Effect of Drugs on Renal Development

Schreuder, Michiel F.; Bueters, Ruud; Huigen, Marleen C. D. G.; Rüssel, Frans G. M.; Masereeuw, Rosalinde; Heuvel, Lambertus P. van den

doi:10.2215/cjn.04740510

Cited by 72 publications

(52 citation statements)

References 51 publications

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“…Extrapolating from animal models, these and other medications may impact nephron number as well as increase the risk of AKI in infants 43 . Interestingly, however, follow up of individuals exposed to betamethasone for 48 hours prior to birth did not reveal any increase in blood pressure at age 30 years compared to controls 44 .…”

Section: Developmental Determinants Of Low Nephron Numbermentioning

confidence: 99%

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

et al. 2013

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Developmental programming of non-communicable diseases is now an established paradigm. With respect to hypertension and chronic kidney disease, adverse events experienced in utero can affect development of the fetal kidney and reduce final nephron number. Low birth weight and prematurity are the most consistent clinical surrogates for a low nephron number, and are associated with increased risk of hypertension, proteinuria and kidney disease in later life. Rapid weight gain in childhood or adolescence further compounds these risks. Low birth weight, prematurity and rapid childhood weight gain should alert clinicians to an individual's life-long risk of hypertension and kidney disease, prompting education to minimize additional risk factors and ensuring follow-up. Birth weight and prematurity are significantly impacted by maternal nutrition and health during pregnancy. Optimization of maternal health and early childhood nutrition could therefore attenuate this programming cycle and reduce the global burden of hypertension and kidney disease in the future.

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Section: Developmental Determinants Of Low Nephron Numbermentioning

confidence: 99%

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

et al. 2013

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“…In addition, most studies have only limited consideration of ethnicity, sex, and the extremes of age (3,93). Human pediatric kidney data remain limited, so what we currently know, especially from a mechanistic standpoint, comes largely from a limited number of rodent studies.…”

Section: Pediatric Developmental Pharmacology and Drug Elimination Inmentioning

confidence: 99%

Handling of Drugs, Metabolites, and Uremic Toxins by Kidney Proximal Tubule Drug Transporters

Nigám¹,

Wu²,

Bush³

et al. 2015

Clinical Journal of the American Society of Nephrology

221

192

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The proximal tubule of the kidney plays a crucial role in the renal handling of drugs (e.g., diuretics), uremic toxins (e.g., indoxyl sulfate), environmental toxins (e.g., mercury, aristolochic acid), metabolites (e.g., uric acid), dietary compounds, and signaling molecules. This process is dependent on many multispecific transporters of the solute carrier (SLC) superfamily, including organic anion transporter (OAT) and organic cation transporter (OCT) subfamilies, and the ATP-binding cassette (ABC) superfamily. We review the basic physiology of these SLC and ABC transporters, many of which are often called drug transporters. With an emphasis on OAT1 (SLC22A6), the closely related OAT3 (SLC22A8), and OCT2 (SLC22A2), we explore the implications of recent in vitro, in vivo, and clinical data pertinent to the kidney. The analysis of murine knockouts has revealed a key role for these transporters in the renal handling not only of drugs and toxins but also of gut microbiome products, as well as liverderived phase 1 and phase 2 metabolites, including putative uremic toxins (among other molecules of metabolic and clinical importance). Functional activity of these transporters (and polymorphisms affecting it) plays a key role in drug handling and nephrotoxicity. These transporters may also play a role in remote sensing and signaling, as part of a versatile small molecule communication network operative throughout the body in normal and diseased states, such as AKI and CKD.

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“…However, NICU patients are commonly exposed to medications that impair nephrogenesis 137 (such as aminoglycoside antibiotics or prostaglandin synthetase inhibitors) and frequently experience AKI. If these are independent risk factors for CKD, avoidance of such medications or efforts to decrease AKI incidence could lead to better long-term outcomes.…”

Section: Nicu Managementmentioning

confidence: 99%

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

2013

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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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Effect of Drugs on Renal Development

Cited by 72 publications

References 51 publications

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease

Handling of Drugs, Metabolites, and Uremic Toxins by Kidney Proximal Tubule Drug Transporters

Short-Term Gestation, Long-Term Risk: Prematurity and Chronic Kidney Disease

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