Pre-treatment considerations in childhood hypertension due to chronic kidney disease

Abstract

Hypertension (HTN) develops very early in childhood chronic kidney disease (CKD). It is linked with rapid progression of kidney disease, increased morbidity and mortality hence the imperative to start anti-hypertensive medication when blood pressure (BP) is persistently > 90(th) percentile for age, gender, and height in non-dialyzing hypertensive children with CKD. HTN pathomechanism in CKD is multifactorial and complexly interwoven. The patient with CKD-associated HTN needs to be carefully evaluated for co-morbidities that frequently alter the course of the disease as successful treatment of HTN in CKD goes beyond life style modification and anti-hypertensive therapy alone. Chronic anaemia, volume overload, endothelial dysfunction, arterial media calcification, and metabolic derangements like secondary hyperparathyroidism, hyperphosphataemia, and calcitriol deficiency are a few co-morbidities that may cause or worsen HTN in CKD. It is important to know if the HTN is caused or made worse by the toxic effects of medications like erythropoietin, cyclosporine, tacrolimus, corticosteroids and non-steroidal anti-inflammatory drugs. Poor treatment response may be due to any of these co-morbidities and medications. A satisfactory hypertensive CKD outcome, therefore, depends very much on identifying and managing these co-morbid conditions and HTN promoting medications promptly and appropriately. This review attempts to point attention to factors that may affect successful treatment of the hypertensive CKD child and how to attain the desired therapeutic BP target.

Keywords: Anaemia; Childhood; Chronic kidney disease; Hyperparathyroidism; Hypertension; Renin-angiotensin; Vascular calcification.

Figure 1

Prevalence of hypertension by chronic kidney disease stage in children. Data for this Figure were obtained from reference[3]. CKD: Chronic kidney disease.

Figure 2

Pathophysiologic mechanisms of hypertension in chronic kidney disease. A: Volume overload is associated with increase in cardiac output (CO) which ultimately leads to hypertension; B: Increase in total peripheral resistance (TPR) due to systemic vasoconstriction leads to hypertension; C: Arterial tunica media calcification causing vascular stiffening and failure of vasodilatation and vasoconstriction are illustrated. Chronic hyperparathyroidism promotes vascular wall mineralization or calcification leading to vascular stiffening and increase in TPR with consequent hypertension. Blood pressure = CO × TPR. RAAS: Renin-angiotensin-aldosterone system; ANG II: Angiotensin II; ET-1: Endothelin 1; PTH: Parathyroid hormone.