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Nefrologia PT > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

NEFROPATIA POR CONTRASTE

acute decline in gfr in cin occurs in ___ and peak crea concentration in ____

A

24 to 48 hours
3 to 5 days

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2
Q

pathophysiology of CIN-nefropatia por contraste

A

hypoxic and renal tubular damage + endothelial dysfunction + altered microcirculation

A IRA induzida por contraste é a principal causa insuficiência renal aguda em pacientes hospitalizados.•IRA não-oligúrica, 24-48 após exposição, com resoluçãoem 1 semana.

vasoconstricão•hipóxia medular•efeito citotóxico direto•hiperosmolaridade

prerenal acute kidney injury

contrast media assoc with lower incidence of aki Low osmolar, isosmolar

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3
Q

IRA POR AMINOGLICOSIDEOS

A

most nephrotoxic amino glycoside neomycin

Obstrucão tubular por debris celulares e AUMENTO pressão intratubular•

DIMINUIÇAO DA TFG e do fluxo sanguíneo renal

  • liberacão de vasoconstritores•contracão mesangial
  • Alt. membrana: proteinúria•Perpetuacão do dano•congestão vascular, marginacao de cel. inflam e liberação de ROS•AUMENTO do aporte distal de H2O e Eletrólitos

•IRA NÃO OLIGÚRICA (7dias após exposicão)•FANCONI-like•

Histologia: NTA tipo isquêmico, em focos; PERDA da borda em escova,vacuolizacão e corpos mieloides

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4
Q

idiosyncratic allergic response to different pharmacologic agents

A

Acute interstitial nephritis

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5
Q

hallmark of AIN

A

inflammatory infiltrates within the interstititium

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6
Q

2nd most common cause of intrinsic AKI

A

nephrotoxic ATN

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7
Q

to limit cast formation and preventive measure in tubular disease with endogenous nephrotoxins

A

volume expansion, alkalinization of urine

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8
Q

what will accelerate and aggravate light chain cast nephropathy

A

reduction in GFR

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9
Q

most common cause for post renal azotemia

A

structural or functional obstruction of the bladder neck

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10
Q

major and most commonly injured epithelial cell involved in AKI related to ischemia, sepsis and or nephrotoxins

A

proximal tubular cell

most susceptible to ischemic injury S3 proximal tubule in the outer stripe of the medulla

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11
Q

primarily responsible for the extension phase of AKI

A

endothelial cell injury and dysfunction

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12
Q

history of atrial fibrillation or recent MI, nausea, vomiting, flank or abdominal pain; mild proteinuria occasional rbcs; elevated LDH, normal transaminase levels

A

renal artery thrombosis

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13
Q

recent manipulation of aorta, retinal plaques, subcutaneous nodules, purpura, livedo reticularis; eosinophiluria; eosinophilia, hypocomplementemia

A

atheroembolism

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14
Q

nephrotic syndrome; pulmonary embolism; flank pain; proteinuria, hematuria

A

Renal vein thrombosis

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15
Q

typical urinalysis findings in HUS/TTP

A

RBCs, mild proteinuria, rarely RBC or granular casts

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16
Q

urine findings in rhabdomyolysis,

A

positive for heme in absence of RBC

sangue= hyperK, hyperphos, hypocalcemia, increased CK, myoglobin

Necrose muscular e liberacão de produtos intracelulares na circulação:

Lesãopela miogobina=toxidade tubular direta, obstrucao por cilindros intraluminais e mioglobina causando vasoconstriccao renal

cascata inflamatoria causando vasocontriccao renal

seuqestro de fluidos , deplecao de volume, e hipoperfuao renal

tudo levando a NTA

CK, dor muscular, mioglobinúria, Dist.Hidroeletrolítico e IRA (15% de todas as causas)

AUMENTO CPK, ALDOLASE, TGO,TGP, POTASSIO E FOSFATO E QUEDA DO CALCIO

•Causas:•Trauma muscular•hipertermia maligna; s. neuroléptica maligna;hipotermia•Infeccão, dist. eletrolíticos, DROGAS e TOXINAS

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17
Q

RABDOMIOLISE

A

Fisiopatologia:obstrução tubular pela mioglobina, vasoconstriccao intra-renal e a tubulotoxicidade direta induzida pelo grupo heme da mioglobina.

Danos mais deletérios na urina acida.

Alcalinização urinaria pode ajudar a prevenir cilindros tubulares de pigmentos.

Deve-se utilizar solução salina isotônica para expansão volêmica almejando um debito de 200-300ml/h ou até que a mioglobinuriadesapareça

Drogas associadas: fibrato, álcool, estatinas, heroína e cocaína

Diagn cpk>15000 para ter irá
FeNa baixa é comum
Aumento de cpk, ldh,aldolase,tgo,tgp

fatores de risco - High initial serum creatinine, low serum calcium, hipofosfatemia

–urine findings in hemolysis, hyperK, hyperphos, hypocal, hyperuricemia and free circulating hgb

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18
Q

urine findings in tumor lysis, myeloma, ethylene glycol

A

urate crystals, dipstick proteinuria, oxalate crystals

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19
Q

calcium oxalate crystals

A

ethylene glycol intoxication

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20
Q

lafbp is detected in the urine within how many hours to ischemic or nephrotoxic injury

A

6 hours

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21
Q

mL of post void residual volume indicative of bladder outlet obstruction

A

100-150 ml

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22
Q

Cairo Bishop definition of tumor lysis syndrome

A

2 of the following achieved in the same 24h interval from 3 days before to 7 days after chemo: uric acid > 8, K >6, phos > 4.6, calcium < 7 mg/dL

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23
Q

definitive therapy for abdominal compartment syndrome

A

surgical laparotomy

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24
Q

contrast agent is associated with acute kidney injury (CA-AKI)

A

at risk outpatients for contrast associated AKI, rate of isotonic sodium chloride 3 ml/kg 1 hour prior to procedure then 6 ml/kg per hr over 2-6 hours after procedure

at risk hospitalized patients for contrast associated AKI rate of isotonic sodium chloride 1 ml/kg per hr for 6-12 hours prior and after procedure 1 ml/kg per hr for 6-12 hours prior and after procedure

Exposure to a contrast agent is associated with acute kidney injury (CA-AKI) and the cause is likely to be multifactorial.

Risk factors for CA-AKI include chronic kidney disease (CKD), old age and hypovolaemia.

Alternative imaging techniques should be considered for patients at high risk of CA-AKI.

Expansion of intravascular volume and using lower osmolality contrast agents reduce the risk of CA-AKI.

–

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25
Q

used to limit uric acid generation with acute urate nephropathy

A

allopurinol 100 mg/m2 every 8 hours (max 800 mg/day)

effective prophylaxis and treatment for acute uric acid mediated tumor lysis syndrome rasburicase

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26
Q

nia

A

Os agentes mais freqüentemente envolvidos com a NIA são os antibióticos beta-lactâmicos (por uma reação de hipersensibilidade) e os anti-inflamatórios. As quinolonas também são imputadas como causa da NIA (também por hipersensibilidade)

pesquisa de eosinófilos na urina

A eosinofilúria, quando realizada com a coloração de Hansel e solicitada até 10 dias após o início do quadro de NIA, apresenta sensibilidade de 70% e especificidade de 90%.

1) a biópsia renal, que continua sendo o padrão-ouro no diagnóstico da NIA.
2) a cintilografia com Gálio67, O citrato de gálio é um radiomarcador que se impregna nos tecidos com processo inflamatório. . Este exame possui sensibilidade de 65% e especificidade de 58% para o diagnóstico de NIA. Apesar dos níveis baixos de sensibilidade e especificidade, a cintilografia com gálio diferencia com precisão a NTA isolada da NIA. Como na NTA isolada o processo inflamatório é praticamente ausente, não há captação do Gálio67 na topografia renal.

Methlypred 250-500 mg/day for 3-4 days then oral pred 1 mkd over 8-12 weeks

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27
Q

if the duration of AKI is short, not extremely catabolic and does not require RRT; dietary protein requirement is

A

0.8-1 g/kg bw/day

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28
Q

If duration of AKI is prolonged, with hypercatabolism or on RRT, dietary protein intake

A

1-1.5 kg/bw/day

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29
Q

total caloric intake with prolonged AKI

A

20-30 kcal/kg/by/day

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30
Q

Kt/V recommended for RRT in AKI

A

3.9/week

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31
Q

effluent volume during CRRT

A

20-25 ml/kg/hr

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32
Q

FeNa in Radio Contrast Induced Nephrotoxicity

A

<1%

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33
Q

AKI resolves within

A

1-2 weeks

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34
Q

biomarker of AKI associated with reducing apoptosis and enhancing normal proliferation of renal tubular cells

A

NGAL

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35
Q

Diagnosis of Clinical Tumor lysis syndrome

A

laboratory + at least one of the ff: 1. Crea more than 1.5x, cardiac arrhythmia/sudden death, seizure

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36
Q

acute worsening of heart function leads to AKI

A

Acute CRS Type 1

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37
Q

chronic abnormalities in heart function result in kidney dysfunction

A

Chronic CRS Type 2

38
Q

AKI precedes cardiac dysfunction

A

Acute renocardiac (Type 3)

39
Q

CKD leads to cardiac dysfunction

A

Chronic renocardiac (Type 4)

40
Q

Systemic conditions result in simultaneous cardiac and renal dysfunction

A

secondary CRS (Type 5)

41
Q

Moderate renal dysfunction (Crea 1.5-2.5) with steady or slowly progressive course

A

Type 2 HRS

42
Q

Early Goal Directed therapy for sepsis

A

MAP > 65, CVP 10-12, UO > 0.5 ml/kg/hr, CVO2 > 70%

43
Q

cardinal manifestation of AKI

A

decreased urine output

44
Q

increase of > 50% developing over 7 days

A

AKI RIFLE

45
Q

Increase of > 0.3 mg/dL or > 50% developing over < 48 hours

A

AKI AKIN

46
Q

Increase of > 0.3 mg/dL over <48 hours or an inc of > 50% developing over < 7 days

A

KDIGO AKI

47
Q

urine output in AKI definition

A

< 0.5 ml/kg/hr for > 6 hours

48
Q

More than 50% (> 0.3 mg/dL) increase in crea stage

A

Risk, Stage 1

49
Q

More than 100% increase in crea stage

A

Injury, Stage 2

50
Q

More than 200% increase in crea stage

A

Failure Stage 3

51
Q

need for RRT for >4 weeks stage of AKI

A

Loss

52
Q

need for RRT for > 3 months stage of AKI

A

End Stage

53
Q

UO in Risk or Stage 1 AKI

A

< 0.5 ml/kg/h for > 6 h

54
Q

UO in Injury or Stage 2 AKI

A

< 0.5 ml/kg/h for > 12 h

55
Q

UO in Failure or Stage 3 AKI

A

< 0.3 ml/kg/h for ? 24h or anuria for >12 h

56
Q

most common cause of AKI

A

prerenal

57
Q

hallmark feature in ATN

A

loss of the apical brush border of PTC

FeNa in ATN >2

A necrose tubular aguda (NTA) é uma LRA intrínseca que se segue a uma condição de hipoperfusão grave e persistente ou lesão tóxica de células epiteliais causando descolamento da membrana basal e disfunção tubular

UNa in Prerenal vs ATN <20 vs >40

Urine-Plasma Crea ratio Prerenal vs ATN > 40 vs < 20

UOsm prerenal vs ATN > 500 vs 300

acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40.

58
Q

organic thiophosphate to ameliorate cisplatin toxicity

A

Amifostine

59
Q

limits acetaminophen induced renal injury if given within 24H of ingestion

A

NAC

60
Q

Chelating agent that may prevent heavy metal nephrotoxicity

A

Dimercaprol

61
Q

inhibits ethylene glycol metabolism to oxalic acid

A

Ethanol

62
Q

inhibitor of alcohol dehydrogenase that decreases production of ethylene glycol metabolites

A

Fomepizole

63
Q

MTA

A

TMA syndromes and other systemic disorders associated with microangiopathic hemolytic anemia (MAHA) and thrombocytopenia

SyndromeClinical featuresLaboratory findings

Primary thrombotic microangiopathy (TMA) syndromes

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.

Shiga toxin-mediated hemolytic uremic syndrome (ST-HUS)Abdominal pain; diarrhea (often bloody); possible history of outbreak or exposure to livestock or contaminated food, although most cases are sporadic.Renal failure is prominent. Stool may be positive for the organism (Escherichia coli or Shigella dysenteriae) or Shiga toxin.

Drug-induced TMAHistory of exposure to quinine or other implicated medication. Immune-mediated forms have an abrupt onset with fever, chills, abdominal pain, nausea, anuric acute kidney injury. Toxic, dose-related etiologies may arise gradually, or onset may be sudden with an intravenous toxic agent (eg, Opana-ER).

Immune mediated: Severe acute kidney injury; drug-dependent antibodies to platelets and/or neutrophils can be demonstrated.

Toxic, dose related: May have gradual or sudden onset of renal failure and hypertension.

Coagulation-mediated TMAInherited, typically presents in children <1 year old.DGKE, thrombomodulin, or plasminogen gene mutation.

Metabolism-mediated TMAInherited, typically presents in children <1 year old, but may also present in adults.Elevated serum homocysteine and methylmalonic acid, and low methionine levels; increased urinary methyl-malonic acid. MMACHC gene mutation.

Systemic disorders that may present with MAHA and thrombocytopenia

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.

Systemic infectionMay include bacterial, viral, rickettsial, or fungal organisms. High fever and shaking chills are common.

Systemic malignancyMay occur with occult systemic malignancy. Breast, prostate, lung, pancreatic, or gastrointestinal tumors are often responsible.Depends on specific tumor.

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.

Systemic rheumatic diseases (eg, SLE, SSc, APS)SLE may be associated with hypertension, renal insufficiency, and autoimmune cytopenias. APS typically presents with arterial and/or venous thromboembolism but can also produce a TMA.Serologic testing may show autoantibodies characteristic of the underlying condition; APS may have prolonged aPTT. Renal biopsy may demonstrate TMA identical to the primary TMA syndromes.

Solid organ transplantMay be associated with calcineurin inhibitor administration. May be associated with infection such as CMV in the setting of immunosuppression. In patients receiving a kidney transplant for a primary TMA syndrome, the syndrome may recur in the transplanted kidney.Renal biopsy may have features of rejection.

Therapy for primary TMAs is directed at the underlying pathophysiology; therapy for other systemic disorders associated with MAHA and thrombocytopenia is focused on the underlying disorder. Refer to UpToDate topics on evaluating patients with suspected TMA and on specific syndromes for additional information on presentation/diagnosis and management.

TMA: thrombotic microangiopathy; ADAMTS13: A Disintegrin And Metalloprotease with a ThromboSpondin type 1 motif, member 13; DGKE: diacylglycerol kinase epsilon; HELLP: hemolysis, elevated liver function tests, and low platelets; BP: blood pressure; PRES: posterior reversible encephalopathy; SLE: systemic lupus erythematosus; SSc: systemic sclerosis (scleroderma); APS: antiphospholipid syndrome; CMV: cytomegalovirus; PT: prothrombin time; aPTT: activated partial thromboplastin time.

64
Q

DOENÇA ATEROEMBOLICA

Suspeitada , principalmente, após intervençao endovascular com quadro de IRA com pico em média 8 semanas após o procedimento.
Elevaçao da creat pode ocorrer até 6 meses após o insulto ateroembolico.

Quadro=inicio agudo com possibilidade de progressão lenta ate mesmo para DRCT.
SINTOMAS: acometimento de múltiplos órgãos por embolos de colesterol com manifestações;
-cutâneas: livedo reticular, dedo azul, petequias, purpuras e ulceras necróticas. áreas necróticas puntiformes
Dor abdominal , náuseas ,vômitos mialgia e febre baixa. A embolia de colesterol ou doença ateroembólica caracteriza-se pela oclusão de pequenas artérias por cristais de colesterol derivados de placas ateroscleróticas rotas da aorta ou de grandes artérias. Pacientes com doença aterosclerótica expostos a algum evento desencadeante para rotura de uma placa aterosclerótica (procedimentos angiográficos, cirurgias cardiovasculares, anticoagulação, trombólise ou eventualmente espontânea) estão predispostos a embolização por cristais de colesterol. Existem três formas de apresentação da doença ateroembólica. Na forma aguda ocorre piora da função renal logo após o evento desencadeante devido embolização maciça. Na forma subaguda a perda de função renal ocorre após dias ou semanas à exposição ao fator desencadeante. Já na forma crônica a embolização de cristais de colesterol poderia ocorrer de forma espontânea, contribuindo para a progressão para IRC em pacientes com perda de função renal prévia.

Dentre os achados laboratoriais podemos encontrar eosinofilia, eosinofilúria, hipocomplementemia, hematúria microscópica, proteinúria não nefrótica e, em caso de acometimento intestinal, elevação de amilase, enzimas hepáticas e CPK. O achado de livedoreticularis ou isquemia/gangrena de um dos dedos do pé sugere o diagnóstico. O tratamento é de suporte, incluindo a prevenção de novos surtos de embolização, suporte nutricional e diálise. Infelizmente a evolução para IRC ocorre na maioria dos casos.

–

3

rabdomiólise:

Fisiopatologia:obstrução tubular pela mioglobina, vasoconstriccao intra-renal e a tubulotoxicidade direta induzida pelo grupo heme da mioglobina.

Danos mais deletérios na urina acida.

Alcalinização urinaria pode ajudar a prevenir cilindros tubulares de pigmentos.

Deve-se utilizar solução salina isotônica para expansão volêmica almejando um debito de 200-300ml/h ou até que a mioglobinuriadesapareça

Drogas associadas: fibrato, álcool, estatinas, heroína e cocaína

Diagn cpk>15000 para ter irá
FeNa baixa é comum
Aumento de cpk, ldh,aldolase,tgo,tgp

fatores de risco - High initial serum creatinine, low serum calcium, hipofosfatemia

A

causada pela oculsao de peqs arterias por embolos de colesterol derivados de placas ateromatosas ulcerada

formas aguda= dias apos o procedimento,subaguda e cronica

pico 8 sems apos, pode ocorrer ate 6m depois

biopsia mostra uns cristais convexos

outros= dedo azul, livedo, dor abdominal e defict neurologico

leve a moderada hematuria, proteinuria e has acelerada ou nova

risk factors include older age, male gender, diabetes, hypertension, hyperlipidemia, and smoking

Complement factors are associated with the inflammatory response secondary to atherosclerosis. Cholesterol crystals trigger both complement pathways, classical and alternative.

65
Q

doenca ateroembolica

A

emboli typically lodge in the arcuate and interlobar arteries and are seen on light microscopy as elongated biconvex transparent needle-shaped clefts

66
Q

Onco-Nephrology

A

mieloma-nefropatia por cilindros , rim do mieloma

normal=immunoglobulin light chains are freely filtered by the glomerulus and taken up by tubular cells by cubilin/megalin receptors and clathrin-dependent endocytosis, where they are subsequently degraded in lysosomes .

The increased production of light chains by neoplastic plasma cell populations overwhelms the proximal tubular capacity to perform this function, and excess light chains bind to Tamm–Horsfall protein in the distal tubule, causing obstruction and a reduction in GFR.

Factors that promote cast formation include a heavy load of serum-free light chains (SFLC) delivered to the distal tubule, acidic urine, concurrent treatment with furosemide or nonsteroidal anti-inflammatory drugs, dehydration, intravenous contrast, and hypercalcemia

Patients should be adequately volume-expanded with intravenous fluids such as isotonic saline or sodium bicarbonate, although this process results in a small decrease in light-chain concentration at best. Urinary alkalinization may help to increase the solubility of SFLC. Antimyeloma agents (bortezomib, dexamethasone, thalidomide, and lenalidomide) should be initiated as soon as safely possible to try to decrease SFLC production, because an early reduction of SFLC portends improved renal recovery in cast nephropathy (29). Nephrotoxic agents, including nonsteroidal anti-inflammatory drugs, intravenous contrast, loop diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and aminoglycosides, should be avoided.

67
Q

sindrome lise tumoral

A

hiperuricemia, hipercalemia, hiperfosfatemia e hipocalcemia

The pathophysiology of AKI in TLS involves the formation of crystals comprised of uric acid, calcium phosphate, and/or xanthine, which can lead to intratubular obstruction and inflammation and a reduction in GFR.

In addition, hyperuricemia can cause AKI through crystal-independent mechanisms, such as renal vasoconstriction, reduced renal blood flow, reactive oxygen species, and inflammation

68
Q

cuasa de ira pós transplante de medula ossea

A

can be divided into those causes occurring early after HCT (within the first 30 days) and those causes occurring later (>3–4 months).

During the peritransplant period, AKI is most commonly caused by sepsis, hypotension, and exposure to nephrotoxic agents (methotrexate, amphotericin B, acyclovir, aminoglycosides, angiotensin-converting enzyme inhibitors, intravenous contrast, and calcineurin inhibitors), which predispose the patient to acute tubular necrosis .

In addition, the administration of antibiotics and/or allopurinol can cause acute interstitial nephritis.

TLS can occur as a result of the conditioning regimen, although the incidence of this occurrence is low in this population.

Hepatic sinusoidal obstruction syndrome presents early post-HCT with clinical and laboratory features similar to hepatorenal syndrome.

Late-onset AKI after HCT has a more limited differential diagnosis, and it is usually attributed to thrombotic microangiopathy or calcineurin inhibitor toxicity (45).

69
Q

ira por cni

A

Routine monitoring of serum creatinine and plasma drug levels (cyclosporine=150–400 ng/ml; tacrolimus≤15 ng/ml

Inibidores da calcineurina, relacionados a disfunçãotubular, IRA e SHU•Incidência de IRA em EstudoCoortede transplantadosnos EUA atingiu 60%, follow-up 36 meses•Patogênese:•dano endotelial, GESF e fibrose intersticia

Formas de apresentação danefrotoxicidade da ciclosporina A• Retardo no funcionamento do enxerto renal• Elevação assintomática da creatinina sérica• Insuficiência renal aguda• Síndrome hemolítico-urêmica• Insuficiência renal crônica• Alterações eletrolíticas (hipomagnesemia,hipercalemia, hipofosfatemia, hiperuricemia)• Alterações da capacidade de concentração urinária• Acidose hiperclorêmica• Hipertensão

Alteracões hidro-eletrolíticas•Hipercalemia/Acidose•Alteração da excreção urinária•Diminui atividade do SRAA•Hiperuricemia e gota•Alteração da excreção urinária de ácido úrico•Alterações glomerulares e tubulares•Hipofosfatemia, hipomagnesemia, hipercalciúria

70
Q

Hepatic Sinusoidal Obstruction Syndrome (Veno-Occlusive Disease)

A

transplante de cels hematopoieticas

hepatomegalia dolorosa, ascite, ictericia, confusao mental , ganho de peso

tender hepatomegaly, fluid retention, weight gain, and jaundice that occurs after the administration of high-dose conditioning regimens, including cyclophosphamide, busulfan, and/or total body irradiation.

The pathophysiology of SOS involves damage to hepatic sinusoidal endothelial cells , which leads to sinusoidal thrombosis and obstruction and portal hypertension. estado pro coagulante, pro inflamatorio, liberacao de citocinas, oculao veia centrolobular

occurs more commonly after myeloablative allogeneic HCT than after autologous HCT

Risk factors:e older age, pre-existing liver disease, medications (methotrexate, itraconazole, sirolimus, and norethisterone), and certain conditioning agents (cyclophosphamide and busulfan)

AKI develops in approximately 50% of patients with SOS and is clinically indistinguishable from the hepatorenal syndrome.

. AKI ensues 10–16 days post-HCT, with approximately one-half of patients requiring dialysis.

More than 70% patients with SOS will recover spontaneously with only supportive therapy, which consists of maintaining sodium and water balance, preserving renal blood flow, and treating symptomatic ascites with repeated paracenteses

outrod ttos-with defibrotide, oligodeoxyribonucleotide with antithrombotic and profibrinolytic properties that has a 46% complete response rate. Infusion of heparin and/or ursodeoxycholic acid administered immediately before induction therapy may also be moderately successful as preventive measures.

71
Q

mat apos tx de medula

A

mat Hematopoietic cell transplant May occur with autologous or allogeneic transplant. May be associated with exposure to cytotoxic chemotherapy, radiation, systemic infection, or a calcineurin inhibitor.

.Thrombotic microangiopathy (TMA) is a common cause of late-onset AKI in patients who have undergone HCT. Previously known as bone marrow transplant nephropathy or radiation nephropathy, TMA after HCT resembles the hemolytic–uremic syndrome and usually occurs 20–99 days post-transplant.

The diagnosis of TMA can be challenging, because characteristic features such as anemia, thrombocytopenia, and renal insufficiency are commonly present in the HCT patient population for other reasons, and evidence of schistocytes or elevated serum lactate dehydrogenase levels is also not entirely reliable (62). Hypertension is often present. Urinalysis can be normal or reveal variable proteinuria and/or hematuria, and cellular casts may be seen on urine sediment. Renal biopsy is rarely needed to establish the diagnosis, except when the presentation is atypical. Typical histology includes mesangiolysis, basement membrane duplication, glomerular endothelial cell swelling, and tubular injury with interstitial fibrosis

72
Q

mat

A

Thrombotic microangiopathy (TMA) is a common cause of late-onset AKI in patients who have undergone HCT. Previously known as bone marrow transplant nephropathy or radiation nephropathy, TMA after HCT resembles the hemolytic–uremic syndrome and usually occurs 20–99 days post-transplant. The diagnosis of TMA can be challenging, because characteristic features such as anemia, thrombocytopenia, and renal insufficiency are commonly present in the HCT patient population for other reasons, and evidence of schistocytes or elevated serum lactate dehydrogenase levels is also not entirely reliable (62). Hypertension is often present. Urinalysis can be normal or reveal variable proteinuria and/or hematuria, and cellular casts may be seen on urine sediment. Renal biopsy is rarely needed to establish the diagnosis, except when the presentation is atypical. Typical histology includes mesangiolysis, basement membrane duplication, glomerular endothelial cell swelling, and tubular injury with interstitial fibrosis

The pathogenesis of TMA after HCT is not well understood, but damage to renal endothelial cells likely plays a central role.

. The management of HCT-associated TMA is otherwise largely supportive. Calcineurin inhibitors are typically discontinued, although there is no substantial evidence that this discontinuation is necessary, especially in patients who require these medications for life-threatening GVHD. Other oral agents that can be used for the prevention and treatment of GVHD include mycophenolate mofetil and corticosteroids (65). Substitution of calcineurin inhibitors with daclizumab, a humanized monoclonal antibody to the α-chain of the IL-2 receptor, has been shown to improve TMA in patients with both GVHD and TMA (66). Rituximab, a monoclonal antibody against CD20, and defibrotide have also shown effectiveness in treating HCT-associated TMA in small, uncontrolled studies (67). Given its important role in the treatment of non-HCT–associated TMA, plasmapheresis is sometimes used to treat HCT-associated TMA, but there is no established proof of benefit with this approach (62). Other experimental therapies for TMA under investigation have focused on attenuating inflammatory endothelial injury and include 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors, prostacyclin analogs, endothelin receptor antagonists, antithrombin III, IgG, and anti-TNF agents (65,67). Patients diagnosed with TMA are at higher risk for transplant-associated complications, including systemic infections and acute GVHD, and they have greater 180-day mortality (65). Renal prognosis in these patients is also poor, with the development of TMA increasing the risk of AKI, CKD, and ESRD requiring long-term dialysis (65).

73
Q

LEPTOSPIROSE

A

Leptospira interrogans-espiroqueta aeróbia obrigatória
Leptospira tem tropismo pelo rim e suas endotoxinas afetam as células tubulointersticiais.
Transmissão direta urina animal ou indireta pela água contaminada
Incubação até 15 dias
Maioria é não ictérica
Geralmente é não oligurica e na maioria das vezes associada a hipoKem razão da FENa e FEk estaem elevadas,o que costuma preceder a diminuição da TFG

Incidencia de IRA na leptospirose varia de 10-80%.

Síndrome de Weil : IRÁ, plaquetopenia e sangramento pulmonar.

Valores de K acima de 4,0 estao associados a maior mortalidade.
Na forma anictérica ocorre recuperação da fc renal espontaneamente após alguns dias e recuperação dos valores de ureia e creat na segunda semana.

Forma ictérica:CLcr, reabs proximal de sódio, acidificação urinaria e proteinuria normalizam no 3 mês após a doença e o déficit de concentração urinaria pode permanecer até o 6 mês.

Fase leptospiremica:3-7 dias, nessa fase igM é negativa , só positiva após 7 dias
Fase imune: meningoencefalite , uveíte

Leptospirose até que se prove o contrário :
Tríade: ictericia rubinica; hiperemia conjuntivas +ictericia IRA não oligurica +hipocalemia Hemorragia alveolar

Outras causas de IRÁ COM HIPOCALEMIA: leptospirose, aminoglicosideo, anfótericina b.

Leptospirose envolvimento na inibição da bomba de nakatpase

Laboratório
Leucocitose,plaquetopenia. , IRÁ, CPK, aumento de bilirrubinas

Diagnóstico: cultura, anticorpos elisa, pcr

Tto:
Hv parcimoniosa
Ceftriaxone ou penicilina b cristalina
Docliciclina pós exposição

74
Q

VANCOMICINA

A

Ação contra bactérias G+, excreção predominantemente renal; poucoeliminada por diálise convencional

  • Na década de 60, detectou-se nefrotoxicidade em até 25% dos pacientes;atribuída as impurezas geradas durante o processo de fermentação da droga
  • Estudos recentes detectam elevações de Crem até 10% dos pacientes•Fatores de risco: combinação com aminoglicosídeos, nível sérico da droga >10 mg/L (até 8 vezes mais nefrotoxicidade), idade, duração do tratamentomaior do que três semanas, creatinina basal elevada e desidratação
  • NIA é pouco freqüente•Recomendacões: correção de dose; MTZ creatinina;teicoplamina

–

75
Q

ACICLOVIR

A

an acute rise in creatinine

  • I/V drug causes crystalline nephropathy(tubular obstruction and damage) in 5-10% pts. usually in dehydration
  • Tx and prevention: Hydration and dose adjustment (slowing I/V infusion)

12-16% dos pacientes, IRA NÃO-OLIGÚRICA

  • Filtrado e secretado na urina, baixa solubilidade, com formação de cristaisintratubulares de aciclovir; poliúria, fosfatúria e hipoP
  • Deterioração da função renal 24-48h após inicio da terapia, “cólica renal”, comrecuperação da função renal 4-9 dias após suspensão da droga.

Hemodiálise podeser indicada se ocorrer neurotoxicidade

•Prevenção:•solução isotônica IV 125ml/hr 1h antes até 6h após início da terapia•cuidado com infusão rápida e dose > 500mg/m2•ganciclovir

–

76
Q

ira drogas por segmentos do nefron

A

Proximal tubule(S1/S2segments:)

Aminoglycosides Cephaloridine Cadmium chloride Potassium dichromate

Proximal straighttubule (S3segment)Cisplatin Mercuricchloride Dichlorovinyl–L–cysteine

Glomeruli Interferon–α Gold Penicillamine

Interstitium Cephalosporins Cadmium NSAID

Renalvessels NSAIDs ACEinhibitors CyclosporinA

77
Q

POLI B

A

Ação contra bactérias Gram- multirresistentes,especialmente Pseudomonas

  • Nefrotoxicidade e neurotoxicidade
  • Relato de IRA em aproximadamente 20% dos pacientestratados. A histologia renal mostra NTA, NIA ou pode sernormal
  • Mesmo após a interrupção do antibiótico pode continuar ahaver queda da filtração glomerular por aproximadamenteuma semana

Alteração na concentração intracelular de cálcio e na produçãode radicais livres, com ativação de cascata inflamatória

  • Aumento de permeabilidade de membrana: influxo de íons eágua provoca edema e lise celular
  • Fatores de risco: hipoalbuminemia e em uso de AINE

A anfotericina B causa vasoconstricão renal e diminuição da TFG;aumento de 50% ou mais nos níveis de creatinina é observada em até28% dos pacientes

  • Idade, associação com outras nefrotoxinas, diuréticos, DRC prévia ,distúrbios de K/Mg e dose diária/acumulada aumentam o risco deIRA (Uptodate, 2014)
  • Injúria tubular; aumento da permeabilidade celular e perda dofeedbacktubulo-glomerular; dist. de K, Mg, ATR distal, DI nefrogênico•deoxycholate - toxicidade direta

PREVENÇÃO•Expansão polêmica (diminuicão dofeedbackTúbulo-glomerular)•Controle hidroeletrolítico•Formulações lipossomais•We suggest using lipid formulations of amphotericin B rather than conventionalformulations of amphotericin B. (2A)•In the treatment of systemic mycoses or parasitic infections, we recommendusing azole antifungal agents and/or the echinocandins rather than conventionalamphotericin B, if equal therapeutic efficacy can be assumed. (1A)•Descontinuação da terapiA

78
Q

IRA POR CRISTAIS

A

inibidores de protease (indinavir, atazanavir)

  • aciclovir
  • sulfonamidas
  • ciprofloxacino
  • metotrexate
  • oxalato (metanol e etilenoglicol; sindrome do intestino curto,orlistat, altas doses de vitamina C)•laxativos de fosfato de sódio

BAIXA SOLUBILIDADE CRISTALÚRIA OLIGÚRIA CÓLICA RENAL

pH alcalinoAlto fluxo urinário

79
Q

INDINAVIR

A

Excreção principalmente hepática (80%), solubilidade urinária é pH-dependente

  • Nefrolitíase
  • Fatores de risco:•baixa massa corporal magra,•associação ritonavir

,•uso concomitante de sulfametoxazol + trimetoprima•co-infecção pelo vírus da hepatite B ou C•influência de fatores ambientais, incluindo temperaturae umidade locais.

–

80
Q

antivirais e antiretrovirais

A

Zidovudina Acidose láctica e rabdomiólise

Didanosina Acidose láctica, aumento de ácido úrico, magnésio

Zalcitabina Insuficiência renal aguda, acidose láctica, hiponatremia, hipocalcemia,gota, cálculo renal

Estavudina Acidose láctica

Lamivudina Acidose láctica

Nevirapina Acidose láctica

Saquinavir Acidose láctica, hipocalcemia, discalemia, magnesemia e fosfatemia,síndrome pancreatorrenal

Ritonavir Insuficiência renal aguda, síndrome pancreatorrenal, hipocalcemia,discalemia, fosfatemia, magnesemia e uricemia

Indinavir Acidose láctica, precipitação intratubular, nefrolitíase, insuficiência renal

Nelfinavir Acidose láctica, hipocalcemia, disfosfatemia e uricemia, nefrolitíase

81
Q

nefropatia por contraste

A

contraste associado com menor risco de IRA- iso ou hipoosmolar

queda da tfg ocorre em 24-48h e o pico em 3-5 dias com recuperaçao apos

fisiopatologia: nefrotox direta para as cets tubulares aumentando a viscosidade do fluido tubular causando apoptose de cels endoteliais,necrose eobstrucao tubular e depois queda da tfg.

efeitos indiretos:diminuicao de substancias vasoativas causando diminuicao do fluxo sang glomerular.tb aumenta a osmolalidade e viscosidade do sangue

FeNa in Radio Contrast Induced Nephrotoxicity <1%

at risk hospitalized patients for contrast associated AKI rate of isotonic sodium chloride 1 ml/kg per hr for 6-12 hours prior and after procedure

at risk outpatients for contrast associated AKI, rate of isotonic sodium chloride 3 ml/kg 1 hour prior to procedure then 6 ml/kg per hr over 2-6 hours after procedure

82
Q

cisplatina

A

Quimioterápico potente, associado a disfunção tubular e IRA

•Fatores de risco•idade avançada, sexo feminino, tabagismo, hipoalbuminemia•pico plasmático alto•uso prévio de cisplatina•DRC•uso concomitante de anfoB e aminoglicosídeos

Patogênese:•toxicidade celular (TCP): S. Fanconi-likee ATR II•vasoconstricão•efeito pró-inflamatório•microangiopatia trombótica

•Prevenção:•dose menor; salina isotônica•amifostine;NAC•carboplatin

–

83
Q

aines

A

Efeitos adversos renais ocorrem em 1-5% (2,5 MILHÃO/ano)dos pacientes em uso de AINE (não-seletivoseinibidores daCox-2), principalmente em pacientes idosos•hipoalbuminemia, menor teor de água corporal

•Normalmente, o aumento na creatinina ocorre nos primeiros 3a 7 dias da terapia, com retenção de Na, H2O e K; semanormalidades do sedimento urinário

Mechanism by which nonsteroidalanti-inflammatorydrugs(NSAIDs) disrupt the compensatory vasodilatation response of renal prostaglandins to vasoconstrictor hormones inpatients with prerenal conditions

. Most of the renal abnormalities encountered clinically as a result of NSAIDs can be attributed to the action oft hesecompoundsonprostaglandinproductioninthekidney[31].SodiumchlorideandwaterretentionarethemostcommonsideeffectsofNSAIDs.Thisshouldnotbeconsidereddrugtoxicitybecauseitrepresentsamodificationofaphysiologiccontrolmechanismwithouttheproductionofatruefunctionaldisorderinthekidney

SÍNDROMES RENAIS•IRA “pré-renal” ou NTA•NIA; nefrite tubulointersticial crônica; Nefropatia do analgésico•S. Nefrótica (DLM; Nefropatia Membranosa)•Necrose de papila•anormalidades hidroeletrolíticas (retencão hidrossalina,hipoNa, hiperK, ATR IV)•Malignidade uroepitelia

84
Q

necrose de papila

A

• Analgesic abuse • Diabetes • Sickle cell anemia • Obstructive uropathy

85
Q

ira pre renal vs renal

A

pre renal vs nta

indice IRA Pré-renal NTA

Osmolaridade urinária > 500 mOsm < 350 mOsm

Osmolaridade urinária/ plasmática > 1,3 < 1,1

Creatinina urinária / plasmática > 40 < 20

Sódio urinário < 20 mEq/l > 40 mEq/l

Excreção fracional de sódio (%) Excreção fracional de uréia (%) < 1 < 35 > 3 >35

feureia

fração de excreção da uréia (FeU), calculada como [(uréia urinária / uréia plasmática) / (creatinina urinária / creatinina plasmática)] x 100 (%), pode ser utilizada para o diagnóstico diferencial da IRA pré-renal versus parenquimatosa em pacientes com doença crítica.

Excreção fracional de uréia (%) < 35 >35

86
Q

ira hepatorenal

A

Critérios Maiores – todos devem estar presentes para o diagnóstico perda de função renal (ClCr < 60 ml/min ou Cr > 1,5 mg/dL)

ausência de outras causas de IRA ausência de melhora após expansão plasmática ausência de melhora após suspensão de diuréticos

proteinúria < 500 mg/dia

ausência de obstrução urinária

ausência de IRA parenquimatosa

Critérios Menores – podem estar presentes ou não diurese < 500 ml/dia sódio urinário < 10 meq/l osmolalidade urinária > plasmática sódio sérico < 130 meq/l hemácias na urina < 50 p/c

–

87
Q

rapid progressive AKI with doubling of the serum crea to > 2.5 in < 2 weeks

A

Type 1 HRS

88
Q

Diagnostic criteria for HRS

A
  1. cirrhosis with ascites
  2. AK

I 3. no improvement of AKI after 2 days of diuretic withdrawal and volume expansion

  1. absence of shock
  2. absence of parenchymal kidney disease
89
Q

amount of albumin per Liter of ascites drained when paracentesis volume exceeds 5L

A

6 to 8 g albumin

90
Q

vasoconstrictive agent combined with volume expansion that may improve kidney function in hrs

A

terlipressin

91
Q

glomerulonefrites na cirrose

A

gnmp hcv

iga secundaria

hepatite b

Nefrologia PT (112 decks)

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