Hostname: page-component-586b7cd67f-rdxmf Total loading time: 0 Render date: 2024-11-26T07:57:18.739Z Has data issue: false hasContentIssue false
  • English
  • Français

Medium-term follow-up of renal function in hypoxaemic congenital heart disease patients

Published online by Cambridge University Press:  18 September 2015

Efrén Martínez-Quintana  and
Fayna Rodríguez-González
Efrén Martínez-Quintana*
Affiliation:
Cardiology Service, Insular-Materno Infantil University Hospital, Las Palmas de Gran Canaria, Spain
Fayna Rodríguez-González
Affiliation:
Dr. Negrín University Hospital of Gran Canaria, Las Palmas de Gran Canaria, Spain
*
Correspondence to: E. M. Quintana, Servicio de Cardiología, Complejo Universitario Insular-Materno Infantil, Avenida Marítima del Sur s/n, 35016 Las Palmas de Gran Canaria, Spain. Tel: +003 492 844 1360; Fax: +0034 928 441853; E-mail: [email protected]
Get access Rights & Permissions [Opens in a new window]

Abstract

Introduction

Hypoxaemic congenital heart disease (CHD) patients are at higher risk of complications. The aim of this study was to compare and follow-up blood and 24-hour urine analytical data in hypoxaemic and non-hypoxaemic CHD patients.

Methods

The inclusion criteria for this study were as follows: patients older than 14 years of age with a structural CHD with or without associated hypoxaemia.

Results

In total, 27 hypoxaemic and 48 non-hypoxaemic CHD patients were included in order to compare blood and 24-hour urine analytical data. Among hypoxaemic patients, 13 (48.1%) were male, two (7.4%) had diabetes mellitus, one of whom was a smoker, one (3.7%) had systemic arterial hypertension, and 11 (40.7%) showed pulmonary arterial hypertension. The mean follow-up time was 3.1±1.9 years. Hypoxaemic CHD patients showed higher proteinuria concentrations (g/24 hours) (0.09 (0.07; 0.46) versus 0.08 (0.07; 0.1), p=0.054) and 24-hour albumin excretion rate (µg/min) (16.5 (11.2; 143.5) versus 4.4 (0.0; 7.6), p<0.001) compared with non-hypoxaemic CHD patients; however, no significant differences were found in the proteinuria levels and in the 24-hour albumin excretion rate in CHD patients with associated hypoxaemia, both at baseline and at follow-up. When divided into groups, hypoxaemic patients with palliative shunts showed significantly higher proteinuria concentrations compared with hypoxaemic patients not operated on or with Fontan procedures (p=0.01). No significant differences were seen in 24-hour proteinuria and 24-hour albumin excretion rate during the follow-up of patients with palliative shunts.

Conclusions

Hypoxaemic CHD patients have significant higher 24-hour proteinuria concentration and 24-hour albumin excretion rate compared with non-hypoxaemic CHD patients. Among hypoxaemic CHD patients, those with palliative shunts showed the highest 24-hour proteinuria concentrations.

Keywords

CHDhypoxaemiaproteinuriaimpaired renal functionfollow-up
Type
Original Articles
Information
Cardiology in the Young , Volume 26 , Issue 6 , August 2016 , pp. 1137 - 1143
Check for updates
Copyright
© Cambridge University Press 2015 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Inatomi, J, Matsuoka, K, Fujimaru, R, Nakagawa, A, Iijima, K. Mechanisms of development and progression of cyanotic nephropathy. Pediatr Nephrol 2006; 21: 1440–1445.Google Scholar
2. Martínez-Quintana, E, Rodríguez-González, F, Fábregas-Brouard, M, Nieto-Lago, V. Serum and 24-hour urine analysis in adult cyanotic and noncyanotic congenital heart disease patients. Congenit Heart Dis 2009; 4: 147–152.Google Scholar
3. Agras, PI, Derbent, M, Ozcay, F, et al. Effect of congenital heart disease on renal function in childhood. Nephron Physiol 2005; 99: 10–15.CrossRefGoogle ScholarPubMed
4. Chiurchiu, C, Remuzzi, G, Ruggenenti, P. Angiotensin-converting enzyme inhibition and renal protection in nondiabetic patients: the data of the meta-analyses. J Am Soc Nephrol 2005; 16 (Suppl 1): S58–S63.Google Scholar
5. The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia). Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, non-diabetic nephropathy. Lancet 1997; 349: 1857–1863.Google Scholar
6. Levey, AS, Greene, T, Kusek, JW, Beck, GJ. A simplified equation to predict glomerular filtration rate from serum creatinine. J Am Soc Nephrol 2000; 11 (Suppl): A08028.Google Scholar
7. Stevens, LA, Coresh, J, Greene, T, Levey, AS. Assessing kidney function – measured and estimated glomerular filtration rate. N Engl J Med 2006; 354: 2473–2483.Google Scholar
8. Quiñones, MA, Otto, CM, Stoddard, M, et al. Recommendations for quantification of Doppler echocardiography: a report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. J Am Soc Echocardiogr 2002; 15: 167–184.CrossRefGoogle ScholarPubMed
9. Naderi, AS, Reilly, RF. Primary care approach to proteinuria. J Am Board Fam Med 2008; 21: 569–574.Google Scholar
10. Dittrich, S, Haas, NA, Bührer, C, Müller, C, Dähnert, I, Lange, PE. Renal impairment in patients with long-standing cyanotic congenital heart disease. Acta Paediatr 1998; 87: 949–954.Google Scholar
11. Perloff, JK. Systemic complications of cyanosis in adults with congenital heart disease—hematologic derangements, renal function, and urate metabolism. Cardiol Clin 1993; 4: 689–699.Google Scholar
12. Burlet, A, Drukker, A, Guignard, JP. Renal function in cyanotic congenital heart disease. Nephron 1999; 81: 296–300.Google Scholar
13. Akita, H, Matsuoka, S, Kuroda, Y. Nephropathy in patients with cyanotic congenital heart disease. Tokushima J Exp Med 1993; 40: 47–53.Google Scholar
14. Perloff, JK, Latta, H, Barsotti, P. Pathogenesis of the glomerular abnormality in cyanotic congenital heart disease. Am J Cardiol 2000; 86: 1198–1204.Google Scholar
15. Gupte, PA, Vaideeswar, P, Kandalkar, BM. Cyanotic nephropathy-a morphometric analysis. Congenit Heart Dis 2014; 9: 280–285.Google Scholar
16. Elsayed, EF, Tighiouart, H, Griffith, J, et al. Cardiovascular disease and subsequent kidney disease. Arch Intern Med 2007; 167: 1130–1136.Google Scholar
17. Metcalf, PA, Baker, JR, Scragg, RK, Dryson, E, Scott, AJ, Wild, CJ. Albuminuria in people at least 40 years old: effect of alcohol consumption, regular exercise, and cigarette smoking. Clin Chem 1993; 39: 1793–1797.Google Scholar
18. Ribstein, J, du Cailar, G, Mimran, A. Combined renal effects of overweight and hypertension. Hypertension 1995; 26: 610–615.Google Scholar
19. Hall, JE, Crook, ED, Jones, DW, Wofford, MR, Dubbert, PM. Mechanisms of obesity-associated cardiovascular and renal disease. Am J Med Sci 2002; 324: 127–137.Google Scholar
20. Iseki, K, Ikemiya, Y, Iseki, C, Takishita, S. Proteinuria and the risk of developing end-stage renal disease. Kidney Int 2003; 63: 1468–1474.Google Scholar
21. Kalantari, K, Bolton, WK. A good reason to measure 24-hour urine creatinine excretion, but not to assess kidney function. Clin J Am Soc Nephrol 2013; 8: 1847–1849.Google Scholar
22. Martínez-Quintana, E, Miranda-Calderín, G, Ugarte-Lopetegui, A, Rodríguez-González, F. Rehabilitation program in adult congenital heart disease patients with pulmonary hypertension. Congenit Heart Dis 2010; 5: 44–50.CrossRefGoogle ScholarPubMed
23. Oterdoom, LH, Gansevoort, RT, Schouten, JP, de Jong, PE, Gans, RO, Bakker, SJ. Urinary creatinine excretion, an indirect measure of muscle mass, is an independent predictor of cardiovascular disease and mortality in the general population. Atherosclerosis 2009; 207: 534–540.CrossRefGoogle ScholarPubMed
24. Martínez-Quintana, E, Rodríguez-González, F. Proteinuria and clinical outcome in CHD patients. Cardiol Young 2015; 25: 1054–1059.CrossRefGoogle ScholarPubMed
25. Sharma, P, Blackburn, RC, Parke, CL, McCullough, K, Marks, A, Black, C. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers for adults with early (stage 1 to 3) non-diabetic chronic kidney disease. Cochrane Database Syst Rev 2011; (10): CD007751.Google Scholar
26. Bolignano, D, Palmer, SC, Navaneethan, SD, Strippoli, GF. Aldosterone antagonists for preventing the progression of chronic kidney disease. Cochrane Database Syst Rev 2014; 4: CD007004.Google Scholar
27. Alfie, J, Aparicio, LS, Waisman, GD. Current strategies to achieve further cardiac and renal protection through enhanced renin-angiotensin-aldosterone system inhibition. Rev Recent Clin Trials 2011; 6: 134–146.Google Scholar