case conference 報告者： r3 潘恆之報告者： r3 潘恆之指導老師：方基存醫師...

Case Conference R3 R3 2010.11.24 2010.11.24

Outline Case report: A 35-year-old female with newly onset of hypertension and proteinuria since the 3 rd trimester suffered from postpartum acute renal failure Differential diagnosis of hypertension disorder related to pregnancy Differential diagnosis of proteinuria Review of preeclampsia Future direction

Case General Data No: 39036654 Gender: female Age: 35-year-old Ethnic: Taiwanese Marriage: married Occupation: Electronics Travel history: denied in recent three months admission date : 2010/10/04

Chief Complaint Progressive dyspnea for 5 days.

Present Illness The 35-year-old woman had pregnancy with estimated date of confinement on 2010/10/11. Pre-partum exam recorded progressively elevated blood pressure up to 130/80 mmHg without proteinuria in third trimester. Progressive bilateral leg edema was noted since 09/14. She was admitted in hospital and received Cesarean section on 09/28.

Present Illness After the operation 1. Post-partum hemorrahge with hypovolemic shock intensive blood transffusion and fluid resuscitation. 2. Acute kidney injury with decreased urine output and pulmonary edema. Furosemide Dyspnea improved gradually after urine output increase transffer to our ER on 10/04.

Past history Maternal History: G2P2A1, delivered 1 female baby with birth body weight:3395 Medical history: Denied any systemic disease Operative history: 1. Left indirect inguinal hernia post herniorrhaphy on 2006/11/23. 2. Primary Cesarean section on 2010/9/28.

Personal history Alcohol usage: denied Cigarette: denied Betel nut: denied OTC drugs: denied Chinese Herbs: denied Food allergy: never Drug allergy: never

Family history Her grandpa, grandma, aunt and uncle had history of hypertension. Pedigree was shown as following figure. ( :male; :female; :dead male; :dead femle; :patient)

Physical examination Vital Sign: T:37.3 degree; P:90bpm; R:16cpm; BP:149/96mmhg Height: 152cm; weight: 42.4kg. HEENT: conjunctiva: non-pale; sclera: anicteric; CHEST: breathing sound: bilateral clear; heart sound: regular heart beats without audible murmur ABD.: soft and flat; no tenderness; surgical scar (+) normoactive bowel sounds no Murphys sign; no McBurney tenderness. EXT.: Free movable without limitation. Bilateral minimal pitting edema.

10/04 Lab Exam at ER Hemogram11/30 WBC1000/uL9.1 Hemoglobing/dL10.6 Hematocrit%29.9 MCVfL120.1 Platelets1000/uL211 Segment%73.4 Lymphocyte%15.9 Monocyte%9.3 Eosinophil%0.6 Basophil%0.8 P.T 12.7 INR 1.1 Biochemistry11/30 BUN (B)mg/dL14.0 Creatininemg/dL1.04 Bilirubin (T)mg/dL6.1 AST (GOT)U/L346 ALT/GPTU/L146 ALK-PU/L149 Sugarmg/dL149 ALBg/dL3.75 Namg/dL125 Kmg/dL1.3 Camg/dL6.8 CRPmg/L60.67 Ammoniamg/dL130

Urinalysis11/30 Color Orange SP.Gravity 1.013 pH 6.5 Leukocyte Trace Nitrite Negative Proteinmg/dLTrace Glucoseg/dLNegative Ketone Trace UrobilinogenEU/dL4.0 H Bilirubin 2+ Blood Negative RBC/uL0 WBC/uL4 Virology11/30 HBsAgtiterNegative Anti-HbstiterNegative Aati-HBctiterNegative Anti-HAVtiterNegative Anti-HCVtiterNegative 10/04 Lab Exam at ER

2010/10/04 CXR A-P view (Supine) Patchy opacities in bil. lower lungs suspect pulmonary edema, r/o pleural effusion or pneumonia Suspect Cariomegaly No obvious fracture No mediastinal widing No large airway anomaly

2010/10/05 Abdominal Sonography Value: Spleen Index:5.1 x 3.1 cm CBD: 0.47 cm Impression: - Parenchymal liver disease, score 6 - Liver nodules - Ascites and right pleural effusion; - Right hydronephrosis; - Cholecystopathy.

2010/10/5 Cardiac 2D echo: Value: IVS(mm) = 10 LVPW(mm) = 9 LVEDD(mm) = 52 LVESD(mm) = 34 LVEF: M-mode(Teichholz)= 63 % Conclusion: - Adequate LV systolic function with normal wall motion - Mild MR,AR and TR - Mild pulmonary hypertension - Dilated LV

ER Impression Acute renal failure with pulmonary congestion Hypokalemia Postpartum hemorrahge

ER Management Medication: Rocephin (500mg/vial) 2PC Q12h Furosemide (20mg/amp) 1PC Q12h Potassium chloride (600mg/tab) 1PC TID Amlodipine (5mg/tab) 1PC QD IVF: N/S 500cc + KCl 15meq run 60cc/hr Admission to Nephro ward on 10/06

2010/10/06 2010/10/07 2010/10/08 2010/10/09 2010/10/10 BU N 39.3 32.0 29.5 Cr 2.80 2.00 1.34 Na 141 142 140 K 2.5 3.6 Ca 8.1 P 2.7 CO2 26.0 Rocephin Amlodipine Isorsobide-5-mononitrate Abd. echo Cardic echo Kidney echo

Ca7.07.58.6 P2.83.23.3 Na141140138 K3.74.24.8 Cl102104 Mg1.51.61.7 Rocephin Amlodipine EKG MBD 2010/10/16 2010/10/12 2010/10/13 2010/10/14 2010/10/152010/10/11 Valsartan Isorsobide-5-mononitrate Chest echo

Impression 1. Acute kidney injury, RIFLE-F, favor due to hypovolemic shock from postpartum hemorrahge 2. Fever with leukocytosis, favor sepsis from post-partum hemorrahge 3. Hypokalemia, favor loop diuretic effect

Outline Differential diagnosis of hypertensive disorder related to pregnancy Differential diagnosis of proteinuria Review of preeclampsia Future direction Review of this case

Hypertensive disorders related to pregnancy Preclampsia Chronic hypertension Preeclampsia superimpsed upon chronic hypertension Gestational hypertension

Hypertensive disorders related to pregnancy Preclampsia --- Hypertension and proteinuria after 20 th wks of gestation in a previously hypertensive disorders related to pregnancy normotensive woman Chronic hypertension --- Hypertension antedates pregnancy or before the 20 th wks of pregnancy or persists longer than 12 th wks postpartum.

Hypertensive disorders related to pregnancy Preeclampsia superimpsed upon chronic hypertension --- a. Preexisting hypertension develops new onset proteinuria after 20 th wks of gestation b. Preexisting hypertension and proteinuria with an exacerbation of blood pressure ( SBP > 160mmhg or DBP > 110mmhg) Gestational hypertension --- It should resolve by 12 th wks postpartum

Etiology of proteinuria

National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol 2000;183:S122.

History of Preeclampsia Eclampsia has been recognized clinically since Hippocrates. Two thousand years ago, Celsus described pregnancy-associated seizures and named eclampsia the Greek word for lightning In 1843, Rayer and Lever described the association of proteinuria with eclampsia. Hippocrates Celsus

History of Preeclampsia In 1884, Schedoff and Porockjakoff first observed the link between hypertension and eclampsia. Twentieth century began to realize that proteinuria and hypertension were strong predictiors for the onset of eclampsia. -- this prequel of eclampsia was termed preeclampsia

Leon Chesley 1908-2000

Introduction of Preeclampsia Pregnancy-associated hypertension, proteinuria and edema A systemic disease that results from placental defects occurs in about 57% of pregnancies worldwide, relate to about 15% of preterm births The incidence is much higher in developing countries. Emergent delivery of the baby alleviates the maternal symptoms, but may lead to increased morbidity for the baby

Definition 1972 recommendations of the American College of Obstetricians and Gynecologists a. Increased blood pressure after 20 weeks of gestation (140/90 mm Hg) or an increase in systolic pressure of 30 mm Hg or in diastolic pressure of 15 mm Hg b. Proteinuria (0.3 g of protein in a 24-hour urine specimen or a urine dipstick result of 1+).

Pathophysiology of preeclampsia Noris M et al. (2005) Mechanisms of Disease: pre-eclampsia Nat Clin Pract Neprol 1: 98114 doi:10.1038/ncpneph0035 Placentation Abnormalities a. Placental tissue is necessary for development of the disease, but the fetus is not. b. Preeclampsia is always cured after delivery of the placenta The Maternal Syndrome a. The abnormal placentation release of secreted factors that enters the mothers circulation. b. All of the clinical features of preeclampsia are maternal responses to generalized endothelial dysfunction

Placentation Abnormalities ( Stage I ) -- Abnormal remodeling of spiral arteries

The Maternal Syndrome (stage II )

VEGF: vascular endothelial growth factor PlGF: placental growth factor FLT-1: fms-like tyrosine kinase 1 sFLT-1:Soluble fms-like tyrosine kinase 1 Membrane bound receptor

Noris M et al. (2005) Mechanisms of Disease: pre-eclampsia Nat Clin Pract Neprol 1: 98114 doi:10.1038/ncpneph0035 Role of the soluble form of Fms-like tyrosine kinase 1 in the maternal syndrome of pre-eclampsia

sEng:Soluble endoglin Glomerular Placenta Liver Peripheral blood Schistocytes & reticulocytosis Multifocal necrosis Diffuse inflammation at the maternalfetal junction Hemorrhagic infarction and fibrinoid necrosis with lumen obstruction of vessel Endolitheosis Nature Medicine - 12, 642 - 649 (2006) Published online: 4 June 2006; | doi:10.1038/nm1429 sFLT-1:Soluble fms-like tyrosine kinase 1

The Maternal Syndrome (stage II ) All of the clinical features of preeclampsia are maternal responses to generalized endothelial dysfunction !! sFlt-1, sEndoglin(sEng )

Other hypotheses Baha Sibai, Gus Dekker, Michael Kupferminc. The Lancet. London: Feb 26-Mar 4, 2005. Vol. 365, Iss. 9461; p. 785

The putative role of COMT, HIF-1a and 2-ME

Biology of preeclampsia

Noris M et al. (2005) Mechanisms of Disease: pre-eclampsia Nat Clin Pract Neprol 1: 98114 doi:10.1038/ncpneph0035 L -Arginine depletion in pre-eclampsia promotes poor placental perfusion and microvascular damage

sFlt-1 hypothesis. Garovic V D et al. Nephrol. Dial. Transplant. 2007;22:1136- 1143 The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: [email protected]

Unifying hypothesis of pre-eclampsia pathophysiology

Clinical feature --- hypertension Plasma renin activity

Clinical feature --- hypertension

Clinical feature --- Proteinuria : J Clin Invest. 2004 November 15; 114(10): 14121414

Clinical feature --- Proteinuria

Method: Renal tissue was obtained from 7 severe preclampsia women

Schematic of the slit diaphragm and other important proteins involved in maintaining foot process assembly. Quaggin S E, Kreidberg J A Development 2008;135:609- 620

Immunocytochemistry for nephrin. Garovic V D et al. Nephrol. Dial. Transplant. 2007;22:1136-1143 Immunocytochemistry for synaptopodin Immunocytochemistry for podocin Control Case 3 Case 2 Case 5 Case 6 Case 7

Blocking of circulating VEGF reduces the expression of nephrin and synaptopodin, but does not affect podocin. Garovic V D et al. Nephrol. Dial. Transplant. 2007;22:1136- 1143

Clinical feature --- Proteinuria The urine sediment is typically benign. Urinary shedding of podocytes may indicate podocyte loss from the glomerulus, which may lead to a disruption of the glomerular filtration barrier and consequent proteinuria.

Clinical feature --- GFR decresed Healthy pregnant women exhibit marked glomerular hyperfiltration due to depression of the plasma oncotic pressure 1. Hypervolemic-induced hemodiltution lower the plasma protein concentration 2. Elevated rate of renal plasma flow In women with preeclampsia a. Glomerular filtration rate (GFR) decreases by 30 to 40 percent in preeclamptics b. Renal plasma flow also decreaseses

Clinical feature --- Other renal findings Renal failure and diabetes insipidus: unusual complication Hyperuricemia unknown mechanism Some thoughts-- 1. reflect increased proximal sodium and urate reabsorption induced by renal ischemia ? 2. underlying metabolic syndrome, tissue damage, oxidative stress, and inflammation Hypocalciuria unknown mechanism

Renal biopsy Atherosis = swelling of glomerular endothelial cells = lipid laden cells in the wall of the artriole fibrinoid necrosis thrombosis, sclerotic narrowing of arterioles and placental infarction => correlation between the severity of the disease and the extent of the lesions. [1,6,16-20]

1.Endothelial cell body 2.Swollen, non-fenestrated endothelium 3.Subendothelial fibrinoid deposition 4.Mesangial cell interposition

Clinical feature --- edema Most pregnant women have edema, so presence of edema is not part of the dignostic criteria However, sudden and rapid weight gain ( > 5 pounds/weeks) and facial edema may occur in women who develop preeclampsia Because of vasoconstriction, the volume reduce and the diuretics should be avoided in the absence of pulmonary edema

Clinical feature --- Eclampsia Seizure with other neurologic symptoms, including headache and visual disturbances, complicate approximately 5 of every 10000 pregnancies. Proposed theories: 1. Cerebral vasospasm 2. Cerebral edema 3. Severe hypertension disturb cerebral autoregularion and disrupt the blood-brain barrier

Cerebral edema prdominantly involves the posterior, parieto- occipital lobes and is similar to images described in reversible posterior leukoencephalopathy syndrome [ Manfredi M, Beltramello A, Bongiovanni LG, Polo A, Pistoia, L, Rizzuto N: Eclamptic encephalopathy: Imaging and pathogenetic considerations. Acta Neurol Scand 96: 277 282, 1997 ] This MRI findings has been noted to correlate with endothelial dysfunction markers, including LDH, RBC morphalogy and creatinine.

CT MRI posterior, parieto- occipital lobes

Clinical feature --- Coagulopathy and HELLP syndrome The HELLP syndrome develops in up to 10% of pregnancies with severe preeclampsia In preeclampsia, endothelial injury may also become low- grade coagulopahty with increaed fibronectin, increased platelet aggregation, shortened platelet survival, and depressed antithrombin III levels. [53]

Risk factor

a. Family history of preeclampsia in a first degree relative is associated with an increase in risk (RR-- 2.90, 95% CI --1.70-4.93) b. Hormonal, hypertension, renin- angiotensin system changes, some links to HLA types c. Fetal genes from the father may contribute to the increased risk [Duckitt, K, Harrington, D. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330:565.[Duckitt, K, Harrington, D. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330:565. ]

Risk factor First pregnancy increases the risks of developing preeclampsia, (RR--2.91, 95% CI-- 1.28-6.61), the mechanism is unclear [Duckitt, K, Harrington, D. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330:565.[Duckitt, K, Harrington, D. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330:565. ]

Risk factor 1.Multiple gestation increases the risk of preeclampsia (RR-- 2.93, 95% CI-- 2.04- 4.21) 2. The risk rises with the number of fetuses. [ Duckitt, K, Harrington, D. Risk factors for preeclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330:565. ] Duckitt, K, Harrington, D. Risk factors for preeclampsia at antenatal booking: systematic review of controlled studies. BMJ 2005; 330:565.

Risk factor a.Medical conditions associated with vascular insufficiency (eg: HTN, DM, SLE, CKD, Acquired and inherited thrombophilias) increase the risk of abnormal placenta and preeclampsia [1,15] b. Obsterical conditions that increase placental mass without increaseing placental blood flow (eg: hydatidiform mole, hydrop fetalis, DM, twin gestation) result in relative ischemia and are associated with preeclampsia.

Predictor of preeclampsia AFP, hCG, uE3, inhibin A, uterine artery Doppler not sufficiently sensitive and specific to be clinically useful as a screening test. Doppler ultrasonography is a useful method to assess the velocity of ulterine blood flow since the second tremester An abnormal velocity wave form high resistence index more than 6 sixfold increase in rate of preeclampsia * Sensitivity: 20-60% * Limited value as a screening test but could be beneficial as a test for high risk gourp [Lancet 2005; 365: 78599]

Predictor of preeclampsia Measurement of angiogenic factors (eg, VEGF, sFIt-1, PlGF, sEng) in blood or urine is the most promising approach for predicting preeclampsia not available for clinical use at present. Large babies in women with obesity and gestational diabetes have been soociated with increased risk of preeclampsia. Fetal /placental weight ratio (FP ration) as an important determinant for the onset of preeclampsia FP increase = placental blood supply decreae + embryo demand increase/normal

Management Hospitalization is useful for making assessment and facilitates rapid intervention to prevent complications Patient offered outpatient monitoring should be able to comply with frequent maternal and fetal evaluation (ever 1 ~ 3 days) and have ready access to medical care. Resticted activity is recommeneded, but there is no ecidence that complete bedrest improves pregnancy outcome. The definitive treatment --- Delivery Indication: Maternal end-organ dysfunction and nonreassuring tests of fetal well-being at any gastational age

Management Laboratory follow-up a. The minimum : patelet count, serum creatinine, serum ALT and AST repeated once or twice weekly b. Other tests: Hct (hemoconcentration or hemolysis ), LDH (hemolysis and HELLP sndrome), blood smear schistocytes and helmet cells ( hemolysis ) c. 24hr daily urine protein and random protein-to-creatinine ratio

Management Treatment of hypertension dose not alter the course of the disease or diminish perinatal morbidity or mortality * Side effect BP drop placenta perfusion drop [ Abalos, E, Duley, L, Steyn, DW, Henderson-Smart, DJ. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy (Cochrane Review). Cochrane Database Syst Rev 2007; :CD002252. ] Abalos, E, Duley, L, Steyn, DW, Henderson-Smart, DJ. Antihypertensive drug therapy for mild to moderate hypertension during pregnancy (Cochrane Review). Cochrane Database Syst Rev 2007; :CD002252. * Indication of treatment a. Neurologic symptoms b. Symptomatic women: SBP >=160mmhg or DBP >= 105 ~ 110 mmhg # goal SBP:130~150 mmhg and DBP:80~100mmhg c. Symptomatic women SBP 150 mmhg or DBP 95~ 100 mmhg.

Management Choice of anti-hypertension medication 1. Labetalol Randomized trial have shown that labetalol is effective and safter than nicardipine or methyldopa). 2. Hydralazine 3. Immediate release nicardipine iv form 4. Sustained release nifedipine oral form Antenatal corticosteroids promote fetal lung maturity should be administered to women less than 34 th wks Routine sodium restriction and diuretics have no role [11] L-arginine failed Plasma volume expansion did not improve failed

Management Lancet 2005; 365: 78599

Prevention Lancet 2005; 365: 78599

Discussion and literature review Result glomerular endotheliosis was found in preclampsia as well as gestational hypertension and normal pregnancies Discussion 1. Pregnancy is a stress test 2. Normal term pregnancy, gestational hypertension and preeclampsia appears to be a continuous process Q: Is glomerular endotheliosis = Pre-clampsia ?

Serial biopsy studies of preeclampstic patient in recovery and have readily demonstrated that these processes reverse themselves. [ KINCAID-SMITH PS: The renal lesion of preeclampsia revisited. Am J Kidney Dis 17:144148, 1991] However, in Japanese biopsy studies, many preeclampsia women have sclerotic injuries that look like FSGS. [OGINO S: An electron microscopic study of the glomerular alterations of pure preeclampsia Am J kidney Dis 1991.] and [ LAFAYETTE RA, DRUZIN M, SIBLEY R, et al: Nature of glomerular dysfunction in pre-eclampsia. Kidney Int 54:12401249, 1998 ] Result both of the renal function and ultrastructural changes recover soon in the postpartum period Discussion the risk of hypertension increase because they lose some nephrons during this illness or because herediatry or other facotrs predipose them to hypertension Discussion and literature review Q: Is glomerular endotheliosis reversible ?

Discussion and literature review Several reports have suggested that women with preeclampsia have an increased risk of later hypertension and associated metabolic disturbance, including higher insulin levels and reduced endothelial function, long-term studies have also suggested increased risks of stroke, ischemic heart disease and tyep2 DM [Wilson BJ, Watson MS, Prescott GJ, et al. Hypertensive diseases of pregnancy and risk of hypertension and stroke in later life: results from cohort study. BMJ 2003;326:845.] [Wikstrm AK, Haglund B, Olovsson M, Lindeberg SN. The risk of maternal ischaemic heart disease after gestational hypertensive disease. BJOG 2005;112:1486-91.] Women with a history of preeclampsia are at increased risk for having a renal biopsy in the future.[ Vikse BE, Irgens LM, Bostad L, Iversen BM. Adverse perinatal outcome and later kidney biopsy in the mother. J Am Soc Nephrol 2006;17:837-45. ]

or Preeclampsia Permanent renal injury ESRD Discussion and literature review Preexisting renal diseasePreeclampsia ESRD If preeclampsia itself causes permanent renal injury ??? What is the relationship between preeclampsia and ESRD ???

HELLP syndrome is not associated with long-term renal complication and does not warrant continuous nephrological follow up. 34patient, 16 HELLP, 18 control followup 5-7yrs follow up 24hr Ccr

The absolute risk of cardiovascular disease in patients with a history of preeclampsia is higher that of ESRD, and there is well-known association between CKD and CV disease

Discussion and literature review Data from the Norwegian Kidney Biopsy Registry and the Medical Birth Registry of Norway. Included women who had had a representative kidney biopsy in 1988-2005 after their last pregnancy Of the 582 included women, 76 develped ESRD 3.9 +- 3.4 yrs. Women with clinical diagnosed preeclampsia had a RR of ESRD of 1.1(95% CI, 0.5-2.6) and women with preterm birth had a RR of 2.4 (95% CI, 1.2-4.6) In women with kidney disease diagnosed by biopsy, previous preeclampsia doest not seem to be a risk marker for progression to ESRD

Data from the Medical Birth Registry of Norway from 1967 to 2004 and Norwegian Renal Registry from 1980 and 2005. Include 570433 women with diagnosis of ESRD who had been pregnant one to three times

1. Having a low-birth-weight or preterm infant increased the relative risk of ESRD. 2. ESRD developed in 477 of 570,433 women with a mean (SD) of 179 years after pregnancy (overall rate, 3.7 per 100,000 women per year). Preeclampsia is a marker for an increased risk of subsequent ESRD

However. of the 477 cases of ESRD among the women, 168 were due to glomerulonephritis, 59 to interstitial nephritis, 100 to hereditary or congetital causes (84 of these patients had ADPKD), 68 to diabetic nephropathy and 82 to other causes. => associated with similar relative risks comparing the development of ESRD in general. ????? Whether previous preeclampsia was associated with progression of established kidney disease----it is limited by the small number ofwomen in each category of ESRD

Conclusion Women with a history of preeclampsia have an increased risk of microalbuminuria with a prevalence similar to the published prevalence in patients with type 1 diabetes mellitus.

How should women with pre-eclampsia be followed up? Preeclampsia is a marker for an increased risk of ESRD Among women with preeclampsia, giving birth to a low- birth-weight or preterm infant further increased the relative risk of ESRD women with a history of preeclampsia should undergo renal follow up eGFR, BP, quantification of proteinuria, lipid profile and glucose tolerance

Characteristics Of PreeclampsiaThis patient Epidemiology Between late second trimester and the first few days postpartum third trimester in pregnancy Risk factors 1.Family history of preeclampsia 2.Nulliparity 3.Multiple gestation 4.Molar pregnancies 5.Older maternal age 6.Obesity 7.Preexisting hypertension 8.Chronic renal disease 9.Diabetes mellitus 10.Throbotic vasular disease Negative ? Negative Postive Negative

Review of this case Characteristics Of PreeclampsiaThis patient clinical features 1. Hypertension 2. Proteinuria 3. Edema 4. Neurologic symptoms 4. Acute renal insufficiency 5. Abnormal liver function tests 6.Thrombocytopenia 7.Hemolysis 8.Elevated LDH 9.Hyperuricemia V X V X V (bleeding related ?) ? V

Review of this case Characteristics Of PreeclampsiaThis patient Differential diagnosis 1. Chronic hypertension 2.Preeclampsia superimpsed upon chronic hypertension 3.Gestational hypertension a.Hypertension and proteinuria occurring at the 3 rd trimester b.Hyperuricemia (?) Delivery Blood pressure normalization Proteinuria normalization Renal function improvement ? 20th day 15th day

Thanks for your attention !!

Circulating angiogenic factores Circulating angiogenic factors, alterations in the renin- angiotensin system, and insulin resistence sFlt-1 in pregancies with trisomy 13 Endoglin (Eng) is an angiogenic receptor that is expressed on the surface of endothelial cell and placental syncytiotrophoblasts. Eng acts as a co-receptor for TGF-B, inhibited trophoblast outgrowth and migration

Risk of Pre-eclampsia in First and Subsequent Pregnancies: Results

Treatment of preelampsia Hypothesis 1. L-Arg decrease NO deficiency a. Give LAME in rat preeclamsia like V b. Give L-Arg to man fail X

Preeclampsia CKD? Endotheliosis seems to be responsible for the decreased GFR After delivery, the glomerular changes usually reverse rapidly, coinciding with resolution of the hypertension and proteinuria

case conference 報告者： r3 潘恆之 報告者： r3 潘恆之 指導老師：方基存醫師...

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case conference 報告者： r3 潘恆之報告者： r3 潘恆之指導老師：方基存醫師...