ACUTE KIDNEY INJURY Flashcards

1
Q

What is acute kidney injury?

A

Spectrum of a disease starting from :

Increased creatinine

Decreased urine output

Progress to failure

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2
Q

what the definition of AKI?

A

Sudden decline in kidney functions
leading to :

Blood urea nitrogen in the kidney

creatinine with 48 H after injury

Urine output less than 0.5

Metabolites and biomarkers in urine

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3
Q

what are 3 basic renal processess?

A

Glomerular filtration

tubular reabsorption

Tubular secretion

Filters 180L per day but excrete 1-2L a day

Reabsorbs 99% water

100% glucose

99.5 Na

50% urea

Most of these occur at the proximal convoluted tubule

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4
Q

what are the markers for AKI?

A

GFR

Urine output

GFR IS better

when GFR is still above 60% , the kidney damage can be reverse

if it is 30% and below = failure and chronic impairment

Serum creatinine is better used in acute settings

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5
Q

what are the requirements to be diagnosed with AKI?

A

less than 0.5 ml urine

Oliguria ( 100-400ml in 24 hours )

Anuria ( less than 100mL in 24 hours )

Increased in serum creatinine ( 1 mg/dl ) IMPORTANT MARKER FOR KIDNEY FUNCTION

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6
Q

what are the causes of acute renal failure?

A

Acute kidney injury will lead to acute renal failure :

Prerenal (HYPOVOLEMIA)

Intrarenal ( glomerular , interstitial, tubular )

Postrenal —(Obstruction by hypertrophy or anything )

But one can lead to each other for example :

Hypovolemia ( prerenal ) will lead to ischemia in kidney ( intrarenal )

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7
Q

what is the relation of covid and AKI?

A

patients with covid 19 were twice as likely to develop AKI compared to non covid patiensts who developed AKI during the same time period in 2019 ( 56.9% ) vs 25.1% respectively

AKI appears to be a marker of covid 19 infection severity and mortality rate is higher for these patients

Various COVID-19 related effects that are thought to contribute to AKI include kidney tubular injury ( Acute tubular necrosis ) with septic shock , microinflammation , increased blood clotting and probable direct infection of kidney

most patients with covid 19 related AKI who recover continue to have low kidney function after discharge from hospital

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8
Q

what causes AKI prerenal?

A

Decreased renal perfusion without cellular injury

60% of community acquired cases ( MOST COMMON )

40% Hospital acquired cases

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9
Q

what causes Acute renal failure in hospital patients?

A

45% —> ACUTE TUBULAR NECROSIS ( ischemia, nephrotoxins by drugs or substances given to patients )—-> MOST COMMON

21% prerenal —> Congestive heart failure, volume depletion , sepsis

10% urinary obstruction

4% glomerulonephritis or vasculitis

2% AIN ( acute interstitial nephritis )

1% Atheroemboli

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10
Q

what causes hypovolemia ( prerenal aetiology )?

A

Hemorrhage, burns, dehydration (IV LOSS )

GI loss : vomiting , diarrhea ( hyponatremia ) –> cholera

Renal loss : Diuresis , hypo adrenalis, osmotic diuresis

Sequestration : Pancreatitis, peritonitis, trauma, low albumin

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11
Q

what causes low cardiac output ( prerenal causes )?

A

kidney gets 25% of CO ( SV X HR )

Myocardial disease

Valvular heart disease

pericardial disease

Tamponade

pulmonary artery hypertension

pulmonary embolus

positive pressure mechanical ventilation

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12
Q

what are other causes of prerenal AKI/AKF?

A

Renal vasoconstriction : hypercalcemia , noradrenaline, cyclosporin, amphotericin B

Systemic vasodilation : sepsis, medication, anesthesia, anaphylaxis

impairment of autoregulation : NSAIDS , ACE1

Hyperviscosity syndrome : Multiple myeloma, polycthemia rubra vera

Cirrhosis in ascites

Increases IAP

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13
Q

what type of urine AND SERUM? u get in cases of prerenal AKF/AKI?

A

during hypovolemia the body compensate by water and sodium retention forming urine with :

No casts and no cells

Concentrated ( cuz low fluid but high solutes )

FeNa less than 1%

Urine Na less than 20

SERUM will have :

high solutes, BUN ( BLOOD UREA NITROGEN) and CREATININE

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14
Q

what are the tubular intrinsic causes of AKI?

A

Acute tubular necrosis

ischemia

nephrotoxic

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15
Q

what are the glomerular intrinsic causes of AKI?

A

Glomerulonephritis (GN )

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16
Q

What are the interstitial intrinsic causes of AKI?

A

acute interstitial nephritis ( AIN )

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17
Q

what are the classifications of acute tubular necrosis ?

A

Ischemic

Nephrotoxic

18
Q

what are the types of nephrotoxic acute tubular necrosis ?

A

Endogenous toxins :

Heme pigments ( myoglobin , hemoglobin )
Myeloma light chains

Exogenous toxins :

Antibiotics ( aminoglycosides , amphotericin B )

Radiocontrast agents

Heavy metal ( Cis platinum ( chemotherapy ), mercury, Lithium )

poisons ( Ethylene glycol )

19
Q

How do we differentiate between acute tubular necrosis and prerenal?

A

Mainly through fraction of excreted sodium

in ATN = high sodium excreted
in prerenal = Low sodium excreted

Also

ATN = has epi cells and granular casts whereas prerenal dont

Prerenal causes improve with IVF
ATN doesnt improve

20
Q

what are the pathological characteristics of ATN?

A

patchy necrosis

Loss of brush borders

Flattening of epithelium

Detachment of Cells

Formation of intratubular casts

Tubular dilation and obstruction

21
Q

what are the two types of intrinsic glomerular AKI?

A

Acute glomerulonephritis

Immune glomerulonephritis

22
Q

what causes acute glomerulonephritis ?

A

Poststrept infection

Rapidly progressive Glomerulonephritis e

23
Q

what causes immune glomerulonephritis ?

A

Immune complex (GN )

anti- glomerular basement membrane ( GBM ) —> GOODPASTURE SYNDROME

Anti neutrophil cytoplasmic antibody associated glomerulonephritis ( ANCA associated GN ), Wegener granulomoatosis, churag strauss syndrome , microscopic polyangiitis

24
Q

what are the characteristics of glomerular disease ?

A

Hematuria ( dysmorphic RBCS )

RBC casts , no nuclie ( in prerenal no cast, in ATN we have muddy brown GRANULAR cast) here we have RED CAST , INTERSTITIAL WOULD HAVE WHITE CAST

Lipiduria ( increased glomerular permeability )

Proteinuria ( Maybe in nephrotic range )

Fever, rash , arthralgias

Elevated ESR

Low complement levels

25
what are types of intrinsic interstitial AKI?
Drug hypersensitivity ---> MOST COMMON 70% Infection ----> 15% ( Legionella. CMV, bact,viruses ) 8% = idiopathic 6% = AUTOIMMUNE ( Sarcoid. tubulointerstitial nephritis )
26
What are the causes of drug hypersensitivity intrinsic interstitial AKI?
30% antibiotic : Methicillin, cephalosporins, cipro Sulfa drug NSAIDS Allopurinol --> for gout
27
Describe AIN from drugs? (Acute intersitital nephritis )
Renal damage is not DOSE DEPENDENT May take weeks after initial exposure to drug but only 3-5 days to develop AIN after second exposure to drug Fever 27% Serum eosinophilia 23% Maculopapular rash 15% Urine : Low urine output with WHITE CASTS Urine eosinophils
28
describe contrast induced AKI?
1-2 days after contrast injection with recovery after 5-7 days Renal insufficiency Diabetes mellitus Multiple myeloma High osmolar ionic contrast media Contrast medium volum : dehydration Rx; fluids , N acetyl cysteine ; 600MG Non ionic low osmolar contrast dye
29
describe contrast induced acute tubular necrosis ?
when contrast induces tubular necrosis it decreases ability kidney to CONCENTRATE URINE as a result the sepcific gravity of urine becomes similar to plasma around 1.010 this is cuz the tubules are less able to reabsorb water and concentrate the urine leading to urine that is : ISOSTHENURIC ( SAME CONCENTRATION AS PLASMA )
30
what are the causes of post renal AKI?
Post renal obstruction; stones obstruction to the urinary outflow tract Prostatic hypertrophy blocked catheter malignancy bilateral pujo post urethral valve (PUV)
31
which patients are in risk ?
age pre existing renal impairment Diabetes hypertension , vascular disease jaundice mulitple myeloma drugs : diuretics , nsaids , acei sepsis , ICU
32
what do we ask for in ARF history?
Nausea, vomiting , diarrhea Hx of DM, heart disease , liver disease , previous renal disease , stones, BPH recent illness ? edema, change in urination new medication Recent radiology studies Rashes
33
what do you see in physical examination ?
Volume status : Mucus membrane , orthostatics CVS : Jugular venous distention ( HF ) , rubs Pulmonary : Decreased breath sounds , rales Rash allergic interstitial nephritis Large prostate Extermities : skin turgor edema
34
signs and symptoms of ARF?
Weight gain Weakness peripheral edema hypertension Nausea vomiting Pulmonary edema breathlessness asicites
35
describe creatinine?
indirect marker of renal function it is not elevated in early stages of kidney disease ( will not raise above normal lvl unless 60% loss of kidney function ) muscle mass Creatinine clearance : Urine creatineine x frequence / Production of creatinine
36
why does hyperkalemia happen in AFR?
impaired excretion of potassium seen in ECG elevation in T wave
37
what are the biomarkers found in glomerular injury?
Cysteine rich 61 matrix metalloprotinase 9 MMP 9
38
What are biomarkers of tubular injury?
Neutrophil gelatinase associated lipocalin NGAL NGAL demonstrated a sensitivity of 85% and sepcificity of 83% IL-18, IL-6 ( early sensitive predictor of AKI which is closely related to severity of AKI and mortality rates
39
whats the treatment?
Volume : ASSES VOL STATUS Replace in prerenal GDT Vol overload Remove offending cause , drugs : Dialysis, aspirin alkalinization , aspirin, antidepressents Antidots NAAC for pracetamol Electrolytes /AB status Diet
40
management of hyperkalemia?
calcium gluconate insulin glucose kayexalate Mg instead of Ca in patient on digoxin Bicarbonate only in concomitant severe acidosis Dialysis
41
what are the indications of continuous renal replacement therapy in certain cases ?
Acidosis ( metabolic ) Electrolytes ( Hyperkalemia ) Ingestion of drugs overload ( fluid ) Uremia