Inulin clearance in the premature infant receiving indomethacin

Catterton, Zack; Sellers, Billy B.; Gray, Bonnie

doi:10.1016/s0022-3476(80)80757-8

Cited by 36 publications

(11 citation statements)

References 8 publications

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“…When administered postnatally to promote the pharmacological closure of a haemodynamically active patent ductus arteriosus, indomethacin may harm the immature newborn kidney. Transient sharp decreases in GFR and urine flow rate have indeed been reported after low and marginally effective doses of indomethacin (0.2 mg/kg given once) with persistant ductal constriction [32][33][34]. The mean duration of the renal abnormalities induced by indomethacin, most often reversible, varies from 2 to 6 days [32].…”

Section: Prostaglmldinsmentioning

confidence: 99%

Vasoactive factors in the immature kidney

Guignard

Gouyon

John³

1991

Pediatr Nephrol

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The newborn infant is in a state of renal insufficiency with a glomerular filtration rate (GFR) as low as 20 ml/min per 1.73 m2 at term, and 10 ml/min per 1.73 m2 at 28 weeks of gestation. While the immature "insufficient" kidney can cope with most of the normal demands, its reserve is limited, and often overwhelmed by commonly occurring neonatal stresses. Various vasoactive systems such as the renin-angiotensin system, intrarenal adenosine, the prostaglandins and the atrial natriuretic peptide, are hyperactive in the neonatal period. Some of these systems appear crucial for the maintenance of GFR. Overstimulation of both angiotensin II and adenosine by an hypoxaemic stress can further impair the GFR, eventually leading to established renal failure. Inhibition of angiotensin II formation by the administration of angiotensin converting enzyme inhibitors can, on the other hand, also lead to renal failure. Prevention of these renal risks requires a precise knowledge of the newborn kidney physiology, physiopathology and pharmacology.

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Section: Prostaglmldinsmentioning

confidence: 99%

Vasoactive factors in the immature kidney

Guignard

Gouyon

John³

1991

Pediatr Nephrol

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“…Indo methacin, a PG synthetase inhibitor, is com monly used to promote the pharmacological closure of a hemodynamically active patent ductus arteriosus (PDA). Transient side ef fects have been described after the use of indomethacin, such as hyponatremia, a 60% decrease in urine flow rate [5,23], a 30-40% decrease in GFR [4,23,29,40], and a vari able decrease in electrolyte excretion. These effects are already observed after low and marginally effective doses of indomethacin (0.2 mg/kg given once) with respect to persis tent ductal constriction [23], The mean du ration of these abnormalities, most often re versible, varies from 2 to 6 days [23].…”

Section: Drugs Given After Birthmentioning

confidence: 99%

Adverse Effects of Drugs on the Immature Kidney

Guignard

Jb²

1988

Neonatology

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The immature kidney may be adversely affected by a variety of vasoactive or diuretic drugs, either administered to the mother during pregnancy, or to the neonate. Inhibitors of the angiotensin-converting enzyme administered to the hypertensive pregnant woman can severely and sometimes definitely impair renal function in the fetus, leading to postnatal anuria. Pathogenesis involves interference with the renin-angiotensin system and the prostaglandins. Beta-adrenergic agents administered during labor depress glomerular filtration rate transiently. Tolazoline, an alpha-adrenergic blocking agent useful in the treatment of persistent pulmonary hypertension of the neonate induces intense renal vasoconstriction with consequent hypoperfusion. Indomethacin, a prostaglandin synthetase inhibitor used for the pharmacological closure of a patent ductus arteriosus, also increases renal vascular resistance, and decreases urine output. Furosemide, the drug most often used in oliguric neonates, may also adversely affect the newborn infant. Its use has been associated with an increase in the incidence of patent ductus arteriosus, hypercalciuria, nephrocalcinosis and secondary hyperparathyroidism. These observations demonstrate that the proper use of drugs requires that the therapeutic endpoint be clearly defined and the predictable side effects be anticipated.

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“…It has been ob served that these changes are associated with a rise in systemic blood pressure and a de crease in plasma renin activity [35], Following birth, the pattern of urinary excretion of prostaglandins and the role played by this system in controlling renal hemodynamics tend to be somewhat differ ent than what has been described during fetal life. First, the rate of urinary PGE2 and PGF2a excretion steadily increases after birth and continues to rise until adult life [1,5,74], Secondly, it has been suggested that prostaglandins may play an important role in the decrease in renal vascular resistance and rise in renal blood flow observed after birth [1,5,9], However, studies by Osborn et al [43] have not been able to demonstrate that inhibition of prostaglandin synthesis in unanesthetized newborn animals affects re nal hemodynamics. Also, despite the fact that renal prostaglandins have been impli cated as mediators of natriuresis in adults [42], changes in prostaglandin excretion rate in children are not related with changes in sodium excretion [1,5] Vasopressin and Vasotocin…”

Section: Kallikrein-kinin Systemmentioning

confidence: 99%

Hormonal Regulation of Renal Function during Development

Robillard¹,

Nakamura²

1988

Neonatology

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The present review summarizes current and new knowledge concerning the major hormonal systems that directly or indirectly affect renal function during development. The role of the renin-angiotensin-aldosterone system in regulating renal function during fetal and postnatal life is reviewed. A summary of the role of this system during fetal and postnatal stresses is also provided. The physiological role of the renal kallikrein-kinin system in the control of renal blood flow, renin release and sodium excretion during development is examined. Possible influences of the prostaglandin system on regulation of renal function and renin secretion during fetal and postnatal maturation are explored. The effect of vasopressin on the ability of the fetal and postnatal kidney to concentrate urine and regulate body fluid homeostasis is reviewed in detail. The physiologic action of vasotocin on renal sodium and water homeostasis is described. New information regarding the role of the sympathetic system in the regulation of renal hemodynamics and in the control of renal function during development is presented. Finally, recent studies demonstrating the effect of atrial natriuretic factor and corticosteroids on the developing kidney are discussed.

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Inulin clearance in the premature infant receiving indomethacin

Cited by 36 publications

References 8 publications

Vasoactive factors in the immature kidney

Vasoactive factors in the immature kidney

Adverse Effects of Drugs on the Immature Kidney

Hormonal Regulation of Renal Function during Development

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