Published online Nov 6, 2015. doi: 10.5527/wjn.v4.i5.500
Peer-review started: May 29, 2015
First decision: August 4, 2015
Revised: August 30, 2015
Accepted: October 1, 2015
Article in press: October 8, 2015
Published online: November 6, 2015
Processing time: 169 Days and 8.8 Hours
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 > 90th 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.
Core tip: Hypertension (HTN) is often difficult to control in chronic kidney disease (CKD). Failure to achieve the desired therapeutic BP target in the hypertensive CKD child could be due to comorbidities and toxic effects of HTN promoting medications. So, before starting or altering anti-hypertensive medications, it is important that patients are evaluated for the roles that HTN promoting medications and co-morbidities like chronic anaemia, hyperphosphataemia, progressive tunica media calcifications, and serum parathyroid hormone levels that are well above the acceptable limits for CKD stage could be playing in the entire process. Ways of solving this important clinical problem are the focus of this article.