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Urinary System > AKI > Flashcards

AKI Flashcards

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?

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?

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?

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?

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?

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?

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
Q

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

A

? nephrotoxins (drugs, sepsis, myoglobin)

? ATN established

? parenchymal renal disease other than ATN (multi-system disease would suggest glomerulonephritis, UTI, drugs)

25
Q

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

A

? 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
Q

What are some signs of volume overload to look for when treating acute kidney injury?

A

Gallop rhythm

BP may be high, normal, or low

Raised JVP

Pulmonary oedema (basal crackles & dyspnoea)

Peripheral oedema (sacral/ankle)

CXR

27
Q

What is the established management for acute kidney injury?

A

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
Q

What is the prognosis for ATN?

A

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
Q

What can cause red/brown urine?

A

Haemoglobinuria

Myoglobinuria

Food dye consumption e.g. beetroot

30
Q

What are some of the causes of microscopic haematuria?

A
  • 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
Q

What are some of the causes of macroscopic haematuria?

A

Glomerular (painless)

IgA nephropathy + upper resp. tract infection

32
Q

What are some of the causes of heavy proteinuria?

A

Reduced oncotic pressure e.g. loss of Igs (due to infection), loss of coagulation cascade proteins (increases thrombus risk)

Urine can appear frothy

33
Q

What is nephritic syndrome?

A

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
Q

What is nephrotic syndrome?

A

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
Q

What is rapidly progressive glomerulonephritis?

A

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
Q

What is the difference in the cause of vascular damage in acute and chronic kidney damage?

A

Expansion on interstitium compresses vascular structures

Acute = due to oedema

Chronic = due to fibrin deposition

37
Q

What are the common primary and the secondary causes of nephrotic syndrome?

A

PRIMARY (disease just targets glomerulus):

  • minimal change glomerulonephritis
  • focal segmental glomerulosclerosis
  • membraneous glomerulonephtritis

SECONDARY (targets other tissues - systemic)

  • diabetes mellitus
  • amyloidosis
38
Q

Outline the mechanism and progression of minimal change glomerulonephritis.

A

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
Q

Outline the mechanism and progression of membranous glomerulonephritis.

A

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
Q

Outline the mechanism and progression of focal change glomerulonephritis.

A

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
Q

How does diabetes mellitus damage the glomeruli?

A

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
Q

Give some examples of diseases which cause haematuria but are not classified as nephritic syndromes.

A

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
Q

What can cause nephritic syndrome?

A

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
Q

Define plasmapheresis.

A

The removal, treatment, and return of plasma to the blood circulation

Urinary System (16 decks)

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