Renal and Urology Flashcards
AKI Staging
1: 1.5-1.9x baseline creatinine or an increase of 26 urology/L
<0.5 ml/kg/hr for 6-12 hours
2: 2-2.9x baseline creatinine
<0.5ml/kg/hr for more than 12 hours
3: 3x baseline creatinine
<0.3 ml/kg/hr for 24 hours or Anuria for 12 hours
SALFORD management of AKI
Sepsis and other causes- treat
ACEi/ARBs and other nephrotoxic drugs - stop
Labs - Cr and urea
Fluid assessment and challenge
Obstruction - identify with USS
Renal/crit care referral if non resolving
Dip the urine
Causes of AKI
Pre renal; sepsis, dehydration, hypotension, shock, severe heart failure
Renal; acute interstitial nephritis , nephrotoxic drugs, rhabdomyolysis
Post renal; obstructed by stones, prostate, cancer
drugs that may have to be stopped in AKI because of risk of toxicity - but not worsening AKI in themselves
Metformin
Lithium
Digoxin
stages/diagnosis of CKD
1 - kidney damage evidence with GFR >90
2 - kidney damage evidence with GFR 60-89
3 - GFR 30-59
4 - GFR 15-29
5 - GFR <15 end stage renal failure
CKD management earlier stages
start an ACEi or ARB
start statin
control HTN and diabetes
CKD complications
Anaemia - EPO deficiency
Vitamin D deficiency –> tertiary hyperparathyroidism; increased PTH with reduced vit D and calcium
when should metformin be stopped in CKD
GFR <30
nephrotoxic drugs
Sulphonylureas
ACEi
Diuretics
Metformin
ARB
NSAID
SGLT2i
what features indicate need for dialysis in kidney failure
refractory hyperkalaemia
metabolic acidosis
uraemic encephalopathy
pulmonary oedema
hyperkalaemia ECG changes
in order…
peaked T waves
P waves widen and flatten then disappear
conduction abnormalities
bradycardia
hyperkalaemia treatment
IV calcium gluconate to protect the heart
rapid insulin in dextrose
salbutamol nebs
insulin + Sal moves potassium into the intracellular space
nephrotic syndrome + management
massive proteinuria with minimal haematuria
salt and fluid restrict
diuretics + ACEi/ARB
anticoagulate if needed
what features indicate need for dialysis in kidney failure
refractory hyperkalaemia
metabolic acidosis
uraemic encephalopathy
pulmonary oedema
hyperkalaemia ECG changes
in order…
peaked T waves
P waves widen and flatten then disappear
conduction abnormalities
bradycardia
hyperkalaemia treatment
IV calcium gluconate to protect the heart
rapid insulin in dextrose
salbutamol nebs
insulin + Sal moves potassium into the intracellular space
nephrotic syndrome + management
massive proteinuria with minimal haematuria
salt and fluid restrict
diuretics + ACEi/ARB
anticoagulate if needed
nephritic syndrome
haematuria + mild proteinuria
most commonly caused by IgA nephropathy
what features indicate need for dialysis in kidney failure
refractory hyperkalaemia
metabolic acidosis
uraemic encephalopathy
pulmonary oedema
hyperkalaemia ECG changes
in order…
peaked T waves
P waves widen and flatten then disappear
conduction abnormalities
bradycardia
hyperkalaemia treatment
IV calcium gluconate to protect the heart
rapid insulin in dextrose
salbutamol nebs
insulin + Sal moves potassium into the intracellular space
nephrotic syndrome + management
massive proteinuria with minimal haematuria
salt and fluid restrict
diuretics + ACEi/ARB
anticoagulate if needed
nephritic syndrome
haematuria + mild proteinuria
most commonly caused by IgA nephropathy
APCKD; features and management
cystic kidneys with extra renal cysts in liver, aneurysms and mitral valve prolapse
management; BP control, screen for CVD, threapies in trial include vasopressin and somatostatin
test for it using USS
what is the anion gap?
metabolic acidosis normal anion gap causes?
raised anion gap causes?
(Na+ + K+) - (Cl- + HCO-3)
normal anion gap:
gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
renal tubular acidosis
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease
raised anion gap:
lactate: shock, sepsis, hypoxia
ketones: diabetic ketoacidosis, alcohol
urate: renal failure
acid poisoning: salicylates, methanol
what is IgA nephropathy?
most common cause of glomerulonephritis classically presenting with macroscopic haematuria in young people following a respiratory tract infection (1-2 days after)
not much proteinuria. usually self resolves
acute interstitial nephritis
cause of renal failure resulting in marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules
Features
-fever, rash, arthralgia
-eosinophilia
-mild renal impairment
-hypertension
caused by drugs, systemic disease, infection
anti-glomerular basement disease
small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis
post streptococcal glomerulonephritis
nephritis affecting young children 1-2 weeks after a streptococcal sore throat
causes malaise, proteinuria and (sometimes visible) haematuria
urology 2WW referral
Aged >= 45 years AND:
unexplained visible haematuria without urinary tract infection, or
visible haematuria that persists or recurs after successful treatment of urinary tract infection
Aged >= 60 years AND have unexplained nonvisible haematuria and either dysuria or a raised white cell count on a blood test
most common cause of nephrotic syndrome in children
minimal change disease
then focal segmental glomerulosclerosis
how does acute interstitial nephritis present
allergic type picture, raised eosinophils, IgE and urinary WCC and impaired renal function
treatment of rhabdomyolysis
rapid IV fluid hydration
normal excretion of protein in urine
<150mg with <30mg albumin
4 causes/types of nephrotic syndrome
- minimal change
- focal segmental glomerulosclerosis
- membranous glomerulonephritis
- membranoproliferative glomerulonephritis
diagnosed/distinguished by renal biopsy
what is rapidly progressive glomerulonephritis?
form of nephritic syndrome where you see glomerular haematuria (RBC casts or dysmorphic RBCs) and rapidly developing kidney injury - fatal if not treated quickly
causes of nephritic syndrome
nephritic syndrome aka acute glomerular nephritis caused mainly by IgA nephropathy
also caused by post streptococcal glomerulonephritis
treatment of minimal change disease
corticosteroids
causes of acquired renal cysts
simple cysts
acquired renal cystic disease
hypokalaemia related cysts
non genetic developmental renal cysts
medullary sponge kidney
multicystic dysplastic kidneys
pyelocalyceal cysts
genetic causes of cystic kidney disease
ADPKD, ARPKD
tuberous sclerosis, von hippel lindau disease, medullary cystic disease (all autosomal dominant)
some X linked disorders
secondary causes of nephrotic syndrome
autoimmune
infections
drugs
toxins
diabetes
tumours
what is vasculitis?
examples of large, medium and small vessel vasculitis
inflammation of blood vessels
large; giant cell arteritis, Takayasu
medium; kawasaki, polyarteritis nodosa
small; ANCA associated or ‘other’ e.g. in SLE
what indicates testicular torsion
management?
- sudden onset pain
- absent cremasteric reflex
- unilateral swollen and retracted testicle
- typically in adolescence
surgical exploration
how does haemolytic uraemic syndrome present? how is it treated
children
acute kidney injury
microangiopathic haemolytic anaemia
thrombocytopenia
treat with supportive care and IV fluids
first line investigation for prostate cancer
multiparametric MRI
causes of transient or spurious haematuria
menstruation
vigorous exercise
UTI
sexual intercourse
drugs e.g. rifampicin
food e.g. beetroot
What pain relief should be used in renal colic
IM diclofenac
acute pyelonephritis management
quinolone e.g. ciprofloxacin or a broad spectrum cephalosporin e.g. cefalexin for 10 days
membranous glomerulonephritis management
all pts should be on an ACEi or ARB
immunosuppression; usually corticosteroids
consider anticoagulation
