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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- Slide 1
- Case Conference R3 R3 2010.11.24 2010.11.24
- Slide 2
- 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
- Slide 3
- 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
- Slide 4
- Chief Complaint Progressive dyspnea for 5 days.
- Slide 5
- 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.
- Slide 6
- 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.
- Slide 7
- 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.
- Slide 8
- Personal history Alcohol usage: denied Cigarette: denied Betel
nut: denied OTC drugs: denied Chinese Herbs: denied Food allergy:
never Drug allergy: never
- Slide 9
- 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)
- Slide 10
- 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.
- Slide 11
- 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
- Slide 12
- 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
- Slide 13
- 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
- Slide 14
- 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.
- Slide 15
- 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
- Slide 16
- ER Impression Acute renal failure with pulmonary congestion
Hypokalemia Postpartum hemorrahge
- Slide 17
- 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
- Slide 18
- 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
- Slide 19
- 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
- Slide 20
- 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
- Slide 21
- Outline Differential diagnosis of hypertensive disorder related
to pregnancy Differential diagnosis of proteinuria Review of
preeclampsia Future direction Review of this case
- Slide 22
- Hypertensive disorders related to pregnancy Preclampsia Chronic
hypertension Preeclampsia superimpsed upon chronic hypertension
Gestational hypertension
- Slide 23
- 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.
- Slide 24
- 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
- Slide 25
- Outline Differential diagnosis of hypertensive disorder related
to pregnancy Differential diagnosis of proteinuria Review of
preeclampsia Future direction Review of this case
- Slide 26
- Etiology of proteinuria
- Slide 27
- National High Blood Pressure Education Program Working Group on
High Blood Pressure in Pregnancy. Am J Obstet Gynecol
2000;183:S122.
- Slide 28
- Outline Differential diagnosis of hypertensive disorder related
to pregnancy Differential diagnosis of proteinuria Review of
preeclampsia Future direction Review of this case
- Slide 29
- 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
- Slide 30
- 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
- Slide 31
- Leon Chesley 1908-2000
- Slide 32
- 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
- Slide 33
- 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+).
- Slide 34
- 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
- Slide 35
- Placentation Abnormalities ( Stage I ) -- Abnormal remodeling
of spiral arteries
- Slide 36
- Slide 37
- The Maternal Syndrome (stage II )
- Slide 38
- 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
- Slide 39
- 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
- Slide 40
- 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
- Slide 41
- The Maternal Syndrome (stage II ) All of the clinical features
of preeclampsia are maternal responses to generalized endothelial
dysfunction !! sFlt-1, sEndoglin(sEng )
- Slide 42
- Other hypotheses Baha Sibai, Gus Dekker, Michael Kupferminc.
The Lancet. London: Feb 26-Mar 4, 2005. Vol. 365, Iss. 9461; p.
785
- Slide 43
- The putative role of COMT, HIF-1a and 2-ME
- Slide 44
- Biology of preeclampsia
- Slide 45
- 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
- Slide 46
- 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:
journals.permissions@oxfordjournals.org
- Slide 47
- Unifying hypothesis of pre-eclampsia pathophysiology
- Slide 48
- Clinical feature --- hypertension Plasma renin activity
- Slide 49
- Clinical feature --- hypertension
- Slide 50
- Slide 51
- Clinical feature --- Proteinuria : J Clin Invest. 2004 November
15; 114(10): 14121414
- Slide 52
- Clinical feature --- Proteinuria
- Slide 53
- Method: Renal tissue was obtained from 7 severe preclampsia
women
- Slide 54
- 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
- Slide 55
- 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
- Slide 56
- 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
- Slide 57
- 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.
- Slide 58
- 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
- Slide 59
- 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
- Slide 60
- Slide 61
- Slide 62
- 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]
- Slide 63
- 1.Endothelial cell body 2.Swollen, non-fenestrated endothelium
3.Subendothelial fibrinoid deposition 4.Mesangial cell
interposition
- Slide 64
- 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
- Slide 65
- 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
- Slide 66
- 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.
- Slide 67
- CT MRI posterior, parieto- occipital lobes
- Slide 68
- 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]
- Slide 69
- Risk factor
- Slide 70
- 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. ]
- Slide 71
- 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. ]
- Slide 72
- 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 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.
- Slide 73
- 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.
- Slide 74
- 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]
- Slide 75
- 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
- Slide 76
- 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
- Slide 77
- 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
- Slide 78
- 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.
- Slide 79
- 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
- Slide 80
- Management Lancet 2005; 365: 78599
- Slide 81
- Prevention Lancet 2005; 365: 78599
- Slide 82
- 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
pre- eclampsia appears to be a continuous process Q: Is glomerular
endotheliosis = Pre-clampsia ?
- Slide 83
- 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 ?
- Slide 84
- 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. ]
- Slide 85
- 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 ???
- Slide 86
- 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
- Slide 87
- 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
- Slide 88
- 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
- Slide 89
- 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
- Slide 90
- 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
- Slide 91
- 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
- Slide 92
- 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.
- Slide 93
- 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
- Slide 94
- Outline Differential diagnosis of hypertensive disorder related
to pregnancy Differential diagnosis of proteinuria Review of
preeclampsia Future direction Review of this case
- Slide 95
- 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
- Slide 96
- 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
- Slide 97
- 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
- Slide 98
- Thanks for your attention !!
- Slide 99
- 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
- Slide 100
- Slide 101
- Risk of Pre-eclampsia in First and Subsequent Pregnancies:
Results
- Slide 102
- Slide 103
- Slide 104
- Slide 105
- 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
- Slide 106
- 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
- Slide 107