Acute Kidney Injury Flashcards

Question

used to limit uric acid generation with acute urate nephropathy

Answer 1

allopurinol 100 mg/m2 every 8 hours (max 800 mg/day) effective prophylaxis and treatment for acute uric acid mediated tumor lysis syndrome rasburicase

Answer 2

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

Answer 3

0.8-1 g/kg bw/day

Answer 4

1-1.5 kg/bw/day

Answer 5

20-30 kcal/kg/by/day

Answer 6

20-25 ml/kg/hr

Answer 7

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

Answer 8

Acute CRS Type 1

Answer 9

Chronic CRS Type 2

Answer 10

Acute renocardiac (Type 3)

Answer 11

Chronic renocardiac (Type 4)

Answer 12

secondary CRS (Type 5)

Answer 13

Type 2 HRS

Answer 14

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

Answer 15

decreased urine output

Answer 16

\< 0.5 ml/kg/hr for \> 6 hours

Answer 17

Risk, Stage 1

Answer 18

Injury, Stage 2

Answer 19

Failure Stage 3

Answer 20

\< 0.5 ml/kg/h for \> 6 h

Answer 21

\< 0.5 ml/kg/h for \> 12 h

Answer 22

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

Answer 23

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.

Answer 24

Amifostine

Answer 25

Dimercaprol

Answer 26

Fomepizole

Answer 27

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.

Answer 28

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.

Answer 29

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

Answer 30

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.

Answer 31

hiperuricemia, hipercalemia, hiperfosfatemia e hipocalcemia The pathophysiology of AKI in TLS involves the formation of c**rystals 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

Answer 32

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 obstructio**n syndrome presents early post-HCT with clinical and laboratory f**eatures 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).

Answer 33

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

Answer 34

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.

Answer 35

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**

Answer 36

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).

Answer 37

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

Answer 38

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 --

Answer 39

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 --

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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. --

Answer 44

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

Answer 45

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

Answer 46

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 --

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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 --

Answer 51

Type 1 HRS

Answer 52

1. cirrhosis with ascites 2. AK I 3. no improvement of AKI after 2 days of diuretic withdrawal and volume expansion 4. absence of shock 5. absence of parenchymal kidney disease

Answer 53

6 to 8 g albumin

Answer 54

terlipressin

Answer 55

gnmp hcv iga secundaria hepatite b