Hypertension in pediatric patients with Chronic Kidney Disease

In contrast to adults where hypertension is a leading cause of chronic kidney disease, in pediatrics, hypertension is predominantly a sequela, however, an important one that, like in adults, is likely associated with a more rapid decline in kidney function or progression of chronic kidney disease to end stage. There is a significant issue with unrecognized, or masked, hypertension in childhood chronic kidney disease. Recent evidence and, therefore, guidelines now suggest targeting a blood pressure of <50th percentile for age, sex, and height in children with proteinuria and chronic kidney disease.

This often cannot be achieved by monotherapy and additional agents need to be added. Blockade of the renin angiotensin aldosterone system represents the mainstay of therapy, although often limited by the side effect of hyperkalemia. The addition of a diuretic, at least in the earlier stages of chronic kidney disease, might help mitigate this problem.

CKD stages in children

Stage	GFR description	eGFR (mL/min/1.73 m2)
I	Normal or elevated	≥90
II	Mildly decreased	60–89
III	Moderately decreased	30–59
IV	Severely decreased	15–29
V	Kidney failure	<15

Abbreviations

CKD, chronic kidney disease; eGFR, estimated glomerular filtration ate; GFR, glomerular filtration rate.

HTN in children is rare, with a prevalence of 3%–9%; however, in children with CKD, the prevalence rises to 50%. Theriology of HTN in children varies depending on the age of diagnosis. Neonates and infants most commonly have HTN due to renovascular diseases such as renal venous thrombosis or renal artery stenosis, and other renal parenchymal diseases. HTN is probably more prevalent in preterm neonates, with the presence of umbilical lines, postnatal acute kidney injury, patent ductus, intraventricular hemorrhage, and chronic lung disease, all being associated with HTN. In children and adolescents, intrinsic renal parenchymal disease and renovascular disease are the most common causes of HTN. Secondary HTN is most common earlier in childhood, while adolescents and adults more commonly present with essential HTN. Primary HTN is strongly correlated with overweight in childhood. Children with CKD most often present with secondary HTN, as BP elevation is a common consequence of renal damage and decreased renal function.

The prevalence of HTN is further increased in children on dialysis. In the NAPRTCS registry cohort, 76% of children on chronic dialysis had HTN, 57% of which were cases of uncontrolled HTN requiring further investigation to direct management.

CKD and HTN are intimately linked to one another, and act synergistically to cause further decline in renal function. Often masked or under-recognized, HTN presents an important target for treatment and renoprotection. ACE inhibitors and other medications affecting the RAAS are the best drug therapies in pediatric patients with HTN and CKD to date. End-organ damage can be detrimental to the patient and should always be screened for. Monitoring BP is essential for tracking progression of CKD, particularly through the ABPM method in the pediatric HTN population.