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Nefrologia PT > farmacologia > Flashcards

farmacologia Flashcards

1
Q

açao dos diureticos ao longo do néfron

A

Acetazolamida é um inibidor da anidrase carbonica e age no TUBULO PROXIMAL

Furosemida bloqueia o canal NaK2Cl na porcao espessa ascendente da alça de henle

hidrochlorothiazide= inhibe o cotransportador de NaCl no tubulo distal

espironolactone =competitively inhibits the aldosterone mineralocorticoid receptor in the cortical collecting duct=inibe a abs de na no túbulo distal e a secreção de k nos túbulos coletores

Amiloride blocks ENaC (epithelial sodium channel) in the cortical collecting duct

DIURETICO EVITAR EM QUEM TEM ALERGIA A SULFA = CUIDADO COM TIAZIDICOS E DIAMOX

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2
Q

Drug induced AIN

Drugs associated with tubular cell toxicity and acute in- terstitial nephropathy

A

– NSAIDs incl Cox-2 inhibitors – Cephalosporins
– Furosemide and Bumetanide – Ciprofloxacin
– Cimetidine
– Allopurinol

aminoglycosides, amphotericin B, cisplatin, beta lactams, quinolones, rifampin, sulfonamides, vancomycin, acyclovir, and contrast agents . These agents induce renal tubular cell injury by impairing mitochondrial function and interfering with tubular transport and increasing oxidative stress and free radicals (6,10). Chronic use of acetaminophen, aspirin, di- uretics and lithium is associated with chronic interstitial nephritis leading to fibrosis and renal scarring

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3
Q

Rituximab

A

Potent anti-B-cell agent
Rapidly clears circulating B-cells
Long half life
of antibody (~ 3 weeks) of B-cell depletion
Virtually no circulating B-cells at 3 months, but with early return by 6 months

Clearance of B-cells does not correlate with clinical response
SLE
RA*

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4
Q

PARICALCITOL

A

Paricalcitol treatment reduced PTH concentrations more rapidly with fewer sustained episodes of hypercalcemia and increased Ca x P product than calcitriol therapy.

estudo VITAL Paricalcitol reduces BAP levels, which may be beneficial for reducing vascular calcification.

Paracalcitol =associacao com niveis elevados de hypercalcemia

Recommended initial dose is 0.04 to 0.1 mcg/kg (2.8 to 7 mcg) administered no more frequently than every other day at any time during dialysis. The maximum daily adult dose is 0.24 mcg/kg.

When converting a patient from calcitriol to paricalcitol, the initial dose of paricalcitol should be four times greater than the patient’s dose of calcitriol.

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5
Q

AINES

A

Prerenal azotemia
• Ischemic acute tubular necrosis
• Allergic interstitial nephritis (AIN)
• AIN plus minimal change nephropathy
• ARF plus bilateral flank pain
• Sodium and water retention
• Hyperkalemia
• CRF and papillary necrosis

Fatores de risco : idade>65 anos; DCV, DM. Homens, dose de ANE e DRC (RFGe<60 mL/min)

Dois tipos de IRA. • Hemodinamicamente mediada e a Nefrite Intersticial Aguda. • Inibição das enzimas da COX-1 com a consequente redução na síntese das PG é o efeito fisiopatológico principal na IRA hemodinamicamente mediada na com o uso de AIE

ANE na IRA • Depleção de volume do EEC • Medicações: IECA, ARA, diuréticos e inibidores da Calcineurina • Cirrose Hepática • Síndrome Nefrótica • Hipercalcemia • DRC • EAR • Idosos

NSAID associated AIN

Quadro Clínico • Aumento incidental da Cr sérica (3 a 7 dias) • Urinalise é geralmente negativa para hematúria e proteinúria. • Sedimento urinário pode apresentar : cilindros hialinos e se há NTA: cilndros epitelias ou granulares. • Cilindros leucocitários e hemáticos não são visualizados na IRA mediada hemodinamicamente

• Heterogenous picture
• Typically, no hypersensitivity reaction
• Usually middle-aged or elderly
• Majority: associated nephrotic syndrome
(MCD)
• Pyuria, hematuria, eosinophiluria (less than
methicillin-associated)

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6
Q

Acute Interstitial Nephritis

Drugs

A

ANTIBIOTICS

Penicillins, cephasporins, others (quinolones, Bactrim)

DIURETICS

Thiazides, furosemide

ANALGESICS
NSAIDS

ANTICONVULSANTS

phenytoin, carbamazepine, phenobarbitol

OTHERS

allopurinol, cimetidine

Clinical Syndromes

• Drug Induced AIN
– Variable
– Full-blown hypersensitivity reaction to
asymptomatic increase in Scr
– Nephritic / Nephrotic / AIN Urine sediment
– Fanconi’s syndrome, hyperkalemeic
hyperchloremic metabolic acidosis,
Nephrogenic DI

Diagnostic features

• Urinalysis
• Impaired concentrating ability (SG, low urine
osmolality)
• Leukocytosis – eosinophilia (10-30%) common
• Increased IgE
• Urine eosinophiluria
• Gallium – high sensitivity, low specificity
• Renal Biopsy

Eosinophiluria

 >1% of white cells in urine stained
 Wright’s and Hansel’s Stain
 Both use eosin-methylene blue combinations
 Hansel’s 4 fold more sensitive, less pH dependent
 Sensitivity 67%, specificity 80%

CAUSES
•Acute Interstitial Nephritis
•UTI
pyelonephritis
prostatitis
Cystitis
•Glomerulonephritis
•Atheroembolic disease

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7
Q

Trimethoprim-Sulfamethoxazole

A

Elevated creatinine, no change in BUN, no
evidence of ARF: inhibition of tubular secretion
• Allergic interstitial nephritis with fever, rash, and
eosinophilia induced by sulfa moiety

• Hyperkalemia with salt wasting due to amiloride-
like action of trimethoprim

• Rarely, crystallization of sulfamethoxazole
metabolite and renal stone formation

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8
Q

Aminoglycoside Nephrotoxicity

A

25% incidence with “therapeutic” levels
• some correlation with cumulative dose
• non-oliguric ARF after 5-10 days
• Toxicity correlates with cationic charge
• Pathology: membrane phospholipidosis
• Prevention: once daily dosing

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9
Q

QUIMIOTERAPICOS

A
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10
Q

IRA INDUZIDA POR DROGAS

A
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11
Q

HIPOCALEMIANTES

A
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12
Q

Cisplatin Nephrotoxicity

A

ARF complicates in 1-25% of cases
• Accumulated by proximal tubules S3 segment
• Mitochondrial injury and free radical toxicity
• Non-oliguric ARF +/- Mg and K wasting
• Prevent by saline loading
• Carboplatin less nephrotoxic, more
myelotoxic

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13
Q

Pentamidine Nephrotoxicity

A
  • Risk factors: hypovolemia and CRF
  • 25-95% incidence of ARF after 7 to 10 days
  • Several reports of ARF after nebulized drug
  • Often pyuria, proteinuria, hematuria, casts
  • Hypomagnesemia / Hypocalcemia, distal RTA
  • Does not appear to be dose dependant
  • Mechanism unknown
  • Recovery usually within weeks
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14
Q

Foscarnet Nephrotoxicity

A

Risk factors: hypovolemia and CRF
• Acute renal azotemia within 7 days
• Associated polyuria and hyperphosphatemia
• ATN, interstitial fibrosis, glomerular crystals
• Dialysis in 10% of patients with ARF
• Slow recovery over weeks - months

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15
Q

Câncer e nefrotoxicidade

A
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16
Q

Mat e drogas qt

A
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17
Q

Mat e qt

A

Continuação

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18
Q

tma

A

Qt e mat

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19
Q

Irá pós tx de cela hematopoiéticas

A
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20
Q

Irá pós tx de cela hematopoiéticas

A
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21
Q

Ira pós tx cels hemato

A
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22
Q

Fármaco nefrotoxicidade

A
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23
Q

Anfotericina b

A

nephrotoxicity is manifested as

azotaemia, renal tubular acidosis, impaired renal concentrating ability and electrolyte abnormalities like hypokalaemia and sodium and magnesium wasting.

Forma lipossônica é menos nefrotóxicq .

The mechanism of nephrotoxicity involves direct cell membrane actions to increase permeability, as well as indirect effects secondary to activation of intrarenal mechanisms (tubuloglomerular feedback) and/or release of mediators (thromboxane A2). The latter effects are presumably responsible for the observed acute decreases in renal blood flow and filtration rate,

DIABETES INSIPIDUS, ATR DISTAL, HIPOCALEMIA, INCAPACIDADE DE CONCENTRAR A URINA

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24
Q

ANFOTERICINA B

A

26 - 83% of patients develop nephrotoxicity
• Increasing incidence b/o greater incidence of fungal
infections
• Chronic renal damage depends on cumulative dose of
ampho
– 44% of patients with CRF if > 4 g of ampho
– 8% with < 1 g ampho
• Azotemia usually reversible

Clinical

• Cumulative dose > 0.6 g (except BMT patients)
• Acute vasoconstriction
• Distal nephron damage
– Loss of urine concentration
– Distal RTA
– Wasting of K and Mg
• Azotemia

Pathology / Pathophysiology

• Vasoconstriction – acute reduction in RBF and GFR
• Histologic damage in distal nephron
– necrosis of tubular epithelial cells
– intracellular and intra-tubular calcium deposits
– tubular atrophy, interstitial edema, fibrosis
– Cytoplasmic vacuolization in smooth muscle cells in media of
renal arterioles

• Proximal and glomerular capillary damage

1)Vasoconstriction - DIMINUI PERFUSAO E tfg =Pre-renal azotemia

2)Distal Tubular Defects-
Acidification defects
Concentrating defects = hipokalemia,Hypomagnesemia,NDI

3) dano renal=Persistent
azotemia
(CRI)

Vasoconstrictive Effects of Amphoterecin B

Reduction in RBF and GFR
Possible Mechanisms
– Endothelin
– Tubulo-glomerular feedback
– Direct vasoconstrictor
– Role of voltage dependent calcium channels
– Role of arachidonic metabolites

Role of Liposomal Amphoterecin B

• Liposomes are small vesicles of phospholipid bilayer
• Taken up preferentially by reticulo-endothelial cells and
macrophages
• Enhanced therapeutic index (20 fold)
• Less toxic to kidneys
• Fewer side-effects

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25
Q

polymixin antimicrobial agents, colistin and polymyxin B Polimixina

A

Nephrotoxicity is related to their D-amino content and fatty acid compo- nent, which increases cellular membrane permeability and allows cation influx (41). This effect leads to tubular cell swelling and lysis with AKI development.

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26
Q
A
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27
Q

acyclic nucleotide phosphonates (adefovir, cidofovir, tenofovir)

A

enter the cell via basolateral human organic anion transporter–1(hOAT-1) and promote cellular injury primarily through disturbing mitochondrial function. Mitochondrial injury is manifested by mitochondrial enlargement, clumped cristae, and convoluted contours that impair cellular ener- getics (8,10,26,43). Tenofovir, which is employed widely to treat hepatitis B virus and HIV infection, is associated with proximal tubulopathy and AKI

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28
Q

Drug-Induced Cast Nephropathy

A

Vancomicina

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29
Q

Fator de risco nefrotoxicidade

A
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30
Q

Gentamicin Nephrotoxicity

A

• Non-oliguric renal failure
• Slow recovery of renal function
• Proximal tubule dysfunction (enzymuria, proteinuria,
aminoaciduria, glucosuria
• Hypomagnesemia
• Hypocalcemia
• Hypokalemia

Damage to proximal tubules
– dense osmiophilic lamellar structures (myeloid bodies) in lysosomes
– loss of microvilli of luminal surfaces
– tubular cell necosis
• Damage to glomerular capillary
– endothelial cell damage (diameter of fenerstrae)

  • Aminoglycosides are freely filtered
  • Proximal renal tubular cells concentrate aminoglycosides
  • Injury evident within hours
  • Tubular cells accumulate gentamicin
  • Enzymuria and proteinuria follow

Enzymuria ->Lysozymuria ->Glycosuria ,Aminoaciduria,Proteinuria,Transport defects->K and Mg wasting ,Polyuria NDI ->Necrosis

Risk Factors for Aminoglycoside Nephrotoxicity

Prolonged course of treatment
• Volume depletion
• Sepsis
• Pre-existing renal disease
• Hypokalemia
• Elderly patient
• Combination therapy with cephalosporins (partic.
Cephalothin)
• Other nephrotoxins
• Gentamicin>amikacin>tobramycin

Factors which combine with Gentamicin to

enhance nephrotoxicity

  • Amphoterecin
  • Contrast
  • Cisplatin
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31
Q

Tumor lysis syndrome

A

– 1 in 400 patients
– Majority of BMT patients with relapse not de novo
disease
– Big problem in bulky rapidly growing radio-chemo
sensitive tumors
– Uric acid, phosphate, xanthine
– Intra-tubular precipitation – obstruction
– Volume repletion, urinary alkalinization, allopurinol

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32
Q

Marrow infusion toxicity

A

Not seen with allogeneic BMT
– Consequence of cryopreservation
• -800C, DMSO (dimethyl sulfoxide)
• Potential disruption of granulocytes and RBCs
– Side-effects: N/V, headache, fever, flushing, chills,
hyper and hypotension, bradycardia, heart block, overt
hemoglobinuria, in-vivo hemolysis

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33
Q

Veno-Occlusive Disease

A

Caused by radio-chemotherapy-induced
endothelial injury of hepatic venules venular
thrombosis collagen and reticular fiber
deposition sinusoidal and portal hypertension
• Hepatic necrosis (zone 3) transaminitis
• Intra-hepatic portal vein - systemic vein shunting
and hepatocyte necrosis jaundice
• ARF in bilirubin b/o excretion

VOD and HRS are similar

• Both share:
– Jaundice and portal HTN prior to ARF
– Sodium avidity
– High BUN / Creat ratio (≈ 30:1)
– Mild hyponatremia
– Low BP (SBP in 90s)
– Autopsy data - no structural lesion in kidneys

34
Q

AINES

A

Distúrbios Metabólicos Hipercalemia • AIE diminuem a secreção de renina.

• Prejudicam a liberação de Aldosterona (via angiotensina II)

CUIDADO: USO DE DROGAS RETENTORAS DE POTÁSSIO IECA, BRA E DIURETICOS POUPADORES DE POTÁSSIO.

Hiponatremia • Efeito inibitório na atividade do ADH • Piorar a Hiponatremia em situações de elevações do ADH (ICC ou hipovolemia) • Aumentam a susceptibilidade em indivíduos idosos da hiponatermia reacionada aos tiazídicos.

• Acidose Metabólica hiperclorêmica (urina, pH >5.5). • Perda Urinária de K não pode ser explicada por uso de diurético ou deficiencia de magnésio. • Parada do uso de Ibuprofeno resulta na resolução completa do distúrbio em pouco dias. • Mecanismo desconhecido.

35
Q

NEFROTOXICIDADE ANTIRETROVIRAIS

A

antiretroviral nephrotoxic effects accounted for 14% of late-onset AKI episodes, occurring after 3 months of initiating HAART

HAART has also been associated with CKD. The major drugs implicated in this include indinavir, atazanavir, and tenofovir

TENOFOVIR=toxicidade tubular, sindrome de fanconi , which carries the potential consequences of calcium and phosphorus dysregulation and osteomalacia TDF-induced renal toxicity is more likely to occur in HIV patients with preexisting kidney disease or poorly controlled HIV disease with longer overall antiviral treatment duration, older age, elevated baseline creatinine concentration, female gender, African American ethnicity, CD4 nadir <200 cells/mm3, and concomitant administration of other nephrotoxic drugs

36
Q

nefrotoxicidade antiretrovirais

A

In a study by Wyatt et al., the major risk factors for AKI and associated mortality included severe immunosupression (CD4 count, <200 cells/mm3) and opportunistic infections [19]. Dehydration, alkaline urine, and a previous history of nephrolithiasis appear to be risk factors for atazanavir-associated kidney stones [32].

The risk factors for hyperlactemia (lactate > 2 mmol/L with or without acidosis) which is common with “d-drugs” like stavudine (d4T) and didanosine (ddI) include extended duration of treatment, old age, female gender, pregnancy, hypertriglyceridemia, obesity, hepatitis C infection, impaired kidney function, treatment with ribavirin, and alcohol use

37
Q

ira por drogas

A

pré renal-AINES, inibidores da calcineurina, BRA/IECA,interlecunas, CAR-T e diureticos

38
Q

ira por drogas

A

cristais=

AZATANAVIR, ACICLOVIR, ORLISTAT, QUINOLONAS,VITAMINA C E METROTREXATE

39
Q

IRA POR DROGAS

A

INJURIA TUBULAR

ANTIBIOTICOS,CONTRASTE, QUIMIOTERAPIA

EX: TENOFOVIR, CISPLATINA, VANCOMICINA, AMINOGLICOSIDEOS, ANFO B, IFOSFAMIDA, mTOR, CNI

40
Q

ira por drogas

A

lesao intersticial

AINES, ATB, QT, IMUNOTERPIA, IBP

41
Q

IRA POR DROGAS

A

DOENCAS GLOMERULARES

VASCULITE INDUZIDA POR DROGAS= Hidralazina,retinoides , cocaina (levemisole)

MAT=quinina, cni, antiVEGF

GESF- bifofonatos, interferon, mtor, esteroides anabolizantes,heroina, inibidores da tiroisna kinase,

dlm= aines

membranosa=aines, ouro, imunoterapia

42
Q

inibidores da calcineurina

A

ciclosporina =has

hipertricose, hiperplasia gengival,hiperuricemia, hipertrigliceridemia

os 2= hipomagnesemia, hipercalciuria,acidose metabolica

tacrolimus=dm,alopecia,hipercalemia

43
Q

Calcineurin inhibitor (CNI) nephrotoxicity

A

·

may occur any time after initiation of therapy, and can affect transplant or native kidneys and present as acute or chronic reductions in kidney function.

Elevated serum CNI help make the diagnosis, although CNI nephrotoxicity is not necessarily dose dependent.

CNI can cause vasoconstriction and increased serum creatinine (Scr) in the absence of morphologic findings

CNI nephrotoxicity–related acute injury is reversible with change in immunosuppression therapy; chronic injury is not reversible.

MO;Vasoconstriction-related CNI nephrotoxicity shows no morphologic changes.

Isometric vacuolization of proximal tubular epithelium, and vascular injury with loss of smooth muscles, myocyte cytoplasmic vacuolization, and dropout from necrosis or apoptosis are characteristic of acute CNI nephrotoxicity.

fibrose cortical estriada ou nova aparecimento de hialinose arteiolar com microcalcificacao

focal nodular hyalinosis and eventual hyalinosis, which can have a distinctive adventitial localization and can extend to the media of the entire vascular wall of arterioles and arteries.

CNI nephrotoxicity can also cause thrombotic microangiopathy (TMA) involving mostly arterioles and glomerular tufts.

Chronic CNI toxicity shows a striped pattern (tb pode aparecer em outras isquemias) interstitial fibrosis with proportional tubular atrophy.

Immunofluorescence microscopy: IgM and C3 staining in arterioles with hyalinosis and fibrinogen staining of thrombi in small arteries, arterioles, and glomeruli involved by thrombotic microangiopathy.

Electron microscopy: Isometric vacuoles in proximal tubular epithelium as dilated endoplasmic reticulum and large lysosomes. Hyaline accumulation within the adventitia or media of arterioles and arteries. Glomerular endothelial swelling, expansion of lamina rara interna, and mesangiolysis are present in cases with TMA.

Histological features of acute CNI-induced nephrotoxicity include early-stage hyalinization and dropout of individual myocytes in afferent arterioles, and isometric vacuolation of proximal straight tubules

replacement of myocytes in afferent arterioles with beads of hyaline that bulge into the adventitia, striped interstitial fibrosis and tubular atrophy

44
Q

nefrotoxidade cni

A

CNI exposure

Morphologic lesions may be absent (with functional CNI-induced vasoconstriction causing reduced kidney function)

Nodular hyalinosis, particularly adventitial hyalinosis, extending to the media of arterioles and arteries

Striped interstitial fibrosis

Thrombotic microangiopathy

Isometric tubular vacuolization (less specific)

45
Q

cni

A

A microangiopatia trombótica é uma patologia classicamente reconhecida em pacientes tratados com inibidores de calcineurina (tacrolimus e ciclosporina) ou mesmo, quando associada a um quadro de rejeição humoral.

a associação de ciclosporina e rapamicina é o único esquema imunossupressor que tem uma atividade pró-necrótica e anti-angiogênica nas células endoteliais da artéria.

a associação de rapamicina e ciclosporina, apresenta um risco relativo de desenvolver microangiopatia trombótica

46
Q

rapamicina

A

A rapamicina é um poderoso imunossupressor que ultimamente integra o arsenal terapêutico no transplante renal.

Entre os efeitos colaterais classicamente conhecidos, como dislipidemia, proteinúria, úlceras orais, aumento da incidência de linfocele entre outros, novos eventos como a pneumonite relacionado a droga , o quadro de anasarca.

incidência de edema generalizado (5,5%), tendo o edema de membros inferiores uma incidência próxima de 57% em pacientes transplantados de fígado, em uso de rapamicina

. A causa de extravasamento de líquido para o terceiro espaço nos pacientes em uso da rapamicina ainda não está bem esclarecida

. A biópsia com rim histologicamente normal, fazia parte da nossa hipótese diagnóstica.

47
Q

vancomincina

A

VANCOCINEMIA=15-20

ototoxicidade

homem vermelho

trombocitopenia

48
Q

gentamicina

A

bearter tipo iv

49
Q

ACIDOSE LATICA DO TIPO B

A

metformina e linezoida

50
Q
A
51
Q

litio

A

INTOXICACAO PELO LITIO USA AMILORIDA, AMILORIDA BLOQUEIA O ENAC. É EFICAZ NO DINEFROGENICO , N TEM RELACAO COM O CENTRAL.É INEFICAZ QUANDO A OSM DA URINA >200

52
Q

ALOPURINOL NÃO PODE FAZER JUNTO COM AZATIOPRINA=PANCITOPENIA

A

pancitopenia

53
Q

mat

A

cocaina

cyclosporine, mitomycin- C, and quinine

54
Q

cetuximab

A

hipomagnesemia

55
Q

fenitoina não é dialisável

A
56
Q

vitamina d

A

. The terms “vitamin D2” and “vitamin D3” do not refer to the hydroxylation status of vitamin D–either D2 or D3 can exist in the (1,25-OH), (25-OH), and unhydroxylated varieties–rather, they refer to whether or not the vitamin D derives from animal (D3, also called cholecalciferol) or plant (D2, also called ergocalciferol).

  1. Ergocalciferol (Vit D2) is the least expensive, is the type of vitamin D with which milk is fortified, and can be given in large enough oral doses to correct vitamin D deficiency relatively rapidly (e.g., 50000 units of ergocalciferol po qweek x 12 weeks).
  2. Cholecalciferol (Vit D3) is better absorbed orally than Vit D2, but is not available as a high dose form like D2 (e.g., 400-800 units po qd of cholecalciferol).
  3. Calcitriol refers to the activated form of vitamin D, which is hydroxylated at both the (1) and (25) positions, and may be either D2 or D3; the medication calcitriol is the D3 form.
  4. Cholecalciferol (VitD3) is produced in the human skin in response to UV light and is initially unhydroxylated at both the (1) and (25) position. Hydroxylation occurs at the (25) position in the liver (an efficient process which generally occurs even in the setting of advanced liver disease) and occurs at the (1) position in the kidney.
  5. Paricalcitol (Zemplar) is a vitamin D2 analogue which is hydroxylated at both (1) and (25) positions.
  6. doxercalciferol (Hectorol) is another vitamin D2 analogue which is hydroxylated only at the (1) position.
57
Q

acetazolamina

A

inibidor da anidrase carbonica-tubulo proximal

These diuretics, or drugs that to promote urine production, act by inhibiting the enzyme for which they are named, carbonic anhydrase (CA). This enzyme assumes two forms in the proximal tubule: one form within the brush border that converts bicarbonate to carbon dioxide and water, and the other intracellular form that converts water and carbon dioxide to carbonic acid which spontaneously dissociates to bicarbonate and a free hydrogen ion.

Inhibition of CA prevents tubular absorption of bicarbonate leading to a disruption in sodium gradients and eventual natriuresis,.CA inhibitors are not first line for hypertension.

These drugs are more commonly used for altitude sickness, by offsetting altitude induced respiratory alkalosis and speeding up the process of acclimatization2, and cerebral edema via inhibition of carbonic anhydrase in the central nervous system and decreased neuronal discharge3.Since there is urinary loss of bicarbonate as well as sodium, a common side effect for these drugs is the development of a proximal (type 2) renal tubular acidosis and thus a metabolic acidosis.

58
Q
A
59
Q

Loop Diuretics (Furosemide, Torsemide, Bumetanide, Ethacrynic Acid)

A

These diuretics lead to natriuresis via inhibition of the Na-K-2Cl cotransporter on the luminal side of ascending loop of Henle cells. Inhibition of sodium reabsorption leads to the profound diuretic response.

These powerful diuretics are useful for management of acute fluid overload and can restore volume balance in patients with heart failure, liver failure, and pulmonary edema. While not first line, they can also be used to manage hypertension especially when associated with diminished kidney function.

Patients using loop diuretics should be monitored for excessive fluid and electrolyte loss as hypokalemia can be an adverse side effect.

60
Q

Thiazide Diuretics (Hydrochlorothiazide, Chlorthalidone)

A

Thiazides produce natriuresis via inhibition of the NaCl symporter in the distal tubule. By lowering intraepithelial Na concentration, activity of the basolateral Na/Ca antiporter is increased facilitating increased Ca reabsorption from the tubular lumen.

These agents are excellent first line agents in managing hypertension in an outpatient setting.

Thiazides, much like loop diuretics, can also cause hypokalemia. Additionally, thiazides can cause an array of metabolic and electrolyte abnormalities such as hyperglycemia, hyperuricemia, hyperlipidemia, hypercalcemia, and hyponatremia.

61
Q
  1. Potassium Sparing Diuretics (Amiloride, Triamterene, Spironolactone, Eplerenone)1
A

Potassium sparing diuretics can largely be divided into two categories based on mechanism of action

-Competitive antagonism of intracellular mineralocorticoid receptors (spironolactone, eplerenone)

Epithelial sodium channel (ENaC) blockers (amiloride, triamterene)

These diuretics have earned their name due to their lack of excretion, or “sparing”, of potassium contrary to their thiazide and loop counterparts. For this reason, these drugs are often paired with the potassium wasting diuretics especially if a patient has had hypokalemia in the past.

The most adverse effect to be aware of is hyperkalemia as this increases the risk for potentially fatal arrhythmias.

62
Q

Sodium Zirconium Cyclosilcate (Lokelma ®)

A

Mechanism not fully understood, exchanges hydrogen and sodium for potassium in small and large intestines

1 hour

No studies conducted on patient with bowel obstruction or impaction. Avoid in patients with severe constipation, bowel obstruction or impaction. Preferred oral potassium binder Monitor for signs of edema, can increase diuretics if indicated.

63
Q

Patiromer (Veltassa ®)

A

Increases potassium removal by fecal excretion, exchanges calcium for potassium in the large intestine. ~7 hours 24 hours Avoid in patient with bowel obstruction or severe constipation. Can cause Hypomagnesemia. May decrease effectiveness of oral Ciprofloxacin. Administer Ciprofloxacin 3 hours before or after Patiromer. Patiromer must be refrigerated or used within 3 days after removed from refrigeration

64
Q

sorcal

A

Exchanges sodium for potassium in the large intestine >2 hours Variable Case reports of colonic necrosis; avoid in setting of bowel obstruction or following bowel injury or surgery; may be of limited utility in setting of severe hyperkalemia Can repeat every 4-6 hours; consider initial dose of 45-60 grams in body weight >80 kg

65
Q

Aminoglycoside antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs), contrast agents, and angiotensin converting enzyme inhibitors (ACEIs) are the most common cause of AKI in hospitalized patients

A

The risk of contrast-induced nephropathy is highest in diabetics and chronic kidney disease diabetes

66
Q

Drugs can cause nephrotoxicity by altering intraglomeu- lar hemodynamics and decreasing GFR

A

ACEI, angiotensin-converting enzyme blockers [ARBs], NSAID, cyclo- sporine, and tacrolimus

67
Q

crystal nephropathy

A

Certain drugs such as ampicillin, ciprofloxacin, sulfonamides, acyclovir, ganciclovir, methotrexate and triam terene are associated with crystal nephropathy

Crystal nephropathy may also results from the use of che- motherapy due to uric acid and calcium phosphate crystal deposition

68
Q

rabdomiolise

A

Statins and alcohol may induce rhabdomyolysis because of a toxic effect on myocyte function

69
Q

risco

A

extracellular volume depletion, sepsis, renal impairment, cardiovascular disease, diabetes, or prior exposure to radio contrast agents

70
Q

drogas removidas dialise

A

Theoretically, drugs with a molecular weight <5000, low plasma protein binding and a small volume of distribution (Vd) can be removed effectively by CRRT

71
Q

has e cni

A

Calcineurin Inhibitor-Induced (CNI) HTN

Cyclosporine > tacrolimus.

CNI-induced salt-sensitive HTN in mice revealed phenotype similar to familial hyperkalemic HTN (FHH), a.k.a. pseudohypoaldosteronism type II or Gordon syndrome: renal sodium (HTN) and potassium retention (hyperkalemia), RTA, hypomagnesemia, ± hypercalciuria.

Likely mechanisms: increased renal expression of the phosphorylated (active) form of the thiazide-sensitive NaCl cotransporter (NCC), along with increases in the expression of kinases that mediate activation of NCC

Likely best treated with thiazide diuretics

72
Q

aumenta creat sem alt fc renal

A
73
Q
A
74
Q

anti has dialisaveis

A

dialisaveis

metildopa, atenolol, metoprolol, captopril, enalapril, ramipril,minoxidil

nao dialisaveis

clonidina

losartana

propanolol , carverdilol

fosinopril

anlodipina,

hidralazina

75
Q

Renal Manifestations of Ipilimumab

tto melanoma

A

granulomatous interstitial nephritis

(induced lupus nephritis.

nia

76
Q

fibrose sist nefrogenica

A

Putative co-factors for NSF

Proinflammatory statesinfectionconnective tissue diseasesmajor surgeryHypercoagulable statesVascular injuryLiver failurehepatorenal syndromeliver transplantationMetabolic abnormalitieshyperphosphatemiahypercalcemiametabolic acidosisiron overloadTherapeutic agentshigh-dosage ESA

77
Q

gadolinio

A

Use only macrocyclic GBCAs; agents with hepaticclearance should be studied further to document safety.

Y

Use the lowest dosage of GBCA required to providequality images.

Y

Avoid intravenous iron and high-dosage erythropoie-sis-stimulating agents before and after the anticipatedexposure.

Y

Optimize calcium, phosphate, and acid-base balancebefore the anticipated exposure.

Y

Consider arranging hemodialysis to follow GBCA ex-posure for patients who are currently on this modality

78
Q

farmacocinetica

A

Ingeneral,dosagereductionisindicatedinpatients with CKD when

>

30% of a drug oran active metabolite appears unchangedin the urine.

Altered Pharmacokinetic Principles

In general, dosage reduction is indicated in pa-tients with chronic kidney disease (CKD) when

30%of a drug or an active metabolite appears unchanged inthe urine.

79
Q

fatores q afetam a dialisancia de uma droga

small (500 Da), water-soluble (appear unchanged in urine), unbound drugswith small distribution volumes would likely be re-moved from the body by dialysis

A

Drugsize (molecular weight)

% protein boundvolume of distribution

water solubility (% of dose appearing “unchanged” inurine)

Membranesize (surface area)

permeability (pore size)composition (polysulfone, cellulose-based,

etc.

)drug-membrane–binding characteristics (if any)Dialysis methoddialysis (drug removal by diffusion)hemofiltration (drug removal by convection)duration of procedureblood and dialysate flow rateultrafiltration ratereplacement solution location (pre- or postfilter)

80
Q

tubulopatias induzidas por atb

A

Aminoglycosides and tetracyclinesproximal RTA or Fanconi syndrome Normal anion gap metabolic acidosis; hypokalemia; uric acid, glucose,amino acid, phospho-wastingBartter-like syndrome Metabolic alkalosis with K

, Ca

, Mg

, Na

wastingAmphotericin B compoundsdistal RTA (H

“backleak”) Normal anion gap metabolic acidosishypokalemia K

wasting; distal RTApolyuria/hypernatremia Nephrogenic diabetes insipidusTrimethoprimdistal RTA Normal anion gap metabolic acidosisblockade of ENaC HyperkalemiaPenicillinshypokalemia High urine K

, low urine Cl

hyperkalemia High K

content in setting of poor kaliuresisLinezolid and tetracyclineslactic acidosis High anion gap metabolic acidosis

81
Q

nia drogas

A

Drugs: Allergic interstitial nephritis Antibiotics: Beta-lactam (PCN, Cephalosporins): remains a frequent reported cause of AIN Quinolones: most often seen with ciprofloxacin Sulfonamide: Sulfamethoxazole/Trimethoprim (bactrim) Others: rifampin, sulfa, vanco, erythromycin, acyclovir, ethambutol (EMB) Diuretics: thiazides, furosemide, bumetanide, triamterene NSAIDS (including selective COX-2 inhibitor): pure interstitial nephritis (ISN) ± papillary necrosis/ minimal change nephropathy (MCN) + ISN (85%) H2 blockers (cimetidine, ranitidine-rare) PPI (omeprazole and lansoprazole) Allopurinol Indinavir 5-aminosalicylates (5-ASA) ( i.e. mesalamine) Others: phenobarbital, phenytoin, nitrofurantoin, IFN, IL-2, Angiotensin converting enzyme inhibitor (ACEI: i.e.captopril) The drug-induced AIN is not dose dependent, and recurrence or exacerbation can occur with a repetitive exposures to the same or a related drug (Up-To-Date)

82
Q

corpos mieloides

A

hidroxicloroquina e aminoglicosideos

Nefrologia PT (112 decks)

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