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Renal 8/6/20 Flashcards

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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
management of membranous glomerulonephritis
- 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
26
causes of nephritic syndrome
- rapidly progressive glomerulonephritis (crescentic glomerulonephritis) due to Goodpasture's, ANCA positive vasculitis, etc. - IgA nephropathy - (usually post viral)
27
post-strep glomerulonephritis vs IgA
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)
28
fibromuscular dysplasia
- cause of renal artery stenosis with 'string of beads' appearance - usually in young females - follows commencement of ACEI
29
rate of infusion of maintenance fluids
Maintenance fluids should be prescribed at a rate of 30 ml/kg/24hr
30
vitamin D deficiency in renal failure management
Alfacalcidol - used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys
31
complications of too much 0.9% saline
hyperchloraemic metabolic acidosis | - too many chloride ions, produces HCl
32
complications of Hartmann's solution
contains K+ so can precipitate cardiac events in patients with deranged K+
33
maximum recommended rate of potassium infusion via a peripheral line is...
10 mmol/hour | - cardiac monitoring above 20mmol/hr (central line)
34
features of goodpasture's syndrome
- pulmonary haemorrhage - haemoptysis - followed by rapidly progressive glomerulonephritis - lethargy - anti-GBM antibodies
35
management of goodpasture's syndrome
- plasmapheresis - corticosteroid therapy - cyclophosphamide
36
features of granulomatosis with polyangiitis (Wegener's )
- 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
investigations for granulomatosis with polyangiitis (Wegener's)
- 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
management of granulomatosis with polyangiitis (Wegener's)
- plasmapheresis - corticosteroid therapy - cyclophosphamide poor prognosis
39
renal features of ADPKD
- hypertension - abdominal pain - chronic kidney disease - renal stones - haematuria - recurrent UTIs
40
extra-renal complications of ADPKD
- 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
screening test for PKD (for family members)
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
ADPKD type 1 or 2
``` Type 1 (chromosome 16) - 85% cases - develop renal failure earlier Type 2 (chromosome 4) - 15% cases ```
43
management of PKD
- symptom relief, eg. ACEIs - tolvaptan slows cyst growth in some - kidney transplant - dialysis
44
ARPKD
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
features of haemolytic uraemic syndrome
- diarrhoea history within previous 2 weeks - acute kidney injury (high creatinine) - microangiopathic haemolytic anaemia - thrombocytopenia
46
cause of haemolytic uraemic syndrome
- shiga-toxin producing E. coli (follows diarrhoea)
47
management of haemolytic uraemic syndrome
- supportive > fluids > dialysis/blood transfusion if required - no role for Abx - plasma exchange in cases of severe HUS without diarrhoea
48
thrombotic thrombocytopenic purpura features
The TRANF Pentad (TTP) - Thrombocytopenia - Renal failure - Anaemia - Neurological symptoms due to microemboli - Fever schistocytes on blood film due to high vWF
49
causes of TTP (thrombotic thrombocytopenic purpura)
- post infection (typically urinary/GI) - pregnancy - drugs - other: tumours, SLE, HIV
50
drugs causing TTP (thrombotic thrombocytopenic purpura)
POCCA - penicillin - oral contraceptive pill - ciclosporin - clopidogrel - aciclovir
51
causes of DIC
- sepsis - trauma - obstetric complications eg. HELLP syndrome - malignancy
52
AKI or dehydration?
higher rise in urea than creatinine = likely dehydration | high rise in creatinine than urea = likely AKI
53
causes of high anion gap acidosis
- diabetic ketoacidosis - lactic acidosis (sepsis, salicylates (aspirin), shock) - methanol poisoning - ethlene glycol poisoning (antifreeze)
54
high anion gap vs normal anion gap
high anion gap = increased organic acid production/ingestion | normal anion gap = loss of bicarbonate (eg. diarrhoea, renal tubular acidosis)
55
causes of acute tubular necrosis
``` 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
features of acute tubular necrosis
``` - features of AKI: > raised urea > creatinine > potassium - muddy brown casts and high sodium in the urine ```
57
causes of normal anion gap acidosis
- renal tubular acidosis - diarrhoea - hyperosmolar hyperglycaemic state - Addison's disease - pancreatic fistula
58
features of renal tubular acidosis (all types)
- hyperchloraemic metabolic acidosis (normal anion gap) - abdo discomfort - Kussmaul breathing
59
renal tubular acidosis type 1 (distal)
- 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
renal tubular acidosis type 2 (proximal)
- 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
renal tubular acidosis type 4 (hyperkalaemic)
- reduction in aldosterone leads to reduction in ammonium excretion - causes hyperkalaemia - causes include hypoaldosteronism (Addison's), diabetes, hypovolaemia
62
Henoch Schonlein Purpura features
- 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
complications of nephrotic disease
1. DVT/PE/Renal vein thrombosis (reduced antithrombin) 2. Infection (Loss of Ig through urine) 3. Thromboembolism
64
drugs to stop in AKI
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
AKI staging by creatinine increase
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
normal anion gap range: | sodium + potassium) - (bicarbonate + chloride
8-14mmol/L
67
features of acute interstitial nephritis (AIN/TIN - tubulointerstitial)
- fever, rash, arthralgia - eosinophilia - mild renal impairment - hypertension - sterile pyuria, white cell casts (leukocytes in urine) uveitis a complication (TINU)
68
causes of acute interstitial nephritis (AIN/TIN - tubulointerstitial)
- drugs/allergy - systemic disease: SLE, sarcoidosis, and Sjögren's syndrome - infection: Hanta virus , staphylococci
69
requirement per day of K+, Na+ and Cl- is...
1 mmol/kg/day
70
management of acute interstitial nephritis (AIN/TIN - tubulointerstitial)
remove/treat cause if identified | corticosteroids may provide benefit
71
features of Alport's syndrome
X-linked inheritance - bilateral sensorineural hearing loss - visual changes (lenticonus) - haematuria/renal signs
72
histological findings of Alport's syndrome (renal biopsy)
splitting of lamina densa ( 'basket-weave' appearance)
73
target haemoglobin for CKD patients
100-120 g/L
74
most common viral infection following renal transplant
cytomegalovirus (EBV common too - prophylaxis should have been given for both)
75
most common cancer risk in transplant patients (due to immunosuppressant meds)
squamous cell carcinoma of skin | - lymphoma and cervical cancer risks are also increased
76
primary vs secondary aldosteronism
``` primary = high aldosterone levels compared to renin in renin:aldosterone ratio secondary = high renin ```
77
causes of primary aldosteronism
- idiopathic adrenal hyperplasia - phaeochromocytoma - Cushing's
78
causes of seconday aldosteronism
- renal hypoperfusion, eg. renal artery stenosis | - heart failure
79
reason for hypercoagulable state in nephrotic syndrome
- antithrombin III is bound to albumin so in proteinuria/hypoalbuminaemia there is a deficiency of antithrombin III - hypercoagulable state
80
proteinuria screening in diabetes
``` use ACR (albumin:creatinine ratio) ACR>2.5 = microalbuminuria - give ACEI if appropriate in CKD ```
81
blood tests for rhabdomyolysis
- very high creatine kinase (>1000U/L) - AKI with high creatinine - myoglubinuria (hypocalcaemia as calcium binds to myoglobin) - metabolic acidosis - hyperkalaemia
82
CKD and calcium/phosphate
- 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
management of CKD secondary parathyroidism
- reduced dietary phosphate (cut down on chocolate, shellfish, nuts, cola) - if ineffective, phosphate binding eg. sevelamer - alfacalcidol (vit D) - parathyroidectomy in resistant cases
84
change in eGFR and creatinine after commencing ACEI
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
CKD staging
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
protein:creatinine ratio conversion to daily protein loss in urine
divide by 100 for g/day from mg/mmol in protein:creatinine ratio eg. P:C = 350mg/mmol = 3.5g/day proteinuria

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