Systemic Arterial Vasodilation, Vasopressin, and Vasopressinase in Pregnancy

Schrier, Robert W.

doi:10.1681/asn.2009060653

Cited by 56 publications

(50 citation statements)

References 16 publications

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“…[19][20][21] Despite stimulation of the RAAS, blood pressure is decreased, particularly in the first trimester, and healthy pregnant women are resistant to the pressor effects of angiotensin II. 22 GFR and renal blood flow increase by 40-65% and 50-85%, respectively, during normal pregnancy.…”

Section: Glomerular Hyperfiltration In Pregnancymentioning

confidence: 99%

Glomerular hyperfiltration: definitions, mechanisms and clinical implications

et al. 2012

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Glomerular hyperfiltration is a phenomenon that can occur in various clinical conditions including kidney disease. No single definition of glomerular hyperfiltration has been agreed upon, and the pathophysiological mechanisms, which are likely to vary with the underlying disease, are not well explored. Glomerular hyperfiltration can be caused by afferent arteriolar vasodilation as seen in patients with diabetes or after a high-protein meal, and/or by efferent arteriolar vasoconstriction owing to activation of the renin-angiotensin-aldosterone system, thus leading to glomerular hypertension. Glomerular hypertrophy and increased glomerular pressure might be both a cause and a consequence of renal injury; understanding the renal adaptations to injury is therefore important to prevent further damage. In this Review, we discuss the current concepts of glomerular hyperfiltration and the renal hemodynamic changes associated with this condition. A physiological state of glomerular hyperfiltration occurs during pregnancy and after consumption of high-protein meals. The various diseases that have been associated with glomerular hyperfiltration, either per nephron or per total kidney, include diabetes mellitus, polycystic kidney disease, secondary focal segmental glomerulosclerosis caused by a reduction in renal mass, sickle cell anemia, high altitude renal syndrome and obesity. A better understanding of the mechanisms involved in glomerular hyperfiltration could enable the development of new strategies to prevent progression of kidney disease.

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Section: Glomerular Hyperfiltration In Pregnancymentioning

confidence: 99%

Glomerular hyperfiltration: definitions, mechanisms and clinical implications

et al. 2012

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“…51 It is hypothesized that the drop in serum sodium is related to the occurrence of vasodilation, arterial underfilling, and subsequent ADH release. 52 Relaxin may play a role here because it has been shown to cause ADH secretion and water drinking in animal studies, and levels are increased during human pregnancy. 53,54 Mild hyponatremia occurs at the same time there is a rise in aldosterone and its antinatriuretic forces.…”

Section: Changes In Tubular Functionmentioning

confidence: 99%

“…It can be managed with desmopressin (DDAVP), which is resistant to degradation by vasopressinase. 52 Although frequent urination is often reported in pregnant women, true polyuria (>3 L/day) is rare.…”

Section: Changes In Tubular Functionmentioning

confidence: 99%

Renal Physiology of Pregnancy

Cheung

Lafayette

2013

Advances in Chronic Kidney Disease

501

314

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Pregnancy involves remarkable orchestration of physiologic changes. The kidneys are central players in the evolving hormonal milieu of pregnancy, responding and contributing to the changes in the environment for the pregnant woman and fetus. The functional impact of pregnancy on kidney physiology is widespread, involving practically all aspects of kidney function. The glomerular filtration rate increases 50% with subsequent decrease in serum creatinine, urea, and uric acid values. The threshold for thirst and antidiuretic hormone secretion are depressed, resulting in lower osmolality and serum sodium levels. Blood pressure drops approximately 10 mmHg by the second trimester despite a gain in intravascular volume of 30% to 50%. The drop in systemic vascular resistance is multifactorial, attributed in part to insensitivity to vasoactive hormones, and leads to activation of the renin-aldosterone-angiostensin system. A rise in serum aldosterone results in a net gain of approximately 1000 mg of sodium. A parallel rise in progesterone protects the pregnant woman from hypokalemia. The kidneys increase in length and volume, and physiologic hydronephrosis occurs in up to 80% of women. This review will provide an understanding of these important changes in kidney physiology during pregnancy, which is fundamental in caring for the pregnant patient.

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“…As the kidneys undergo the gestational process, a corresponding physiological compensation, such as glomerular hypertrophy and hyper-filtration, would occur to meet the excessive requirements of pregnancy, which is a consequence of increased renal blood flow [7, 8]. In healthy women, the changes in the kidneys as a result of pregnancy would stabilize naturally without any sequel after the delivery of a child [7–9].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Outcomes of Systemic Lupus Erythematous Patients after Pregnancy: A Nationwide Population-Based Cohort Study

et al. 2016

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BackgroundData on long-term maternal outcomes in patients with systemic lupus erythematosus (SLE) are lacking. The study aimed to explore the relationships among SLE, pregnancy, outcomes of end-stage renal disease (ESRD), and overall mortality.MethodsWe established a retrospective cohort study consisting of four cohorts: pregnant (case cohort) and nonpregnant SLE patients, as well as pregnant and nonpregnant non-SLE patients. One case cohort and three comparison cohorts were matched by age at first pregnancy and index date of pregnancy by using the Taiwan National Health Insurance Research Dataset. All study subjects were selected based on the index date to the occurrence of ESRD or overall death. Cox proportional hazard regression models and Kaplan–Meier curves were used in the analysis.ResultsSLE pregnant patients exhibited significantly increased risk of ESRD after adjusting for other important confounders, including immunosuppressant and parity (HR = 3.19, 95% CI: 1.35–7.52 for pregnant non-SLE; and HR = 2.77, 95% CI: 1.24–6.15 for nonpregnant non-SLE patients). No significant differences in ESRD incidence were observed in pregnant and nonpregnant SLE patients. Pregnant SLE patients exhibited better clinical condition at the baseline and a significantly lower risk of overall mortality than nonpregnant SLE patients.ConclusionsOur data support current recommendations for SLE patients to avoid pregnancy until disease activity is quiescent. Multicenter recruitment and clinical information can be used to further examine the association of SLE and ESRD (or mortality) after pregnancy.

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Systemic Arterial Vasodilation, Vasopressin, and Vasopressinase in Pregnancy

Cited by 56 publications

References 16 publications

Glomerular hyperfiltration: definitions, mechanisms and clinical implications

Glomerular hyperfiltration: definitions, mechanisms and clinical implications

Renal Physiology of Pregnancy

Long-Term Outcomes of Systemic Lupus Erythematous Patients after Pregnancy: A Nationwide Population-Based Cohort Study

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