Strict Blood-Pressure Control and Progression of Renal Failure in Children

Trivelli, Antonella; Picca, Stefano; Litwin, Mieczysław; Peco-Antić, Amira; Testa, Sara; Emre, Sevinç; Afonso, Alberto Caldas; Niaudet, Patrick; Bakkaloğlu, Ayşı̇n; Montini, Giovanni; Wingen, A.-M.; Sartipy, Peter; Jeck, Nikola; Berg, Ulla; Çalışkan, Salim; Wygoda, Simone; Hohbach-Hohenfellner, Katharina; Dušek, Jiří; Urasiński, Tomasz; Arbeiter, Klaus; Neu, Thomas R.; Gellermann, Jutta; Fischbach, Michel; Möller, Kristina; Wigger, Marianne; Peruzzi, Licia; Mehls, Otto; Schaefer, Franz

doi:10.1056/nejmoa0902066

Cited by 812 publications

(259 citation statements)

References 26 publications

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“…A larger randomized study showed that both losartan and enalapril decreased proteinuria in 268 children with normal or high blood pressure [16]. The ESCAPE trial [17] found that 5-year intensified BP control in 385 children with CKD who received a fixed dose of an ACE inhibitor, delayed the time to 50 percent reduction in glomerular filtration rate (GFR) or progression to ESKD more effectively than conventional BP control. Proteinuria decreased by more than 50 percent during the firs six months, but, unexpectedly, gradually increased thereafter towards baseline values despite good BP control in both treatment groups.…”

Section: Introductionmentioning

confidence: 99%

Achieving remission of proteinuria in childhood CKD

et al. 2016

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Background A multidrug treatment titrated to proteinuria by maximum tolerated doses of an angiotensin converting enzyme (ACE) inhibitor and an angiotensin receptor blocker (ARB) combined with intensified blood pressure (BP) control prevented renal function loss in adults with proteinuric nephropathies. Herein, we investigated the effects of this program in children. Methods From May 2002 to September 2014 we included in this observational, longitudinal, cohort study twenty consecutive children with chronic nephropathies and 24-h proteinuria >200mg who received ramipril and losartan up-titrated to maximum approved doses (2.48±1.37 mg/m2 and0.61±0.46 mg/kg daily, respectively). The primary efficacy endpoint was more than 50% 24-h proteinuria reduction to <200 mg (Remission). Secondary outcomes included changes in proteinuria, serum albumin, BP, and glomerular filtration rate (GFR). Results Mean (±SD) patient age at inclusion was 13.8±2.8 years, median (IQR) serum creatinine 0.7 (0.6-1.0) mg/dl and proteinuria 690 (379-1270) mg/24h [or 435 (252-711) mg/m2/24h]. Proteinuria significantly decreased by month six and serum albumin levels increased over a follow-up period of 78 (39-105) months. In the nine children who achieved remission, proteinuria reduction persisted throughout the whole follow-up without rebounds. GFR improved in the children with remission and worsened in those without. Mean±SD GFR slopes (+0.023±0.15 vs. -0.014±0.23 ml/min/1.73m2/month, respectively) significantly (p<0.05) differed, whereas BP control was similar between the two groups. We observed hyperkalemia in two children. Conclusions Combination therapy with maximum approved doses of ACE inhibitors and ARBs may achieve proteinuria remission with kidney function stabilization or even improvement in a substantial proportion of children with proteinuric nephropathies, and is safe.

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Section: Introductionmentioning

confidence: 99%

Achieving remission of proteinuria in childhood CKD

et al. 2016

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“…They were thus not treated with RAS inhibitors. Hypertensive patients with hypodysplasia were reported to benefit from strict control of BP with angiotensin converting enzyme inhibitors [13]. Also, albuminuria and proteinuria are correlated with disease progression in children with CKD [14].…”

Section: Discussionmentioning

confidence: 99%

Trajectory of Estimated Glomerular Filtration Rate Predicts Renal Injury in Children with Multicystic Dysplastic Kidney

Matsumura¹,

Sugii²,

Awazu³

2018

Nephron

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Background/Aims: Children with a solitary functioning kidney have a risk of renal injury caused by hyperfiltration. Timely intervention with renin-angiotensin inhibitors may be beneficial. We examined whether trajectory of estimated glomerular filtration rate (eGFR) would predict renal injury, defined as microalbuminuria/proteinuria, hypertension, and/or a decline in eGFR. Methods: Seventeen patients (male 7, female 10) with multicystic dysplastic kidney (MCDK; median age 13 years, range 6–19 years) followed in our clinic were examined retrospectively. An eGFR decline was defined as a fall to < 90 mL/min/1.73 m² or a decline of > 5 mL/min/1.73 m²/year for those with baseline eGFR of ≥90 or < 90 mL/min/1.73 m² respectively. Results: Nine patients had renal injury at the time of investigation. Compared with 8 patients without renal injury, those with renal injury tended to be older (14.7 ± 4.2 vs. 11.4 ± 4.6 years) and the birth weight was smaller (2,538 ± 281 vs. 2,966 ± 361 g, p < 0.05). The frequency of contralateral congenital anomaly of kidney and urinary tract (cyst, hydronephrosis, or vesicoureteral reflux) were not different. The trajectory of eGFR in those without renal injury was either an increase (n = 3) or unidentifiable (n = 5), whereas that in the renal injury group was exclusively an increase followed by decline (p < 0.05). The average age of the onset of eGFR decline was 9.4 ± 4.2 years and that of the start of renal injury (albuminuria/proteinuria 5, eGFR decline 4, hypertension 1) was 12.5 ± 4.2 years. Conclusion: All the children with MCDK who developed renal injury had eGFR trajectory of increase followed by decline. Renal injury followed the peak eGFR by 3 years on average. This observation is in agreement with the hyperfiltration theory and underscores the importance of following eGFR trajectory closely.

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“…A number of studies found that aggressive blood pressure control delays the progression of chronic kidney disease (CKD). These include the ESCAPE study, which found that aggressive blood pressure control in children with CKD resulted in better GFR and reduced progression to ESRD [14]; also a study conducted on an elderly population in Denmark concluded that a reduced incidence of ESRD in this population was associated with an increase in the prescription rates for anti-hypertensive drugs, especially RAAS blockade with angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockade (ARB). Other studies such as the MDRD study found limited benefit in aggressive versus normal blood pressure control [15,] while other studies found no benefit beyond that of normal blood pressure control [16,17].…”

Section: Hypertension and Polycystic Kidney Diseasementioning

confidence: 99%

Renin-Angiotensin-Aldosterone System Antagonism and Polycystic Kidney Disease Progression

Hian

Lee

Thomas³

2016

Nephron

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Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a systemic disease characterised by the formation of multiple renal cysts that adversely affect renal function. ADPKD shows significant progression with age when complications due to hypertension are most significant. The activation of the renin-angiotensin-aldosterone system (RAAS) occurs in progressive kidney disease leading to hypertension. The RAAS system may also contribute to ADPKD progression by stimulating signalling pathways in the renal cyst cells to promote growth and deregulate epithelial transport. This mini review focuses on the contribution of the RAAS system to renal cyst enlargement and the potential for antagonists of the RAAS system to suppress cyst enlargement as well as control ADPKD-associated hypertension.

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Strict Blood-Pressure Control and Progression of Renal Failure in Children

Cited by 812 publications

References 26 publications

Achieving remission of proteinuria in childhood CKD

Achieving remission of proteinuria in childhood CKD

Trajectory of Estimated Glomerular Filtration Rate Predicts Renal Injury in Children with Multicystic Dysplastic Kidney

Renin-Angiotensin-Aldosterone System Antagonism and Polycystic Kidney Disease Progression

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