Gravidez Flashcards

Question 1

Q

O Rim na gestação

Answer

A

Aumento do tamanho do rim.
Dilatação do trato urinário.
Aumento do fluxo sanguíneo renal.
Aumento da filtração glomerular

expansao do volume aumenta 1,5 l

aumenta hemacias

reduçao da creat sericaaumento da excrecao do acido urico=hipouricemia

menor reabs proteica= certo grau de proteinuria mas nao aumenta 300mg/dia

glicosuria= aumento da carga filtrada de glicose por conta do hiperfluxo e reducao da capacidade de reabs max da glicose

aumento da calciuria mas vem acompanhada tb de mg citrato glicoptns acidas

alcalose respiratoria

retencao de sodio =até 1000mg

retençao de k= 320meq

Question 2

Q

O Rim na gestação

Answer

A

Aumento da Aldosterona
Aumento da reabsorção de sódio
Aumento da reabsorção de água
Diminuição do Sódio sérico e osmolaridade sérica.
Aumento da Glicosúria
Aumento da Amino-acidúria
Aumento da Renina
Diminuição da reabs do ácido úrico.
Vasodilatação renal
Aumento da Filtração Glomerular Aumento do fluxo sanguíneo renal Diminuição da creatinina sérica
Aumento da Proteína urinária

Question 3

Q

Alterações renais na gestação

Answer

A

Dilatação do trato urinário:
Aumento do risco de infecções do trato urinário. Uropatias obstrutivas.

Aumento da filtração glomerular. aumento da vasodilatacao, aumento do óxido nitrico induzido pela relaxina

Diminuição da Creat serica, BUN e ácido úrico.
Metabolismo da água: diminuição da osm serica 270 e sódio sérico
Ácido-Base : Diminuição do Bicarbonato sérico.

Question 4

Q

Como a Gestação pode
influenciar a doença renal ?

Answer

A

Alterações hemodinâmicas – Hiperfiltração.
Aumento da proteinúria.
Pre-eclampsia.
Possibilidade de perda permanente da
função.

Question 5

Q

Como a doença renal influencia a
gestação ?

Answer

A

Incidência de pre-eclampsia aumentada

Incidência de prematuridade aumentada

Incidência de Crecimento intra-utero
retardado aumentada.

Question 6

Q

IRC e Gestação

Answer

A

Favorável se Creat
<1,5 mg/dl.
Favorável na ausência de Hipertensão .
Poucas evidências relacionam diagnóstico histológico e prognóstico.

Question 7

Q

Gerenciamento da Nefropatia
Diabética antes e durante a gestação

Answer

A

Controle rígido da glicemia com multiplas aplicações e supervisão dietética.
Prognóstico fetal relacionado com a HbAc1
Parar iECA e ARAII.
Metildopa, labetolol, Bloq dos Canais de Ca e diuréticos.
Avaliação cardíaca pré-parto
Exames laboratoriais mensais, no mínimo.

Question 8

Q

Nefropatia lúpica e a gestação

Answer

A

Pouco prognóstico se : Doença ativa na concepção.
A Doença aparece pela primeira vez na gestação.
Níveis de anticorpos antifosfolípede
aumentado.
Hipertensão, azotemia e proteinúria no 1o Trimestre,
* Curso imprevisível durante a gestação

Question 9

Q

Anticorpo antifosfolípede na
Gestação

Answer

A

Perda fetal.
Vasculite renal, microangiopatia trombótica.
pré-eclâmpsia
Trombose arterial e venosa.
Tratamento : Aspirina e Heparina.

Question 10

Q

Tratamento da nefrite lúpica na
Gestação

Answer

A

Alta dose diária PO de corticóide
Prednisona

Azatioprina é segura.Experiência da gestação em transplantadas.

Ciclofosfamida e Micofenolato usados
Azatioprina é segura.

Ciclofosfamida e Micofenolato usados
apenas quando o risco maternal é alto.

Parto – componente múltiplo, difícil dx
entre pré-eclâmpsia e Lupus flare.

Question 11

Q

Lupus flare x pré-eclâmpsia

Answer

A

Lúpus flare
Proteinúria + Hipertensão +
Cilindros Hemáticos+Azotemia+
C3 e C4 baixos+
Plaquetas baixas +Leucócitos baixos+
Função Hepática NORMAL

Pré eclampsia
Proteinúria + Hipertensão + Azotemia +
Cilindros Hemáticos NÃO TEM
e C3 e C4 baixos NÃO TEM
Função Hepática anormal +/-
Plaquetas baixas +/-
Leucócitos baixos NAO TEM

Question 12

Q

Doença Policística na Gestação

Answer

A

Aumento da incidência de ITUs
Hipertensão materna associada com pior prognóstico.

Complicações extra-renais:
Hemorragia subaracnóide – aneurismas
Cistos hepáticos – estimulados pelo estrogênio.
Múltiplas gestações podem ser problemáticas

Question 13

Q

Doença Renal Intrínsica x pré-
eclâmpsia

Question 14

Q

IRA na gestação e puerpério

Answer

A

NTA: Hemodinâmica, toxinas, sépse, etc.
Nefrite Túbulo-Intersticial Aguda
Fígado Gorduroso Aguda
pré-eclâmpsia / HELLP
Síndromes Microangiopáticos.
Necrose Cortical Aguda em sangramento
Obstétrico maciço

Question 15

Q

HELLP – Fígado Gorduroso
PTT e SHU

Question 16

Q

Diálise e Gestação

Answer

A

Bom prognóstico Antigos estudos : 23 %
Dados recentes : 40 – 70 %
Alta incidência de perda no 2
Trimestre
Prematuridade na maioria (média de 32 semanas)
Melhor prognóstico se houver função renal residual.
EPO, controle de PA e pouca heparina.
Alta incidência de problemas congênitos e de desenvolvimento. Sem diferença entre HD e CAPD.
Gerenciamento : > 20h diálise melhora prognóstico.

Question 17

Q

Transplante e Gestação

Answer

A

Prognóstico depende da PA e função renal de base.
Ainda existe controvérsia se a gestação acelera a perda do enxerto.

Pacientes são aconselhados a aguardar 2 anos
após transplante.

Question 18

Q

Conseqüências maternas da
hipertensão na gestação

Answer

A

Morte
Abruptio Placentae (DPP)
Insuficiência Renal Aguda
Ruptura hepática

Question 19

Q

Conseqüências fetais da
hipertensão na gestação

Answer

A

5 – 15 x a incidência de crescimento intra-útero retardado.

3 – 6 x a incidência de feto natimorto.
(?) Problemas a longo prazo de
desenvolvimento e neurológicos.

Question 20

Q

Classificação
HAS na gravidez

Answer

A

HAS primária ou secundária
pré-eclâmpsia e eclampsia
Hipertensão crônica
Preeclamsia superajuntada com hipertensão crônica.HAS pré - 25% de pré-eclâmpsia HAS
Hipertensão gestacional

Question 21

Q

Classificação da Hipertensão
gestacional

Answer

A

Diagnóstico da Hipertensão gestacional Detectada pela primeira vez após a metade da gestação
Sem proteinúria

Se a pré-eclâmpsia não se desenvolver e
PA retornar ao normal pela 12 sem. pós parto:Hipertensão transitória.
PA manter-se alta no pós-parto
=Hipertensão crônica.

Question 22

Q

Diagnóstico de Hipertensão na
gestação

Answer

A

< 20 semanas – Hipertensão Crônica.pa >140x90mmhg

> 20 semanas ou ate 6 apos o parto –duas medidas espaçada sde 4-6 horas =has gestacional

pré-eclâmpsia: has gestacional +lesao de orgao alvo ; proteinuria ou nao

Hipertensão crônica
Hipertensão crônica com pré-eclâmpsia e
hipertensão transitória.

Question 23

Q

Fatores de risco para pré-eclâmpsia

Answer

A

Fetais/Placentários:
Primeira gestação
Múltiplas gestações
Mola Hidatiforme

Maternais
Doença vascular pré existente:Hipertensão, Diabetes, doença renal.

Síndrome metabólica :Obesidade, resistência a insulina e dislipidemia.

Trombofilias:
Fator V de Leiden
Anticorpo Anti-fosfolípede.

Question 24

Q

Pré-eclâmpsia

Answer

A

Síndrome gestacional
Diagnosticada após a 20 sem. de gestação
Hipertensão
Proteinúria
Cefaléia, distúrbios visuais, dor abdominal e torácica.
Edema de mãos e face
Ganho de peso abrupto
Alterações laboratoriais.

preeclampsia is new-onset hypertension with systolic blood pressure >140 mm Hg or diastolic BP≥90 mm Hg after 20 weeks’ gestation, together with one or more symptoms of maternal organ dysfunction and fetal growth restriction. Soluble fms-like tyrosine kinase-1 (sFlt-1) levels which antagonize angiogenic placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) are higher in women with preeclampsia. In some studies of women without CKD sFLT:PlGF ratio or PlGF levels helped guide management (especially as a test to rule-out preeclampsia). Aspirin (75-150 mg/day) from the beginning of pregnancy is recommended for all women with CKD as it significantly decreases the risk of preeclampsia. When severe features of preeclampsia are absent expectant management is feasible up to 37 weeks of gestatio

Question 25

Q

Exames laboratoriais na pré-
eclâmpsia

Answer

A

↑ creatinina > 0,8, < 1,5 mg/dl (nl 0,6 mg/dl).
↑ ácido úrico > 5,5 mg/dl (nl < 4,5 mg/dl).
↑ proteinúria > 300 mg/24h
↓ Cálcio urinário < 150 mg/24h (nl 250 mg/24h).
Trombocitopenia < 100.000 plaquetas Enzimas hepáticas elevadas.
HELLP – Hemolysis, Elevated Liver enzymes, Low Platelets

Question 26

Q

O Rim na pré-eclâmpsia

Answer

A

↓ Renina
↓ Vasodilatação (vasoconstrição)
↓ Ritmo de Filtração Glomerular
↓ Fluxo Sanguíneo Renal
↓ Excreção de Sódio (Hipocalciúria)
↓ Excreção de Urato
Proteinúria

Question 27

Q

Terapia Anti-hipertensiva na pré-eclâmpsia

Answer

A

Parto Iminente
Hidralazina (IV ou IM)
Labetolol (IV)
Bloqueadores de Canais de Ca.
Diazoxide (IV)

Parto Adiado
Metildopa
Labetolol ou outro βBloq
Bloqueadores de Canais de Ca.
Hidralazina
α Bloqueadores
Clonidina

Question 28

Q

Avaliação pós-parto

Answer

A

Quem ?
Precoce ( < 34 semanas ), pré-eclâmpsia severa.
Pré -eclâmpsia Recorrente
Proteinúria persistente ( > 6 semanas )
Hipertensão persistente ( > 6 semanas )

Como ?
Avaliação pós-parto:
Descarte :
1. DoençaRenal.
2. Hipertensão primária ou secundária.
3. Síndrome do anticorpo antifosfolípede.
4. ProteínaS.
5. Deficiência de proteína C
6. Fator V de Leiden
7. Hiperhomocisteínemia

Question 29

Q

Hypertensive Disorders in Pregnancy

Answer

A

The spectrum of disorders includes:

transient (“gestational”) hypertension,

chronic hypertension,

preeclampsia,

HELLP syndrome, eclampsia,

and chronic hypertension with superimposed preeclampsia

Question 30

Q

Clinical Presentation and Diagnosis of Preeclampsia

Answer

A

Patients present with new onset hypertension after 20 weeks gestation, often with proteinuria.

 Preeclampsia itself rarely leads to acute kidney injury (1%).

 Degree of proteinuria does not correspond to degree of edema/anasarca

o This is likely due to a high renin/aldosterone sodium avid state.

 Most recent (2016) diagnostic criteria include:

o Systolic blood pressure >ou =140mmHg or diastolic blood pressure>ou =90mmHg

o With proteinuria of 0.3g or greater on a 24-hour urine collection

o In the absence of proteinuria diagnostic criteria include hypertension with

any of the following: thrombocytopenia, AKI, impaired liver function,pulmonary edema, or cerebral/visual symptoms

Question 31

Q

Mechanism of Disease in Preeclampsia:

Answer

A

Preeclampsia is a vascular disease that can affect any vascular bed.

 Risk factors include: First pregnancy, prior history of preeclampsia, history of HTN,

obesity, maternal age (>40 y), multiple gestation, ethnicity, maternal family history

of preeclampsia, history of a variety of system or renal limited disorders such as

diabetes, lupus, scleroderma, sickle cell disease and others, and pregnancies from

in vitro fertilization.

 Glomerular endotheliosis, a hall mark of preeclampsia, is found in a spectrum of

thrombotic microangiopathies.

 There are two stages of preeclampsia:

o Abnormal placentation

 Factors associated include: genetics, preexisting chronic disease,

inadequate vasodilatory hormones, absent endothelial growth

factors, circulating autoantibodies and abnormal cytotrophoblast

generation.

o Oxidative stress in the placenta leading to the clinical phenotype

 Factors associated include: increased circulating soluble FLT

(sFLT1) and soluble endoglin (sENG), decreased circulating

placental growth factor (PIGF) and vascular endothelial growth

factor (VEGF).

 Elevation of sFLT1 leads to procoagulation and

vasoconstriction

 The above factors lead to the vascular dysfunction, capillary leak

and vasospasm and the associated clinical findings of hypertension,

proteinuria, glomerular endotheliosis, coagulation abnormalities,

pulmonary edema, neurologic symptoms and hepatic dysfunction.

Question 32

Q

Treatment of Preeclampsia and future directions in diagnosis and therapy

Answer

A

The only current definitive therapy is delivery.

 In high risk women daily aspirin is recommended for prevention.

o Studies have not demonstrated clear morbidity or mortality benefits,

however have demonstrated risk reduction in the development of

preeclampsia.

 Several studies have demonstrated the potential for measuring and monitoring the

biomarker, sFLT1.

o Use in clinical practice is not currently available however it may prove a

useful tool for diagnosis and management in the future.

 Targeted approaches have been reported or are in development.

o The use of plasmapheresis for removal of sFLT1, however is lacking robust

data on use and efficacy.

o Animal models using short interfering RNA to impair sFlt-1 are in

development

Question 33

Q

Other causes of endotheliosis

Answer

A

A potential side effect of the anticancer drug, Bevacizumab, is proteinuria and

edema.

o Pathologically it demonstrates endothelial swelling very similar to the

nephropathology seen in preeclampsia.

 Idiopathic endotheliosis is a reported entity with measured antibodies to VEGF.

 Both of the aforementioned entities can occur regardless of sex or gestational

status

Question 34

Q

ITU

Answer

A

Urocultura na primeira semana de pre natal

bacteriuria assintomatica =tto -> complicacoes trabalho de parto pre termo e pielonefrite

nao pode usar quinolona

fofomicina =liberado

macrodantina=liberado , so nao pode depois da 35 semana

cefalexina 7 dias, bactrim pode reduzir a oferta de acido folico mas pode

>2 infeccoes = avaliacao mensal de urocultura e profilaxia

=macrodantina ate 35 e depois substitui cefalexina

PIELONEFRITE= compica c sepse 40% dos casos = tratar hospitalar e atb sistemico

profilaxia ate o parto

fat de risco= glicosuria, relaxamento do ureter, alteracoes da imunidade na gravidez

Question 35

Q

estimativa da tfg na gravidez

Answer

A

Endogenous creatinine clearance, measured by 24-hour urine collection, remains the standard of care for estimation of GFR in pregnancy

All creatinine-based formulas to estimate GFR, including the Modification of Diet in Renal Disease Study (MDRD) and Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations, consistently underestimate GFR in pregnancy

se of cystatin C to estimate GFR has not been validated for use in pregnant individuals. In one prospective study including 12 healthy pregnant patients, serum cystatin C did not correlate with GFR measured by inulin clearance, indicating it is unlikely to be a useful marker of GFR in pregnancy

Question 36

Q

proteinuria na gravidez

Answer

A

Proteinuria — Urinary protein excretion rises in normal pregnancy, from the nonpregnant level of approximately 100 mg/day to approximately 150 to 200 mg/day in the third trimester.

This may result in a positive dipstick result when a concentrated urine sample is examined. Urinary protein excretion greater than 300 mg/day is considered abnormal and should prompt further evaluation

Urine protein excretion is even higher in uncomplicated twin pregnancy, which can lead to diagnostic confusion when evaluating a patient for preeclampsia because values greater than 300 mg/day are considered abnormal

Question 37

Q

alteracoes do ureter na gestacao

Answer

A

Progesterone reduces ureteral tone, peristalsis, and contraction pressure.

●More prominent involvement of the right ureter may be due to dextrorotation of the uterus by the sigmoid colon, kinking of the ureter as it crosses the right iliac artery, and/or proximity to the right ovarian vein.

●Enlarged vessels in the suspensory ligament of the ovary may compress the ureter at the brim of the bony pelvis.

●Uterine enlargement may cause the ureters to become elongated, tortuous, and displaced laterally as pregnancy advances.

Vesicoureteral reflux — Bladder flaccidity may cause incompetence of the vesicoureteral valve. This change, combined with increased intravesical and decreased intraureteral pressure, appears to result in intermittent vesicoureteral reflux

Question 38

Q

POSTPARTUM

Answer

A

The pregnancy-induced physiologic changes described above return to the nonpregnant state by four to six weeks following delivery

Question 39

Q

gravidez e DRC

Answer

A

Women with significant chronic kidney disease (CKD), particularly those with advanced CKD, are much less likely to become pregnant or have an uncomplicated pregnancy compared with women with normal kidney function. Even mild CKD is associated with a higher risk of adverse maternal and fetal outcomes, including worsening of maternal kidney function, proteinuria, and hypertension, as well as preterm birth and fetal growth restriction

Question 40

Q

Impact of pregnancy in women with CKD

Answer

A

Maternal

Worsening kidney function and/or proteinuria

Potential flare of underlying disease

Hypertensive disorders of pregnancy

Gestational hypertension

Preeclampsia

HELLP syndrome

Complications of immunosuppression

Miscarriage

Fetal

Preterm birth

Stillbirth or neonatal death

Low birth weight

Fetal growth restriction

Small for gestational age

Question 41

Q

Pregnancy pode acelerar

the progression of CKD. The risk is dependent upon the baseline GFR, proteinuria, and hypertension

Question 42

Q

drc e gravidez

Answer

A

even mild reductions in glomerular filtration rate (GFR) may increase the risk of preeclampsia, gestational hypertension, and possibly premature delivery. The risk increases as GFR declines and in the settings of proteinuria and hypertension. Higher levels of proteinuria also adversely affect pregnancy outcomes. Fetal survival is lower when hypertension is uncontrolled (ie, >140/90 mmHg) preconception.

Question 43

Q

ieca/bra e gravidez

Answer

A

Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) should not be used during pregnancy, since they are associated with fetal abnormalities. In general, as soon as a patient expresses desire for pregnancy, we stop the ACE inhibitors or ARBs and transition her to other medication (eg, nifedipine, labetalol, methyldopa) for blood pressure control. However, for CKD patients who have significant proteinuria and no immunological treatment options (eg, diabetic kidney disease or kidney scarring), we continue ACE inhibitors or ARBs up until the detection of conception (at which time they are stopped).

Question 44

Q

aas e pré eclampsia

Answer

A

Patients with CKD are considered to be at high risk for preeclampsia. Low-dose aspirin therapy has been shown to decrease the risk of preeclampsia in women at moderate to high risk of the disease, but studies have not included patients with CKD. In pregnant patients with CKD, we weigh the potential risks and benefits of low-dose aspirin therapy and offer treatment to those without any contraindications to aspirin use.

Question 45

Q

indicacao d ehd na gravidez

Answer

A

Management of CKD should continue throughout pregnancy with ongoing attention to complications such as hypertension, metabolic bone disease, and anemia.

If the estimated GFR (eGFR) declines below 20 mL/min/1.73 m2 or the blood urea nitrogen (BUN) increases >50 to 60 mg/dL (18 to 21 mmol/L), we consider the elective initiation of dialysis. This is different from the approach for nonpregnant CKD patients in whom there is no minimum eGFR or threshold BUN that provides an absolute indication to begin dialysis in the absence of symptoms. However, this decision must be individualized

Question 46

Q

pré eclampsia

Answer

A

Systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg on at least 2 occasions at least 4 hours apart after 20 weeks of gestation in a previously normotensive patient AND the new onset of 1 or more of the following*:

Proteinuria ≥0.3 g in a 24-hour urine specimen or protein/creatinine ratio ≥0.3 (mg/mg) (30 mg/mmol) in a random urine specimen or dipstick ≥2+ if a quantitative measurement is unavailable

Platelet count <100,000/microL

Serum creatinine >1.1 mg/dL (97.2 micromol/L) or doubling of the creatinine concentration in the absence of other renal disease

Liver transaminases at least twice the upper limit of the normal concentrations for the local laboratory

Pulmonary edema

New-onset and persistent headache not accounted for by alternative diagnoses and not responding to usual doses of analgesics¶

Visual symptoms (eg, blurred vision, flashing lights or sparks, scotomata)

Question 47

Q

pré eclampsia sobreposta

Answer

A

desenvolvimento de pre eclampsia em pac has cronica

fatores de risco= has previa, drc, proteinuria previa

piora do edema/ aumento do acido urico

agressao a orgao alvo

Question 48

Q

ira na gravidez

Answer

A

Causes of AKI early in pregnancy (before 20 weeks) include pre-kidney disease due to hyperemesis gravidarum and acute tubular necrosis (ATN) resulting from a septic abortion or other bacterial or viral infections

Causes of AKI in late pregnancy (after 20 weeks) include preeclampsia, thrombotic thrombocytopenic purpura (TTP), complement-mediated thrombotic microangiopathy (C-TMA), acute fatty liver of pregnancy (AFLP), ATN or acute cortical necrosis, acute pyelonephritis, and, rarely, urinary tract obstruction. Nonsteroidal antiinflammatory drugs (NSAIDs) may cause AKI in the postpartum period.

Question 49

Q

The evaluation of pregnancy-associated AKI

Answer

A

urinalysis and microscopic analysis of sediment;

quantitation of protein excretion by either 24-hour urine collection or by protein-to-creatinine ratio; urine culture;

hemoglobin level and platelet count with peripheral blood smear;

total, direct, and indirect bilirubin concentration;

serum haptoglobin; serum lactate dehydrogenase (LDH);

serum aspartate aminotransferase (AST) and/or alanine aminotransferase (ALT); and a kidney ultrasound

Question 50

Q

The specific treatment for pregnancy-associated AKI depends on the underlying etiology:

Answer

A

Preeclampsia-associated AKI is an indication for delivery. Delivery generally results in completely recovery of kidney function, although moderately increased albuminuria (formerly called “microalbuminuria”) may persist.
TTP-associated AKI is primarily treated with plasma exchange, and C-TMA may be treated with plasma exchange, and possibly, eculizumab.
AFLP-associated AKI includes the treatment of disseminated intravascular coagulation (DIC) and delivery of the fetus.
In addition to targeted therapies of specific underlying disorders, the treatment of AKI is supportive. Dialysis should be initiated based on the usual criteria for patients in the nonobstetric setting.

Question 51

Q

Preeclampsia is the most common cause of AKI during pregnancy

Answer

A

Preeclampsia refers to the new onset of hypertension and either proteinuria or other signs of systemic disease (including thrombocytopenia, elevated liver enzymes, AKI, pulmonary edema, cerebral and/or visual disturbances), usually after 20 weeks of gestation in a previously normotensive woman

Question 52

Q

pré eclampsia

Answer

A

Preeclampsia may occur with or without features of the HELLP syndrome.

HELLP = hemolysis, low platelet count, and elevated liver enzymes are present

AKI is more common when preeclampsia is accompanied by features of the HELLP syndrome

AKI is often multifactorial in such cases since, in addition to the renal changes characteristic of preeclampsia such as endothelial cell swelling and injury, there is associated coagulopathy, which may result in bleeding, placental abruption, and ATN.

In some cases, preeclampsia is first diagnosed in the postpartum period, without documentation of antepartum hypertension and proteinuria should be distinguished from microangiopathic disorders, particularly C-TMA.

Question 53

Q

tratamento pre eclampsia grave

Answer

A

grave preeclampsia is an indication for urgent delivery

pa>160x100-> lesao de orgao alvo = HELLP, plaq<100.000, aumento transaminases, insuf renal, eap, emergencia hipertensiva= avaliacao do feto

controle da pa= nifedipino vo/hidralazina ev/nitroprussiato em casos selcionados

sulfato de mgnesio= ataque 4g iv, manutencao 1g/hora

na drc - só prescreve a manutencao

24-37 semanas = adiar o parto se possivel

induzir o parto

. The renal and extrarenal abnormalities typically begin to resolve spontaneously within two to three days postpartum, and complete recovery of GFR occurs within eight weeks postpartum.

Occasionally, if proteinuria is severe, it may take several months to resolve completely. Moderately increased albuminuria may persist

. Women who develop preeclampsia may be at increased risk of developing end-stage kidney disease (ESKD) later in life, but the absolute risk is small.

pré eclampsia grave = pa>160x100

eclampsia=crise convulsiva

hellp= hemolise microangiopatica, aumento de enzimas hepaticas , plaquetopenia

Question 54

Q

Primary thrombotic microangiopathy (TMA) syndromes

Answer

A

Thrombotic thrombocytopenic purpura (TTP)

May have severe neurologic abnormalities. Inherited; may present in a newborn infant, a child with thrombocytopenia, or, less commonly, an adult. Among adults, a common presentation is during a first pregnancy.

Acquired autoimmune: Uncommon in children.

Severe MAHA and thrombocytopenia; acute kidney injury is rare.

Severe deficiency of ADAMTS13 (activity <10%). Acquired cases often have a detectable ADAMTS13 inhibitor (autoantibody).

Inherited TTP has ADAMTS13 gene mutation.

Complement-mediated TMA

Inherited and acquired disorders may present in children or adults.

Renal failure is prominent.

Inherited disorders usually have a heterozygous mutation in a gene encoding a regulatory protein in the alternate complement pathway (eg, CFH, CFI, CD46/MCP, C3, CFB, CFHRs).

Acquired disorder has antibodies to complement factor H or I.

Disseminated intravascular coagulation (DIC)May be caused by infection, malignancy, postpartum hemorrhage with hypotension, or a vascular abnormality such as a giant hemangioma (eg, Kasabach-Merritt syndrome).Thrombocytopenia, decreased fibrinogen, and elevated D-dimer are typical with acute or chronic DIC. MAHA may occur. Prolongation of the PT and aPTT are seen in acute DIC.

Pregnancy-related syndromes (eg, severe preeclampsia, HELLP)Typically present in third trimester or postpartum. Severe hypertension and liver involvement are often present. Abnormalities resolve with delivery.Elevated hepatic transaminases. Acute kidney injury is uncommon.

Severe hypertensionTypically, systolic BP >200 mm Hg and diastolic BP >100 mm Hg. Neurologic features including PRES may be present. Hypertension may also occur in primary TMAs with severe renal involvement, so the temporal relationship is important. Abnormalities resolve with control of the BP.Often associated with severe renal failure. Renal biopsy demonstrates TMA identical to the primary TMA syndromes.

Question 55

Q

sFLT1= fator soluvel do sflt

Answer

A

elevacao desse marcador para diferenciar pre eclampsia

Question 56

Q

Rim da toxemia gravídica – endoteliose:

Answer

A

A endoteliose é a lesão glomerular específica da pré-eclâmpsia. Gestação múltipla, doença renal crônica e hipertensão, entre outros, são fatores de risco para o desenvolvimento da pré-eclâmpsia, doença caracterizada por hipertensão e proteinúria, geralmente durante o último trimestre da gestação, associada com edema e hiperuricemia. Na microscopia ótica da endoteliose, o glomérulo apresenta-se aumentado e o lúmen do capilar glomerular estreito e sem sangue. Esta ausência de trombos no lúmen capilar difere a endoteliose da microangiopatia trombótica, complicação também relacionada com a pré-eclâmpsia. Glomeruloesclerose focal e segmentar pode estar presente em até 50% das endotelioses e também pode ser encontrada tardiamente na microangiopatia trombótica.

Question 57

Q

Microangiopatia trombótica:

Answer

A

Microangiopatia trombótica = quadro agudo de anemia hemolítica microangiopática, trombocitopenia e sinais variáveis de disfunção orgânica secundária à trombose plaquetária na microcirculação.

É secundária à lesão endotelial que pode ser causada por diversos agentes como exotoxinas, endotoxinas, auto-anticorpos, imunocomplexos e drogas

. Quando associada com a gravidez, pode ser manifestada clinicamente como Púrpura Trombocitopênica Trombótica, Síndrome Hemolítica Urêmica ou Síndrome HELLP, como no caso desta paciente.

Os achados na microscopia óptica são de microtrombos na luz dos capilares glomerulares, arteríolas e artérias, com proliferação miointimal e duplicação de lâmina elástica destas em alguns casos, levando à isquemia glomerular e retração do seu tufo, alterações descritas na biópsia renal desta paciente. Na microscopia eletrônica, a lesão da microangiopatia trombótica consiste em alargamento da parede do vaso (capilar e arteríola), com edema e destacamento das células endoteliais da membrana basal, depósitos subendoteliais de material e debris celulares, trombo plaquetário intraluminal com obstrução parcial ou completa do lúmen dos vasos. O encontro destas alterações no fragmento renal da biópsia, e sua associação com as manifestações clínicas já amplamente descritas, nos levaram ao diagnóstico final de microangiopatia trombótica no contexto da Síndrome HELLP.

Question 58

Q

ATN and acute cortical necrosis

Answer

A

are suggested by the history (sepsis or hemorrhage) and by microscopic analysis of urinary sediment, which often shows pigmented granular casts and renal tubular epithelial cells. The diagnosis of cortical necrosis can usually be established by ultrasonography or computed tomography (CT) scanning, which demonstrate hypoechoic or hypodense areas in the renal cortex

Question 59

Q

HELLP syndrome

Answer

A

hemolysis with a microangiopathic blood smear, elevated liver enzymes, and low platelet count)

The most common clinical presentation is abdominal pain and tenderness in the midepigastrium, right upper quadrant, or below the sternum. Many patients also have nausea, vomiting, and malaise, which may be mistaken for a viral illness. Hypertension and proteinuria are present in approximately 85 percent of cases

Most cases of HELLP are diagnosed between 28 and 36 weeks of gestation, but symptoms may present up to 7 days postpartum.

Question 60

Q

HELLP DIAGNOSTICO

Answer

A

We require the presence of all of the following criteria to diagnose HELLP (Tennessee classification)

Hemolysis, established by at least two of the following:

Peripheral smear with schistocytes and burr cells (picture 2)
Serum bilirubin ≥1.2 mg/dL (20.52 micromol/L)
Low serum haptoglobin (≤25 mg/dL) or lactate dehydrogenase (LDH) ≥2 times the upper level of normal (based on laboratory-specific reference ranges)
Severe anemia, unrelated to blood loss

●Elevated liver enzymes:

•Aspartate aminotransferase (AST) or alanine aminotransferase (ALT) ≥2 times the upper level of normal (based on laboratory-specific reference ranges)

●Low platelets: <100,000 cells/microL

The use of twice the upper limit of normal threshold was chosen, in part, to avoid problems related to differences in assays, which may result in an elevated absolute value in one hospital that is considered near normal in another.

In HELLP, an elevated LDH level is a nonspecific marker that can be associated with severe hemolysis, acute hepatocellular injury, or both. The total bilirubin level is increased as a result of an increase in the indirect (unconjugated) fraction from hemolysis. Haptoglobin level is a specific marker of hemolysis: 25 mg/dL provides the best cutoff between hemolytic and non-hemolytic disorders. (See “Diagnosis of hemolytic anemia in adults”, section on ‘High LDH and bilirubin; low haptoglobin’.)

Severe anemia in pregnancy can be defined as hemoglobin level <8 to 10 g/dL, depending on the trimester. (See “Anemia in pregnancy”, section on ‘Definition of anemia’.)

The American College of Obstetricians and Gynecologists suggests slightly different diagnostic criteria and acknowledges the absence of clinical consensus among experts [22]:

●LDH ≥600 IU/L, and

●AST and ALT elevated more than twice the upper limit of normal, and

●Platelet count <100,000 cells/microL

Subclassification — Although not commonly used, some clinicians subclassify HELLP based on severity of thrombocytopenia (Mississippi classification) [23]:

●Class 1 – Platelet count ≤50,000 cells/microL plus LDH >600 IU/L and AST or ALT ≥70 IU/L

●Class 2 – Platelet count >50,000 but ≤100,000 cells/microL plus LDH >600 IU/L and AST or ALT ≥70 IU/L

●Class 3 – Platelet count >100,000 but ≤150,000 cells/microL plus LDH >600 IU/L and AST or ALT ≥40 IU/L

Question 61

Q

Question 62

Q

HELLP DIAGNOSTICO

Answer

A

The diagnosis of HELLP is based on the presence of all of the following criteria (Tennessee classification)

Hemolysis, established by at least two of the following:

Peripheral smear with schistocytes and burr cells (picture 2)
Serum bilirubin ≥1.2 mg/dL (20.52 micromol)
Low serum haptoglobin or lactate dehydrogenase (LDH) ≥2 times the upper level of normal (based on laboratory-specific reference ranges)
Severe anemia, unrelated to blood loss

•Elevated liver enzymes:

-Aspartate aminotransferase (AST) or alanine aminotransferase (ALT) ≥2 times the upper level of normal (based on laboratory-specific reference ranges)

•Low platelets: <100,000 cells/microL.

●Differential diagnosis – The four major disorders in differential diagnosis are acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura, pregnancy-related hemolytic-uremic syndrome, and systemic lupus erythematosus. All have features that overlap with HELLP (table 3A-B). (See ‘Differential diagnosis’ above.)

Question 63

Q

HELLP

Answer

A

Management

Initial management – The initial steps are to assess the mother, stabilize patients who are unstable, and assess gestational age and fetal status (nonstress test, ultrasound examination for biophysical profile and fetal presentation). Because of the potential for severe maternal complications, which can develop rapidly, patients with HELLP should be managed at a tertiary care center with appropriate levels of maternal and neonatal intensive care. Our general approach to management is illustrated in the algorithm (algorithm 1). (See ‘Management of patients presenting before delivery’ above.)
Treatment of severe hypertension – Patients with severe hypertension should receive antihypertensive therapy (eg, intravenous labetalol (table 4)) promptly to reduce the risk of stroke. (See ‘Patients requiring urgent assessment or intervention’ above.)
Treatment of hepatic bleeding – Although uncommon, severe right upper quadrant/epigastric pain may be due to hepatic bleeding, which may remain contained or rupture the liver capsule. The management of a hematoma is to support the patient with volume replacement and transfusion of blood and blood products, as needed. Prompt delivery is indicated once they are hemodynamically stable and severe anemia and coagulopathy, if present, have been corrected. A team experienced in liver trauma surgery should be consulted during maternal stabilization and prior to delivery.
Magnesium sulfate – Magnesium sulfate is given intravenously to patients on the labor and delivery unit to prevent convulsions and for fetal/neonatal neuroprotection in pregnancies between 24 and 32 weeks of gestation with a live fetus. (
Antenatal corticosteroids. – Antenatal corticosteroids to enhance fetal lung maturation are administered when the gestational age is above the lower limit of viability and <34 weeks of gestation. We recommend not administering dexamethasone for treatment of HELLP syndrome (Grade 1B). Dexamethasone does not accelerate resolution of laboratory abnormalities or reduce the risk of maternal complications

Question 64

Q

PROTEINURIA EM GRAVIDAS

Answer

A

In nonpregnant individuals without kidney disease, normal urinary protein excretion is less than 150 mg daily. In pregnancy, urinary protein excretion normally increases substantially; hence, urinary protein excretion is considered abnormal in pregnant people when it exceeds 300 mg daily

Proteinuria is one of the cardinal features of preeclampsia (table 1), a common and potentially severe complication of pregnancy. Proteinuria in pregnancy can also indicate primary kidney disease or kidney disease secondary to systemic disorders, such as diabetes mellitus or primary hypertension. Adding to the complexity, 20 to 25 percent of pregnant people with chronic hypertension, diabetes mellitus, or chronic kidney disease develop superimposed preeclampsia

Glomerular filtration rate (GFR) and renal blood flow rise markedly during pregnancy, resulting in a physiologic fall in the serum creatinine concentration. Urinary protein excretion increases substantially due to a combination of increased GFR and increased permeability of the glomerular basement membrane [7]. Additionally, tubular reabsorption of filtered protein is reduced in pregnancy, along with other nonelectrolytes, such as amino acids, glucose, and beta-microglobulin.

Answer 61

A

The spot urine protein-to-creatinine ratio (UPCR; mg protein/mg creatinine) is an accurate, convenient, and relatively rapid method to quantify proteinuria in pregnancy. A UPCR less than 0.15 mg/mg may be considered normal (predictive of less than 300 mg protein in a 24-hour collection), and values above 0.7 mg/mg are very likely to indicate significant proteinuria (more than 300 mg protein in a 24-hour collection). A UPCR greater than 0.3 mg/mg after 20 weeks gestation is one of the diagnostic criteria for preeclampsia

The gestational age at which proteinuria is first documented is important in establishing the likelihood of preeclampsia versus other kidney disease. Proteinuria documented before 20 weeks of gestation suggests preexisting renal disease. Proteinuria beginning after 20 weeks gestation is usually due to preeclampsia, especially in the presence of hypertension or other features of severe preeclampsia

Nephrotic syndrome is associated with an increased risk of deep venous thrombosis (DVT). Patients with severe nephrotic syndrome (particularly those with membranous nephropathy) and very low serum albumin levels who are not at high risk for bleeding may benefit from prophylactic anticoagulation. However, there is no high quality evidence to guide the optimal approach to prophylactic anticoagulation in this patient population.

Bile acid sequestrants and fibrates can be safely used in pregnancy to treat severe hyperlipidemia due to nephrotic syndrome; statins should be avoided

Preeclampsia is considered superimposed when it occurs in a woman with chronic hypertension. It is characterized by worsening or resistant hypertension (especially acutely), the new onset of proteinuria or a sudden increase in proteinuria, and/or significant new end-organ dysfunction after 20 weeks of gestation in a woman with chronic hypertension.

Answer 62

A

Biópsia renal, que revelou endoteliose glomerular.

A incidência de toxemia varia de 3 a 15% das gestações.

As primigestas jovens apresentam maior risco, mas também há incidência aumentada após os 35 anos de idade.

já se sabe que este processo se inicia em fase precoce da gestação, tendo se observado que, dentre outros fatores, não ocorreria a segunda onda de invasão trofoblastica, responsável pela destruição da camada muscular das artérias espiraladas. Como conseqüência, os vasos permaneceriam obliterados e hiperreativos aos agentes vasopressores. No decorrer da gestação, com necessidade de aumento do fluxo sangüíneo, poderia então ocorrer disfunção placentária. A isquemia placentária pode ser responsável pela liberação de produtos que alteram a função endotelial, levando às alterações características da pré-eclampsia, tais como vasoespasmo, ativação da coagulação e perda de fluido do intravascular.

O diagnostico da toxemia é clinico, e a definição clássica inclui: aparecimento de hipertensão, proteinúria e edema significante.

Em algumas pacientes sem diagnostico prévio de hipertensão, o diferencial entre pré-eclampsia e hipertensão crônica pode ser dificultado, tendo em vista a habitual redução da PA que ocorre nos primeiros trimestres da gestação. O sedimento urinário é geralmente normal e a creatinina sérica pode ou não estar um pouco aumentada. A proteinúria tende a aumentar no decorrer da gestação, podendo chegar a níveis nefróticos.

Answer 63

A

Durante a gestação, diante de um quadro de microangiopatia trombótica, duas entidades devem ser lembradas:
1- SHU/PTT (Síndrome Hemolítico Urêmica / Púrpura Trombocitopênica Trombótica)
2- Toxemia gravídica grave (geralmente com síndrome HELLP- hemólise, anemia microangiopática, aumento de enzimas hepáticas e plaquetopenia)

Para o diagnóstico diferencial, o mais importante é a história e o início do quadro. A toxemia geralmente ocorre no final do 3o trimestre, incluindo o período intraparto e uma pequena parcela nas primeiras 48h de puerpério e, NÃO OCORRE antes de 20 semanas de gestação em gestações não molares. SHU e PTT freqüentemente ocorrem no puerpério, o início dos sintomas pode ser retardado em cerca de 48h ou mais após o parto. Quando a SHU e a PTT ocorrem pré-parto podem ocorrer em qualquer fase da gestação, geralmente antes de 20 semanas de gestação. A SHU periparto pode ser precedida por sinais indistingüíveis de pré-eclâmpsia.

Toxemia gravídica grave é bem mais comum que SHU e PTT; geralmente é precedida por hipertensão, proteinúria, e edema importante. Insuficiência renal costuma ser pouco usual mesmo nos casos mais graves, exceto na situação de instabilidade hemodinâmica por sangramento ou, no caso de CIVD. A toxemia gravídica grave é uma indicação de resolução da gestação urgente, conforme foi realizada no caso descrito. O quadro renal e extrarenal tipicamente começa a resolver-se cerca de 2 a 3 dias pós parto e atinge recuperação completa cerca de 8 semanas após o parto. CIVD pode estar presente na toxemia quando em associação com descolamento prematuro de placenta, ruptura hepática e insuficiência hepática. Fatores de coagulação costumam estar baixos na toxemia e normais na SHU.

A SHU/PTT é caracterizada por uma combinação de trombocitopenia e anemia microangiopática, geralmente associada a doença renal. A associação de SHU/PTT com gravidez é sugerida pela observação em séries de casos. Geralmente a distinção entre SHU e PTT era dado por predomínio de acometimento renal ou neurológico, respectivamente; porém trata-se de método impreciso e provavelmente irrelevante com relação à tomada de conduta.

O diagnóstico diferencial entre a toxemia com síndrome HELLP e a SHU/PTT é difícil uma vez que AMBAS são caracterizadas por microangiopatia e plaquetopenia. A presença de enzimas hepáticas elevadas sugere fortemente HELLP.

Answer 64

A

Gestational hypertension

New onset of systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on at least 2 occasions 4 hours apart after 20 weeks of gestation in a previously normotensive individual

And:

No proteinuria /No severe features of preeclampsia (thrombocytopenia, renal insufficiency, elevated liver transaminases, pulmonary edema, cerebral or visual symptoms)

Preeclampsia

New onset of systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on at least 2 occasions at least 4 hours apart after 20 weeks of gestation in a previously normotensive individual or systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg confirmed within a short interval (minutes) to facilitate timely antihypertensive therapy

And:

Proteinuria (≥300 mg per 24-hour urine collection [or this amount extrapolated from a timed collection], or protein:creatinine ratio ≥0.3, or urine dipstick reading ≥2+ [if other quantitative methods are not available])

Or, in the absence of proteinuria, new-onset hypertension with the new onset of any of the following:

Thrombocytopenia (platelet count <100,000/microL)

Renal insufficiency (serum creatinine of >1.1 mg/dL [97 micromol/L] or a doubling of the serum creatinine concentration in the absence of other renal disease)

Impaired liver function as indicated by liver transaminase levels at least twice the normal concentration

Pulmonary edema

Persistent cerebral or visual symptoms

Preeclampsia with severe featuresAny of these findings in a patient with preeclampsia:

Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg on 2 occasions at least 4 hours apart (unless antihypertensive therapy is initiated before this time)

Thrombocytopenia (platelet count <100,000/microL)

Impaired liver function as indicated by liver transaminase levels at least twice the normal concentration or severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses, or both

Progressive renal insufficiency (serum creatinine concentration >1.1 mg/dL [97 micromol/L] or a doubling of the serum creatinine concentration in the absence of other renal disease)

Pulmonary edema

Persistent cerebral or visual disturbances

Eclampsia

In a patient with preeclampsia, generalized seizures that cannot be attributed to other causes

HELLP syndrome

Presence of Hemolysis, Elevated Liver enzymes, and Low Platelet count; hypertension may be present (HELLP in such cases is often considered a variant of preeclampsia)

Chronic (preexisting) hypertensionHypertension diagnosed or present before pregnancy or before 20 weeks of gestation. Hypertension that is first diagnosed during pregnancy and persists for at least 12 weeks post-delivery is also considered chronic hypertension.

The blood pressure criteria are systolic blood pressure ≥140 mmHg, diastolic blood pressure ≥90 mmHg, or both. Ideally, this diagnosis is based on at least 2 elevated blood pressure measurements taken at least 4 hours apart. In the setting of severe hypertension, the diagnosis can be confirmed in a shorter interval to facilitate timely treatment.

Chronic hypertension with superimposed preeclampsia*Any of these findings in a patient with chronic hypertension:

A sudden increase in blood pressure that was previously well-controlled or an escalation of antihypertensive therapy to control blood pressure

New onset of proteinuria or sudden increase in proteinuria in a patient with known proteinuria before or early in pregnancy

Chronic hypertension with superimposed preeclampsia with severe featuresAny of these findings in a patient with chronic hypertension and superimposed preeclampsia:

Systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg despite escalation of antihypertensive therapy

Thrombocytopenia (platelet count <100,000/microL)

Impaired liver function as indicated by liver transaminase levels at least twice the normal concentration or severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses, or both

New-onset or worsening renal insufficiency

Pulmonary edema

Persistent cerebral or visual disturbances

Answer 65

A

Preeclampsia/eclampsia/HELLP syndrome (hemolysis, elevated liver enzymes, low platelets)

●Gestational hypertension

●Chronic hypertension

●Preeclampsia superimposed on chronic hypertension

Answer 66

A

We suggest hemodialysis rather than peritoneal dialysis for women who wish to become, or are, pregnant (Grade 2B). The pregnancy rate is lower among patients on peritoneal dialysis compared with hemodialysis, and there appears to be a higher rate of small for gestational age (SGA) pregnancies among peritoneal dialysis compared with hemodialysis patients

Answer 67

A

Modification of the maintenance immunosuppression regimen is frequently necessary prior to conception. All immunosuppressive medications carry some risk in pregnancy. The use of mycophenolate mofetil/sodium and mammalian (mechanistic) target of rapamycin (mTOR) inhibitors (sirolimus and everolimus) is contraindicated in pregnancy because of reports of severe structural malformations associated with these agents

Answer 68

A

Nutrition — Attention to nutritional considerations and proper weight gain are essential for a successful pregnancy [26]. Evaluation and follow-up by a dietician familiar with the requirements of pregnancy and ESKD may be helpful.

The diet should be modified among dialysis patients:

●Daily protein intake of 1.5 to 1.8 g/kg per day – This is higher than the recommended amount for nonpregnant CKD patients (0.8 g/kg) and for pregnant women without CKD (approximately 1.1 g/kg) in order to account for amino acid losses with dialysis.

●Double doses of water-soluble vitamins and folic acid supplementation of 5 mg/day – The folic acid requirement is higher than for nondialysis individuals because folic acid is cleared by dialysis.

●Liberalization of dietary phosphate – Pregnant women who are on dialysis should not be on any phosphate restriction and generally do not require phosphate binders due to intensification of hemodialysis. In fact, phosphate supplementation may be necessary during dialysis.

●Assessment of dry weight – In general, women should gain approximately 2 to 4 pounds during the first three months of pregnancy and 1 pound per week thereafter, necessitating regular adjustments to dry weight. Careful clinical assessment of volume status is advised to determine ultrafiltration goals.

Answer 69

A

Many women get magnesium sulfate before delivery, either to prevent seizures in preeclampsia or to reduce the risk of cerebral palsy before preterm birth of an infant <32 weeks. Magnesium is renally excreted, and toxicity is potentially life threatening due to respiratory depression, arrhythmias, and central nervous system (CNS) depression.

For women who require magnesium sulfate before delivery, we reduce both the loading dose and the infusion rate by one-half. We closely monitor serum levels and follow the patient clinically for evidence of magnesium toxicity.

Answer 70

A

In addition, there appears to be a higher rate of small for gestational age (SGA) pregnancies among peritoneal dialysis compared with hemodialysis patients.

Intensive dialysis – Providing more frequent and/or longer dialysis decreases the risk of polyhydramnios, helps control hypertension, increases birth weight and gestational age, improves maternal nutrition, and increases the chances of live birth

Most clinicians would increase the frequency of hemodialysis to five or six times per week.

The specific dose varies depending on the residual kidney function.

Among patients without residual kidney function, we provide ≥36 hours of dialysis per week.

Further studies will be necessary to refine dialysis dose and determine if less intensive regimens can be safely prescribed as this study had too few patients that received between 30 and 36 hours of dialysis.

Among patients with residual kidney function, we target a blood urea nitrogen (BUN) under 50 mg/dL UREIA MENOR QUE 100

Potassium – We advise using a dialysate potassium of ≥3 mEq/L. This lessens the risk of hypokalemia, which should be avoided. Hyperkalemia is uncommon because of intensive dialysis, and dialysate concentrations <3 mEq/L are rarely required.

●Calcium – We use a dialysate calcium concentration of 1.5 mmol/L (6 mg/dL) in order to avoid the risk of hypocalcemia. 1,75-2,5?

●Bicarbonate – We use a dialysate concentration of 30 mEq/L, which is generally sufficient to avoid metabolic acidosis in patients undergoing intensive dialysis. If metabolic acidosis develops, the dialysate bicarbonate may be increased to 35 mEq/L.devido a alcalose respiratoria da gravidez pode haver necessidade de diminuir o bic para 25

●Phosphate – If hypophosphatemia develops despite a liberal dietary phosphorus intake (and no phosphate binders), we add sodium phosphate to the dialysate to aim for a concentration of up to 4.5 mg/dL (1.5 mmol/L). The dialysate phosphate concentration is adjusted to maintain pre- and postdialysis phosphate concentrations within the normal range

aumentar o acido folico para 5mg/dia

Answer 71

A

Anticoagulation – Heparin is considered safe to use for anticoagulation in pregnancy.

Peritoneal dialysis — During early stages of pregnancy, intensive dialysis may be provided by increasing the volume and number of exchanges. In later stages, the number of exchanges must be increased (preferably with the use of a cycler) to provide sufficient dialysis since the volume is limited by the expanding uterus. In one report, dialysis was provided using an overnight cycler with 8 to 12 one-liter exchanges over 12 to 16 hours, with four additional manual exchanges during the day [32]. By 30 weeks, the overnight cycler provided up to 20 exchanges of 750 mL over 18 hours.

As with hemodialysis patients, hypokalemia, hypocalcemia, metabolic acidosis, hypophosphatemia, and hypotension should be avoided. These complications are uncommon with peritoneal dialysis. We limit the use of hypertonic solutions (either 4.25 percent or icodextrin) as much as possible.

Hypertension — Specific blood pressure targets for pregnant dialysis patients have not been defined [33]. The postdialysis target for nonpregnant dialysis patients is <140/90 mmHg. In a 2015 trial (Control of Hypertension in Pregnancy Study [CHIPS]) that randomly assigned pregnant women with gestational or chronic hypertension to diastolic blood pressure treatment targets of 85 or 100 mmHg, there were no differences in maternal, fetal, or neonatal outcomes for the two blood pressure targets, although fewer women in the lower diastolic blood pressure target group developed severe hypertension [34]. However, this study did not include dialysis patients. (See “Treatment of hypertension in pregnant and postpartum patients”.)

Answer 72

A

meta pressorica

metas 120x160 80-100

140x90

Answer 73

A

he optimal time for conception after kidney transplantation is uncertain. We agree with the 2005 American Society of Transplantation (AST) report on the Consensus Conference on Reproductive Issues and Transplantation, which states that the kidney transplant recipient can safely proceed with pregnancy, provided that the following conditions are met [31]:

●It has been more than one year since kidney transplantation.

●Graft function is optimal, defined as a serum creatinine of <1.5 mg/dL (133 micromol/L), with no or minimal proteinuria.

●There have been no episodes of rejection in the previous year.

●There are no concurrent fetotoxic infections, such as cytomegalovirus (CMV).

●The patient is not on known teratogenic or fetotoxic medications.

●The immunosuppressive regimen is stable at maintenance levels.

In addition, patients who have a history of recent (but not currently active) CMV disease should be advised to wait at least six months and preferably one year from the resolution of disease before trying to conceive. There are no high-quality data to guide the optimal timing of pregnancy after CMV infection. At our center, we advocate waiting one year following complete resolution of infection.

While we, and most experts, recommend avoiding pregnancy during the first posttransplant year (when the risk of rejection and infection is highest), the timing of pregnancy may need to be individualized in certain patients, such as those who are older and have a limited number of reproductive years. Successful pregnancies within the first posttransplant year have been reported, with no difference in pregnancy outcomes, maternal and fetal complications, or graft survival compared with pregnancies that occurred after one year [51,65].

Even when the above conditions are met, pregnancy presents some risk to the patient, allograft, and fetus. The major risks to the patient include the risk of rejection and allograft failure due to changes in the metabolism of immunosuppressive medications and increased filtration that occurs during pregnancy. (See ‘Effect of pregnancy on graft function and outcomes’ above and ‘Rejection’ below.)

Answer 74

A

following baseline evaluation prior to planned conception:

●Assessment of the patient’s medical history to identify any important clinical events (eg, episodes of rejection, potentially fetotoxic infections such as CMV) in the preceding year

●Assessment of the patient’s medication history for potential teratogenic or fetotoxic medications (discontinue and/or substitute medications that have been identified to be potentially teratogenic or fetotoxic [eg, angiotensin-converting enzyme (ACE) inhibitors])

●Assessment of the patient’s maintenance immunosuppression regimen (see ‘Management of immunosuppression’ below)

●Assessment of vaccination status (see ‘Vaccination’ below)

●Assessment of blood pressure (see ‘Hypertension’ below)

●Measurement of serum creatinine, bicarbonate, and electrolytes

●Measurement of fasting plasma glucose and hemoglobin glycated hemoglobin (A1C) (see ‘Gestational diabetes’ below)

●Liver function tests (see ‘Preeclampsia’ below)

●Complete blood count (see ‘Anemia’ below)

●Plasma polymerase chain reaction (PCR) testing for CMV and BK virus (see “Clinical manifestations, diagnosis, and management of cytomegalovirus disease in kidney transplant patients” and “Kidney transplantation in adults: BK polyomavirus-associated nephropathy”)

●Urinalysis and spot urine protein-to-creatinine ratio from a first or second morning void (and, if proteinuria is present, a 24-hour urine collection for protein)

●Ultrasound with Doppler of the kidney allograft

Answer 75

A

modification of the maintenance immunosuppression regimen is frequently necessary prior to conception.

The immunosuppressive medications used in transplantation pass through the maternal-fetal barrier to varying degrees, and all carry some risk in pregnancy

The recommended maintenance immunosuppression regimen in pregnant transplant recipients is the combination of a CNI (either tacrolimus or cyclosporine), azathioprine, and low-dose prednisone.

The use of mycophenolate mofetil/sodium and mammalian (mechanistic) target of rapamycin (mTOR) inhibitors (sirolimus and everolimus) is contraindicated in pregnancy.

Mycophenolate mofetil/sodium should be discontinued at least six weeks prior to conception because of reports of severe structural malformations associated with these agents

. Patients taking sirolimus should be advised to continue contraception for at least 12 weeks after sirolimus therapy has been stopped, while those taking everolimus should continue contraception for at least eight weeks after everolimus has been stopped.

We typically switch all patients taking mycophenolate mofetil/sodium or an mTOR inhibitor to azathioprine.

All patients undergoing adjustment of immunosuppression should have close monitoring of allograft function for a few months to ensure stability of the allograft.

In addition, patients should be informed of the increased risk of rejection following changes in immunosuppression.

The safety of belatacept use during pregnancy is still unknown [68].

The true impact of the immunosuppressive regimen on the developing fetus is not well defined, and the long-term risks are unknown. There are possible concerns about neurocognitive disorders and immunologic disturbances in addition to structural congenital anomalies. Evidence on the effects of these agents on pregnancy outcomes are discussed elsewhere.

Vaccination — Patients should ideally be vaccinated pretransplant against influenza, Pneumococcus, hepatitis B, human papillomavirus (HPV), and tetanus. If not, the patient should receive these vaccines before pregnancy. Live vaccines should not be administered posttransplant.

Answer 76

A

There are no definitive recommendations to guide the optimal blood pressure goal in pregnant kidney transplant recipients. The 2005 AST report on the Consensus Conference on Reproductive Issues and Transplantation states that blood pressure should be maintained close to normal [31], although it was noted that this target differs from higher blood pressure goals of existing guidelines for pregnant women with chronic hypertension without end-organ damage. In pregnant kidney transplant recipients with preexisting hypertension, our treatment target is a systolic pressure of 120 to 140 mmHg and diastolic pressure of 80 to 90 mmHg. In those who do not have preexisting hypertension, we initiate antihypertensive therapy when the blood pressure is consistently >140/90 mmHg. (See “Treatment of hypertension in pregnant and postpartum patients”.)

The treatment of hypertension in pregnant transplant recipients is similar to that in pregnant nontransplant patients

Methyldopa, beta blockers (particularly labetalol), hydralazine, and dihydropyridine calcium channel blockers can all be safely used in hypertensive pregnant transplant patients.

Nondihydropyridine calcium channel blockers (such as diltiazem and verapamil) can increase CNI levels and should be avoided if possible.

ACE inhibitors, angiotensin II receptor blockers (ARBs), and direct renin inhibitors are associated with significant fetal risk and are contraindicated during pregnancy. Women who are taking any of these agents should discontinue them as soon as they are contemplating pregnancy and should be discouraged from conceiving for at least six weeks after discontinuation.

Answer 77

A

tients who are found on routine testing to have an increase in serum creatinine or proteinuria should be promptly evaluated for allograft dysfunction. Common causes of allograft dysfunction among pregnant recipients include rejection, preeclampsia, volume depletion, and CNI toxicity;

although less common, obstruction should also be considered.

The evaluation and diagnosis of kidney allograft dysfunction in pregnant transplant recipients are similar to that in nonpregnant recipients. In some cases, a kidney allograft biopsy may be necessary to determine the cause of graft dysfunction. Although data are limited, ultrasound-guided kidney allograft biopsies are generally safe and well tolerated during pregnancy

Answer 78

A

reported rates of kidney allograft rejection are generally comparable between pregnant and nonpregnant kidney transplant recipients

although the risk of rejection may be higher in sensitized recipients (ie, panel reactive antibody [PRA] levels >0 percent) Risk factors for the development of rejection during pregnancy include an elevated prepregnancy serum creatinine level and fluctuating immunosuppressive drug levels caused by pregnancy-related changes in the distribution and clearance of these agents.

As discussed above, we recommend closely monitoring CNI levels every two to four weeks and maintaining them at the same levels as they were prior to pregnancy. (

The clinical presentation of acute rejection in pregnant recipients is similar to that in nonpregnant recipients .While most patients are asymptomatic, presenting only with an elevation in serum creatinine and/or proteinuria, those with more serious rejection may present with fever, oliguria, and graft pain or tenderness. Occasionally, the diagnosis may be missed in patients with subtle increases in serum creatinine and/or proteinuria, which can be masked by the normal pregnancy-related changes in GFR and proteinuria.

Rejection must also be distinguished from preeclampsia which can also present with an increase in serum creatinine and proteinuria, and acute pyelonephritis, which can present with fever and graft tenderness.

In patients who are suspected of having acute rejection, an ultrasound-guided kidney allograft biopsy should be performed to establish the diagnosis and guide treatment. This procedure is generally safe and well tolerated in pregnancy, although data regarding kidney allograft biopsies in pregnancy are limited

Treatment options are limited because of the potential fetotoxicity of many of the agents normally used to treat acute rejection.

Augmentation of baseline immunosuppression and glucocorticoids are generally safe and are considered first-line therapy for both acute T cell-mediated (TCMR) and antibody-mediated rejection (ABMR) in pregnant recipients.

In patients who are suspected of having rejection but cannot un

dergo a kidney allograft biopsy, glucocorticoids can be given as empiric treatment for rejection. Rabbit antithymocyte globulin (rATG), which is used to treat more severe forms of acute TCMR, is not recommended during pregnancy, as there are insufficient data regarding risk to the fetus.

Patients with acute ABMR can receive intravenous immune globulin (IVIG), rituximab, and plasmapheresis, which have been used to treat pregnant patients with idiopathic thrombocytopenic purpura and acquired thrombotic thrombocytopenic purpura, respectively.

In patients with rejection who are treated with high-dose glucocorticoids, we do not routinely give antibiotic prophylaxis against Pneumocystis pneumonia (PCP), since the risk of PCP in this setting is low and trimethoprim-sulfamethoxazole (TMP-SMX), dapsone, and inhaled pentamidine should all be avoided in pregnancy.

Answer 79

A

Some, but not all, studies have suggested higher rates of gestational diabetes in the pregnant transplant population. According to the TPR 2016 annual report, gestational diabetes can be seen in 8 percent of pregnant kidney transplant recipients taking a CNI, compared with approximately 2 to 5 percent of the general pregnant population [44]. Another study from the United Kingdom, however, reported rates of gestational diabetes in the transplant population that were comparable with that of the general population (approximately 3 percent) [33]. Factors that contribute to the development of gestational diabetes in transplant recipients include CNI use, glucocorticoids, obesity, and insulin resistance that can be seen after transplantation [29,34,46]. Uncontrolled blood glucose levels during the first trimester have been associated with a higher incidence of congenital anomalies.

Answer 80

A

MF, mycophenolate sodium, and mTOR inhibitors (sirolimus and everolimus) should be avoided during pregnancy and in patients who may become pregnant. Azathioprine has been used safely in pregnant transplant patients. Cyclosporine, tacrolimus, and prednisone also appear to be safe. Pharmacokinetic factors, such as volume of distribution and metabolism, are altered with pregnancy, and drug levels require more frequent monitoring and adjustment

Answer 81

A

Hydroxychloroquine (HCQ) (

●Sulfasalazine (SSZ)

●Low-dose aspirin

●Azathioprine (AZA) and 6-mercaptopurine (6-MP) (

●Colchicine

Low-dose glucocorticoid (eg, 5 to 15 mg of prednisone per day) is compatible with pregnancy, although higher doses and use later in pregnancy increases the risk of gestational diabetes and pregnancy-induced hypertension.

Tumor necrosis factor (TNF)-alpha inhibitors, cyclosporine, tacrolimus, and intravenous immune globulin (IVIG) are compatible with use during pregnancy. Some experts discontinue TNF-alpha blockers during the third trimester, although use of these drugs can be extended, if necessary, to a later gestational age if benefits outweigh potential risks for an individual patient. Certolizumab is compatible with use throughout pregnancy.

Abatacept, anakinra, belimumab, ixekizumab, rituximab, secukinumab, and tocilizumab may be used up until conception. While there are limited or no data on other biologics, one can consider continuing these medications through conception. Tofacitinib and the other small molecules should be avoided in pregnant and lactating women. (See ‘Limited information’ above.)

●In pregnant women, we limit the use of high-dose glucocorticoids, cyclophosphamide (CYC), and rituximab only to women with life-threatening rheumatologic autoimmune disease in whom the benefits of these agents is felt by the patient and clinician to outweigh the risks. (See ‘Glucocorticoids’ above and ‘Cyclophosphamide’ above and ‘Rituximab’ above.)

●Leflunomide (LEF), methotrexate (MTX), and mycophenolate mofetil (MMF) should be avoided in pregnant women with autoimmune disease, and counseling should be offered in the setting of inadvertent exposure.

Answer 82

A

Severe blood pressure elevation:

Systolic blood pressure ≥160 mmHg and/or diastolic blood pressure ≥110 mmHg on 2 occasions at least 4 hours apart while the patient is on bedrest; however, antihypertensive therapy generally should be initiated upon confirmation of severe hypertension, in which case criteria for severe blood pressure elevation can be satisfied without waiting until 4 hours have elapsed

Symptoms of central nervous system dysfunction:

New-onset cerebral or visual disturbance, such as:

Photopsia, scotomata, cortical blindness, retinal vasospasm

Severe headache (ie, incapacitating, “the worst headache I’ve ever had”) or headache that persists and progresses despite analgesic therapy with acetaminophen and not accounted for by alternative diagnoses

Hepatic abnormality:

Impaired liver function not accounted for by another diagnosis and characterized by serum transaminase concentration >2 times the upper limit of the normal range or severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by an alternative diagnosis

Thrombocytopenia:

<100,000 platelets/microL

Renal abnormality:

Renal insufficiency (serum creatinine >1.1 mg/dL [97.2 micromol/L] or a doubling of the serum creatinine concentration in the absence of other renal disease)

Pulmonary edema

Seizure prophylaxis – For patients with preeclampsia with features of severe disease, we recommend intrapartum and postpartum seizure prophylaxis with magnesium sulfate (Grade 1A). Seizure is an infrequent occurrence in patients without severe features of preeclampsia; however, some clinicians and patients may feel the benefit of treatment is justifiable given the low cost and toxicity of the treatment. (See ‘Seizure prophylaxis’ above.)

•Initial and maintenance magnesium sulfate dosing – The most common dose is 4 to 6 g magnesium sulfate intravenously over 15 to 20 minutes followed by 1 to 2 g/hour as a continuous infusion. The maintenance dose is only given when a patellar reflex is present (loss of reflexes is the first manifestation of symptomatic hypermagnesemia), respirations exceed 12 breaths/minute, and urine output exceeds 100 mL over four hours. (See ‘Dosing’ above.)

The maintenance dose (but not the loading dose) should be adjusted in patients with renal insufficiency. We use 1 g/hour if the serum creatinine is >1.2 and <2.5 mg/dL (106 to 221 micromol/L) and no maintenance dose if the serum creatinine is ≥2.5 mg/dL (221 micromol/L). (See ‘Dosing in renal insufficiency’ above.)

•Magnesium toxicity – Magnesium toxicity is uncommon in patients with good renal function. Toxicity is related to serum magnesium concentration: loss of deep tendon reflexes occurs at 7 to 10 mEq/L (8.5 to 12 mg/dL or 3.5 to 5.0 mmol/L), respiratory paralysis at 10 to 13 mEq/L (12 to 16 mg/dL or 5.0 to 6.5 mmol/L), cardiac conduction is altered at >15 mEq/L (>18 mg/dL or >7.5 mmol/L), and cardiac arrest occurs at >25 mEq/L (>30 mg/dL or >12.5 mmol/L). (See ‘Signs of magnesium toxicity’ above.)

Clinical assessment for magnesium toxicity should be performed every one to two hours. We obtain serum magnesium levels every six hours as an adjunct to clinical assessment in patients who have a seizure while receiving magnesium sulfate, clinical signs/symptoms suggestive of magnesium toxicity, or renal insufficiency. (See ‘When to check magnesium levels’ above.)

•Management of toxicity – Calcium gluconate 15 to 30 mL of a 10 percent solution intravenously over 2 to 5 minutes is administered to patients with cardiac arrest or severe cardiac toxicity related to hypermagnesemia. A starting dose of 10 mL of a 10 percent solution is used for patients with less severe but life-threatening cardiorespiratory compromise. (See ‘Antidote’ above.)

●Delivery

Route – Preeclampsia is not an indication for cesarean delivery. Most patients with preeclampsia with or without severe features can be delivered vaginally. Cesarean delivery should be reserved for usual obstetric indications. (See ‘Route of birth’ above.)
Patients with thrombocytopenia – For severely thrombocytopenic patients (platelets <50,000/microL), we notify the blood bank and have platelets readily available for transfusion in case excessive bleeding develops at vaginal delivery or excessive oozing is observed at the time of skin incision at cesarean. The decision for prophylactic platelet transfusion in patients with severe preeclampsia-related thrombocytopenia but no excessive bleeding depends on patient-specific factors; consultation with the hematology service may be helpful. (See ‘Management of thrombocytopenia’ above.)
Fluid balance – Fluid balance should be monitored closely to avoid excessive administration, which can lead to pulmonary edema. A maintenance infusion of a balanced salt or isotonic saline solution at approximately 80 mL/hour is often adequate. Oliguria that does not respond to a modest trial of increased fluids (eg, a 300 mL fluid challenge) suggests renal insufficiency. (See ‘Fluids’ above.)

●Prognosis

Recurrence in future pregnancies – There is an increased risk of preeclampsia recurrence in subsequent pregnancies. Early-onset preeclampsia with severe features has a higher risk of recurrence than milder disease with onset at term. (See ‘Prognosis’ above.)
Risk for development of cardiovascular disease – The American Heart Association considers a history of preeclampsia or pregnancy-induced hypertension a major risk factor for development of cardiovascular disease (coronary heart disease, stroke, and heart failure)

Answer 83

A

is a rare event, usually presenting in the second or third trimester with acute flank pain radiating to the groin or lower abdomen and hematuria. Normal pregnancy is associated with a mild increase in urine calcium excretion and a rise in urine pH; these are risk factors for calcium phosphate stones, which appear to be the most common kidney stone in pregnancy. Urinary stasis, due both to increased progesterone and a diminished fluid intake associated with reduced bladder capacity, may also contribute to stone formation.

Answer 84

A

creat baixa= clearance medido

ptnuria ate 300mg

acido urico baixo

sodio e k normais

elevacao do calcio urinario

hidronefrose d>E

Answer 85

A

presence of renal insufficiency at the time of conception is the most important risk factor for progression of disease.

In women with preserved kidney function, the potential for pregnancy to hasten progression has only been noted in women with hypertension or histological damage (cortical tubulointerstitial scarring and arteriosclerosis) on renal biopsy

factors like hypertension, proteinuria and/or the type of underlying kidney disease are likely important

Answer 86

A

interromper 6 sems antes concepcao

morte fetal, ma formacao

trocar por AZA

Answer 87

A

pregnancy itself increases the potential of a disease flare during any trimester or the early postpartum

Predictors of a renal flare during pregnancy in women with lupus include evidence of disease activity (e.g. low complement levels) as well as evidence of renal activity with a partial remission (proteinuria <1 g/day) increasing the risk of renal deterioration 3-fold as compared with 9-fold in women with >1 gram of urine protein per day

As such, 6 months of sustained disease quiescence prior to considering a pregnancy has been recommended based on studies that show the disease flared in 7% of patients with inactive disease as compared with 61% of patients with active disease at the time of conception

Disease quiescence is clinically defined as an absence of clinical symptoms, normal or stable serology and a urine protein <500 mg–1 g/day, with similar remission and stability criteria applied to patients with vasculitis to improve pregnancy outcomes

Answer 88

A

a protein:creatinine ratio >500 mg/g or a urinary albumin-to-creatinine ratio >300 mg/g due to non-diabetic nephropathy resulted in higher rates of preeclampsia and preterm delivery than in those with less proteinuria or those with proteinuria secondary to diabetes, suggesting glomerular disease may result in particularly poor pregnancy outcomes

Answer 89

A

Preferred medication choices in pregnancy

DrugUS FDA categoryDoseAdverse events in pregnancyComments

Hydroxychloroquine N 200–400 mg daily Stomach upset, vision changes =SEGURO women who discontinue hydroxychloroquine prior to or during pregnancy have been reported to have more antenatal lupus activity and disease flares and require more prednisone use during pregnancy

Prednisone C 1 mg/kg pre-pregnancy body weight (max of 80 mg/day) Possible increase in cleft lip and palate
Increased potential for gestational diabetes, hypertension, avascular necrosis and bone loss, irritability and mood issues often more pronounced in pregnancy Vitamin D and calcium supplementation should be coadministered .

Azathioprine D 2 mg/kg pre-pregnancy body weight Maternal leukopenia and infection

Calcineurin inhibitors C Target based May potentiate maternal hypertension and diabetes Often requires higher doses
Maintain lower trough levels to avoid nephrotoxicity

Rituximab C As per local protocols, no pregnancy dose adjustment required Maternal infection and neonatal B cell depletion with increased potential for infection Avoid administration in the third trimester if possible

Methyldopa (PO) B 500 mg–3 g in 2 divided doses Drowsiness, dry mouth Longest clinical safety experience

Labetalol (PO) C 100–1200 mg/day in 2–3 divided doses Fetal bradycardia, hypotension, neonatal hypoglycemia, asthma, decreased uteroplacental flow First-line in many practices

Nifedipine (PO) C 30–120 mg/day Hypotension especially if used with magnesium sulfate Avoid short-acting versions

Hydralazine (PO) C 50–300 mg/day in 2–4 divided doses Hypotension, neonatal thrombocytopenia, drug-induced lupus, tachycardia

Thiazide (PO) B 25–50 mg/day Volume contraction, hypokalemia, metabolic alkalosis Not a first-line agent, but can continue if patient well controlled previously with no signs of volume contraction; avoid in preeclampsia

Labetalol (IV) C 10–20 mg; repeat 20–80 mg IV every 30 min or 1–2 mg/min, max 300 mg/day Same as Labetalol (PO) Preferred agent for hypertensive crisis, contraindicated in asthma

Hydralazine (IV) C 5–10 mg IV/IM, may repeat every 20–30 min to a maximum of 20 mg Same as hydralazine (PO) Preferred agent for hypertensive crisis; careful with maternal hypotension

Furosemide (PO or IV) C Start 20–40 mg IV and titrate up as necessary, maximum 200 mg/day Volume contraction, hypokalemia, metabolic alkalosis, ototoxicity Use only in pulmonary edema or significant edema; careful monitoring to avoid volume contraction

Enoxaparin B 40 mg daily Increased bleeding, especially in patients with advanced CKD Continue for at least 6 weeks postpartum

Answer 90

A

orientacao pre gestacional =engravidar quando tiver

dose baixa de corticoide 10mg/dia de pred

ausencia de ativ de dç por no minimo 6meses =proteinuria <500mg/24h

biopsia renal?

suspender medicacoes teratogenicas 3 meses antes

Answer 91

A

MMF is associated with high rates of spontaneous pregnancy loss and is highly teratogenic, with up to one in five infants exposed reported to have congenital abnormalities.

Birth defects include cleft lip and palate, absent auditory canals, hypertelorism and microtia [53]. Women taking MMF should switch to an alternative agent (usually azathioprine) approximately 3 months prior to conception to ensure disease stability. Cyclophosphamide and chlorambucil are also teratogenic [54] and are associated with increased risk of fetal loss [55] and hence should be avoided in pregnancy

Answer 92

A

The use of an ACE inhibitor during the second and third trimesters of pregnancy has been associated with a number of serious foetal malformations including oligohydramnios, foetal and neonatal renal failure, bony malformations, limb contractures, pulmonary hypoplasia, prolonged hypotension and neonatal death.

trocar para labetalol nifedipina e metildopa

aldosterona tbm nao pode

Answer 93

A

aas= 80-150mg dia

hidroxicloroquina 400mg dia

monitorar= complemento , exame de urina, proteinuria eanti dna

antiro e anti la positivos = les neonatal=associado a alteracao cardiacas fetais

monitoramento cardiaco fetal 18-24sems

Answer 94

A

maior fator de risco para pre eclampsia

marcadores positivos= anti coagulante lupico, anticardiolipina

clinica=abortamento >10 sems, tres perdas fetais, insuf placentaria ou sofrimento ffetal <34 sems

evento trombotico arterial ou venoso de causa nao identificada

indica anticoagulacao

Answer 95

A

We recommend that low dose aspirin, low molecular weight heparin, labetalol, nifedipine, methyldopa, prednisolone, azathioprine, ciclosporin, tacrolimus and hydroxychloroquine are safe for use in pregnancy (1B).

We recommend pregnant women taking prednisolone and/or calcineurin inhibitors are screened for gestational diabetes

We recommend women with CKD are offered low-dose aspirin (75-150 mg) in pregnancy to reduce the risk of pre-eclampsia

We recommend labetalol, nifedipine and methyldopa can be used to treat hypertension in pregnancy

METILDOPA , LABETALOL, NIFEDIPINA E HIDRALAZINA

CALCIO E VIT D

Answer 96

A

in a woman with non-proteinuric CKD, if she develops new hypertension (systolic BP > 140 mmHg and/or diastolic BP > 90 mmHg) and proteinuria (uPCR > 30 mg/mmol or uACR > 8 mg/mmol) or maternal organ dysfunction after 20 weeks’ gestation (1B).

in a women with proteinuric CKD if she develops new hypertension (systolic BP > 140 mmHg and/or diastolic BP > 90 mmHg) or maternal organ dysfunction after 20 weeks’ gestation (1B)

in a women with chronic hypertension and proteinuria, if she develops maternal organ dysfunction after 20 weeks’ gestation (1B).

Guideline 4.4.6

We suggest in women with chronic hypertension and proteinuria that the development of sustained severe hypertension (systolic BP > 160 mmHg and/or diastolic BP > 110 mmHg or doubling of antihypertensive agents) and/or a substantial rise in proteinuria (doubling of uPCR or uACR compared to early pregnancy) should prompt clinical assessment for superimposed pre-eclampsia (2D).

Answer 97

A

We recommend erythropoietin stimulating agents are given if indicated in pregnancy (1C).

Bone health

Guideline 4.7.1

We recommend women with CKD who are vitamin D deficient be given vitamin D supplementation in pregnancy (1B).

Guideline 4.7.2

We recommend calcimimetics are discontinued in pregnancy (1D).

Guideline 4.7.3

We recommend non-calcium based phosphate binders are discontinued in pregnancy (

Answer 98

A

teratogenico

descontinuar 6 meses antes

pode fazer cni

plasmaferese?

Answer 99

A

deplecao de cels b neonatais

melhor nao

se usar , usar antes de 16 sems

Answer 100

A

ENGRAVIDAR apos 1-2 anos de tx

preditores de bom desfecho materno e fetal

creat <1,5

funcao do enxerto estavel sem RAC recente

proteinuria <500mg/dia

PA normal ou controlada

idade materna jovem

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