated after certain observations in patients CRID showing absence of coronary disease, and where an unspecific elevation of TnT between 10% - 20% was evident (37,43). In our diabetic patients, the dialysis would elevate the prevalence of positive TnT from 20% to 55% or from 16% to 40% according to the value of cut considered (0.05 ng/ml or 0.10 ng/ml. emphasizing that such elevation turned out to be apparently unspecific, that is to say, without relation to clinical coronary events, although it could be an expression of a minor myocardial damage, since there are some concrete evidences that the elevated second generation TnT in dialysis is cardiospecific (3,30,56).

   In spite of the fact that the dialysis might be modifying the quantitative value of TnT, this sporadic or persistent increase could also show a significative prognostic value for cardiovascular event or mortality. (24, 26-28, 31-36). However, in these studies the TnT would go on being sensible but less specific in patients without renal failure and taking into consideration that the time of dialysis in these patients is much higher than in our patients.

   In order to avoid or limit the effect of the interference, some authors suggest to elevate the cut point of TnT from 0.10ng/ml to 0.15-0.20 ng/ml (28,50,56); take the values before the dialysis session (8) and/or doing a serial measurement of the marker (45).

   In our case, even by elevating the value of the TnT cut to the conventional >0.10ng/ml in patients with CRID no relation with the cardiac events was found (the data are not shown); however, we have not studied other higher cuts.

   The main cause of morbidity and mortality in patients with CRI seems to be the cardiovascular complications (58), may be due to the close relation with atherosclerosis, and the principal reasons of atherosclerosis in these patients would be diabetes and age (46). Also, our patients CRID-D showed a larger number of events in a year than the CRID-ND patients (20% versus 9%), even though it is not significant because of the limited number of patients. This could suggest that TnT would be useful as a prognostic factor in patients CRID, particularly if they are diabetics (28).

   According to this, the literature says that patients with chronic renal insufficiency undergoing dialysis have a larger frequency of high TnT values in patients with diabetes nephropathy than in those who have nephropathy without diabetes, and in general it is related to the events rate (24,28,46,47). Our patients with diabetes nephropathy receiving dialysis also had higher values than the nondiabetic ones, and then, the frequency of the positive tests were significantly more frequent; yet those elevated values of TnT did not relate to a larger rate of an ischemic event clinically shown.

   Since we do find relation among diabetes nephropathy-TnT- ischemic events in patients CRI but without dialysis; since we assume cardioespecificity of the antibodies of the third generation TnT assay (3, 30, 56), and with the evidence that CRID-D patients show higher values than CRID-ND patients in similar dialysis conditions, we could then conclude that there is an interaction between diabetes nephropathy and the dialysis process in generating a moderate elevation of TnT (average term of 0.06ng/ml) without having a necessary relation to clinical events presented but, at least, as an expression of a chronic minor myocardial damage.

   If we think that the clearance of TnT is interfered in the dialysis process 24 and because of this, we could explain the moderate elevated values without relation to ischemic events, then, this interference would have been the same in patients with CRID-D and CRID-ND.

   In general, the reasons given for the elevation of TnT without relation to myocardial ischemia in chronic renal patients are multiple and still controversial.

   A possible explanation for higher values of TnT in diabetic patients than in the nondiabetic ones without relation to clinical events might be the presence of silent myocardial ischemia, due to an autonomic neuropathy (59). This hypothesis would justify the lack of relation between the moderate elevated values of TnT observed and the absence of evidence of clinical ischemic events. Also, it was established that the more frequent diabetic complications associated to TnT elevation in CRID was the neuropathy (47).

   In the absence of myocardial necrosis and clinical symptoms, a silent ischemia or a minor myocardial damage would probable come out in chronic renal patients, mainly in those that show moderate elevated values of TnT (>0.01 and < 0.10 ng/ml), in close relation to short and repeated episodes of ischemia/ reperfusion. A group of Spanish investigators (60-62), have observed in a canine model how very short ischemia episodes followed by short-term reperfusions -that might be equivalent to silent ischemic episodes- are able to produce stunned myocardial when they are repeated and such process would be reversible. The analysis of the ultraestructure of this tissue, in absence of necrosis, showed damage and mitochondria fusion that predict alterations in the core of the cardiomuscle. This silent ischemia produces an increase among 320% to 571% on the basal value of TnT, and these values in human beings would be the equivalent of a TnT 0.03-0.06ng/ml.

   From another point of view, the common point between the diabetic nephropathy and CRI would be the high concentration of final products of glycosilation (47) and the cause of many diabetic complications (63) and suggested as inductors of genetic expression. We might speculate then, that they induce a genetic expression of TnT in noncardiac cells. The increase of TnT in patients with multiple diabetic complications refers to the greater sensitivity and exposition of the tissues to these products (47).

   We might suggest a genetic re-expression of cardiac TnT isoforms in skeletal muscle associated to necrosis and regeneration (64-68), nevertheless, an obvious clinical miopathy is not common in patients with dialysis treatment (47). But also, a fetal re-expression of TnT in skeletal muscle after the denervation (69) has been described and then it is again suggested the relation between diabetic nephropathy and unspecific increase of TnT.

   The objective presence of cardiac TnT in noncardiac tissues is still a subject that admits discussion. There is evidence that there is not cardiac TnT in skeletal muscles in patients with CRID and with high xeric levels (50). However, Ricchiuti and et al, (30,43,70) detect a second generation of cardiac TnT expression in skeletal muscles biopsies of patients with CRID, though they say that these unspecific isoforms are not simultaneously detected by the two monoclonals antibodies used in second and third generation TnT tests (BM Mabs M11.7 and M7) and thus, the assay of TnT does not suffer alterations and proves to be specific for the adult cardiac muscle.

   According to our results, the TnT in patients with CRID would not show prognostic usefulness for ischemic events either in patients with or without diabetes nephropathy; however, this marker would allow to identify those patients with CRIwD-D who have a high risk of ischemic events within the next 6 months.

We thank to:
English Teacher : Miss Olga Bonetti
Statistic Analysis: Daniel Senestrari MD
Assistant Reachers: Miss Mariella Focaccia


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2nd Virtual Congress of Cardiology

Dr. Florencio Garófalo
Steering Committee
Dr. Raúl Bretal
Scientific Committee
Dr. Armando Pacher
Technical Committee - CETIFAC

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