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Renal and Urology > Acute Kidney Injury > Flashcards

Acute Kidney Injury Flashcards

1
Q

What tests are done to determine if there is a problem with the kidneys?

A

-Bloods
=Serum creatinine-reference range 60-110 micromole/L
=Calculates estimated glomerular filtration rate- reference range >60 mL/min
-Urine
=Urine output
=Urinalysis- blood and/or protein in urine

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2
Q

What is acute kidney injury?

A

-An abrupt decrease in kidney function
=Retention of waste products
=Impaired fluid balance
=Abnormal electrolyte balance (potassium)
-Staging system to stratify in studies (based in serum creatinine and urine output)

AKI is defined as any of the following:

  • Increase in serum creatinine by > 26.5 μmols/L in 48 hours or,
  • Increase in serum creatinine by > 1.5x baseline creatinine within last 7 days or
  • Urine volume < 0.5ml/kg/hr for 6 hours
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3
Q

Describe diagnosis of AKI

A
  • Diagnosis relies on assessment of renal function/ urine output
  • Many patients will have pre-existing CKD
  • Review of clinical events will normally identify cause
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4
Q

Describe Stage 1 AKI

A

Serum creatinine:
=1.5-1.9 times baseline/ >/26.5 micromoles/L increase
Urine Output:
=<0.5ml/kg/hour for 6-12 hours

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5
Q

Describe Stage 2 AKI

A

-SC:
=2.0-2.9 times baseline
-UO:
=<0.5ml/kg/hour for >/12 hours

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6
Q

Describe Stage 3 AKI

A 
-SC:
=3.0 times baseline/ increase in serum creatinine to >/353.6 micromoles/L / Initiation of renal replacement therapy
-UO:
=<0.3ml/kg/hour for >/24 hours
OR
=Anuria for >/12 hours
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7
Q

What are the causes of AKI?

A

-Pre-renal
=Reduced perfusion
=Blood supply problem
=Cardiac failure, sepsis, blood loss, dehydration, vascular occlusion
-Renal
=Within kidney
=Glomerulonephritis, small-vessel vasculitis, acute tubular necrosis, interstitial nephritis
-Post-renal
=Obstruction
=Stones, prostatic enlargement, prostatic cancer, retroperitoneal fibrosis, ureteral valve stenosis

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8
Q

Describe pre-renal causes of AKI

A

-Volume depletion/ Hypovolaemia
=Diarrhoea, bleeding, third space loss (ascites), diuresis, sepsis
-Hypotension
=Heart failure, sepsis, oedematous states, drugs, liver failure
-Renal ischaemia
=Hepatorenal syndrome, arterial occlusions, dissection of abdominal aorta, severe renovascular disease, renal artery stenosis
-Drugs
=NSAIDs, calcineurin inhibitors, ACE/ARBs

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9
Q

What mechanisms lead to AKI?

A
  • Reduced glomerular perfusion
  • Glomerular filtration rate is reduced
  • Constriction of efferent arteriole
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10
Q

What mechanisms are activated in hypovolaemia?

A 
-Sympathetic NS
=Tachycardia, vasoconstriction
-Renin-aldosterone axis
=vasoconstriction
=aldosterone stimulates salt and water retention
-Neuroendocrine axis
=increased antidiuretic hormone (ADH)
=Reduced urine output
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11
Q

What is the hypovolaemia-initial fluid resuscitation?

A

-IV fluid challenge
=500mL 0.9% sodium chloride or plasmalyte over 15 minutes
=Reasonable to repeat if no response
=Do not give more than 2000mL as resuscitation fluid without senior input

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12
Q

What are the drugs that make AKI worse?

A
  • ACE inhibitors and Angiotensin receptor blockers
  • Blood pressure lowering drugs (beta blockers, amlodipine/ calcium channel blockers)
  • Diuretics
  • Non-steroidal anti-inflammatory drugs
  • Radiocontrast agents
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13
Q

What is the initial treatment of AKI?

A
  • IV fluids
  • Stop nephrotoxins (withhold lisinopril and other blood pressure lowering treatments, NSAIDs)
  • Physiological monitoring (pulse, bp, fluid input and output)
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14
Q

Why is hyperkalaemia life-threatening?

A

-Can lead to abnormalities in electrical conduction system of the heart (main intracellular cation)
=cardiac arrest
=asystole/ ventricular fibrillation

  • Broad QRS complexes
  • Tenting of T wave
  • Loss of p wave
  • Abnormal rhythms
  • Sine wave
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15
Q

What is the most appropriate initial treatment for hyperkalaemia?

A

-Intravenous calcium chloride/ gluconate
=protects heart from hyperkalaemia effects
=stabilises myocardium for 20-30 minutes

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16
Q

What is the treatment for hyperkalaemia?

A

-IV calcium salts if ECG abnormal (lasts 30 mins)
-Insulin/ glucose and nebulized salbutamol
=Pushes potassium into cells, lasts 4-6 hours
-Treat underlying cause
=Need to get kidneys working to excrete potassium

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17
Q

What does acute tubular injury cause?

A

-Ischaemia (even less oxygen to hypoxic medulla so disrupts cellular energetics)
-Tubular injury and cell death
=Back leak of glomerular filtration
=Tubular obstruction by cellular casts (sloughed cells block)
=Inflammation (neutrophils and macrophages)
=REDUCED GLOMERULAR FILTRATION

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18
Q

Describe acute tubular injury

A

-Diagnosis of exclusion
=Is there is a treatable cause of renal failure?
-Follows many different causes of AKI (most common cause)
=Currently no preventative strategies
-Recovery is normal outcome with support but long-term consequences

19
Q

What suggests a glomerular cause of AKI?

A

-Urinalysis of protein and blood (active urinary sediment)
-Creatinine raised
=Glomerular nephritis (inflammatory crescent= mass of inflammatory cells)

20
Q

How is systemic vasculitis diagnosed?

A

-Dipstick urinalysis (protein and blood)
-Serum anti-neutrophil cytoplasmic antibodies (ANCA)
-Often present with coincident infection
-Tissue diagnosis
=Kidney most common
=Lung
=Nerve

21
Q

What is the treatment for systemic vasculitis?

A

-Glucocorticoids
=Oral prednisolone
-Plasma exchange
=Significant renal disease and/or pulmonary haemorrhage
-Cyclophosphamide (kill lymphocytes)/ Rituximab (monoclonal antibodies aimed at B cells)

22
Q

What are the common intrarenal causes of AKI in a ITU setting?

A
  • Acute tubular injury (may follow severe hypotension)
  • Rhabdomyolysis (crush injury/ long lie on floor after fall- myoglobin released from damaged muscles and taken up by tubular cells but cant be removed)
  • Contrast nephropathy
  • Interstitial nephritis (drugs- penicillin, NSAIDs)
  • Systemic vasculitis
  • Myeloma (tumour of plasma cells)
  • Haemolytic uraemia syndrome (E Coli 0157 infection)
23
Q

How can post-renal causes be diagnosed?

A

-Ultrasound renal tract (shows hydronephrotic kidney)/ bladder scan (estimate volume in bladder)
=renal pelvis seems larger and darker, causes kidney to be dilated

24
Q

Describe hydronephrosis

A
  • Renal pelvis seems larger and darker, causes kidney to be dilated (pressure of fluid)
  • Pressure over time built up= persists so damage to kidney cortex
25
Q

What are the lower urinary tract symptoms?

A
  • Urgency
  • Frequency
  • Nocturia
  • Incontinence
  • Hesitancy
  • Poor stream
  • Terminal dribbling
26
Q

What are the sphincters of the bladder?

A

-Internal urethral sphincter (involuntary)
=under control of alpha-1 adrenoceptor
-External urethral sphincter (voluntary)
*prostatic between

27
Q

What are the treatments for hydronephrosis?

A

-Insert a urinary catheter
=allow decompression of renal tract
=may become polyuric (cant concentrate as well)
-Start an alpha-blocker (Tamsulosin)
=sphincter more capable of relax (less retention)
=trial without catheter (TWOC)
-May need transurethral prostatic resection (TURP) surgery due to renal impairment

28
Q

What are causes of post-renal AKI?

A
  • Pelvis cancer= cervical, ovarian
  • Bladder lesions/ tumours can occlude ureteric orifice
  • Blood clot in bladder
  • needs to block both kidneys
  • Prostate hypertrophy, cancer
  • Ureter= calculi, tumour, extrinsic compression (retroperitoneal fibrosis, tumour)
29
Q

Describe normal renal structure

A
  • Glomeruli (filtering units)
  • Tubules (reabsorption)
  • Interstitium (bit in between tubules)= mainly comprises microvascular capillaries in health
  • Mesangium (structural support)
30
Q

Why is AKI important?

A

AKI is COMMON (affects 7% of hospital inpatients) and has adverse consequences:

  • Increased length of stay in hospital
  • Increased morbidity
  • Increased hospital & post-discharge mortality
  • Very costly (~£500 million/annum)
31
Q

What adverse renal outcomes in severe AKI independently associated with?

A
  • Increased incidence of chronic kidney disease

- Increased incidence of end-stage renal disease

32
Q

How does myeloma lead to intrarenal obstruction?

A

-Lumen of nephron tubules obstruction
-Bone marrow tumour
-Proliferation of B cells= many single antibodies (paraproteins)
=precipitates in nephron- casts cause complete obstruction

33
Q

What are the tubulointerstitial causes of AKI?

A

-Acute allergic interstitial nephritis (AIN)
=DRUG-RELATED e.g. PPIs, (omeprazole) antibiotics, diuretics, NSAIDs
=May have an eosinophilia (no rash)
=Often respond well to steroids

34
Q

What are the causes of cesentric RPGN (rapidly progressing Glomerular nephritis)?

A

-Goodpasture’s syndrome: anti-GBM Ab (collagen in glomerular basement membrane)
-Wegener’s granulomatosis: PR3 Ab
-Microscopic polyarteritis (MPA): MPO Ab
=both have auto-antibodies to proteins in neutrophils
=vasculitis
-SLE: Anti-nuclear Ab (ANA), anti-dsDNA Abs (young women)

35
Q

What is a disease of the vasculature of the kidney?

A

-Haemolytic uraemic syndrome (HUS)
=E coli related (E coli O157)
=Familial cases (genetic aetiology, complement)
=Glomerular microvascular thrombosis

36
Q

Describe a clinical history in AKI

A
  • Renal history – pre-existing renal disease, diabetes, family history
  • Urine volume - ?acute oliguria
  • Drug history – ? New drugs, nephrotoxic drugs (NSAIDs, ACEI, antibiotics)
  • Systemic symptoms – diarrhoea, rashes etc
  • Fluid status (JVP, postural BP) ?dehydrated
  • ?evidence of infection
  • ?rash, joint pathology
  • Arterial bruits ?underlying renovascular disease
  • Palpable bladder (obstruction)
  • Check drug chart!
37
Q

What investigations are down in suspected AKI?

A
  • Urine dipstick – simple BUT important (blood, protein)
  • Urine culture
  • Renal Ultrasound - if obstructed then decompress
  • Renal biopsy (AKI and normal sized kidneys)
  • Angiography ± intervention
38
Q

What blood tests are don is suspected AKI?

A
  • FBC, blood film, clotting screen
  • Biochemistry including Ca2+, PO42- LFTs and albumin
  • Creatinine kinase (rhabdomyolysis)- statins, long lie
  • Blood cultures
  • Virology and serology e.g Hep B, ASOT
39
Q

What immunological tests are done in AKI?

A

-IgGs and serum electrophoresis (myeloma)
-Complement levels (SLE, post strep GN)
-Autoantibodies e.g.
=Anti-nuclear factor (ANA) - SLE
=Anti-neutrophil Ab (ANCA) - vasculitis
=Anti-GBM Ab - Goodpasture’s syndrome,

40
Q

What are the other tests that can be done in suspected AKI?

A
  • Urine: Bence Jones protein = light chains (myeloma)
  • Chest X ray (cardiac size, pulmonary oedema or haemorrhage)
  • ECG especially if hyperkalaemia
41
Q

Describe the general treatment for AKI

A
  • Optimise fluid balance and circulation
  • Stop exacerbating factors e.g. nephrotoxic drugs (check drug charts)
  • Appropriate prescribing (check BNF, discuss with pharmacist) e.g. opiates accumulate in AKI
  • Supportive treatment e.g. dialysis, nutrition
42
Q

Describe the specific treatment of AKI

A
  • Obstruction - drain renal tract
  • Sepsis - effective antibiotics
  • RPGN e.g. SLE - immunosuppression
  • Goodpasture’s syndrome - Plasma exchange
  • Compartment syndrome - fasciotomy
43
Q

When do we start dialysis

A

-Severe Uraemia
=no prospect of immediate improvement
=uraemic encephalopathy or seizures
=uraemic pericarditis
-Hyperkalaemia unresponsive to medical treatment (>6.5)
=ECG changes
-Fluid overload, especially pulmonary oedema, resistant to treatment with diuretics/fluid restriction
-Severe acidosis (results in myocardial depression and hypotension)

44
Q

What are the risks associated with haemodialysis?

A

-Vascular access related complications -
=Pneumothorax
=Infection
=Bleeding

  • Anticoagulation required which may be problematic in patients with bleeding.
  • Hypotension may be troublesome in some patients (sepsis, IHD, diabetes)

Renal and Urology (43 decks)

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