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Rein et grossesse. Cours des internes 7 avril 2014 Charlotte Laurent Philippe Thorel. Rappels Grossesse modifications multiples. Modifications anatomiques. Augmentation de la taille des reins. Augmentation de la vascularisation du volume interstitiel Nb de nphrons identique. - PowerPoint PPT Presentation


Rein et grossesse

Rein et grossesseCours des internes 7 avril 2014Charlotte LaurentPhilippe Thorel

Rappels Grossesse modifications multiples

Modifications anatomiquesAugmentation de la vascularisation du volume interstitiel Nb de nphrons identiqueUp to date

+ 1 1.5 cm + 30%Augmentation de la taille des reins3Modifications anatomiquesFandes et al. American Journal of Obstetrics and gynecology. Volume 178, Issue 5, May 1998, 1082-1086Dilatation des cavits pylocaliciellesCompression des uretres (D>G) par utrus gravideChangement intrinsque de luretre par progestrone (rduction tonus et pristaltisme)A ne pas confondre avec dilatation pathologique !Compression des uretres (surtout droit par utrus gravide pouss par sigmode, qui va tre comprim par artre iliaque droite ou veine ovarienne droite ou ligament ovarien) , chgt intrinsque de luretre et effet de la progestrone (rduction du tonus urtral, du pristaltisme) vont dilater les uretres, plus droite (peux contenir jusqu 200-300 mL durines !Reflux vsico urtral possible car modification du tonus de la vessie et des uretresAttention aux lithiases qui peuvent mimer la dilatation

4Modifications de lhmodynamique rnaleRENAL HEMODYNAMICSNormal pregnancy is characterized by widespread vasodilation, with increased arterial compliance and decreased systemic vascular resistance (figure 1). These global hemodynamic changes are accompanied by increases in renal perfusion and glomerular filtration rate (table 1). In late gestation, assumption of the left lateral position is associated with increases in glomerular filtration rate and sodium excretion [20].Humoral factors that contribute to volume regulation during pregnancy and cardiovascular and hemodynamic changes related to pregnancy are discussed separately. (See "Maternal endocrine and metabolic adaptation to pregnancy" and "Maternal cardiovascular and hemodynamic adaptations to pregnancy".)Several authors have published normal reference ranges for laboratory results in pregnant women, which vary slightly [21-23]. The following table represents one example (table 2).Increase in GFRGlomerular filtration rate (GFR) rises markedly during pregnancy, primarily due to elevations in cardiac output and renal blood flow. Studies in both rodents and humans suggest that the increase in GFR results from enhanced glomerular plasma flow, rather than increased intraglomerular capillary pressure.The increase in GFR is observed within one month of conception and peaks at approximately 40 to 50 percent above baseline levels by the early second trimester and then declines slightly toward term [24]. Renal blood flow increases by 80 percent above nonpregnant levels.The physiologic increase in GFR during pregnancy results in a decrease in serum creatinine concentration, which falls by an average of 0.4 mg/dL (35 micromol/L) to a normal range of 0.4 to 0.8 mg/dL (35 to 70 micromol/L). Thus, a serum creatinine of 1.0 mg/dL (88 micromol/L), while normal in a non-pregnant individual, reflects renal impairment in a pregnant woman. Blood urea nitrogen (BUN) levels fall to approximately 8 to 10 mg/dL (2.9 to 3.9 mmol/L) for the same reason.MechanismsThe mechanisms for decreased vascular resistance and increased renal plasma flow during pregnancy are not fully understood. Reduced vascular responsiveness to vasopressors such as angiotensin 2, norepinephrine, and vasopressin is well-documented [25]. Nitric oxide synthesis increases during normal pregnancy and may contribute to the systemic and renal vasodilation and the fall in blood pressure [26,27].The ovarian hormone and vasodilator relaxin appears to be a key upstream mediator of enhanced nitric oxide signaling in pregnancy. Relaxin is a peptide hormone in the insulin family; it is normally produced in the corpus luteum, and in pregnancy is secreted in large amounts by the placenta and decidua in response to human chorionic gonadotropin (hCG) [28]. Relaxin increases endothelin and nitric oxide production in the renal circulation, leading to generalized renal vasodilation, decreased renal afferent and efferent arteriolar resistance, and a subsequent increase in renal blood flow and GFR.Chronic administration of relaxin to conscious male and castrated female rats mimics the renal hemodynamic changes of pregnancy (20 to 40 percent increase in GFR and renal plasma flow); these changes can be abolished by the administration of a nitric oxide synthase inhibitor [29]. In pregnant rats, increases in GFR and renal plasma flow can also be abolished by the administration of antirelaxin antibodies or by ovariectomy [30].Estimation of GFRManagement of pregnant women with preeclampsia or preexisting kidney disease requires an understanding of whether the GFR (and therefore, disease severity) is changing or stable; knowledge of the absolute value of the GFR is not usually needed. Changes in GFR are best identified by monitoring changes in the serum creatinine concentration. A rising serum creatinine concentration implies a reduction in GFR, a falling level indicates improvement, and a stable value usually reflects stable function. Among women with a normal or near normal serum creatinine at baseline, a small rise in serum creatinine can reflect a marked reduction in GFR. (See "Assessment of kidney function".)Assessment of renal function with a 24-hour urine collection for creatinine clearance is cumbersome for the patient, and is of limited accuracy in pregnancy [31]. Overcollection and undercollection of 24-hour urine samples appear to be more common in pregnancy than in nonpregnant women [31]. This may be due, in part, to urinary stasis from dilatation of the lower urinary tract in pregnancy; several hundred milliliters of urine can be trapped in the dilated ureters, resulting in a significant lapse between urine formation and urine collection. Estimates of GFR based on the Modification of Diet in Renal Disease (MDRD) equation are also inaccurate during pregnancy; studies of GFR with measured values obtained by inulin clearance in early and late normal pregnancy and in pregnancies complicated by renal disease or preeclampsia show that MDRD substantially underestimates GFR during pregnancy and cannot be recommended for use in clinical practice [32,33]. (See "Assessment of kidney function", section on 'Limitations of using creatinine clearance' and "Assessment of kidney function", section on 'Estimation equations'.)Up to dateAugmentation compliance artrielleDiminution des rsistances artriellesAugmentation de la perfusion rnaleDs 1 mois Max 50% dbut 2T puis retour la normal progressifAugmentation du dbit cardiaqueRduction de la rponse aux vasopresseurs ?Angiotensine 2/ Vasopressine/ Norpinphrine Augmentation de la synthse de NO ?PlacentaRelaxine ?Reproduit sur modle murinAttention : une petite augmentation de la cratinine srique peut reflter une rduction marque du DFGExcrtion sode et DFG sont meilleurs en dcubitus latral gauche qdla grossesse est avance !Modif du DFG ds 1 mois de grossesse et augmente jusqu 40-50% jusquau dbut du 2 trimestre puis diminueDiminution de la cratinine sanguine de 35 mol/L pour une normale de base 35-70 mol/LMcanismes non totalement connus : rduction de la rponse aux vasopresseurs (angiotensine2, vasopressine, norpinphrine, augmentation de la synthse de NO Favorisant la vasodilatation. Relaxine, hormone ovarienne stimulant la synthse doxyde nitrique et dendothline est scrte par le placenta en rponse BHCGChronic administration of relaxin to conscious male and castrated female rats mimics the renal hemodynamic changes of pregnancy (20 to 40 percent increase in GFR and renal plasma flow); these changes can be abolished by the administration of a nitric oxide synthase inhibitor [29]. In pregnant rats, increases in GFR and renal plasma flow can also be abolished by the administration of antirelaxin antibodies or by ovariectomy [30].Les variations de taux de filtration glomrulaire sont mieux identifis par des changements dans la concentration de cratinine srique de surveillance. Une concentration croissante de la cratinine srique implique une rduction de la filtration glomrulaire, un niveau en baisse indique une amlioration, et une valeur stable reflte gnralement la fonction stable. Parmi les femmes ayant une normale ou prs de la cratinine srique normale au dpart, une petite augmentation de la cratinine srique peut reflter une rduction marque du DFGLes estimations de la DFG bases sur la modification de l'alimentation dans la maladie rnale ( MDRD ) quation sont galement inexactes pendant la grossesse , les tudes de GFR avec les valeurs de mesure obtenues par la clairance de l'inuline au dbut et la fin d'une grossesse normale et dans les grossesses compliques par la maladie rnale ou pr-clampsie montrent que MDRD sous-estime sensiblement GFR pendant la grossesse et ne peut tre recommand pour une utilisation en pratique clinique

5Modifications de la pression artrielle

American Society of Hypertension 2009PA va baisser les 2 premiers trimestres et remonter aux valeurs habituelles au 3 trimestre et ventuellement rvler une HTA prsente avant la grossesse mais non connue car non suivie si elle persiste aprs la grossesse

6Autres ModificationsWomen, kidney disease, and pregnancy.Smyth A, Radovic M, Garovic VD.Adv Chronic Kidney Dis. 2013 Sep;20(5):402-10. doi: 10.1053/j.ackd.2013.06.004.Dysfonction tubulaire proximaleRduction de la rabsorption du glucose/phosphate/A. urique..Diminution uricmieNadir 119-178 mol/L 22-24 SA (hmodilution +augmentation du DFG) Nouveau pt dquilibre du NaDiminution de la natrmie de 4 5 mqDiminution de losmolalit = 270 mosm/kgImmunitdiminution de la voie TH1 pour tolrer le ftus et Augmentation de lactivit TH2 (risque pousse maladie mdie par TH2 => lupus)Augmentation de la Pu physiologiqueMax 300 mg/jHyponatrmieDiminution de losmolalit avec normale vers 270 mosm/kgDiminution de la natrmie de 4 5 mq/lC