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AKI Flashcards

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0
Q

What is the aetiology for acute kidney injury?

A

Occurs in ~5% of hospitalised patients & ~25%-30% of ICU patients (UK)

UK: > 85% due to prerenal AKI or ATN (potentially reversible) & > 90% of intrinsic AKI cases due to ATN

Global:

  • infective causes (haemorrhagic fevers)
  • diarrhoeal illnesses
  • obstetric causes (sepsis, post-partum haemorrhage, etc.)
  • spider/snake bites
  • copper sulfate poisoning
  • herbal remedies

AKI mortality increases if dialysis is required

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1
Q

What is the definition of acute kidney injury?

A

Abrupt and sustained decrease in kidney function characterised by: an abrupt decline in actual GFR (days-weeks); upset of ECF volume, electrolytes, and acid/base homeostasis; and the accumulation of nitrogenous waste products.

Defined by any of the following:

  • increase in serum creatinine by >26.5umol/l within 48hrs
  • increase in serum creatinine by >1.5 x baseline within 7 days
  • urine volume < 0.5ml/kg/hr for 6hrs (indicates risk of developing AKI)
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2
Q

What is the general cause of pre-renal acute kidney injury?

A

Reduction in renal perfusion (past point of autoregulation)

note: normally unable to regulate below 80mmHg, but hypertensive patients unable to regulate at higher BP than this (curve shifts to the right)

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3
Q

How does the glomerulus increase renal perfusion?

A

Intrarenal prostacyclin reduces afferent tone (more blood reaches glomerulus) (inhibited by NSAIDs)

Circulating vasoconstrictors (e.g. angiotensin II) increase efferent tone (increased pressure in glomerulus maintains GFR) (inhibited by ACE inhibitors & angiotensin II receptor antagonists)

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4
Q

What are some of the causes of pre-renal AKI?

A

Reduced effective ECF -> reduced perfusion to glomerulus

  • hypovolaemia (blood/fluid loss, “third spacing” - fluid moved out of blood)
  • systemic vasodilatation (sepsis, cirrhosis, anaphylaxis)
  • cardiac failure (LV dysfunction, valve disease, tamponade)

Impaired renal autoregulation (unable to correct perfusion)

  • pre-glomerular vasoconstriction (sepsis, hypercalcaemia, hepatorenal syndrome, NSAIDs)
  • post-glomerular vasodilatation (ACE inhibitors, angiotensin II receptor antagonists)
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5
Q

Will pre-renal acute kidney injury respond to fluid resuscitation?

A

No cell damage in the kidney so there is reabsorption of sodium and water in an attempt to increase perfusion to the glomerulus (aldosterone & ADH released)

Therefore fluids will aid this process

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6
Q

What are the investigations and typical laboratory findings in pre-renal acute kidney injury?

A

Urinalysis:

  • specific gravity: measure of concentration of all solutes in the urine (urine density:water density) - provides information on kidney’s ability to concentrate urine
  • osmolality high (dilute urine)
  • urinary sodium low (sodium reabsorbed)
  • fractional excretion of sodium low (sodium reabsorbed)
  • increased urea & creatinine (confirms acute kidney injury)
  • no haematuria
  • no proteinuria

Blood test:

  • ?hyperkalaemia
  • ?hyponatraemia
  • ?hypocalcaemia/hypophosphataemia
  • normal microscopy
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7
Q

How is the fractional excretion of sodium calculated? What can affect this apart from acute kidney injury?

A

[Na+]urine/[Na+]plasma
——————————— x 100
[creatinine]urine/[creatinine]plasma

Fe(Na+) < 1

  • early post-renal acute kidney injury
  • hepatorenal syndrome
  • acute glomerulonephritis (renal acute kidney injury)
  • early rhabdomyolysis (renal acute kidney injury)
  • hypercalcaemia
  • vasoactive drugs e.g. contrast, cyclosporin, (nor)adrenaline

Fe(Na) > 1 (impaired concentrating ability)

  • elderly
  • chronic kidney injury
  • diuretics
  • glycosuria
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8
Q

Can pre-renal acute kidney injury develop into renal acute kidney injury?

A

Yes

Acute tubular necrosis caused by hypoxia

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9
Q

What are some of the causes of renal acute kidney injury?

A

Tubular (ATN - acute tubular necrosis)

  • sepsis
  • ischaemia
  • nephrotoxins

Glomerular

  • acute glomerulonephritis
  • thrombosis
  • (haemolytic) uraemic syndrome

Interstitial

  • autoimmune (SLE, vasculitis, Wegener’s granulomatosis, cryoglobulinaemia, etc.)
  • infection
  • drugs e.g. NSAIDs

Vascular

  • malignant hypertension
  • renal artery stenosis/obstruction
  • cryoglobulinaemia
  • vasculitis (associated with anti-neutrophil cytoplasmic antibody - ANCA)

Eclampsia

Diabetes

Haematological malignancies

+ anti-rejection drugs e.g. cyclosporin, tacrolimus (calcineurin inhibitor nephrotoxicity)

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10
Q

Does renal acute kidney injury caused by ATN respond to fluid resuscitation?

A

No

Damaged cells cannot reabsorb sodium and water efficiently OR expel excess water

Aggressive fluid resuscitation causes fluid overload

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11
Q

Why are renal tubular cells vulnerable to hypoxia?

A

ATP-dependent processes

Medulla is normally hypoxic anyway

note: tubular cells are present in urine in ATN due to falling off the basement membrane (but not due to necrosis; as the cells are apoptotic, which requires energy)

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12
Q

What symptoms are present in ATN?

A

Impaired tubular function:

  • increased frequency of urination
  • nocturia (altered diurnal concentrating ability)
  • acidosis
  • glycosuria with normal [glucose]blood (not due to glucose exceeding the renal threshold, due to reduced reabsorption of glucose in PCT)
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13
Q

What investigations and typical laboratory findings are found in ATN?

A

Urinalysis:

  • specific gravity normal
  • low osmolality (concentrated urine)
  • high [Na+]urine (sodium not reabsorbed)
  • high Fe(Na) (sodium not reabsorbed)
  • increased urea and creatinine (diagnosis of acute kidney injury)

Blood:

  • ?hyperkalaemia
  • ?hyponatraemia
  • ?hypocalcaemia/hyperphosphataemia
  • microscopy: muddy brown granular casts
  • renal biopsy
  • +++ haematuria
  • +++ proteinuria
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14
Q

What are some nephrotoxins which can cause ATN?

A

Endogenous:

  • myoglobin (rhabdomyolysis)
  • urate
  • bilirubin

Exogenous:

  • endotoxin
  • X-ray contrast (by expanding volume)
  • drugs e.g. ACE inhibitors, aminoglycosides (gentamicin), NSAIDs (by compromising autoregulation)
  • weedkillers, antifreeze
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15
Q

What is rhabdomyolysis? What is the treatment?

A

Muscle necrosis (e.g. due to crush injury) causes myoglobin release

Causes ATN due to nephrotoxic effect & obstruction

Aetiology:

  • earthquakes
  • drug users (unconscious and don’t move)
  • elderly (fall and can’t get up)

Myoglobinuria - “coca-cola” coloured urine

Treatment: forced alkaline diuresis

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16
Q

What is acute glomerulonephritis? What are the typical laboratory findings?

A

Inflammation of glomerulus caused by autoimmune disorders

Primary: disease only affects kidneys e.g. IgA nephropathy

Secondary: systemic autoimmune disease affects kidneys e.g. SLE, vasculitis, Wegener’s granulomatosis

+++ haematuria
+++ proteinuria
RBC casts on microscopy (RBCs stick to the tubular protein Tamm-Horsfall protein)

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17
Q

What is haemolytic uraemic syndrome? How does this compare to non-haemolytic uraemic syndrome?

A

Sudden, rapid destruction of RBCs causes acute kidney injury due to obstruction of small arteries in kidneys

Causes:

  • septicaemia
  • eclampsia
  • drugs
  • microangiopathic haemolytic anaemia
  • thrombocytopenia

MEDICAL EMERGENCY

  • diarrhoea associated HUS (E. coli) = supportive (fluid & electrolyte balance, antihypertensives, dialysis)
  • pneumococcus associated HUS (S. pneumoniae) = avoid plasmapheresis & wash blood products
  • atypical/non-diarrhoea associated HUS = plasmapheresis

Increased [urea] in blood

Non-haemolytic uraemic syndrome due to impaired excretion of urea

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18
Q

What can cause acute tubulo-interstitial nephritis?

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A

Infection (acute pyelonephritis)

Toxins e.g. antibiotics, NSAIDs

note: toxin-dependent acute tubulo-interstitial nephritis is not dose-dependent (can occur with low doses/a long time after the first dose)

19
Q

What is cryoglobulinaemia?

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A

Presence of cryoglobulins in serum (Igs which precipitate reversibly at low temperatures) which can cause systemic inflammation and vasculitis (affecting kidneys & skin)

e.g. purpura, weakness, arthralgia

20
Q

What can cause post-renal acute kidney injury?

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A

Obstruction with continuous urine production -> increased intraluminal pressure -> dilatation of renal pelvis (hydronephrosis) -> reduced renal function

Obstruction within lumen:

  • calculi (must be in both renal pelves or ureters, neck of bladder, or in urethra)
  • thrombus
  • papillary necrosis (infection/ischaemia damages papillae via coagulative necrosis -> sloughed papillae cause obstruction)
  • tumour (renal pelvis, ureter, bladder)

Obstruction within wall of tubule (more freq. cause CKD):

  • congenital (pelviureteric neuromuscular dysfunction, megaureter, neurogenic bladder)
  • ureteric stricture e.g. post-TB

Pressure from outside lumen:

  • prostatic hypertrophy
  • tumours
  • aortic aneurysm (causes fibrosis which constricts around ureter)
  • diverticulitis
  • accidental ligation of ureter
21
Q

What investigation is required in post-renal acute kidney injury?

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A

Ultrasound to detect obstruction

[K+]urine & [K+]blood (!risk of asystole)

22
Q

What are some additional systemic systems which can be caused by acute kidney injury?

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A

Metabolic bone disease (vitamin D not being hydroxylated by kidney)

Anaemia (reduced EPO secretion -> reduced erythropoiesis)

Hypertension (increased renin secretion)

UTIs

Acidosis -> Kussmaul’s breathing (slow, deep respiration associated with acidosis)

Oedema

note: 5l of fluid needs to be retained before oedema will result

23
Q

What are some of the important management concerns in pre-renal acute kidney injury?

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A

? severe vascular disease

? hypovolaemic shock = cool peripheries, increased bpm, reduced BP, postural hypertension, low JVP, increased skin turgor, dry axillae

? cardiogenic shock

? septic shock = pyrexia, rigors, vasodilatation = warm peripheries, rapid capillary refill, hypotension, bounding pulse

24
What are some of the important management concerns in renal acute kidney injury?
? nephrotoxins (drugs, sepsis, myoglobin) ? ATN established ? parenchymal renal disease other than ATN (multi-system disease would suggest glomerulonephritis, UTI, drugs)
25
What are some of the important management concerns in post-renal acute kidney injury?
? renal tract obstruction: - ?anuria - ?prostatism (rectal exam) ? bladder catheter obstruction ? pain ? urine flow disturbance ? single functioning kidney ? history of renal stones ? previous pelvic/abdominal surgery ? palpable bladder ? pelvic/abdominal masses
26
What are some signs of volume overload to look for when treating acute kidney injury?
Gallop rhythm BP may be high, normal, or low Raised JVP Pulmonary oedema (basal crackles & dyspnoea) Peripheral oedema (sacral/ankle) CXR
27
What is the established management for acute kidney injury?
Volume overload hyperkalaemia: - restrict dietary sodium & water - ?diuretics (nephrotoxicty, K+ sparing) Hyperkalaemia: - calcium gluconate (stabilises heart- check ECG after admission) - restrict dietary potassium - stop K+ sparing diuretics - exchange resin - dextrose + insulin (insulin drives K+ into cells - buys time; dextrose prevents resultant hypoglycaemia) - beta-2-agonists? Acidosis: - sodium bicarbonate (if low) - restrict proteins Nutrition: enteral/paraenteral nutrition Dialysis indicated when: - hyperkalaemia not corrected by treatment - metabolic acidosis & sodium bicarbonate cannot be given - fluid overload not corrected by diuretics - presence of nephrotoxins e.g. aspirin overdose, antifreeze (ethylene glycol) - signs of uraemia present (pericarditis, reduced consciousness, intractable nausea & vomiting)
28
What is the prognosis for ATN?
Mortality: ~30%-80%, increased risk lasts for a year afterwards, risk of developing CKD Uncomplicated ATN: 2-3 weeks recovery (if no additional kidney insult e.g. episodes of hypotension) ATN + hypotension + dialysis: prolongs recovery (ischaemic lesions)
29
What can cause red/brown urine?
Haemoglobinuria Myoglobinuria Food dye consumption e.g. beetroot
30
What are some of the causes of microscopic haematuria?
- urinary infection - polycystic kidneys - renal calculi - renal/bladder tumours - arteriovenous malformations - kidney/glomerular disease (brown/smoky coloured urine, clots unusual, urinary stream entirely red)
31
What are some of the causes of macroscopic haematuria?
Glomerular (painless) IgA nephropathy + upper resp. tract infection
32
What are some of the causes of heavy proteinuria?
Reduced oncotic pressure e.g. loss of Igs (due to infection), loss of coagulation cascade proteins (increases thrombus risk) Urine can appear frothy
33
What is nephritic syndrome?
Inflammation of glomerulus which can be caused by post-streptococcal glomerulonephritis (children) or by other glomerulonephritides Renal biopsy required to diagnose - rapid onset - oliguria - hypertension - generalised oedema - haematuria (smoky brown) (therefore more damage required to cause than nephrotic syndrome) Level of damage required to cause inevitably reduces GFR
34
What is nephrotic syndrome?
Glomerular disease which causes proteinuria (hypoalbuminaemia -> oedema) and hyperlipidaemia (due to damaged foot processes -> "leaky filter") note: no orthopnoea (can lie down, therefore oedema can appear in the face and the ankles) Renal biopsy required to diagnose
35
What is rapidly progressive glomerulonephritis?
Glomerular injury so severe that renal function deteriorates over days, causing a uraemic emergency Associated with cresenteric glomerulonephritis Can be associated with systemic vasculitis (inflammatory response crushes glomerulus so fibrin leaks out) Renal biopsy required for diagnosis
36
What is the difference in the cause of vascular damage in acute and chronic kidney damage?
Expansion on interstitium compresses vascular structures Acute = due to oedema Chronic = due to fibrin deposition
37
What are the common primary and the secondary causes of nephrotic syndrome?
PRIMARY (disease just targets glomerulus): - minimal change glomerulonephritis - focal segmental glomerulosclerosis - membraneous glomerulonephtritis SECONDARY (targets other tissues - systemic) - diabetes mellitus - amyloidosis
38
Outline the mechanism and progression of minimal change glomerulonephritis.
Unknown circulating factor damages podocytes which retreat into the cytoplasm, causing proteinuria - no immune complex deposition - basement membrane still intact (no haematuria) - usually occurs in childhood/adolescence (incidence increases with age) Progression: - responds to steroids (large dose of steroids given to children with proteinuria without need to investigate cause) - usually does not progress to renal failure - may recur
39
Outline the mechanism and progression of membranous glomerulonephritis.
Immune complexes (IgG-antibody) deposit in basement membrane of glomerulus/already present in basement membrane of glomerulus bind to antibodies, causing damage ``` PRIMARY = antigens present in basement membrane SECONDARY = circulating antigens deposit in basement membrane (associated with autoimmune disorders e.g. lymphoma, SLE, malaria) ``` Progression: - commonest cause of nephrotic syndrome in adults in UK - 1/3 of patients improve, 1/3 have proteinuria, 1/3 develop renal failure - does not respond to steroids - new basement membrane laid down -> causes "spiky" irregular basement membrane on silver stain histology
40
Outline the mechanism and progression of focal change glomerulonephritis.
Circulating factors damage podocytes, causing segmental scarring Progression: - occurs in adults - causes proteinuria, not haematuria (nephrotic) - develops into renal failure - kidney transplant would also be damaged (circulating factor)
41
How does diabetes mellitus damage the glomeruli?
In general reduces kidney function Accumulation of collagen in basement membrane of glomeruli (due to microvascular effects of disease) ---> basement membrane thickening - mesangial sclerosis ---> characteristic nodules - scarring causes progressive proteinuria (by affecting turnover of collagen in the basement membrane, despite overall thickening) - develops into renal failure
42
Give some examples of diseases which cause haematuria but are not classified as nephritic syndromes.
IgA nephropathy = IgA deposits are trapped in glomeruli (IgA not as easily cleared as IgG) causing (in)visible haematuria +/- proteinuria - most common glomerular cause of haematuria - associated with mucosal infections (due to IgA) - variable histological features e.g. expansion of mesangium -> fibrin deposition - significant proportion progress to renal failure - no effective treatment Thin glomerular basement membrane disease = benign, familial condition causing an abnormally thin basement membrane in glomeruli ---> isolated haematuria Hereditary nephropathy (Alport's syndrome) = X-linked disorder causing abnormal collagen IV (found in basement membrane) ---> deafness & abnormal glomerular basement membrane (split & laminated) ---> renal failure
43
What can cause nephritic syndrome?
Goodpasture's syndrome (anti-GBM) = autoantibody to collagen IV causes acute onset of severe nephritic syndrome and rapid kidney failure - classically described in association with pulmonary haemorrhage in smokers (anti-GBM worsens damage caused by smoking in lungs) - treated EARLY with immunosuppression and plasmapheresis - IgG deposits in glomerulus Vasculitis = group of systemic disorders (e.g. Wegener's granulomatosis, microscopic polyangitis, etc.) which destroy blood vessels by inflammation - no immune complex deposition - associated with anti-neutrophil cytoplasmic antibody (ANCA) ---> inappropriate neutrophil activation ---> vessel damage - appears with segmental necrosis & cresenteric glomerulonephritis - treatable EARLY
44
Define plasmapheresis.
The removal, treatment, and return of plasma to the blood circulation

Urinary System (16 decks)

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