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Year 3 Metabolic -Gemma > Kidneys > Flashcards

Kidneys Flashcards

1
Q

top 3 most common causes of AKI

A

1) sepsis, 2) major surgery, 3) cardiogenic shock

(4) hypovolaemia, 5)drugs, 6) hepatorenal syndrome)

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2
Q

What is the following:
a subset of acute renal railure due to acute, irreversible damage to the kidney parenchyma whether in the de novo acute setting or in addition to a previously existing kidney disease.

A

intrinsic renal failure

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3
Q

name some risk factors for acute kidney injury

A

preexisting CKD/kidney impairment, age, male sex, comorbidity(cancer, cardiovascular disease, diabetes, hypertension etc)

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4
Q

what 3 life-threatening conditions can arise due to AKI?

A

volume overload
hyperkalaemia
metabolic acidosis

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5
Q

name the 4 principal prerenal causes of AKI

A

1) hypovolaemia (haemorrhage, vomiting, diarrhoea)
2) renal hypoperfusion(NSAIDs/selective COX 2 inhibs, ACE inhibs/Angiotension 2r blockers, AAA, renal artery stenosis/occlusion, hepatorenal syndrome)
3) hypotension(cardiogenic shock, distributive shock (anaphylaxis, sepsis)
4) oedematous states (cardiac failure, hepatic cirrhosis, nephrotic syndrome)

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6
Q

name 4 drugs that can lead to renal hypoperfusion (pre-renal cause of AKI)

A

NSAIDs (e.g. paracetamol, aspirin, diclofenac, ibuprofen)
Selective COX 2 inhibitors (celebrex, celecoxib–>reduce risk of peptic ulceration)
ACE inhibitors (-prils, e.g. ramipril)
Angiotensin 2 receptor antagonists (ARBs) (losartan, candesartan, valsartan)

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7
Q

name the 4 principal instrinsic (renal) causes of AKI

A

1) glomerular disease(inflammatory or thrombotic)
2) interstitial nephritis (drug induced, infiltrative, granulomatous, infection related)
3) tubular injury (ischaemia, toxins, metabolic, crystals)
4) vascular (vasculitis, cryoglobulinaemia, polyarteritis nodosa, thrombotic microangiography, cholesterol emboli, renal artery/vein thrombosis)

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8
Q

name the 2 principal postrenal causes of acute renal failure

A

intrinsic(intraluminal, intramural)

extrinsic(pelvic malignancy, retroperitoneal fibrosis)

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9
Q

what urinanalysis investigations are most useful in AKI?

A

Microscopy: red cell casts=glomerularnephritis
Dipstick: blood and/or protein on suggests inflammatory process

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10
Q

What biochemistry investigations are most useful in AKI?

A

serial urea and creatinine= monitor progress
serial electrolytes= check for metabolic consequences of AKI, including hyperkalaemia, hpocalcaemia, hyperphosphataemia, and metabolic acidosis.
blood gases, serum bicarbonate= check for metabolic acidosis
creatine kinase, myoglobinuria= very high creatine kinase and myoglobinuria suggests rhabdomyalsis
C reactive protein=non specific marker of infection/inflammation
serum immunoglobulins, serum protein electrophoresis, Bence Jones proteinuria=immune paresis, monoclonal band on serum electrophoresis and bence jones proteinuria all suggest myeloma.

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11
Q

What haematology investigations are most useful in AKI?

A

FBC, blood film=oesinophilia may be present in acute interstitial nephritis, or vasculitis. Thrombocytopenia and red cell fragments suggest thrombotic microangiopathy.
Coagulation studies= DIC associated with sepsis.

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12
Q

what immunology investigations are most useful in AKI?

A

ANA(antinuclear antibodies) +ve in SLE and some other autoimmune disorders.
anti-dsDNA antibodies=specific for SLE
Prescence of :ANCA (antineutrophil cytoplasmic antibodies); also antiproteinase 3 (PR3) and antimyeloperoxidase antibodies (MPO) are alll assoc with systemic vasculitis.
Low complement concentrations (hypocomplementaemia)=low in SLE< acute postinfectious glomerulonephritis and cryoglobulinaemia.
antiglomerular basement(anti-GBM) antibodies=present in goodpasture’s disease

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13
Q

what radiological investigation is most useful in AKI?

A

renal ultrasound scan=checks renal size, symmetry, and for evidence of obstruction.

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14
Q

what are the 4 classifications of intrinsic renal failure?

A

1) glomerular-immune mediated (nephrotic syndromes), drugs
2) tubular-acute tubular necrosis, drugs
3) interstitial-pyelonephritis, autoimmune disease (e.g. SLE), malignancy
4) vascular-vasculitis, thromboembolic disease, malignant HTN

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15
Q

what is the most common cause of intrinsic renal failure in hospital?

A

acute tubular necrosis (usually ischaemic).

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16
Q

what leads to acute on chronic renal failure?

A

diabetic nephropathy
hypertension-related intrinsic renal failure
nephrotoxicity

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17
Q

what do these 3 histological features appear in?

1) expansion of mesangium (due to hyperglycaemic accumulation of tissue)
2) thickening of GBM
3) glomerular sclerosis (due to intraglomerular hypertension)

A

diabetic nephropathy

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18
Q

what leads to diagnosis of diabetic nephropathy?

A

A long-standing diabetic (type 1 or 2) develops all 3 of the following:

1) persistent albuminuria(more than 300mg/24 hours at least 2 occasions, 3-6 months apart)
2) progressive reduction of eGFR
3) hypertension

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19
Q

what is the clinical presentation of diabetic nephropathy?

A 
foamy urine
persistent proteinuria in a diabetic
diabetic retinopathy
fatigue
foot oedema assoc with hypoalbuminaemia
other diabetes assoc disorders (PVD, HTN, coronary artery disease)
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20
Q

what is the difference between the management of type 1 and type 2 diabetics with diabetic nephropathy?

A

type 1= microalbuminuria in the early phase may be reduced with ACEi
type 2=most important goal is to achieve BP and blood sugar control ASAP.

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21
Q

what are the four different ways in which glomerularnephritis can present?

A

nephritic syndrome (haematuria and some proteinuria)
nephrotic syndrome (no haematuria and lots of proteinuria)
AKI with mild hypertension
chronic nephritic syndrome(e.g. lupus, amyloid)

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22
Q

what is the pharaoh mnemonic for nephritic syndrome?

A 
Proteinuria
Haematuria
Azotaemia
RBC casts- 5 RBC/high powered microscope
Anti-streptoclysin O titres(if post-strep)
Oliguria
Hypertension (salt and water retention)
23
Q

Name 5 conditions that manifest as nephritic syndrome.

A 
post-strep glomerulonephritis
rapid progressive glomerulonephritis
berger's disease (IgA nephropathy)
henoch-schonlein purpura
multiple myeloma
24
Q

Name 4 conditions that manifest as nephrotic syndrome.

A

minimal change disease
focal segmental glomerulosclerosis
membranous glomerulonephritis
membranoproliferative glomerularnephritis

25
Q

which 2 drug classes are absolutely contraindicated in renal artery stenosis?

A

ACE inhibitors and ARBs (angiotensin receptor blockers)

26
Q

disease that affected the small vessels of the kidneys predominantly. There is inflammatory infiltrate within the walls of vessels.
It is classified by serological markers (is ANCA present/absent? Are there specific immune complexes involved?)
Diagnosis is made as a last resort (rule out all other causes of symtoms).

A

vasculitis.
Treatment=steroids.

Small vessels vasculitudes:

ANCA-assoc:
wegener's granulomatosis
microscopic polyangiitis
churg-strauss syndrome
renal limited vasculitis
non-ANCA assoc:
goodpasture's syndrome
cryoglobulinaemia
lupus
henoch-schonlein purpura
27
Q

nephritic syndrome presentation
classically occurs after strep pyogenes infection
immunofluorescence shows coarse granular IgG or C3 deposits
labs show increased red cells and casts, increased ISO titer

A

post-streptococcal glomerulonephritis

28
Q

nephritic syndrome presentation
goodpasture’s disease is in this category
immunofluorescence shows smooth and linear IgG deposits
treat with prednisolone and plasmapharesis

A

rapidly progressive glomerulonephritis(aka crescentic glomerularnephritis)

29
Q

nephritic syndrome presentation
IgA deposits in the mesangium
presents with recurrent haematuria and low grade proteinuria
25% can progress to renal failure, otherwise harmless
treat with prednisolone

A

berger’s disease(aka IgA nephropathy)

30
Q

nephritic syndrome presentation
always in children
type of IgA nephropathy
presents with abdo pain, GI bleed, vomiting and haematuria
classically can find palpable purpura on buttocks and legs
self-limiting disease, requires no steroids

A

henoch-scholein purpura

31
Q 
nephritic syndrome presentation
bence jones protein in the urine
assoc with hypercalcaemia
susceptible to encapsulated bacteria (due to defect in antibody production)
treatment depends on the underlying type
A

multiple myeloma

32
Q

nephrotic syndrome presentation
occurs in young children
treat with prednisolone

A

minimal change disease

33
Q

nephrotic syndrome presentation
similar to minimal change disease, but occurs in adults
common in young, hypertensive males
treat with prednisolone and cyclophosphamide

A

focal segmental glomerulosclerosis

34
Q

nephrotic syndrome presentation
most common primary nephritic syndrome in adults
slowly progressive disorder
many causes (HBV, HCV, syphilis, malignancies, SLE)
treat with prednisolone and cyclophosphamide
50% of cases progress to end-stage renal failure

A

membranous glomerulonephritis

35
Q

nephrotic syndrome presentation
type 1 is slowly progressive, whilst type 2 is aggressive
autoantibody against C3 convertase(low C3 levels)
treat with prednisolone and plasmapharesis

A

membranoproliferative glomerulonephritis

36
Q

what are the 2 classifications of nephrotic syndrome?

A 
primary glomerular disease (idiopathic), eg. minimal change disease, focal segmental glomerulosclerosis, etc.
secondary disease(systemic disease (e.g. DM, SLE, amyloidosis), cancer (esp. membranous nephrotic syndrome), severe systemic infection.
37
Q 
what syndrome is this?
haematuria
limited proteinuria
slight oedema
hypertension
oliguria
damage to podocytes, deposition of matrix
A

nephritic syndrome

38
Q 
what syndrome is this?
no haematuria
proteinuria >3.5g/day (significant)
gross oedema
decreased albumin
hypercoagulation
hyperlipidaemia
inflammation of glomeruli and blood vessels
A

nephrotic syndrome

39
Q

name the 5 functions of the kidneys.

A
  1. excretion of waste products
  2. regulation of acid-base balance (and water homeostasis)
  3. endocrine functions (RAAAS, EPO, ADH-aldosterone complex)
  4. metabolism of vit D and calcium
  5. gluconeogenesis in fasting state (involving small molecular weight proteins)
40
Q

findings in urine microscopy when diagnosing type of renal failure: scant hyaline casts

A

pre-renal AKI

41
Q

findings in urine microscopy when diagnosing type of renal failure: many hyaline casts, RBC present.

A

post-renal AKI

42
Q

findings in urine microscopy when diagnosing type of renal failure: epithelial cells, muddy-brown, coarsely granular casts, WBCs present, low-grade proteinuria

A

Acute tubular necrosis

43
Q

findings in urine microscopy when diagnosing type of renal failure: WBCs and RBCs present, epithelial cells, eosinophils, low-moderate proteinuria

A

allergic interstitial nephritis

44
Q

findings in urine microscopy when diagnosing type of renal failure: RBC casts, dysmorphic red cells, moderate-severe proteinuria

A

glomerulonephritis

45
Q

what antibiotics are nephrotoxic?

A

aminoglycosides (gentamicin, neomycin, tsreptomycin). Act on gram -ve bacteria. Broad spectrum. Cause renal vasoconstriction. This can cause (ischaemic) acute tubular necrosis.

46
Q 
which intrinsic renal disease does this indicate?
eosinophilia
haematuria
pyuira(pus in urine)
WBCs
RBCs
white cell casts
A

acute interstitial nephritis

47
Q

which intrinsic renal disease does this indicate?
muddy brown, granular, epithelial cell casts
tubular cells

A

acute tubular necrosis

48
Q

which intrinsic renal disease does this indicate?
haematuria
proteinuria
dysmorphic RBCs

A

glomerulonephritis

49
Q

how do you distinguish between acute and chronic renal failure?

A

long duration of symptoms, nocturia, absence of acute illness, anaemia, hyperphosphataemia, hypocalcaemia= all suggest chronic renal failure (although similar findings can occur in AKI as complications).
reduced renal size and cortical thickness on renal US scan=characteristic of chronic renal failure; however renal size is typically preserved in diabetics.
BASICALLY: history and examination previous creatinine measurements, small kidneys on USS.

50
Q

how do you exclude diagnosis of obstruction as a cause of AKI?

A

-check for palpable bladder
-ask about previous stones, and bladder outflow obstruction symptoms(weak stream, feeling of incomplete emptying, hesitancy)
-renal US scan checks for renal dilatation and calyces; however obstruction can still be present without dilation (esp in malignancy).
COMPLETE ANURIA=suggests renal tract obstruction
BASICALLY: complete anuria?, palpable bladder, renal ultrasound

51
Q

how do you find out the patient’s volume status?

A

hypovolaemia=postural hypotension and low venous pressure
hypervolaemia=high venous pressure, pulmonary crepitations.

high levels of ADH-->increased tubular reabsorption of water and urea, and disproportionate rise in urea:creatinine ratio.
increased catabolism(e.g. sepsis) also raises urea concentrations, as well as ingestion of protein (e.g. upper GI bleed)
use of diuretics often makes interpretation of urinary indices uninterpretable.

BASICALLY=pulse, JVP, postural BP, daily weghts, fluid balance, disproportional increase in urea:creatinine ratio, urinary sodium concentration(unless on diuretics), fluid challenge(=rapid administration of fluid bolus to critically ill patient. Response to this must be assessed.)

52
Q

how do you check if other renal parenchymal disease exists (other than acute tubular necrosis)?

A

Ask about rashes, arthralgia, myalgia.
Use of antibiotics and NSAIDs->can lead to acute interstitial nephritis.

blood and urine on dipstick, as well as dysmorphic cells and red cell casts indicates glomerulonephritis

eosinophils indicates acute interstitial nephritis

BASICALLY: history and examination(systemic features?), urine dipstick and microscopy(red cells/red cell casts, eosinophils, proteinuria)

53
Q

how do you check if a major vascular occlusion has occured?

A

occlusion of normal renal artery=>loin pain and haematuria
occlusion of previously stenosed renal artery=>can be asymptomatic, leaving the patient dependent on one functioning kidney.
check for renal asymmetry on imaging: especialy when a patient is known to have vascular disease elsewhere.
cholesterol embolism=> can occur after angiography/vascular surgery/anticoagulation/thrombolysis.
Characterised by the classic triad of livedo reticularis (rash), acute renal failure, and eosinophilia. Onset 1-4 weeks post-intervention.

BASICALLY: is there: atherosclerotic vascular disease, renal asymmetry, loin pain, macroscopic haematuria or complete anuria?

Year 3 Metabolic -Gemma (7 decks)

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