renal investigations + findings Flashcards

1
Q

Nodular glomerulosclerosis (Kimmelstein- Wilson lesions)

A

Diabetic nephropathy

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2
Q

management of diabetic nephropathy?

A
  • tight glycemic control
  • ACEI/ ARB (aim for BP <130/80)
  • statins
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3
Q

investigations chronic pyelonephritis?

A
  • micturating cystography
  • renal USS
  • CT urogram

may all be useful

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4
Q

most common cause of chronic pyelonephritis?

A
  • reflux nephropathy
  • vesico ureteric reflex (genetic disposition) usually presenting in childhood with recurrent infection but often asymptomatic
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5
Q

investigations renal artery stenosis?

A

1st= MR angiography or CT angiography

Duplex USS (difficult in obese patients)

-renin: aldosterone (both high)

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6
Q

renal artery stenosis treatment

A
  • ACEI (contraindicated in bilateral disease)
  • statin
  • antiplatelets

surgical angioplasty +/- stent in severe cases

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7
Q

string bean appearance on angiography

A

fibromuscular dysplasia

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8
Q

string bean appearance on angiography

-what treatment?

A

-this is fibromuscular dysplasia (rare cause of renal artery stenosis)

treatment= surgical stenting

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9
Q

diabetic nephropathy on USS

A

bilaterally enlarged kidneys

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10
Q

what type of glomerulonephritis causes haematuria

A

nephritic syndrome

-mesangial cell damage/ endothelial (vasculitis) is proliferative leading to haematuria

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11
Q

what type of glomerulonephritis causes proteinuria?

A
  • nephrotic syndrome

- prodocyte damage (non priliferative atrophy) causes proteinuria

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12
Q

nephrotic syndrome presentation?

A
  • proteinuria (>3g/day)
  • hypo albuminaemia (<30g/l)
  • eodema
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13
Q

nephritic syndrome presentation?

A
  • oliguria
  • haematura (red cell casts in urine)
  • hypertension
  • some proteinuria/ fluid retention
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14
Q

light microscopy shows mesengial cell proliferation + immunofluorescence shows IgA and C3 deposits

A

IgA nephropathy

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15
Q

podocyte fusion and foot process effacement?

A

minimal change

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16
Q

minimal change treatment

A

1st- steroids

cyclophophamide= if steroid resistant

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17
Q

IgA nephropathy treatment?

18
Q

minimal change- nephritic or nephrotic?

19
Q

FSGS- nephritic or nephrotic

20
Q

light microscopy= focal/ segmental sclerosis + hyalinosis

electron microscopy= effacement of foot processes

immunofluorescence= minimal Ig/ complement deposition

A

focal segmental glomerulosclerosis

21
Q

focal segmental glomerulosclerosis treatment

A

steroids +/- immunosuppression

22
Q

membranous nephropathy- nephritic or nephrotic

23
Q

electron microscopy= thick BM with sub epithelial electron complex depositions (spike and dome appearance)

A

-membranous nephropathy

24
Q

treatment- membranous nephropathy

A
  • ACEI/ ARBs
  • immunosuppression (steroids + cyclophosphamide +/- B cell monoclonal antibodies)

1/3rd spontaneously resolve, 1/3rd respond to immunosuppression, 1/3 rd end stage renal failure

25
patient just started amoxicillin, presents with fever, rash, arthralgia, elevated creatinine urine test: - raised eosinophils - white cell casts - sterile pyuria
acute interstitial nephritis
26
urinary ACR >30mg/mmol + hypertension treatment?
ACIE (ramipril)
27
what formula is used to help estimate GFR?
Modification of Diet in Renal Disease Equation (MDRD): - serum creatinine - age - gender - ethnicity used as serum creatinine may not provide an accurate estimate of renal function due to differences in muscle mass
28
- nephritic | - rapid decline in renal function + glomerular epitherlial crescent formation on biopsy
-rapidly progressive glomerulonephritis
29
treatment- radpidly progressive glomerulonephritis
-immunosuppression (steroids + cyclophosphamide + azathioprine) +/- plasma + temporary RRT
30
congo red staining | -apple green birefringence under polarised light
amyloidosis
31
longitudinal splitting of lamina densa seen on electron microscopy (characterised by basket weave appearance) - microscopic haematuria - progressive renal failure - bilateral sensorineural deafness - ocular manifestations - proteinuria
Alport's syndrome (X linked dominant defect in type IV collagen)
32
indications for dyalisis?
AEIOU - Acidosis (PH <7.15) - Electrolyte abnormalities (K > 7 or resistant to treatment) - Intoxication (overdose of certain meds) - Oedema (severe and unresponsive pulmonary oedema) - Uraemia > 40 (seizures, loss of conscioussness)
33
causes of interstitial nephritis?
``` Drugs: (Not All Pills Fuck Renals) NSAIDS Allopurinol Penicillin Furesomide Rifampicin ``` Infection: -TB Systemic: -sarcoidosis
34
causes of tubular injury?
- iscaemia (prolonged renal hypoperfusion) - drugs (gentamycin) - contrast - rhabdomyolysis
35
treatment- hyperkalaemia?
- ECG + IV access - 10 ml 10% calcium gluconate (protect myocardium) - insulin actrapid 10 units + 50ml 50% dextrose or nebuliser salbutamol (short term shift)
36
hyperkalaemia- ECG findings
- tall tented T waves - small p waves - wide QRS
37
hypokalaemia- ECG findings
- U waves - small or absent T waves - prolonged PR interval - ST depression
38
findings of acute tubular necrosis
- AKI - muddy brown casts in urine - high urine sodium + low urine sodium (with poor response to fluid challenge)
39
findings in rhabdomyolysis?
- AKI - disproportionall raised creatinine - raised CK - metabolic acidosis - hyperkalaemia - high phosphate - low calcium - myoglobinuria Patient often has had a fall or been immobile for hours + is associated with statins
40
rhabdomyolysis treatment?
IV fluids +/- urinary alkalinisation
41
Drugs that should be stopped/avoided in AKI
- ARB - Diuretics - Trimethoprin (co trimoxazole) - Contrast - Gentamycin - NSAIDs - ACEI Avoid Drugs That Can Give Nasty AKIs
42
ascites treatment
spironolactone