Cardiac morphology and function in patients with and without residual diuresis on hemodialysis

Araujo, Salustiano; Lemes, Helton P.; Cunha, Danny A.; Queiroz, Vinicius S.; Nascimento, Daniela D.; Ferreira Filho, Sebastião Rodrigues

doi:10.1590/S0101-28002011000100011

Abstracts

In patients with chronic renal failure on hemodialysis, left ventricular hypertrophy is related to the increase in total peripheral vascular resistance and volume overload. The presence of residual diuresis enables greater control of the volemia of these. We evaluated the morpho-functional changes of the left ventricle in patients with chronic kidney disease on hemodyalisis treatment with and without residual diuresis. A total of 31 non diabetic patients were studied and they were divided into two groups: with residual diuresis (RD+) (n = 17) and without residual diuresis (RD-) (n = 14). In both groups, RD+ vs. RD-, using data from a Doppler echocardiogram differences were found, respectively, in the cardiac index (3.9 ± 0.2 vs. 3.0 ± 0.2 L/min/m²; p = 0.0056), systolic index (54 ± 2.9 vs. 45 ± 3.3 mL/b/m²; p = 0.04), end diastolic volume (141 ± 6.7 vs. 112 ± 7.6 mL; p = 0.008), end diastolic diameter (52 ± 0.7 vs. 48 ± 1.1 mm; p = 0.0072) and total peripheral resistance index (1121 ± 56 vs. 1529 ± 111 dyne.sec.cm-5; p = 0.001). RD+ had lower relative wall thickness than RD- (0.38 ± 0.01 vs. 0.45 ± 0.01; p = 0.0008). The ejection fraction and the left ventricular mass index were similar in both groups. The urinary 24-hour volume correlated with the relative wall thickness (r = -0.42; p = 0.0186) and with peripheral resistance index (r = -0.48; p = 0.0059). In conclusion, there were distinct ventricular geometric patterns and different functional performances between RD+ and RD- groups. The presence of residual diuresis can be responsible by these modifications in systolic function.

chronic kidney failure; ventricular remodelling; stroke volume

Em pacientes com doença renal crônica (DRC) em hemodiálise (HD), a hipertrofia ventricular esquerda (HVE) está relacionada ao aumento do índice de resistência vascular periférica (IRVP) total e à sobrecarga de volume. A presença da diurese residual (DR) nesses pacientes possibilita maior controle volêmico. Avaliamos as modificações morfofuncionais do ventrículo esquerdo (VE) em pacientes com DRC em HD com e sem diurese residual. Trinta e um pacientes não diabéticos foram divididos em dois grupos: com diurese residual (DR+) (n = 17) e sem diurese residual (DR-) (n = 14). Em ambos os grupos, DR+ vs. DR-, ocorreram diferenças no índice cardíaco (3,9 ± 0,20 vs. 3,0 ± 0,21 L/min/m²; p = 0,0056), no índice sistólico (54 ± 2,9 vs. 45 ± 3,3 mL/b/m²; p = 0,04), no volume diastólico final (141 ± 6,7 vs. 112 ± 7,6 mL; p = 0,008), no diâmetro diastólico final (52 ± 0,79 vs. 48 ± 1,12 mm; p = 0,0072) e no IRVP total (1.121 ± 56 vs. 1.529 ± 111 dina.seg.cm-5; p = 0,001). O grupo DR+ apresentou menor espessamento relativo de parede (ERP) do que o DR- (0,38 ± 0,01 vs. 0,45 ± 0,01; p = 0,0008). A fração de ejeção (66,00 ± 1,24 vs. 66,0 ± 1,46%; p = 0,873) e o índice de massa ventricular esquerda (132 ± 6,0 vs. 130 ± 8,3 g/m; p = 0,798) foram similares em ambos os grupos. O volume de diurese residual correlacionou-se com o espessamento da parede ventricular (r = 0,42; p = 0,0186) e com o índice de resistência vascular periférica (r = -0,48; p = 0,0059). Em conclusão, a presença ou não da diurese residual, em pacientes com doença renal crônica e em hemodiálise, pode ser responsável por modificações na função cardíaca sistólica.

insuficiência renal crônica; remodelamento ventricular; diurese

ORIGINAL ARTICLE

Universidade Federal de Uberlândia - UFU, Uberlândia, MG, Brasil

Corresponding author

ABSTRACT

In patients with chronic renal failure on hemodialysis, left ventricular hypertrophy is related to the increase in total peripheral vascular resistance and volume overload. The presence of residual diuresis enables greater control of the volemia of these. We evaluated the morpho-functional changes of the left ventricle in patients with chronic kidney disease on hemodyalisis treatment with and without residual diuresis. A total of 31 non diabetic patients were studied and they were divided into two groups: with residual diuresis (RD+) (n = 17) and without residual diuresis (RD-) (n = 14). In both groups, RD+ vs. RD-, using data from a Doppler echocardiogram differences were found, respectively, in the cardiac index (3.9 ± 0.2 vs. 3.0 ± 0.2 L/min/m²; p = 0.0056), systolic index (54 ± 2.9 vs. 45 ± 3.3 mL/b/m²; p = 0.04), end diastolic volume (141 ± 6.7 vs. 112 ± 7.6 mL; p = 0.008), end diastolic diameter (52 ± 0.7 vs. 48 ± 1.1 mm; p = 0.0072) and total peripheral resistance index (1121 ± 56 vs. 1529 ± 111 dyne.sec.cm^-5; p = 0.001). RD+ had lower relative wall thickness than RD- (0.38 ± 0.01 vs. 0.45 ± 0.01; p = 0.0008). The ejection fraction and the left ventricular mass index were similar in both groups. The urinary 24-hour volume correlated with the relative wall thickness (r = -0.42; p = 0.0186) and with peripheral resistance index (r = -0.48; p = 0.0059). In conclusion, there were distinct ventricular geometric patterns and different functional performances between RD+ and RD- groups. The presence of residual diuresis can be responsible by these modifications in systolic function.

Keywords: chronic kidney failure, ventricular remodelling, stroke volume.

INTRODUCTION

Although glomerular filtration rate is rather low in patients with chronic kidney disease (CKD), daily residual diuresis volumes can vary from anuria to polyuria in different individuals. The preservation of residual diuresis (RD) assists in the purification of low-to medium-molecular-weight substances, allowing for even greater liquid removal¹ and improvement of the patient's nutritional state^2,3 and quality of life,⁴ in addition to maintaining the endocrine functions of the kidney.⁵ During the conservative management of patients with CKD,⁶ it was observed that the decline in the glomerular filtration rate was associated with left ventricular hypertrophy (LVH).^7-11 The presence of LVH, in turn, constitutes an important independent factor for cardiovascular risk in patients with CKD.^7,8,12,13 Patients in renal replacement therapy (stage V)⁶ may have larger or smaller residual renal function (RRF) declines depending on the diastolic method used.¹⁴ Thus, patients on hemodialysis (HD) had more rapid reductions in their RRF than those on peritoneal dialysis (PD).^14-17 The progressive reduction in renal function is associated with LVH and greater cardiovascular mortality in PD patients.^12,18,19 In various studies, the presence of LVH was related to hemodialysis treatment;^{9,10,12,20,21} however, few studies have reported a relationship between LVH and the morphological and functional aspects of the left ventricle with different volumes of residual diuresis. Accordingly, the objectives of this study were to verify possible cardiac morphological and functional differences in the left ventricle in patients with or without residual dieresis on chronic hemodialysis treatment.

PATIENTS AND METHODS

PATIENTS/PROTOCOL

This is a cross-sectional study whose patients were recruited in a private hemodialysis clinic. CKD patients who received regular hemodialysis treatment three times a week and agreed to participate in the study met the inclusion criteria. The exclusion criteria were patients in hemodialysis treatment for less than three months, patients with a previous clinical history of cardiovascular disease, diabetic patients and uncontrolled blood pressure. Using the echocardiogram, those patients with an ejection fraction < 55% and with segmental changes in LV contractility were also excluded ^22,23. Thus, two groups were created: RD+ comprised patients with daily residual diuresis > 100 mL/24 hrs (n = 17; 11♂ and 6♀), and RD- comprised patients with daily residual diuresis < 100 mL/24 hrs (n = 14; 9♂ and 5♀) (Table 1). The following clinical and laboratory data of the groups were assessed: systolic arterial pressure (SAP), diastolic arterial pressure (DAP), length of hemodialysis treatment (LHT), urinary 24-hour volume (UV_24hs), hemoglobin (Hb), serum calcium (Ca), parathormone (PTH), serum albumin (Alb) and total peripheral vascular resistance index (TPVRi). This study was previously approved by the Ethics Committee of the Universidade Federal de Uberlândia.

Thumbnail

METHODS

The SAP and DAP were immediately obtained before the HD session using the arm opposite the AV fistula and represented the average of the last ten HD sessions. Mean arterial blood pressure (MAP) was calculated using the formula DAP + (SAP-DAP/3), and the total peripheral vascular resistance index (TPVRi) was calculated using the formula (MAP-CVP/CD) x 80, where CVP is the central venous pressure, which was always considered a zero value (dyne.seg.cm^-5).^24;25 The pressure values were expressed in mmHg. The UV_24hs (mL) was collected during the interdialytic period. Interdialytic weight gain (iWG) represents the difference between body weight immediately after the HD session, and the weight obtained immediately before the next HD session. The iWG value was considered the arithmetic average of the last ten HD sessions. The assessment of adequacy of dialysis was done using the Kt/V index. Kt/V is defined as the dialyzer clearance of urea (K, obtained from the manufacturer in mL/min), multiplied by the duration of the dialysis treatment (t, in minutes) divided by the volume of distribution of urea in the body (V, in mL). Biochemical plasma values were obtained using standardized methods that have been previously described.^26-28 The Doppler echocardiogram used the Acuson-Aspen ^® C2-4 Mhz transducer conducted in the interdialytic period. The exam was performed twenty hours after finishing the hemodialysis session, in the interdialytic period, by an experienced examiner unaware of the protocol. The Doppler echocardiographic variables were analyzed according to the criteria from the American Society of Echocardiography.^22;29-31 For determination of posterior relative wall thickness (RWT) it was used the measurement of posterior wall thickness (PWT) of the left ventricle.^32-35 The following parameters were also evaluated: the ejection fraction (EF), systolic index (SI), cardiac index (CI), end diastolic volume of the left ventricle (EDV), end diastolic diameter of the left ventricle (EDD), interventricular septum thickness (IVS) and left ventricular mass index (LVMi) ^22,24,35. Additionally, the blood flow of the arteriovenous fistula (BF_AV) was assessed with the same echocardiograph equipment.^37;38

STATISTICAL ANALYSIS

For the statistical analysis, we used the GraphPad Prism program, version 5.0, for Windows (GraphPad Software, San Diego California USA). We conducted t-tests and Wilcoxon tests to compare averages between the groups. Values lower than 0.05 were considered significant. The correlation coefficient used was Pearson's correlation coefficient. The data were presented in average ± standard error (Χ ± SE). A multiple regression test was performed when H0: vascular resistance was not a dependent variable of treatment time and/or residual diuresis and/or PTH and/or mean arterial pressure; while H1: vascular resistance was dependent on at least one of those variables cited above. For these calculations, the Bioestat 5.0 was used and alpha error = 0.05 was considered as a decision level.

RESULTS

Clinical and laboratory characteristics of both groups are presented in Tables 1 and 2.

Thumbnail

MORPHOLOGICAL DATA OF THE LEFT VENTRICLE

The relative wall thickness was significantly lower in group RD+ than in group RD- (0.38 ± 0.01 vs. 0.45 ± 0.01; p = 0.0008) (Figure 1). Significant correlations were found between relative wall thickness and: hemodialysis time (r = 0.40; p = 0.024), systolic index (r = - 0.61; p = 0.0003), cardiac index (r = -0.56; p = 0.001) and UV_24hs (r = -0.42; p = 0.01). The end diastolic diameter was higher in RD+ (52 ± 0.7 vs. 48 ± 1.1; p = 0.0072), and we found significant positive correlations between end diastolic diameter and UV_24hs (r = 0.41; p = 0.022) and negative correlations between end diastolic diameter and relative wall thickness (r = -0.60; p = 0.0003).

LEFT VENTRICULAR FUNCTION AND HEMODYNAMIC DATA

The cardiac index of the patients was significantly higher in group RD+ than in group RD- (3.9 ± 0.2 vs. 3.0 ± 0.2 L/min/m2; p = 0.0056). A significant negative correlation between the cardiac index and relative wall thickness was observed (r = - 0.56; p = 0.001). The systolic index was significantly higher in group RD+ (54 ± 2.9 vs. 45 ± 3.3 mL/b/m2; p = 0.0403), as was the end diastolic volume (141 ± 6 vs. 112 ± 7 mL; p = 0.0081). The total peripheral resistance index was significantly lower in group RD+ (1121 ± 56 vs. 1529 ± 111 dina. seg.cm-5; p = 0.001) (Figure 1, Table 1). The BFAV was not statistically different between groups RD+ and RD- (1.8 ± 0.6 vs. 1.4 ± 0.6 L/min/m2; p = ns).

It was observed a significant positive correlation between the systolic index and left ventricular mass index (r = 0.51; p = 0.0039), between the total peripheral resistance index and relative wall thickness (r = 0.51; p = 0.0036) and systolic index and relative wall thickness (r = - 0.61; p = 0.0003). The TPVRi correlated with the CI, SI, RWT and UV_24h (Figures 2 and 3) (Table 2). For the multiple regression analysis the TPVRi was considered as a dependent variable while time of treatment, residual diuresis, PTH and MAP were considered as variables that could influence the peripheral resistance index. We found that F regression = 4.26, p = 0.041, rejected H0 and the following partial coefficients: time (t: -1.47; p = 0.152); residual diuresis (t: -3.35; p = 0.0023); MAP (t: 0.490; p = 0.490) and PTH (t: = 0.498 p = 0.6225).

DISCUSSION

Relative wall thickness constitutes one of the variables used to define the geometric pattern of the left ventricle.^22;32;39 Thus, in our study, we observed that the patients in groups RD+ and RD- had similar left ventricular masses and different values of relative wall thickness (Table 2). This data suggested that both groups would have distinct ventricular morphologies and the load resistance and volume imposed on the left ventricle would be of different magnitudes. This fact becomes more evident, as we found a correlation between peripheral resistance and relative wall thickness, suggesting that, for different values of resistance, there are different values of thickness on the posterior wall (Figure 2). The absence of residual diuresis may have contributed to higher peripheral resistance values and hypervolemic status in the anuric group. Although the interdialytic weight gain was not significant between the groups due to the small size of this sample, the group without diuresis were about 20 per cent heavier than the group with urinary volume. Our data also showed that low-volume diuresis coexisted with high values of peripheral resistance (Figure 2). Wang et al. found that left ventricular mass increased in peritoneal dialysis patients who had lower glomerular filtration rates.⁹ However, these authors found similar end diastolic diameters among the assessed groups, which differs from the findings in our study. One of the possible reasons for these different findings could be due to the type of dialysis, while another reason may be that the authors did not correlate modifications in the left ventricle with the residual 24-hour urinary volume of their patients.

With respect to the functional characteristics of the left ventricle, we observed that CI and SI were lower in the anuric patients (RD-) (Table 2). This finding could be explained by the lower values found in the end ventricular diastolic diameter in RD- (Table 2). The morphological differences of left ventricles between the two groups were responsible for distinct values of cardiac and systolic indexes. Therefore, CKD patients on hemodialysis treatment who lose residual diuresis may have changes in the geometry and function of the left ventricle.

Although Faguli et al. demonstrated LVH in the majority of the hemodialyzed patients studied, these authors did not exclude patients with pathologies that could interfere with the myocardium remodeling process, such as diabetes mellitus, ischemic cardiomyopathy or systemic arterial hypertension; further, they did not correlate their findings with the residual urinary volume.⁴⁰

In CKD patients, RD progressively decreased with time in replacement therapy. In our study, the anuric group (RD-) spent more time in HD treatment than the group with dieresis (RD+), and the loss of urinary volume only happened in patients with the largest length time on treatment. The reasons for losing the residual diuresis may be explained by the changes related to the underlying disease that caused the CKD or by a continuous inflammatory process, anemia and associated co-morbidities.^12,17,41-43 The length of time spent on hemodialysis could increase the potential risks to the left ventricle. These risks come from the treatment itself and from the progression of the illness. However, applying multiple regression and defining the load imposed on the left ventricle as a dependent variable we found a statistical significance only for residual diuresis (p = 0.05). The length of time spent on dialysis therapy, PTH and mean arterial pressure did not have significant values. These data were more relevant because patients were normotensive, thus the volume component of blood pressure could be greater than the resistive component in these patients.

In this study, the morpho-functional cardiac changes could not be attributed to the blood pressure levels found, because the groups RD+ and RD- demonstrated similar diastolic and systolic blood pressure values (Table 1). The same could be said with regard to the use of anti-hypertensive drugs, as there was no difference in the number of hypertensive medications used in both groups (Table 1). Gunal et al. demonstrated that the use of anti-hypertensive drugs contributed to LVMi reductions in only 6% of the patients on hemodialysis (11). However, our results demonstrated that both groups RD+ and RD- did not show differences in their LVMi values (p > 0.05) (Table 2), indicating that the effect of the drugs used did not substantially interfere with our results.

The presence of anemia is another factor that could be related to the presence of LVH.^44;45 The role of anemia as a cause of LVH in patients undergoing dialysis has been well established; correction of anemia with erythropoietin results in the partial regression of LVH (46). In this study, the Hb level remained relatively normal, and there was no difference in Hb level between the groups studied (Table 2).

It has already been shown that hypoalbuminemia is involved in ventricular hypertrophy and dilatation, and in heart failure, and, ultimately decreases patients' survival.^47-51 The CANUSA study demonstrated that serum Alb concentration strongly correlated with mortality.^3,52 In our study, the serum Alb values were normal; we did not find significant differences between the two groups (Table 2). Therefore, we believe that the cardiac changes found in our study could not have been caused by this variable. Persistent hypocalcemia is considered a pathogenic factor in the reduction of left ventricular systolic function.⁵³ However, serum calcium in our study remained at normal values; there was no difference between the two groups (Table 2). Secondary hyperparathyroidism is common in uremic patients, and this complication has contributed to the development of left ventricular systolic dysfunction⁵⁴ and LVH.⁵⁵ PTH serum levels between the groups were statistically non significant (Table 2). The BF_AVis another important factor that contributes to cardiac morphology and function.^38;56 In our study, all fistulas were examined by using their blood flows; there was no statistically significant difference between the groups (Table 2). In addition, morphological and functional changes may be attributed to the different removal rates of solutes in the hemodialysis process; however, they were not different in RD+ and RD-. It is worth noting that the Kt/V measurement in our study did not take into account solute removals promoted by residual diuresis (Table 2).

Based on our study findings, we conclude that the different CI and SI values found in these groups can be attributed to distinct ventricular geometric patterns that are determined by total peripheral resistance and by the presence of residual diuresis. Therefore, the preservation of diuresis appears to influence left ventricular morphology and function in patients with chronic kidney failure.

As limitations of this study it is necessary to observe that it is a cross sectional study and the data of the patients represent the moment when the variables were observed, and they could not express the exactly progression of the patient disease. Beside this, the small size of samples could induce an alpha error in its statistics analyses.

We believe that more prospective studies should be conducted in order to confirm such a hypothesis.

REFERENCES

1. Wang AY. The "heart" of peritoneal dialysis. Perit Dial Int 2007;2:S228-S232.
2. Maiorca R, Brunori G, Zubani R et al Predictive value of dialysis adequacy and nutritional indices for mortality and morbidity in CAPD and HD patients. A longitudinal study. Nephrol Dial Transplant 1995; 10:2295-305.
3. Adequacy of dialysis and nutrition in continuous peritoneal dialysis: association with clinical outcomes. Canada-USA (CANUSA) Peritoneal Dialysis Study Group. J Am Soc Nephrol 1996; 7:198-207.
4. Termorshuizen F, Korevaar JC, Dekker FW, van Manen JG, Boeschoten EW, Krediet RT. The relative importance of residual renal function compared with peritoneal clearance for patient survival and quality of life: an analysis of the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD)-2. Am J Kidney Dis 2003; 41:1293-302.
5. Nolph KD, Prowant BF, Moore HL, Reyad SE. Hematocrit and residual renal creatinine clearance in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Perit Dial Int 1990; 10:279-82.
6. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39:S1-266.
7. Foley RN, Parfrey PS, Harnett JD, Kent GM, Murray DC, Barre PE. The prognostic importance of left ventricular geometry in uremic cardiomyopathy. J Am Soc Nephrol 1995; 5:2024-31.
8. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990; 322:1561-6.
9. Wang AY, Wang M, Woo J et al A novel association between residual renal function and left ventricular hypertrophy in peritoneal dialysis patients. Kidney Int 2002; 62:639-47.
10. Parfrey PS, Harnett JD, Griffiths SM et al The clinical course of left ventricular hypertrophy in dialysis patients. Nephron 1990; 55:114-20.
11. Gunal AI, Kirciman E, Guler M, Yavuzkir M, Celiker H. Should the preservation of residual renal function cost volume overload and its consequence left ventricular hypertrophy in new hemodialysis patients? Ren Fail 2004; 26:405-9.
12. Wang AY, Wang M, Woo J et al Inflammation, residual kidney function, and cardiac hypertrophy are interrelated and combine adversely to enhance mortality and cardiovascular death risk of peritoneal dialysis patients. J Am Soc Nephrol 2004; 15:2186-94.
13. Verdecchia P, Carini G, Circo A et al Left ventricular mass and cardiovascular morbidity in essential hypertension: the MAVI study. J Am Coll Cardiol 2001; 38:1829-35.
14. Lang SM, Bergner A, Topfer M, Schiffl H. Preservation of residual renal function in dialysis patients: effects of dialysis-technique-related factors. Perit Dial Int 2001; 21:52-7.
15. Horinek A, Misra M. Does residual renal function decline more rapidly in hemodialysis than in peritoneal dialysis? How good is the evidence? Adv Perit Dial 2004; 20:137-40.
16. Lysaght MJ, Vonesh EF, Gotch F et al The influence of dialysis treatment modality on the decline of remaining renal function. ASAIO Trans 1991; 37:598-604.
17. Marron B, Remon C, Perez-Fontan M, Quiros P, Ortiz A. Benefits of preserving residual renal function in peritoneal dialysis. Kidney Int Suppl 2008; 108:S42-S51.
18. Levin A. Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis. Semin Dial 2003; 16:101-5.
19. McMahon LP, Roger SD, Levin A. Development, prevention, and potential reversal of left ventricular hypertrophy in chronic kidney disease. J Am Soc Nephrol 2004; 15:1640-7.
20. Harnett JD, Parfrey PS, Griffiths SM, Gault MH, Barre P, Guttmann RD. Left ventricular hypertrophy in end-stage renal disease. Nephron 1988; 48:107-15.
21. London GM, Parfrey PS. Cardiac disease in chronic uremia: pathogenesis. Adv Ren Replace Ther 1997; 4:194-211.
22. Lang RM, Bierig M, Devereux RB et al. Recommendations for chamber quantification: a report from the American Society of Echocardiographys Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005; 18:1440-63.
23. Nishimura RA, Tajik AJ, Shub C, Miller FA, Jr. , Ilstrup DM, Harrison CE. Role of two-dimensional echocardiography in the prediction of in-hospital complications after acute myocardial infarction. J Am Coll Cardiol 1984; 4:1080-7.
24. Marchais SJ, Guerin AP, Pannier BM, Levy BI, Safar ME, London GM. Wave reflections and cardiac hypertrophy in chronic uremia. Influence of body size. Hypertension 1993; 22:876-83.
25. Ferreira Filho SR, de Castro Rodrigues FF, Oliveira PC, Nery MA. Systemic hemodynamic changes in older hypertensive patients after drinking water or eating a meal. Hypertension 2007;49:e31.
26. Burnett RW, Covington AK, Fogh-Andersen N et al Use of ion-selective electrodes for blood-electrolyte analysis. Recommendations for nomenclature, definitions and conventions. International Federation of Clinical Chemistry and Laboratory Medicine (IFCC). Scientific Division Working Group on Selective Electrodes. Clin Chem Lab Med 2000; 38:363-70.
27. Chromy V, Rozkosna K, Sedlak P. Determination of serum creatinine by Jaffe method and how to calibrate to eliminate matrix interference problems. Clin Chem Lab Med 2008; 46:1127-33.
28. Javed MU, Michelangeli F. Enzymatic method for assaying calcium in serum with Ca++ -ATPase. Exp Mol Med 2003; 35:17-22.
29. Harnett JD, Murphy B, Collingwood P, Purchase L, Kent G, Parfrey PS. The reliability and validity of echocardiographic measurement of left ventricular mass index in hemodialysis patients. Nephron 1993; 65:212-4.
30. Schiller NB, Shah PM, Crawford M et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2:358-67.
31. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978; 58:1072-83.
32. Ganau A, Devereux RB, Roman MJ et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol 1992; 19:1550-8.
33. Ford LE. Heart size. Circulation Res 1976; 39:297-303.
34. Gaash WH. LV radius to wall thickness ratio. Am J Cardiol 1979;43:1189-94.
35. Fast JH. Limits of reproducibility of left ventricular wall thickness and mass by M-mode echocardiography. Neth J Med 1989; 34:297-301.
36. Zoccali C, Benedetto FA, Mallamaci F et al. Prognostic impact of the indexation of left ventricular mass in patients undergoing dialysis. J Am Soc Nephrol 2001; 12:2768-74.
37. Miller PE, Tolwani A, Luscy CP et al. Predictors of adequacy of arteriovenous fistulas in hemodialysis patients. Kidney Int 1999; 56:275-80.
38. Robbin ML, Chamberlain NE, Lockhart ME et al Hemodialysis arteriovenous fistula maturity: US evaluation. Radiology 2002; 225:59-64.
39. de SG. Left ventricular geometry and hypotension in end-stage renal disease: a mechanical perspective. J Am Soc Nephrol 2003; 14:2421-7.
40. Fagugli RM, Pasini P, Quintaliani G et al. Association between extracellular water, left ventricular mass and hypertension in haemodialysis patients. Nephrol Dial Transplant 2003; 18:2332-8.
41. Jacobs LH, van de Kerkhof JJ, Mingels AM et al Inflammation, overhydration and cardiac biomarkers in haemodialysis patients: a longitudinal study. Nephrol Dial Transplant 2010; 25:243-8.
42. Krediet RT. How to preserve residual renal function in patients with chronic kidney disease and on dialysis? Nephrol Dial Transplant 2006; 21:42-ii46.
43. Yang PY, Lin JL, Lin-Tan DT et al Residual daily urine volume association with inflammation and nutrition status in maintenance hemodialysis patients. Ren Fail 2009; 31:423-30.
44. Silberberg JS, Rahal DP, Patton DR, Sniderman AD. Role of anemia in the pathogenesis of left ventricular hypertrophy in end-stage renal disease. Am J Cardiol 1989; 15:64:222-4.
45. Stojimirovic B, Petrovic D, Obrenovic R. Left ventricular hypertrophy in patients on hemodialysis: importance of anemia. Med Pregl 2007; 60:155-9.
46. Silberberg J, Racine N, Barre P, Sniderman AD. Regression of left ventricular hypertrophy in dialysis patients following correction of anemia with recombinant human erythropoietin. Can J Cardiol 1990; 6:1-4.
47. Foley RN, Parfrey PS, Harnett JD, Kent GM, Murray DC, Barre PE. Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. J Am Soc Nephrol 1996; 7:728-36.
48. Moon KH, Song IS, Yang WS et al Hypoalbuminemia as a risk factor for progressive left-ventricular hypertrophy in hemodialysis patients. Am J Nephrol 2000; 20:396-401.
49. Suda T, Hiroshige K, Ohta T et al. The contribution of residual renal function to overall nutritional status in chronic haemodialysis patients. Nephrol Dial Transplant 2000; 15:396-401.
50. Fine A, Cox D. Modest reduction of serum albumin in continuous ambulatory peritoneal dialysis patients is common and of no apparent clinical consequence. Am J Kidney Dis 1992; 20:50-4.
51. Struijk DG, Krediet RT, Koomen GC, Boeschoten EW, Arisz L. The effect of serum albumin at the start of continuous ambulatory peritoneal dialysis treatment on patient survival. Perit Dial Int 1994; 14:121-6.
52. Bargman JM, Thorpe KE, Churchill DN. Relative contribution of residual renal function and peritoneal clearance to adequacy of dialysis: a reanalysis of the CANUSA study. J Am Soc Nephrol 2001; 12:2158-62.
53. Feldman AM, Fivush B, Zahka KG, Ouyang P, Baughman KL. Congestive cardiomyopathy in patients on continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1988; 11:76-9.
54. Drueke T, Fauchet M, Fleury J et al Effect of parathyroidectomy on left-ventricular function in haemodialysis patients. Lancet 1980; 1:112-4.
55. London GM, De Vernejoul MC, Fabiani F et al Secondary hyperparathyroidism and cardiac hypertrophy in hemodialysis patients. Kidney Int 1987; 32:900-7.
56. Anderson CB, Codd JR, Graff RA, Groce MA, Harter HR, Newton WT. Cardiac failure and upper extremity arteriovenous dialysis fistulas. Case reports and a review of the literature. Arch Intern Med 1976; 136:292-7.

Cardiac morphology and function in patients with and without residual diuresis on hemodialysis

Salustiano Araujo; Helton P. Lemes; Danny A. Cunha; Vinicius S. Queiroz; Daniela D. Nascimento; Sebastião Rodrigues Ferreira Filho

Publication Dates

Publication in this collection
11 Apr 2011
Date of issue
Mar 2011

History

Accepted
06 Jan 2011
Received
01 Oct 2010

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

[1] 1. Wang AY. The "heart" of peritoneal dialysis. Perit Dial Int 2007;2:S228-S232.

[2] 2. Maiorca R, Brunori G, Zubani R et al Predictive value of dialysis adequacy and nutritional indices for mortality and morbidity in CAPD and HD patients. A longitudinal study. Nephrol Dial Transplant 1995; 10:2295-305.

[3] 3. Adequacy of dialysis and nutrition in continuous peritoneal dialysis: association with clinical outcomes. Canada-USA (CANUSA) Peritoneal Dialysis Study Group. J Am Soc Nephrol 1996; 7:198-207.

[4] 4. Termorshuizen F, Korevaar JC, Dekker FW, van Manen JG, Boeschoten EW, Krediet RT. The relative importance of residual renal function compared with peritoneal clearance for patient survival and quality of life: an analysis of the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD)-2. Am J Kidney Dis 2003; 41:1293-302.

[5] 5. Nolph KD, Prowant BF, Moore HL, Reyad SE. Hematocrit and residual renal creatinine clearance in patients undergoing continuous ambulatory peritoneal dialysis (CAPD). Perit Dial Int 1990; 10:279-82.

[6] 6. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39:S1-266.

[7] 7. Foley RN, Parfrey PS, Harnett JD, Kent GM, Murray DC, Barre PE. The prognostic importance of left ventricular geometry in uremic cardiomyopathy. J Am Soc Nephrol 1995; 5:2024-31.

[8] 8. Levy D, Garrison RJ, Savage DD, Kannel WB, Castelli WP. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 1990; 322:1561-6.

[9] 9. Wang AY, Wang M, Woo J et al A novel association between residual renal function and left ventricular hypertrophy in peritoneal dialysis patients. Kidney Int 2002; 62:639-47.

[10] 10. Parfrey PS, Harnett JD, Griffiths SM et al The clinical course of left ventricular hypertrophy in dialysis patients. Nephron 1990; 55:114-20.

[11] 11. Gunal AI, Kirciman E, Guler M, Yavuzkir M, Celiker H. Should the preservation of residual renal function cost volume overload and its consequence left ventricular hypertrophy in new hemodialysis patients? Ren Fail 2004; 26:405-9.

[12] 12. Wang AY, Wang M, Woo J et al Inflammation, residual kidney function, and cardiac hypertrophy are interrelated and combine adversely to enhance mortality and cardiovascular death risk of peritoneal dialysis patients. J Am Soc Nephrol 2004; 15:2186-94.

[13] 13. Verdecchia P, Carini G, Circo A et al Left ventricular mass and cardiovascular morbidity in essential hypertension: the MAVI study. J Am Coll Cardiol 2001; 38:1829-35.

[14] 14. Lang SM, Bergner A, Topfer M, Schiffl H. Preservation of residual renal function in dialysis patients: effects of dialysis-technique-related factors. Perit Dial Int 2001; 21:52-7.

[15] 15. Horinek A, Misra M. Does residual renal function decline more rapidly in hemodialysis than in peritoneal dialysis? How good is the evidence? Adv Perit Dial 2004; 20:137-40.

[16] 16. Lysaght MJ, Vonesh EF, Gotch F et al The influence of dialysis treatment modality on the decline of remaining renal function. ASAIO Trans 1991; 37:598-604.

[17] 17. Marron B, Remon C, Perez-Fontan M, Quiros P, Ortiz A. Benefits of preserving residual renal function in peritoneal dialysis. Kidney Int Suppl 2008; 108:S42-S51.

[18] 18. Levin A. Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis. Semin Dial 2003; 16:101-5.

[19] 19. McMahon LP, Roger SD, Levin A. Development, prevention, and potential reversal of left ventricular hypertrophy in chronic kidney disease. J Am Soc Nephrol 2004; 15:1640-7.

[20] 20. Harnett JD, Parfrey PS, Griffiths SM, Gault MH, Barre P, Guttmann RD. Left ventricular hypertrophy in end-stage renal disease. Nephron 1988; 48:107-15.

[21] 21. London GM, Parfrey PS. Cardiac disease in chronic uremia: pathogenesis. Adv Ren Replace Ther 1997; 4:194-211.

[22] 22. Lang RM, Bierig M, Devereux RB et al. Recommendations for chamber quantification: a report from the American Society of Echocardiographys Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005; 18:1440-63.

[23] 23. Nishimura RA, Tajik AJ, Shub C, Miller FA, Jr. , Ilstrup DM, Harrison CE. Role of two-dimensional echocardiography in the prediction of in-hospital complications after acute myocardial infarction. J Am Coll Cardiol 1984; 4:1080-7.

[24] 24. Marchais SJ, Guerin AP, Pannier BM, Levy BI, Safar ME, London GM. Wave reflections and cardiac hypertrophy in chronic uremia. Influence of body size. Hypertension 1993; 22:876-83.

[25] 25. Ferreira Filho SR, de Castro Rodrigues FF, Oliveira PC, Nery MA. Systemic hemodynamic changes in older hypertensive patients after drinking water or eating a meal. Hypertension 2007;49:e31.

[26] 26. Burnett RW, Covington AK, Fogh-Andersen N et al Use of ion-selective electrodes for blood-electrolyte analysis. Recommendations for nomenclature, definitions and conventions. International Federation of Clinical Chemistry and Laboratory Medicine (IFCC). Scientific Division Working Group on Selective Electrodes. Clin Chem Lab Med 2000; 38:363-70.

[27] 27. Chromy V, Rozkosna K, Sedlak P. Determination of serum creatinine by Jaffe method and how to calibrate to eliminate matrix interference problems. Clin Chem Lab Med 2008; 46:1127-33.

[28] 28. Javed MU, Michelangeli F. Enzymatic method for assaying calcium in serum with Ca++ -ATPase. Exp Mol Med 2003; 35:17-22.

[29] 29. Harnett JD, Murphy B, Collingwood P, Purchase L, Kent G, Parfrey PS. The reliability and validity of echocardiographic measurement of left ventricular mass index in hemodialysis patients. Nephron 1993; 65:212-4.

[30] 30. Schiller NB, Shah PM, Crawford M et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989; 2:358-67.

[31] 31. Sahn DJ, DeMaria A, Kisslo J, Weyman A. Recommendations regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurements. Circulation 1978; 58:1072-83.

[32] 32. Ganau A, Devereux RB, Roman MJ et al. Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension. J Am Coll Cardiol 1992; 19:1550-8.

[33] 33. Ford LE. Heart size. Circulation Res 1976; 39:297-303.

[34] 34. Gaash WH. LV radius to wall thickness ratio. Am J Cardiol 1979;43:1189-94.

[35] 35. Fast JH. Limits of reproducibility of left ventricular wall thickness and mass by M-mode echocardiography. Neth J Med 1989; 34:297-301.

[36] 36. Zoccali C, Benedetto FA, Mallamaci F et al. Prognostic impact of the indexation of left ventricular mass in patients undergoing dialysis. J Am Soc Nephrol 2001; 12:2768-74.

[37] 37. Miller PE, Tolwani A, Luscy CP et al. Predictors of adequacy of arteriovenous fistulas in hemodialysis patients. Kidney Int 1999; 56:275-80.

[38] 38. Robbin ML, Chamberlain NE, Lockhart ME et al Hemodialysis arteriovenous fistula maturity: US evaluation. Radiology 2002; 225:59-64.

[39] 39. de SG. Left ventricular geometry and hypotension in end-stage renal disease: a mechanical perspective. J Am Soc Nephrol 2003; 14:2421-7.

[40] 40. Fagugli RM, Pasini P, Quintaliani G et al. Association between extracellular water, left ventricular mass and hypertension in haemodialysis patients. Nephrol Dial Transplant 2003; 18:2332-8.

[41] 41. Jacobs LH, van de Kerkhof JJ, Mingels AM et al Inflammation, overhydration and cardiac biomarkers in haemodialysis patients: a longitudinal study. Nephrol Dial Transplant 2010; 25:243-8.

[42] 42. Krediet RT. How to preserve residual renal function in patients with chronic kidney disease and on dialysis? Nephrol Dial Transplant 2006; 21:42-ii46.

[43] 43. Yang PY, Lin JL, Lin-Tan DT et al Residual daily urine volume association with inflammation and nutrition status in maintenance hemodialysis patients. Ren Fail 2009; 31:423-30.

[44] 44. Silberberg JS, Rahal DP, Patton DR, Sniderman AD. Role of anemia in the pathogenesis of left ventricular hypertrophy in end-stage renal disease. Am J Cardiol 1989; 15:64:222-4.

[45] 45. Stojimirovic B, Petrovic D, Obrenovic R. Left ventricular hypertrophy in patients on hemodialysis: importance of anemia. Med Pregl 2007; 60:155-9.

[46] 46. Silberberg J, Racine N, Barre P, Sniderman AD. Regression of left ventricular hypertrophy in dialysis patients following correction of anemia with recombinant human erythropoietin. Can J Cardiol 1990; 6:1-4.

[47] 47. Foley RN, Parfrey PS, Harnett JD, Kent GM, Murray DC, Barre PE. Hypoalbuminemia, cardiac morbidity, and mortality in end-stage renal disease. J Am Soc Nephrol 1996; 7:728-36.

[48] 48. Moon KH, Song IS, Yang WS et al Hypoalbuminemia as a risk factor for progressive left-ventricular hypertrophy in hemodialysis patients. Am J Nephrol 2000; 20:396-401.

[49] 49. Suda T, Hiroshige K, Ohta T et al. The contribution of residual renal function to overall nutritional status in chronic haemodialysis patients. Nephrol Dial Transplant 2000; 15:396-401.

[50] 50. Fine A, Cox D. Modest reduction of serum albumin in continuous ambulatory peritoneal dialysis patients is common and of no apparent clinical consequence. Am J Kidney Dis 1992; 20:50-4.

[51] 51. Struijk DG, Krediet RT, Koomen GC, Boeschoten EW, Arisz L. The effect of serum albumin at the start of continuous ambulatory peritoneal dialysis treatment on patient survival. Perit Dial Int 1994; 14:121-6.

[52] 52. Bargman JM, Thorpe KE, Churchill DN. Relative contribution of residual renal function and peritoneal clearance to adequacy of dialysis: a reanalysis of the CANUSA study. J Am Soc Nephrol 2001; 12:2158-62.

[53] 53. Feldman AM, Fivush B, Zahka KG, Ouyang P, Baughman KL. Congestive cardiomyopathy in patients on continuous ambulatory peritoneal dialysis. Am J Kidney Dis 1988; 11:76-9.

[54] 54. Drueke T, Fauchet M, Fleury J et al Effect of parathyroidectomy on left-ventricular function in haemodialysis patients. Lancet 1980; 1:112-4.

[55] 55. London GM, De Vernejoul MC, Fabiani F et al Secondary hyperparathyroidism and cardiac hypertrophy in hemodialysis patients. Kidney Int 1987; 32:900-7.

[56] 56. Anderson CB, Codd JR, Graff RA, Groce MA, Harter HR, Newton WT. Cardiac failure and upper extremity arteriovenous dialysis fistulas. Case reports and a review of the literature. Arch Intern Med 1976; 136:292-7.