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Resistant hypertension in pediatric end stage renal disease.

Chronic kidney disease (CKD) is defined as the irreversible loss of kidney function, producing progressive decrease in glomerular filtration up to achieve the so-called end stage renal disease (ESRD)1. The long-term survival in children with ESRD has improved but mortality is still about 30 times higher than expected for age. This increases the need for extreme vigilance to achieve the best therapeutic results with less risk2. According to The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines, CKD is classified into five stages of increasing severity3. The renal disease progression to ESRD is largely due to secondary factors that may vary, such as hypertension and proteinuria, whose control is vital because it can prevent the progression of kidney damage. The tight control of blood pressure (BP) is crucial. Initially antihypertensive therapy was performed empirically. Subsequent data in adults suggest superiority of angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) as compared to other antihypertensive agents (diuretics, calcium channel blockers, β-blockers) resulting in a change of pharmacotherapeutic strategy4. Following the results of the ESCAPE trial5 , which established the need of strict control of BP, the European Society of Hypertension6 set new standards in treating hypertension in children with CKD: target of BP of the 75th percentile in patients without proteinuria and of the 50th percentile in children with proteinuria. It is called resistant hypertension when BP is above the target value despite treatment with three antihypertensive drugs4. Proteinuria is not only a marker of kidney disease but also a risk factor for progression of CKD. Data from the European Study Group of Nutritional Treatment of Chronic Renal Failure in Childhood show that urinary protein excretion greater than 60mg/m2/h represents a high risk of progression of CKD7. Drugs that block the renin-angiotensin-aldosterone system have shown to reduce proteinuria. Consequently, it has been suggested that even normotensive patients should be treated with ACE inhibitors or ARBs if proteinuria is present8.