Hypertension and CKD
Division of Nephrology and Hypertension, Cincinnati Children's Hospital Medical Center, OH 45229-3039, USA.Advances in chronic kidney disease (Impact Factor: 2.05). 09/2011; 18(5):355-61. DOI: 10.1053/j.ackd.2011.03.003
Hypertension is found in more than 50% of pediatric patients with CKD. However, its prevalence varies according to the cause of CKD. It is relatively infrequent in children with structural disorders. Acquired renal disorders are associated with an increased prevalence of hypertension, similar to that of adults. Recent studies using ambulatory blood pressure monitoring indicate that children with CKD also have a high prevalence of masked hypertension. Similar to adults, long-standing and uncontrolled hypertension in children is associated with the progression of CKD and development of end-organ damage including early cardiomyopathy and premature atherosclerosis. Aggressive treatment of hypertension should be an essential part of pediatric CKD care, not just to prevent the development of symptomatic cardiovascular disease but also to delay progression of CKD. Recent findings from the European Effect of Strict Blood Pressure Control and ACE Inhibition on Progression of Chronic Renal Failure in Pediatric Patients (ESCAPE) trial have shown that the aggressive treatment of blood pressure, to below the 50th percentile, has even greater benefit in children with CKD, unlike results seen in adult studies.
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ABSTRACT: Autosomal recessive polycystic kidney disease (ARPKD) is a severe, typically early onset form of renal cystic disease. The care of ARPKD patients has traditionally been the purview of pediatric nephrologists for management of systemic hypertension and progressive renal insufficiency. However, the disease has multisystem manifestations and a comprehensive care strategy frequently requires a multidisciplinary team. In severely affected infants, the diagnosis often is first suspected by obstetricians when enlarged, echogenic kidneys and oligohydramnios are detected on prenatal ultrasounds. Neonatologists are central to the care of these infants, who may have respiratory compromise due to pulmonary hypoplasia and massively enlarged kidneys. Among neonatal survivors, a subset of ARPKD patients has clinically significant congenital hepatic fibrosis, which can lead to portal hypertension, requiring close monitoring by pediatric hepatologists. Surgical consultation may be sought to access pre-emptive nephrectomy to relieve mass effect, placement of dialysis access, surgical shunting procedures, and kidney and/or liver transplantation. Recent data suggest that children with ARPKD may be at risk of neurocognitive dysfunction, and may require neuropsychological referral. In addition to these morbidities, families of patients with ARPKD face decisions regarding genetic testing of affected children, testing of asymptomatic siblings, or consideration of preimplantation genetic diagnosis for future pregnancies. These issues require the input of genetic counselors, geneticists, and reproductive endocrinologists. As a result, the management of ARPKD requires the involvement of multiple subspecialists, as well as the general pediatrician, in a complex care network. In this review, we discuss the genetics of this disorder and provide an overview of the associated pathobiology; outline the spectrum of clinical manifestations of ARPKD and the management of organ-specific complications; discuss other disorders that involve genes encoding cilia-associated proteins that can clinically mimic ARPKD; review the animal models available for preclinical studies; and finally, consider future directions for potential targeted therapies.
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ABSTRACT: Although hypertension (HTN) is a predictor of mortality, recent data have questioned the link between baseline HTN and mortality in incident hemodialysis (HD) patients. We used Taiwan's National Health Insurance claim data (NHRI-NHIRD-99182) to investigate the association. In 1999, this longitudinal cohort study enrolled 5752 new HD patients. Follow-up began from the initiation of HD until death, the end of HD, or the end of 2008. A Kaplan-Meier survival analysis was done. Cox proportional hazard analysis was used to identify the risk factors for mortality. The prevalence of baseline HTN was 75.47%. Patients with HTN had a higher prevalence of diabetic mellitus (DM) and cardiovascular diseases. The 1-, 5-, and 9-year cumulative survival rates were 95.5, 63.7 and 41.8% in patients with HTN, and 95.5, 71.0, and 52.0% in those without HTN (log-rank test: P <0.001). Multivariate analysis showed that patients with baseline HTN may have a higher survival rate (hazard ratio (HR) 0.901, 95% confidence interval (CI): 0.819-0.992). After stratification by age and DM, only elderly (≥65) patients without DM had a significantly higher survival rate (HR 0.769, 95% CI: 0.637-0.927). HTN predicts lower mortality with increasing age in patients with congestive heart failure (CHF) or coronary artery disease (CAD). There is a reverse (counterintuitive) association between baseline HTN and mortality in elderly HD patients without DM and a clear tendency for a reverse association with increasing age in patients with CHF or CAD. Further study of the association between HTN and mortality in older HD patients may be warranted.
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ABSTRACT: Thanks to remarkable advances in neonatal intensive care, infants who once had little chance for survival can now enter adulthood. Yet the consequences of premature birth or low birth weight (LBW) on nephrogenesis, final nephron number, and long-term kidney function are unclear. This review focuses on the theory, experimental evidence, and observational data that suggest an increased risk of chronic kidney disease (CKD) for infants born prematurely. Many premature and LBW infants begin life with an incomplete complement of immature nephrons. They are then exposed to a variety of external stressors that can hinder ongoing kidney development or cause additional nephron loss such as hemodynamic alterations, nephrotoxic medications, infections, and suboptimal nutrition. Acute kidney injury, in particular, may be a significant risk factor for the development of CKD. According to Brenner's hypothesis, patients with decreased nephron number develop hyperfiltration that results in sodium retention, hypertension, nephron loss, and CKD due to secondary focal segmental glomerulosclerosis. Because the risk of CKD in premature and LBW infants has not been accurately determined, there are no evidence-based recommendations for screening or management. Yet with the first generation of infants from the surfactant era only now reaching adulthood, it is possible that there is already an unrecognized epidemic of CKD. We suggest individualized, risk-based assessments of premature and LBW infants due to the increased risk of CKD and call for additional research into the long-term risk for CKD these infants face.
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