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WFH > Renal 8/6/20 > Flashcards

Renal 8/6/20 Flashcards

1
Q

diagnostic criteria of AKI

A
  1. Rise in creatinine of 26 micromol/L or more in 48 hours
    OR
  2. ≥ 50% rise in creatinine over 7 days
    OR
  3. Fall in urine output to less than 0.5ml/kg/hour (for more than 6 hours in adults, 8 hours in children)
    OR
  4. ≥ 25% fall in eGFR in children / young adults in 7 days
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2
Q

symptoms of AKI

A

often asymptomatic at first

  • reduced urine output
  • pulmonary and peripheral oedema
  • arrhythmias (secondary to changes in potassium and acid-base balance)
  • features of uraemia (pericarditis/encephalopathy/pruritis)
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3
Q

normal urine output

A

1.5-2ml/kg/hr

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4
Q

causes of AKI

A

PRE-RENAL
- hypovolaemia secondary to dehydration/D&V/decreased cardiac output/sepsis
- renal artery stenosis
RENAL
- vascular eg. vasculitis
- tubular eg. rhabdomyolysis/tumour lysis/acute tubular necrosis/myeloma
- glomerular eg. glomerulonephritis
- interstitial eg. interstitial nephritis
POST-RENAL
- kidney stones
- compression of ureter/BPH

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5
Q

drug causes of AKI

A 
DIRECT EFFECT ON KIDNEY
- NSAIDs
- antibiotics (esp. aminoglycosides eg. gentamicin)
- chemo drugs
ACCUMULATION WITH RENAL DYSFUNCTION
- metformin
EFFECT ON RENAL/FLUID/ELECTROLYTE PHYSIOLOGY
- diuretics
- ACEIs
- ARBs
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6
Q

management of hyperkalaemia

A
  • insulin and dextrose (extracellular –> intracellular K+)
  • IV calcium gluconate (stabilises cardiac membrane)
  • salbutamol nebuliser (extracellular –> intracellular K+)
  • calcium resonium enema or oral (enema better) (slow working - not for emergency mx - aids K+ excretion)

treat underlying cause
haemodialysis if persistent

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7
Q

indications for dialysis

A
  • CKD5
  • refractory pulmonary oedema/fluid overload
  • persistent hyperkalaemia
  • severe metabolic acidosis
  • uraemia (encephalopathy/pericarditis)
  • drug overdose (BLAST - barbiturates, lithium, alcohol/ethylene glycol (antifreeze), salicylate (aspirin), theophylline)
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8
Q

risk factors for AKI

A
  • elderly
  • comorbidity eg. DM, HF, liver disease
  • previous AKI
  • CKD
  • cancer
  • post operative
  • medications
  • neuro/cog impairment - more prone to dehydration etc.
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9
Q

causes of false positive AKI

A
  • pregnancy
  • drugs - trimethoprim
  • contaminated sample
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10
Q

components of Fanconi syndrome

A

PPP AGO

  • type 2 (proximal) renal tubular acidosis
  • polyuria
  • phosphaturia
  • aminoaciduria
  • glycosuria
  • osteomalacia
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11
Q

causes of Fanconi syndrome

A
  • cystinosis (most common cause in children)
  • Sjogren’s syndrome
  • multiple myeloma
  • nephrotic syndrome
  • Wilson’s disease
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12
Q

cANCA with haematuria

A

Wegener’s - crescentic glomerulonephritis

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13
Q

sjogren’s autoantibodies

A

Mr Sjogren is a high (anti-)Ro(anti-)La

  • Anti-Ro
  • Anti-La
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14
Q

test for Wilson’s syndrome

A

high caeruloplasmin (copper carrying protein)

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15
Q

membranous glomerulonephritis markers

A
  • antiphospholipase A2 antibodies
  • basement membrane thickening on light microscopy
  • subepithelial spikes
  • low total T4
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16
Q

haemolytic uraemic syndrome markers

A 
Increased
- fragmented red cells
Decreased
- serum haptoglobins
- platelet count
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17
Q

nephrotic syndrome features

A
  1. Proteinuria (> 3g/24hr) causing
  2. Hypoalbuminaemia (< 30g/L) (& hyperlipidaemia)
  3. Oedema
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18
Q

causes of nephrotic syndrome

A
  • minimal change disease
  • membranous glomerulonephritis
  • focal segmental glomerulosclerosis
  • diabetic nephropathy
  • amyloidosis
  • post-streptococcal glomerulonephritis (CAN PRESENT AS NEPHRITIC TOO)
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19
Q

causes of minimal change disease

A
  • idiopathic
  • drugs: NSAIDs, rifampicin
  • malignancy: Hodgkin’s lymphoma, thymoma
  • infective: infectious mononucleosis
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20
Q

management of minimal change disease

A

steroid responsive - cyclophosphamide in resistant cases

2/3 will relapse

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21
Q

histology of minimal change disease

A
  • normal glomeruli on light microscopy

- fusion of podocytes and effacement of foot processes

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22
Q

causes of focal segmental glomerulosclerosis

A

typically affects young adults

  • idiopathic
  • secondary to other renal pathology e.g. IgA nephropathy, reflux nephropathy (kidney scarring secondary to vesicoureteric reflux)
  • HIV
  • heroin
  • Alport’s syndrome
  • sickle-cell
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23
Q

histology findings for focal segmental glomerulosclerosis

A
  • focal and segmental sclerosis and hyalinosis

- effacement of foot processes

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24
Q

causes of membranous glomerulonephritis

A
  • idiopathic: anti-phospholipase A2 antibodies
  • infections: hepatitis B, malaria, syphilis
  • malignancy: lung cancer, lymphoma, leukaemia
  • drugs: gold, penicillamine, NSAIDs
  • autoimmune diseases: systemic lupus erythematosus, thyroiditis, rheumatoid
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25
Q

management of membranous glomerulonephritis

A
  • fluid balance monitoring
  • ACEI/ARB (reduce proteinuria), then often resolves spontaneously
  • rituximab
  • corticosteroid AND cyclophosphamide (not needed unless progressive/severe)
  • anticoagulation in high risk pts
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26
Q

causes of nephritic syndrome

A
  • rapidly progressive glomerulonephritis (crescentic glomerulonephritis) due to Goodpasture’s, ANCA positive vasculitis, etc.
  • IgA nephropathy - (usually post viral)
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27
Q

post-strep glomerulonephritis vs IgA

A

both preceded by illness
- IgA = illness 1-2 days prior
- PSGN = illness ~2 weeks prior (and associated with proteinuria)
(post-strep GN = longer name longer onset)

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28
Q

fibromuscular dysplasia

A
  • cause of renal artery stenosis with ‘string of beads’ appearance
  • usually in young females
  • follows commencement of ACEI
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29
Q

rate of infusion of maintenance fluids

A

Maintenance fluids should be prescribed at a rate of 30 ml/kg/24hr

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30
Q

vitamin D deficiency in renal failure management

A

Alfacalcidol - used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys

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31
Q

complications of too much 0.9% saline

A

hyperchloraemic metabolic acidosis

- too many chloride ions, produces HCl

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32
Q

complications of Hartmann’s solution

A

contains K+ so can precipitate cardiac events in patients with deranged K+

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33
Q

maximum recommended rate of potassium infusion via a peripheral line is…

A

10 mmol/hour

- cardiac monitoring above 20mmol/hr (central line)

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34
Q

features of goodpasture’s syndrome

A
  • pulmonary haemorrhage - haemoptysis
  • followed by rapidly progressive glomerulonephritis
  • lethargy
  • anti-GBM antibodies
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35
Q

management of goodpasture’s syndrome

A
  • plasmapheresis
  • corticosteroid therapy
  • cyclophosphamide
36
Q

features of granulomatosis with polyangiitis (Wegener’s )

A
  • URT: epistaxis, sinusitis, nasal crusting
  • LRT: dyspnoea, haemoptysis
  • rapidly progressive glomerulonephritis
  • saddle nose deformity
  • also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
37
Q

investigations for granulomatosis with polyangiitis (Wegener’s)

A
  • cANCA positive in > 90%, pANCA positive in 25%
  • chest x-ray: wide variety of presentations eg. cavitating lesions
  • renal biopsy: epithelial crescents in Bowman’s capsule
38
Q

management of granulomatosis with polyangiitis (Wegener’s)

A
  • plasmapheresis
  • corticosteroid therapy
  • cyclophosphamide

poor prognosis

39
Q

renal features of ADPKD

A
  • hypertension
  • abdominal pain
  • chronic kidney disease
  • renal stones
  • haematuria
  • recurrent UTIs
40
Q

extra-renal complications of ADPKD

A
  • cysts: most commonly in liver but can get cysts in other organs particularly pancreas, seminal vesicles and vasculature
  • berry aneurysms: SAH risk
  • cardiovascular system: valvular dysfunction, murmur
41
Q

screening test for PKD (for family members)

A

US abdomen

  • 2 cysts, unilateral or bilateral, if aged < 30 years
  • 2 cysts in both kidneys if aged 30-59 years
  • 4 cysts in both kidneys if aged > 60 years
42
Q

ADPKD type 1 or 2

A 
Type 1 (chromosome 16)
- 85% cases
- develop renal failure earlier
Type 2 (chromosome 4)
- 15% cases
43
Q

management of PKD

A
  • symptom relief, eg. ACEIs
  • tolvaptan slows cyst growth in some
  • kidney transplant
  • dialysis
44
Q

ARPKD

A

chromosome 6

  • rare compared to ADPKD
  • ESRF in childhood, may have oligohydramnios due to poor kidney function in utero, can lead to Potter’s syndrome
  • commonly congenital hepatic fibrosis - varices/splenomegaly
  • picked up on US antenatal screening
45
Q

features of haemolytic uraemic syndrome

A
  • diarrhoea history within previous 2 weeks
  • acute kidney injury (high creatinine)
  • microangiopathic haemolytic anaemia
  • thrombocytopenia
46
Q

cause of haemolytic uraemic syndrome

A
  • shiga-toxin producing E. coli (follows diarrhoea)
47
Q

management of haemolytic uraemic syndrome

A
  • supportive
    > fluids
    > dialysis/blood transfusion if required
  • no role for Abx
  • plasma exchange in cases of severe HUS without diarrhoea
48
Q

thrombotic thrombocytopenic purpura features

A

The TRANF Pentad (TTP)

  • Thrombocytopenia
  • Renal failure
  • Anaemia
  • Neurological symptoms due to microemboli
  • Fever

schistocytes on blood film due to high vWF

49
Q

causes of TTP (thrombotic thrombocytopenic purpura)

A
  • post infection (typically urinary/GI)
  • pregnancy
  • drugs
  • other: tumours, SLE, HIV
50
Q

drugs causing TTP (thrombotic thrombocytopenic purpura)

A

POCCA

  • penicillin
  • oral contraceptive pill
  • ciclosporin
  • clopidogrel
  • aciclovir
51
Q

causes of DIC

A
  • sepsis
  • trauma
  • obstetric complications eg. HELLP syndrome
  • malignancy
52
Q

AKI or dehydration?

A

higher rise in urea than creatinine = likely dehydration

high rise in creatinine than urea = likely AKI

53
Q

causes of high anion gap acidosis

A
  • diabetic ketoacidosis
  • lactic acidosis (sepsis, salicylates (aspirin), shock)
  • methanol poisoning
  • ethlene glycol poisoning (antifreeze)
54
Q

high anion gap vs normal anion gap

A

high anion gap = increased organic acid production/ingestion

normal anion gap = loss of bicarbonate (eg. diarrhoea, renal tubular acidosis)

55
Q

causes of acute tubular necrosis

A 
There are two main causes of ATN; ischaemia and nephrotoxins:
- ischaemia
     > shock
     > sepsis
- nephrotoxins
     > aminoglycosides eg. gentamicin
     > myoglobin secondary to rhabdomyolysis/compartment syndrome
     > radiocontrast agents
56
Q

features of acute tubular necrosis

A 
- features of AKI: 
     > raised urea
     > creatinine
     > potassium
- muddy brown casts and high sodium in the urine
57
Q

causes of normal anion gap acidosis

A
  • renal tubular acidosis
  • diarrhoea
  • hyperosmolar hyperglycaemic state
  • Addison’s disease
  • pancreatic fistula
58
Q

features of renal tubular acidosis (all types)

A
  • hyperchloraemic metabolic acidosis (normal anion gap)
  • abdo discomfort
  • Kussmaul breathing
59
Q

renal tubular acidosis type 1 (distal)

A
  • inability to secrete H+ in distal tubule so less acidification of urine (urine pH >5.5 with systemic acidosis)
  • leads to hypokalaemia
  • complications include nephrocalcinosis and renal stones
  • causes include idiopathic, autoimmune, drugs
60
Q

renal tubular acidosis type 2 (proximal)

A
  • decreased HCO3- reabsorption in proximal tubule
  • leads to hypokalaemia
  • complications include osteomalacia
  • causes include Fanconi syndrome, Wilson’s disease, cystinosis, carbonic anhydrase inhibitors (acetazolamide, topiramate)
61
Q

renal tubular acidosis type 4 (hyperkalaemic)

A
  • reduction in aldosterone leads to reduction in ammonium excretion
  • causes hyperkalaemia
  • causes include hypoaldosteronism (Addison’s), diabetes, hypovolaemia
62
Q

Henoch Schonlein Purpura features

A
  • palpable purpuric rash (with localized oedema)
  • abdominal pain
  • polyarthritis
  • features of IgA nephropathy may occur e.g. haematuria, renal failure
  • raised ESR and WCC
63
Q

complications of nephrotic disease

A
  1. DVT/PE/Renal vein thrombosis (reduced antithrombin)
  2. Infection (Loss of Ig through urine)
  3. Thromboembolism
64
Q

drugs to stop in AKI

A

STOP THE ‘DAMN’ DRUGS
Diuretics
ACE inhibitors/ARBs (reno-protective in non-acute setting but can lead to cardiac arrest in AKI)
Metformin
NSAIDs (except low dose/cardio-protective aspirin)

65
Q

AKI staging by creatinine increase

A

Stage 1 = increase of 1.5-1.9x baseline
Stage 2 = increase of 2.0-2.9x baseline
Stage 3 = increase of 3.0+ x baseline OR creatinine is >354

stage 1 in the 1s
stage 2 in the 2s
stage 3 in the 3s and over

66
Q

normal anion gap range:

sodium + potassium) - (bicarbonate + chloride

A

8-14mmol/L

67
Q

features of acute interstitial nephritis (AIN/TIN - tubulointerstitial)

A
  • fever, rash, arthralgia
  • eosinophilia
  • mild renal impairment
  • hypertension
  • sterile pyuria, white cell casts (leukocytes in urine)

uveitis a complication (TINU)

68
Q

causes of acute interstitial nephritis (AIN/TIN - tubulointerstitial)

A
  • drugs/allergy
  • systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
  • infection: Hanta virus , staphylococci
69
Q

requirement per day of K+, Na+ and Cl- is…

A

1 mmol/kg/day

70
Q

management of acute interstitial nephritis (AIN/TIN - tubulointerstitial)

A

remove/treat cause if identified

corticosteroids may provide benefit

71
Q

features of Alport’s syndrome

A

X-linked inheritance

  • bilateral sensorineural hearing loss
  • visual changes (lenticonus)
  • haematuria/renal signs
72
Q

histological findings of Alport’s syndrome (renal biopsy)

A

splitting of lamina densa ( ‘basket-weave’ appearance)

73
Q

target haemoglobin for CKD patients

A

100-120 g/L

74
Q

most common viral infection following renal transplant

A

cytomegalovirus (EBV common too - prophylaxis should have been given for both)

75
Q

most common cancer risk in transplant patients (due to immunosuppressant meds)

A

squamous cell carcinoma of skin

- lymphoma and cervical cancer risks are also increased

76
Q

primary vs secondary aldosteronism

A 
primary = high aldosterone levels compared to renin in renin:aldosterone ratio
secondary = high renin
77
Q

causes of primary aldosteronism

A
  • idiopathic adrenal hyperplasia
  • phaeochromocytoma
  • Cushing’s
78
Q

causes of seconday aldosteronism

A
  • renal hypoperfusion, eg. renal artery stenosis

- heart failure

79
Q

reason for hypercoagulable state in nephrotic syndrome

A
  • antithrombin III is bound to albumin so in proteinuria/hypoalbuminaemia there is a deficiency of antithrombin III - hypercoagulable state
80
Q

proteinuria screening in diabetes

A 
use ACR (albumin:creatinine ratio)
ACR>2.5 = microalbuminuria
- give ACEI if appropriate in CKD
81
Q

blood tests for rhabdomyolysis

A
  • very high creatine kinase (>1000U/L)
  • AKI with high creatinine
  • myoglubinuria (hypocalcaemia as calcium binds to myoglobin)
  • metabolic acidosis
  • hyperkalaemia
82
Q

CKD and calcium/phosphate

A
  • CKD leads to reduced vit D due to hydroxylation occurring in kidneys, low vit D therefore low Ca2+
  • kidneys normally excrete phosphate, CKD kidneys do not effectively excrete phosphate, high phos in CKD
  • high phosphate drags Ca2+ from bones, causing osteomalacia
83
Q

management of CKD secondary parathyroidism

A
  • reduced dietary phosphate (cut down on chocolate, shellfish, nuts, cola)
  • if ineffective, phosphate binding eg. sevelamer
  • alfacalcidol (vit D)
  • parathyroidectomy in resistant cases
84
Q

change in eGFR and creatinine after commencing ACEI

A

a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, although any rise should prompt careful monitoring and exclusion of other causes

85
Q

CKD staging

A

15, 30, 60, 90

Stage eGFR Comments
1 90+ normal function but signs of
kidney disease in urine etc.
2 60-89 mildly reduced function
3 30-59 moderate dysfunction (can be
divided into a and b based on
eGFR<45 or not)
4 15-29 severe dysfunction
5 <15 very severe, dialysis

86
Q

protein:creatinine ratio conversion to daily protein loss in urine

A

divide by 100 for g/day from mg/mmol in protein:creatinine ratio

eg. P:C = 350mg/mmol = 3.5g/day proteinuria

WFH (18 decks)

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