Arterial hypertension in renal transplant recipients warrants antihypertensive treatment. The preferable choice of antihypertensives that should be used in patients after kidney transplantation remains a matter of debate; however, calcium channel blockers (CCB) and angiotensin-converting enzyme inhibitors (ACEI) are currently the most commonly used antihypertensives. This educational review summarizes the current evidence about the effects of these two classes of medications in transplant recipients. Several studies have demonstrated that both classes of drugs can reduce blood pressure (BP) to similar extents. Meta-analyses of adult randomized controlled trials have shown that graft survival is improved in patients treated with ACEIs and CCBs, and that CCBs increase, yet ACEIs decrease, graft function. Proteinuria is usually decreased by ACEIs but remains unchanged with CCBs. In children, no randomized controlled study has ever been performed to compare BP or graft survival between CCBs and ACEIs. Post-transplant proteinuria could be reduced in children along with BP by ACEIs. The results of the most current meta-analyses recommend that due to their positive effects on graft function and survival, along with their lack of negative effects on serum potassium, CCBs could be the preferred first-line antihypertensive agent in renal transplant recipients. However, antihypertensive therapy should be individually tailored based on other factors, such as time after transplantation, presence of proteinuria/albuminuria, or hyperkalemia. Furthermore, due to the difficulty in controlling hypertension, combination therapy containing both CCBs and ACEIs could be a reasonable first-step therapy in treating children with severe post-transplantation hypertension.

• Klíčová slova
• Angiotensin-converting enzyme inhibitors, Calcium channel blockers, Children, Graft function, Hypertension, Proteinuria, Renal transplantation,
• MeSH
• antihypertenziva farmakologie   terapeutické užití   MeSH
• blokátory kalciových kanálů farmakologie   terapeutické užití   MeSH
• dítě MeSH
• dospělí MeSH
• hypertenze * farmakoterapie   etiologie   MeSH
• inhibitory ACE farmakologie   terapeutické užití   MeSH
• krevní tlak účinky léků   MeSH
• lidé MeSH
• proteinurie farmakoterapie   etiologie   MeSH
• Check Tag
• dítě MeSH
• dospělí MeSH
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• antihypertenziva MeSH
• blokátory kalciových kanálů MeSH
• inhibitory ACE MeSH

Proteinuria is a relatively frequent complication in children after renal transplantation (40-80 %). It is usually mild and non-nephrotic in nature and predominantly tubular in origin. The major causes of post-transplant proteinuria are recurrence of primary glomerulonephritis [mostly focal segmental glomerulosclerosis (FSGS)], rejection (acute and chronic), mTOR inhibitors or hypertension. Proteinuria is a risk factor for graft loss and patient death in adults, and even a mild proteinuria (0.1-0.2 g/day) is associated with impaired graft and patient survival. In children, proteinuria seems to be associated with graft but not patient survival. Proteinuria (protein/creatinine ratio) should be assessed regularly in all children. In children with prior chronic kidney disease due to idiopathic FSGS, proteinuria should be assessed daily during the first month after transplantation to enable early diagnosis of recurrence. The cause of proteinuria should be identified, and graft biopsy should be considered in children with unexplained proteinuria, especially with new onset proteinuria or deterioration of previously mild proteinuria. Treatment must be primarily targeted at the cause of proteinuria, and in normotensive children symptomatic antiproteinuric therapy with angiotensin-converting enzyme inhibitors/angiotensin II receptor antagonists should also be initiated. Other antihypertensive drugs should be used to achieve target blood pressure of <75th percentile. Target proteinuria should be <20 mg/mmol creatinine.

• MeSH
• antagonisté receptorů pro angiotenzin terapeutické užití   MeSH
• antihypertenziva terapeutické užití   MeSH
• časové faktory MeSH
• chronické selhání ledvin diagnóza   etiologie   chirurgie   MeSH
• fokálně segmentální glomeruloskleróza komplikace   diagnóza   MeSH
• hypertenze komplikace   diagnóza   farmakoterapie   MeSH
• imunosupresiva škodlivé účinky   MeSH
• inhibitory ACE terapeutické užití   MeSH
• lidé MeSH
• přežívání štěpu MeSH
• proteinurie diagnóza   etiologie   patofyziologie   terapie   MeSH
• recidiva MeSH
• rejekce štěpu diagnóza   etiologie   terapie   MeSH
• renin-angiotensin systém účinky léků   MeSH
• rizikové faktory MeSH
• TOR serin-threoninkinasy antagonisté a inhibitory   MeSH
• transplantace ledvin škodlivé účinky   MeSH
• věkové faktory MeSH
• výsledek terapie MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• antagonisté receptorů pro angiotenzin MeSH
• antihypertenziva MeSH
• imunosupresiva MeSH
• inhibitory ACE MeSH
• MTOR protein, human MeSH Prohlížeč
• TOR serin-threoninkinasy MeSH