Effect of Congenital Heart Disease on Renal Function in Childhood

Ağras, Pınar Işık; Derbent, Murat; Özçay, Figen; Baskın, Esra; Türkoğlu, Suna; Aldemir, Derya; Tokel, Kürşad; Saatçi, U

doi:10.1159/000081797

Cited by 40 publications

(42 citation statements)

References 28 publications

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“…45 Cyanotic patients with CHD have unique risk factors for developing CKD. These include direct hypoxia leading to early renal tubular injury 46,47 and reactive erythrocytosis. This erythrocytosis induces secondary hyperviscosity leading to engorgement of the glomerular capillary beds, which in turn increases the efferent glomerular arteriolar resistance.…”

Section: Overviewmentioning

confidence: 99%

Diagnosis and Management of Noncardiac Complications in Adults With Congenital Heart Disease: A Scientific Statement From the American Heart Association

Lui¹,

Saïdi²,

Bhatt³

et al. 2017

Circulation

180

136

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ABSTRACT:Life expectancy and quality of life for those born with congenital heart disease (CHD) have greatly improved over the past 3 decades. While representing a great advance for these patients, who have been able to move from childhood to successful adult lives in increasing numbers, this development has resulted in an epidemiological shift and a generation of patients who are at risk of developing chronic multisystem disease in adulthood. Noncardiac complications significantly contribute to the morbidity and mortality of adults with CHD. Reduced survival has been documented in patients with CHD with renal dysfunction, restrictive lung disease, anemia, and cirrhosis. Furthermore, as this population ages, atherosclerotic cardiovascular disease and its risk factors are becoming increasingly prevalent. Disorders of psychosocial and cognitive development are key factors affecting the quality of life of these individuals. It is incumbent on physicians who care for patients with CHD to be mindful of the effects that disease of organs other than the heart may have on the well-being of adults with CHD. Further research is needed to understand how these noncardiac complications may affect the long-term outcome in these patients and what modifiable factors can be targeted for preventive intervention.

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Section: Overviewmentioning

confidence: 99%

Diagnosis and Management of Noncardiac Complications in Adults With Congenital Heart Disease: A Scientific Statement From the American Heart Association

Lui¹,

Saïdi²,

Bhatt³

et al. 2017

Circulation

180

136

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“…However, only a small number of clinical studies have been conducted with the aim of clarifying this hypothesis [6,7]. Tubular injury as well as glomerular injury have also been reported [8]. One of the aims of the present study, therefore, was to retrospectively analyze clinical and laboratory findings in order to clarify the risk factors and the mechanisms of the development and progression of CN.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of development and progression of cyanotic nephropathy

et al. 2006

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Cyanotic nephropathy (CN) is often accompanied by congenital cyanotic heart diseases (CCHD). The purpose of this study was to clarify the risk factors and the mechanisms of involved in the development and progression of CN. Thirty patients with CCHD were examined. We analyzed the risk factors for the development of CN on the basis of the clinical and laboratory findings. We also examined ten renal biopsy specimens obtained from patients with CN. Patients with CN showed significantly higher hematocrit levels than those without CN (P=0.025), although there was no difference between the two groups in terms of oxygen saturation. The renal plasma flow (RPF) in patients both with and without CN was low. However, the filtration fraction (FF) was significantly lower in patients with CN than in those without CN (P=0.001). The glomeruli of biopsy specimens with significant proteinuria (n=7) were larger than those of biopsy specimens without significant proteinuria, and there were more capillaries per glomerulus in the former than in the latter (n=3) and the control specimens (n=6) (glomerular size: P<0.01; number of glomerular capillaries: P<0.01). In conclusion, hyperviscosity by polycythemia may be responsible for the development of CN. This pathological condition may induce an angiogenic increase in the glomerular capillary beds, in turn leading to glomerulomegaly. In addition, the failure of a compensatory mechanism to respond to reduced RPF by hyperfiltration may be accompanied by the development and progression of CN.

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“…Previous reports have demonstrated that congestive heart failure patients were complicated with glomerular injury as indicated by increased albuminuria and decreased GFR. Therefore, the urinary microalbumin (mALB) level has been used to evaluate the glomerular functions (Agras et al 2005).…”

Section: Introductionmentioning

confidence: 99%