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Medicina Interna > 30. Lesión renal aguda > Flashcards

30. Lesión renal aguda Flashcards

1
Q

What is Acute kidney injury (AKI) ?

A

A sudden loss of renal function with a subsequent rise in creatinine and blood urea nitrogen (BUN).

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2
Q

What are the most common causes of AKI?

A

It is most frequently caused by decreased renal perfusion (prerenal) but may also be due to direct damage to the kidneys (intrarenal or intrinsic) or inadequate urine drainage (postrenal).

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3
Q

What is prerenal acute kidney injury?

A

Prerenal causes include any condition that leads to decreased renal perfusion (60% of cases of AKI).

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4
Q

Mention 5 causes of prerenal acute kidney injury

A
  1. Hypovolemia
  2. Hypotension
  3. Decreased circulating volume (↓ effective arterial volume)
  4. Renal artery stenosis
  5. Drugs that affect glomerular perfusion
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5
Q

How does hypercalcemia contribute to hypovolemia?

A

Hypercalcemia —Polyuria— Inhibition of sodium and chloride reabsorption —reduction of kidney’s urinary concentrating ability —volume depletion.

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6
Q

Which etiologies can contribute to hypotension and prerenal AKI?

A
  • Sepsis
  • Cardiogenic shock (decreased cardiac output)
  • Anaphylactic shock
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7
Q

Which etiologies can contribute to a decreased circulating volume and a prerenal AKI?

A
  1. Cardiorenal syndrome: e.g., in congestive heart failure
  2. Hepatorenal syndrome: e.g., in cirrhosis, liver failure
  3. Abdominal compartment syndrome
  4. Nephrotic syndrome
  5. Acute pancreatitis
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8
Q

Give 4 examples of drugs that affect glomerular perfusion

A
  1. Cyclosporine
  2. Tacrolimus
  3. NSAIDs
  4. ACE inhibitors
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9
Q

How do NSAIDs affect glomerular perfusion?

A

They constrict the afferent arteriole, reducing intraglomerular hydrostatic pressure and thereby decreasing glomerular filtration rate (GFR).

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10
Q

How do ACE-Is affect glomerular perfusion?

A

They inhibit angiotensin II-mediated vasoconstriction of the efferent arterioles, reducing intraglomerular hydrostatic pressure and thereby decreasing GFR.

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11
Q

What percentage of AK injuries are intrinsic or renal?

A

35%

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12
Q

What are the 4 causes of intrinsic AKI?

A
  1. Acute tubular necrosis
  2. Acute interstitial nephritis
  3. Vascular diseases
  4. Glomerulonephritis
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13
Q

What are 3 acute tubular necrosis causes?

A
  1. Ischemia: due to prolonged hypotension
  2. Nephrotoxic drugs: radiographic contrast agents, aminoglycosides, cisplatin, methotrexate, ethylene glycol, amphotericin B.
  3. Endogenous toxins: hemoglobin in intravascular hemolysis, myoglobin in rhabdomyolysis, uric acid in TLS, Bence-Jones protein light chains in multiple myeloma
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14
Q

What is the most common etiology for intrinsic AKI?

A

85% of intrinsic AKIs correlate to acute tubular necrosis.

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15
Q

What are the 3 main causes of acute intestitial nephritis?

A
  1. Medications
  2. Infections
  3. Infiltrative diseases like sarcoidosis or amyloidosis
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16
Q

Which medications can lead to acute interstitial nephritis?

A
  • Antibiotics: penicillin, cephalosporins, sulfonamides, ciprofloxacin, acyclovir, and rifampin
  • Phenytoin
  • Interferon, PPIs, NSAIDs, cyclosporine
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17
Q

What kind of infections can lead to acute interstitial nephritis?

A
  • Bacterial: Legionella spp., Streptococcus spp.
  • Fungi: Candida, Histoplasma.
  • Viral: Hepatitis C virus, cytomegalovirus, HIV
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18
Q

What kind of vascular diseases can cause intrinsic AKI?

A
  • Hemolytic uremic syndrome
  • Thrombotic thrombocytopenic purpura
  • Hypertensive emergency
  • Vasculitis
  • Scleroderma renal crisis
  • Renal vein thromboses
  • Renal atheroemboli
  • Renal infarction
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19
Q

What is postrenal acute kidney injury?

A

An AKI caused by any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra

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20
Q

What are the 3 main causes of postrenal AKI?

A
  1. Adquired obstructions
  2. Neurogenic bladder
  3. Congenital malformations (posterior urethral valves)
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21
Q

What are some potential causes of adquired obstructions that could lead to postrenal AKI?

A
  1. Benign prostatic Hyperplasia
  2. Iatrogenic (catherter)
  3. Tumors (prostate, bladder, metastases, cervical)
  4. Stones
  5. Blood clots
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22
Q

What are some potential causes of neurogenic bladder that could lead to postrenal AKI?

A
  • Multiple sclerosis
  • Spinal cord lesions
  • Peripheral neuropathy
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23
Q

True/False: “Even if the ureteral obstruction is unilateral, patients will typically present with elevated serum creatinine levels”

A

FALSE: As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels.

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24
Q

Mention 6 nephrotoxic antibiotics

A
  1. Aminoglycosides
  2. Vancomycin
  3. Cephalosporins
  4. Colistin
  5. Sulfonamides
  6. Streptomycin
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25
Q

Mention 4 nephrotoxic antivirals

A
  1. Acyclovir
  2. Foscarnet
  3. Ciclofovir
  4. Tenofovir
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26
Q

Mention a nephrotoxic antifungal

A

Amphotericin B

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27
Q

Mention 2 nephtotoxic antimetabolites

A
  1. Methotrexate
  2. Cladribine
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28
Q

What is anuria?

A

Urine output that is less than 50 milliliters per 24 hours.

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29
Q

What is oliguria?

A

Urine output of < 400 mL per 24 hours in adults (less than 0.5 mL/kg/h in children).

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30
Q

What are some signs of volume depletion (in prerenal AKI caused by volume loss)?

A
  • Orthostatic or frank hypotension and tachycardia
  • Reduced skin turgor
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31
Q

What are some signs of fluid overload (from Na+ and H2O retention)?

A
  • Peripheral and pulmonary edema
  • Hypertension
  • Heart failure
  • Shortness of breath
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32
Q

What are some signs of uremia?

A
  • Anorexia
  • Nausea
  • Encephalopathy
  • Asterixis
  • Pericarditis
  • Platelet dysfunction
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33
Q

Mention 2 nephrotoxic chmetherapeutic agents

A
  • Cisplatin
  • Carboplatin
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34
Q

Is lithium nephrotoxic?

A

Yes

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35
Q

Mention antiinflammatories and immunosuppresants that are nephrotoxic

A
  1. NSAIDS (aspirin, ibuprofen, diclofenac, ketorolac, piroxicam, and naproxen)
  2. Cyclosporine
  3. Calcineurine inhibitors
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36
Q

What are some signs of renal obstruction (in postrenal AKI)?

A
  • Distended bladder
  • Incomplete voiding
  • Pain over the bladder or flanks
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37
Q

¿En qué diagnóstico podemos pensar niveles estables de creatinina, anemia crónica y riñones pequeños hiperecóicos en la ecografía?

A

Enfermedad renal crónica.

38
Q

What are the diagnostic criteria of acute kidney injury?

A

Acute kidney injury is defined as the presence of any of the following criteria:

  1. Increase in serum creatinine by ≥ 0.3 mg/dL (26.5 μmol/L) within 48 hours.
  2. Increase in serum creatinine to ≥ 1.5 times baseline level within 7 days.
  3. Decrease in urine output to < 0.5 mL/kg/hour for ≥ 6 hours.
39
Q

What is the management for pre-renal AKI caused by hypovolemia?

A

IV fluid resuscitation with isotonic crystalloids to restore fluid losses

40
Q

What is the management for pre-renal AKI caused by shock?

A

Immediate hemodynamic support and identification of the cause of shock

41
Q

What is the management for pre-renal AKI caused by drugs that affect glomerular perfusion?

A

Discontinuation of offending medications (e.g., ACE-Is, ARBs, NSAIDs) and ensuring adequate hydration.

42
Q

What is the management for intrinsic AKI caused by acute tubular necrosis?

A
  1. Discontinuation of potential nephrotoxins
  2. IV fluid therapy with isotonic crystalloids
  3. Oliguric phase: strict fluid balance monitoring to avoid fluid overload
  4. Polyuric phase: matching of fluid and electrolyte losses to prevent a secondary kidney insult from hypovolemia
43
Q

What is the management for intrinsic AKI caused by acute intesrstitial nephritis?

A
  1. Discontinuation of potential nephrotoxins
  2. Treatment of the underlying etiology
  3. Glucocorticoid therapy may be considered.
44
Q

What is the management for intrinsic AKI caused by glomerulonephritis?

A

Glucocorticoids and/or other immunosuppressive therapy may be considered.

45
Q

What is the management for intrinsic AKI caused by vascular causes?

A

Management of hypertensive crises: IV antihypertensives.
TTP or HUS management: Plasma exchange therapy.

46
Q

What is acute kidney injury?

A

Increase in SCr of greater than or equal to 0.3 mg/dL within 48 hours or an increase in SCr greater than 1.5 times baseline within 7 days of decreased urine output for 6 hours.

47
Q

In which patients should we consider postrenal sources of AKI?

A

Patients with signs of nocturia, or urinary frequency. Cancer or trauma patients, solitary kidney patients.

48
Q

What are the risk factors for acute kidney injury?

A
  • 65 years or older
  • Chronic diseases (HTA, DM, FC, aterosclerosis, ERC, uropatía obstructiva)
  • Surgical procedures
  • Sepsis or acute infections
  • Nephrotoxic agents
49
Q

What causes glomerulonephritis?

A

Autoimmune damage to the kidneys themselves, that progress to inflammatory changes, that then ñeads to subsequent fibrosis.

50
Q

What is nephritic syndrome?

A

Hematuria, proteinuria, decreased renal function and high blood pressure.

51
Q

Mention 4 examples of the various types of acute glomerulonephritis

A
  1. Postinfectious glomerulonephritis
  2. IgA nephropathy
  3. Microscopic polyangiitis
  4. Lupues nephritis
52
Q

What is nephrotic syndrome?

A

Hypertension, periorbital swelling or lower leg edema, AKI

53
Q

¿En qué pacientes sospechamos una glomerulonefritis post-infecciosa?

A

Pacientes que reportaron dolor de garganta o infección cutánea, típicamente 1-12 semanas antes de la presentación clínica. Además, se presenta más comúnmente en niños varones de 2-12 años.

54
Q

¿En qué etiologías podemos pensar ante un paciente con: infecciones respiratorias, purpura, artritis, con signos de síndrome nefrítico?

A
  • Granulomatosis de Wegener
  • Poliangiitis microscópica.
55
Q

¿Cuál es el tratamiento para la glomerulonefritis aguda?

A
  1. Supportive care (Cristaloides isotónicos, suspender nefrotóxicos, blood pressure control, dialysis, diuretics, management of hyperkalemia, acidosis, uremia)
  2. Immunosuppressive therapies. (Steroids)
56
Q

¿Cuál es la principal causa de muerte en pacientes con LRA?

A

Sepsis, más del 40% de la mortalidad.

57
Q

¿Cuál es el pilar del tratamiento de los pacientes con sepsis?

A
  • Resucitación agresiva con líquidos (Soluciones isotónicas) en la primera hora.
  • Inicio de agentes vasoactivos en las primeras 6 horas.
58
Q

¿Cuál es la definición de lesión renal aguda?

A

Cumplir con cualquiera de los siguientes 3 criterios:
a) Aumento de 0,3 mg/dl o más los niveles de creatina en menos de 48 horas.
b) Aumento de más de 1.5 veces la creatinina basal en menos de 7 días.
c) Disminución del gasto urinario a menos de 0,5 cc/kg/hora por más de 6 horas.

59
Q

¿Qué hacemos si llega a urgencias un paciente con ERC, y desconocemos su creatinina basal, pero queremos determinar si hizo LRA?

A

Tomamos como creatinina de base el límite superior de normalidad. Es decir, 1.3. Y si aumenta 0.3 mg/dl o más, está cursando con LRA.

60
Q

¿Qué porcentaje de los pacientes hospitalizados hacen LRA?

A

30%

61
Q

¿Que porcentaje de los pacientes hospitalizados en UCI hacen LRA?

A

50%

62
Q

¿Cuáles son los dos trastornos hidroelectrolíticos y metabólicos más comúnmente relacionados a la LRA?

A

Hiperkalemia, hiperfosfatemia, hipocalcemia.

Acidosis metabólica, uremia.

63
Q

¿Qué caracteriza un Sx nefrótico?

A
  • Edemas
  • Hipoalbuminemia
  • Proteinuria mayor a 3-3.5 gr en 24 horas.
64
Q

¿Qué caracteriza un Sx nefrítico?

A
  • Proteinuria (no siempre)
  • Hematuria (origen glomerular): se pueden ver los eritrocitos crenados o los cilindros de eritrocitos en el uroanálisis.
  • Tasa de filtración glomerular muy baja
  • Hipertensión
65
Q

¿Qué manifestaciones puede generar la hiperkalemia?

A
  • Arritmias
  • Palpitaciones
  • Síntomas musculares (debilidad, parálisis)
66
Q

¿Cómo es el abordaje diagnóstico de la LRA?

A
  1. Anamnesis completa: infecciones, medicamentos.
  2. Uroanálisis con sedimento
  3. Relación proteinuria/creatinuria
  4. Ecografía vías urinarias
  5. Si tengo alta sospecha de urolitiasis: urotac
67
Q

¿Qué enfermedad renal sugiere un patrón urinario de: hematuria con eitrocitos dismórficos, cilindros hemáticos, diferentes grados de albuminuria?

A

Glomerulonefritis proliferativa:
- Nefropatía IgA
- Vasculitis ANCA
- Nefritis lúpica

68
Q

¿Qué enfermedad renal sugiere un patrón urinario de: albuminuria severa con hematuria mínima o ausente?

A

Glomerulopatía no proliferativa:
- Diabetes
- Amiloidosis
- Nefropatía membranosa
-Glomeruloesclerosis focal y segmentaria
- Enfermedad de cambios mínimos.

69
Q

¿Qué enfermedad renal sugiere un patrón urinario de: cilindros múltiples granulares y epiteliales con células epiteliales libres?

A

Necrosis tubular aguda en pacientes con LRA subyacente

70
Q

¿Qué enfermedad renal sugiere un patrón urinario de: piuria aislada?

A

Infección:
- Bacteriana
- Mycobacterias

Enfermedad tubulointersticial

71
Q

¿Qué enfermedad renal sugiere un patrón urinario de: función renal anormal, tiras reactivas normales, sedimento con pocas células, sin cilindros, proteinuria mínima o ausente?

A
  • LRA pre-renal por depleción de volumen
  • Hipercalcemia
  • Nefropatía con cilindros de cadena ligera en mieloma múltiple
  • Sx de lisis tumoral
  • Enf. Vascular que produce isquemia glomerular, pero no infarto (Emergencia hipertensiva, esclerodermia, microangiopatía trombótica) o que afecta vasos extraglomerulares (heteroembolia del colesterol, poliartritis nodosa)
  • Obstrucción del tracto urinario
72
Q

¿Qué significa tener una relación BUN/CREAT mayor a 20?

A

Etiología pre-renal

73
Q

¿A qué pacientes se les tomará biopsia renal?

A
  • Deterioro severo desde el principio o progresivo
  • Glomerulonefritis rápidamente progresiva (Px que duplican niveles de creatinina, pero en imágenes tienen riñones normales)
  • Sospecha de lupus
74
Q

¿En qué etiología pensamos si hallamos una proteinuria anormal y/o hematuria?

A

Glomerulonefritis (nefrótico, nefrítico, mixto)

75
Q

¿En qué etiología pensamos si hallamos una piuria estéril?

A

Nefritis intersticial aguda, infecciones.

76
Q

¿En qué etiología pensamos si hallamos cilindros pigmentados granulares y/o células epiteliales de túbulo renal?

A

Necrosis tubular aguda

77
Q

¿En qué etiología pensamos si hallamos una HC o EF sugestivos de sepsis, choque, hipotensión o exposición a nefrotóxicos?

A

Necrosis tubular aguda

78
Q

¿Cuáles son algunas causas menos frecuentes de LRA?

A
  1. Disección aórtica
  2. Lisis tumoral
  3. Hipertensión maligna
79
Q

¿Cuáles son los criterios de una urgencia dialítica?

A
  1. KDIGO 3 y oligoanuria mayor a 48 horas
  2. BUN mayor a 112
  3. Sobrecarga hídrica con edema pulmonar refractaria a manejo
  4. Emergencia hiperkalémica refractaria a manejo
  5. Acidosis metabólica refractaria a manejo
  6. “Envenenamiento” (Intoxicación con litio, con salicilatos)
80
Q

¿A qué pacientes voy a hospitalizar en el contexto de una LRA?

A
  1. KDIGO 2 o KDIGO3, o KDIGO1 con etiología no clara.
  2. Ausencia de posibilidad de valoración temprana por un nefrólogo
  3. Sospecha de glomerulonefritis
  4. Refractariedad a manejo inicial
81
Q

¿Cómo se maneja la LRA?

A
  1. Identificación y manejo etiológico
  2. Corrección de causas reversibles (Hipovolemia, obstrucción)
  3. Eliminar nefrotóxicos
  4. Determinar necesidad de TRR a largo plazo
82
Q

¿Aparte de eliminar nefrotóxicos, qué otras medidas podemos tomar en el paciente hospitalizado con LRA?

A
  • Ajustar medicamentos según TFG
  • Evitar hipotensión
  • No realizar estudios con contraste yodado
83
Q

¿Cómo se maneja una acidosis metabólica en el contexto de una LRA?

A
  1. TRR si se asocia a hipervolemia, y el pH es menor a 7,1 con refractariedad al manejo.
  2. Bicarbonato cuando el pH es menor a 7,2
84
Q

¿Cómo se maneja una alcalosis metabólica en el contexto de una LRA?

A

Suele resolver con SSN

85
Q

¿Qué consideraciones debemos tener en cuanto a la nutrición de los pacientes que cursan con LRA?

A
  1. Si es AKIN3 debe ser dirigida por un especialista
  2. Aliviar el estado catabólico
  3. Restricción hídrica, de sodio, potasio y fósforo
  4. Requerimientos: 25-30 kcal/día y una ingesta de proteínas elevadas de hasta 1,2-1,5 g/kg/día
86
Q

¿Qué combinación de medicamentos me puede llevar a LRA?

A

Bloqueadores de canales de calcio + Macrólidos

87
Q

What is the normal GFR in healthy young adults?

A

90- 120 mL/min

88
Q

The presence of muddy brown casts of epithelial cells found in urine is pathognomonic for …

A

Acute tubular necrosis

89
Q

¿Qué tipo de LRA sospecharemos en un paciente con una concentración urinaria de sodio menor a 20 mEq/L?

A

LRA pre-renal

90
Q

¿Qué exámenes mandar si sospechamos una causa postrenal?

A
  • Ultrasound of kidneys
  • Postvoid bladder volumes
91
Q

¿A partir de qué nivel de

A

Medicina Interna (42 decks)

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