Abstract

Sympathetic activation, hypertension, hyperlipidemia, and immunosuppressive treatment are risk factors for vascular damage in children with glomerulopathies. Aim: To perform pulse wave analysis in children with glomerulopathies. Material and Methods: We studied 33 children (22♂, 11♀) aged 13.3 ± 3.9 years with glomerulopathies: Henoch-Schonlein nephropathy 9 patients, IgA nephropathy 7 patients, membranoproliferative glomerulonephritis 4 patients, mesangioproliferative glomerulonephritis 3 patients, minimal change disease 3 patients, focal segmental glomerulosclerosis (FSGS) 3 patients, and other nephropathies 4 patients. We evaluated age at the disease onset, development of hypertension, body mass index (BMI) Z-score, selected biochemical variables, glomerular filtration rate (ac. to Schwartz formula), and pulse wave parameters determined using a SphygmoCor device (AtCor Medical, Australia): aortic systolic pressure (AoSP), diastolic pressure (AoDP) and pulse pressure (AoPP), augmentation pressure (AP), augmentation index (AIx), augmentation index corrected for heart rate of 75 beats per minute (AIx-75HR) [%], and an index of myocardial oxygen supply and demand, subendocardial viability ratio (SEVR) [%]. The control group included 20 healthy children matched for age and gender. Results: Children with glomerulopathies showed trends for higher mean AP (P=0.08) and AIx (P=0.07), and a significantly higher mean AIx-75HR (P<0.05). Patients with hypertension (n=13) showed higher mean AoDP (P<0.05) and AIx-75HR (P<0.05) compared to normotensives (n=20). Six (18.2%) overhydrated patients had significantly (P<0.05) higher diastolic peripheral and aoritc diastolic blood pressure, as well as aortic systolic blood pressure than 27 (81.8%) normovolemic children. In 33 children, AoSP and AoDP correlated positively with proteinuria (r=0.44, P<0.05; and r=0.57, P<0.05, respectively); AoDP showed negative correlations with albumin (r=-0.42, P<0.05), total protein (r=- 0.36, P<0.05), calcium level (r=-0.47, P<0.05). AoPP correlated positively with BMI Z-score (r=0.43, P<0.05), and SEVR negatively with total cholesterol level (r=-0.43, P<0.05). Conclusions: i. Patients with glomerulopathies show increased arterial stiffness compared to their healthy peers. ii. In children with glomerulonephritis, hypertension is a risk factor for increased aortic stiffness, and hypercholesterolemia may be a risk factor for future myocardial ischemia. iii. Overhydration in children with glomerulonephritis can increase peripheral and central blood pressure without influencing arterial stiffness.

Highlights

  • Glomerulonephritis is an immune-mediated renal disease that presents with isolated asymptomatic proteinuria or erythrocyturia, overt hematuria, nephrotic syndrome, or nephritic syndrome

  • Patients with glomerulopathies show increased arterial stiffness compared to their healthy peers

  • We evaluated the following parameters: aortic systolic pressure (AoSP) [mmHg], aortic diastolic pressure (AoDP) [mmHg], aortic pulse pressure (AoPP) [mmHg], augmentation pressure (AP) [mmHg], augmentation index (AIx) [%], augmentation index corrected for heart rate of 75 beats per minute (AIx-75HR) [%], and an index of myocardial oxygen supply and demand, subendocardial viability ratio (SEVR) [%]

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Summary

Introduction

Glomerulonephritis is an immune-mediated renal disease that presents with isolated asymptomatic proteinuria or erythrocyturia, overt hematuria, nephrotic syndrome, or nephritic syndrome. Adult patients with glomerulonephritis show an increased cardiovascular risk related to lipid abnormalities, coagulation abnormalities, increased sympathetic activity, and the treatment of the underlying disease [4,5]. Pulse waveform is the sum of a wave generated by contraction of the left ventricle and propagating away from the heart within the arterial tree, and a reflected wave returning from the peripheral vessels [6]. Pulse wave velocity is large and the return of reflected wave coincides with the systolic phase of primary pulse wave, resulting in augmentation of late systolic aortic pressure [7]. The size of this augmentation of the central aortic pressure, expressed either as an absolute augmentation pressure (AP)

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