Renal 8/6/20 Flashcards
diagnostic criteria of AKI
- Rise in creatinine of 26 micromol/L or more in 48 hours
OR - ≥ 50% rise in creatinine over 7 days
OR - Fall in urine output to less than 0.5ml/kg/hour (for more than 6 hours in adults, 8 hours in children)
OR - ≥ 25% fall in eGFR in children / young adults in 7 days
symptoms of AKI
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)
normal urine output
1.5-2ml/kg/hr
causes of AKI
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
drug causes of AKI
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
management of hyperkalaemia
- 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
indications for dialysis
- 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)
risk factors for AKI
- elderly
- comorbidity eg. DM, HF, liver disease
- previous AKI
- CKD
- cancer
- post operative
- medications
- neuro/cog impairment - more prone to dehydration etc.
causes of false positive AKI
- pregnancy
- drugs - trimethoprim
- contaminated sample
components of Fanconi syndrome
PPP AGO
- type 2 (proximal) renal tubular acidosis
- polyuria
- phosphaturia
- aminoaciduria
- glycosuria
- osteomalacia
causes of Fanconi syndrome
- cystinosis (most common cause in children)
- Sjogren’s syndrome
- multiple myeloma
- nephrotic syndrome
- Wilson’s disease
cANCA with haematuria
Wegener’s - crescentic glomerulonephritis
sjogren’s autoantibodies
Mr Sjogren is a high (anti-)Ro(anti-)La
- Anti-Ro
- Anti-La
test for Wilson’s syndrome
high caeruloplasmin (copper carrying protein)
membranous glomerulonephritis markers
- antiphospholipase A2 antibodies
- basement membrane thickening on light microscopy
- subepithelial spikes
- low total T4
haemolytic uraemic syndrome markers
Increased - fragmented red cells Decreased - serum haptoglobins - platelet count
nephrotic syndrome features
- Proteinuria (> 3g/24hr) causing
- Hypoalbuminaemia (< 30g/L) (& hyperlipidaemia)
- Oedema
causes of nephrotic syndrome
- minimal change disease
- membranous glomerulonephritis
- focal segmental glomerulosclerosis
- diabetic nephropathy
- amyloidosis
- post-streptococcal glomerulonephritis (CAN PRESENT AS NEPHRITIC TOO)
causes of minimal change disease
- idiopathic
- drugs: NSAIDs, rifampicin
- malignancy: Hodgkin’s lymphoma, thymoma
- infective: infectious mononucleosis
management of minimal change disease
steroid responsive - cyclophosphamide in resistant cases
2/3 will relapse
histology of minimal change disease
- normal glomeruli on light microscopy
- fusion of podocytes and effacement of foot processes
causes of focal segmental glomerulosclerosis
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
histology findings for focal segmental glomerulosclerosis
- focal and segmental sclerosis and hyalinosis
- effacement of foot processes
causes of membranous glomerulonephritis
- 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
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
causes of nephritic syndrome
- rapidly progressive glomerulonephritis (crescentic glomerulonephritis) due to Goodpasture’s, ANCA positive vasculitis, etc.
- IgA nephropathy - (usually post viral)
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)
fibromuscular dysplasia
- cause of renal artery stenosis with ‘string of beads’ appearance
- usually in young females
- follows commencement of ACEI
rate of infusion of maintenance fluids
Maintenance fluids should be prescribed at a rate of 30 ml/kg/24hr
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
complications of too much 0.9% saline
hyperchloraemic metabolic acidosis
- too many chloride ions, produces HCl
complications of Hartmann’s solution
contains K+ so can precipitate cardiac events in patients with deranged K+
maximum recommended rate of potassium infusion via a peripheral line is…
10 mmol/hour
- cardiac monitoring above 20mmol/hr (central line)
features of goodpasture’s syndrome
- pulmonary haemorrhage - haemoptysis
- followed by rapidly progressive glomerulonephritis
- lethargy
- anti-GBM antibodies
management of goodpasture’s syndrome
- plasmapheresis
- corticosteroid therapy
- cyclophosphamide
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
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
management of granulomatosis with polyangiitis (Wegener’s)
- plasmapheresis
- corticosteroid therapy
- cyclophosphamide
poor prognosis
renal features of ADPKD
- hypertension
- abdominal pain
- chronic kidney disease
- renal stones
- haematuria
- recurrent UTIs
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
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
ADPKD type 1 or 2
Type 1 (chromosome 16) - 85% cases - develop renal failure earlier Type 2 (chromosome 4) - 15% cases
management of PKD
- symptom relief, eg. ACEIs
- tolvaptan slows cyst growth in some
- kidney transplant
- dialysis
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
features of haemolytic uraemic syndrome
- diarrhoea history within previous 2 weeks
- acute kidney injury (high creatinine)
- microangiopathic haemolytic anaemia
- thrombocytopenia
cause of haemolytic uraemic syndrome
- shiga-toxin producing E. coli (follows diarrhoea)
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
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
causes of TTP (thrombotic thrombocytopenic purpura)
- post infection (typically urinary/GI)
- pregnancy
- drugs
- other: tumours, SLE, HIV
drugs causing TTP (thrombotic thrombocytopenic purpura)
POCCA
- penicillin
- oral contraceptive pill
- ciclosporin
- clopidogrel
- aciclovir
causes of DIC
- sepsis
- trauma
- obstetric complications eg. HELLP syndrome
- malignancy
AKI or dehydration?
higher rise in urea than creatinine = likely dehydration
high rise in creatinine than urea = likely AKI
causes of high anion gap acidosis
- diabetic ketoacidosis
- lactic acidosis (sepsis, salicylates (aspirin), shock)
- methanol poisoning
- ethlene glycol poisoning (antifreeze)
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)
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 agentsfeatures of acute tubular necrosis
- features of AKI:
> raised urea
> creatinine
> potassium
- muddy brown casts and high sodium in the urinecauses of normal anion gap acidosis
- renal tubular acidosis
- diarrhoea
- hyperosmolar hyperglycaemic state
- Addison’s disease
- pancreatic fistula
features of renal tubular acidosis (all types)
- hyperchloraemic metabolic acidosis (normal anion gap)
- abdo discomfort
- Kussmaul breathing
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
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)
renal tubular acidosis type 4 (hyperkalaemic)
- reduction in aldosterone leads to reduction in ammonium excretion
- causes hyperkalaemia
- causes include hypoaldosteronism (Addison’s), diabetes, hypovolaemia
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
complications of nephrotic disease
- DVT/PE/Renal vein thrombosis (reduced antithrombin)
- Infection (Loss of Ig through urine)
- Thromboembolism
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)
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
normal anion gap range:
sodium + potassium) - (bicarbonate + chloride
8-14mmol/L
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)
causes of acute interstitial nephritis (AIN/TIN - tubulointerstitial)
- drugs/allergy
- systemic disease: SLE, sarcoidosis, and Sjögren’s syndrome
- infection: Hanta virus , staphylococci
requirement per day of K+, Na+ and Cl- is…
1 mmol/kg/day
management of acute interstitial nephritis (AIN/TIN - tubulointerstitial)
remove/treat cause if identified
corticosteroids may provide benefit
features of Alport’s syndrome
X-linked inheritance
- bilateral sensorineural hearing loss
- visual changes (lenticonus)
- haematuria/renal signs
histological findings of Alport’s syndrome (renal biopsy)
splitting of lamina densa ( ‘basket-weave’ appearance)
target haemoglobin for CKD patients
100-120 g/L
most common viral infection following renal transplant
cytomegalovirus (EBV common too - prophylaxis should have been given for both)
most common cancer risk in transplant patients (due to immunosuppressant meds)
squamous cell carcinoma of skin
- lymphoma and cervical cancer risks are also increased
primary vs secondary aldosteronism
primary = high aldosterone levels compared to renin in renin:aldosterone ratio secondary = high renin
causes of primary aldosteronism
- idiopathic adrenal hyperplasia
- phaeochromocytoma
- Cushing’s
causes of seconday aldosteronism
- renal hypoperfusion, eg. renal artery stenosis
- heart failure
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
proteinuria screening in diabetes
use ACR (albumin:creatinine ratio) ACR>2.5 = microalbuminuria - give ACEI if appropriate in CKD
blood tests for rhabdomyolysis
- very high creatine kinase (>1000U/L)
- AKI with high creatinine
- myoglubinuria (hypocalcaemia as calcium binds to myoglobin)
- metabolic acidosis
- hyperkalaemia
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
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
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
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
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
