Nephrology & Urology Flashcards
Indications for IV fluids?
Resuscitation
Maintenance
Replacement
Management of fluid resuscitation?
500mL 0.9% NaCl or Hartmann’s STAT
→ 250mL if at risk of fluid overload
250-500mL boluses up to 2000mL if needed
Daily water vs Na/K/Cl vs glucose requirement?
Water = 25-30mL/kg/day
Na/K/Cl = 1mmol/kg/day
Glucose = 50-100g/day
A 1L bag of IV fluid e.g. 0.9% NaCl contains how much water?
1L (you dumbass)
Caution with 0.9% NaCl vs Hartmann’s vs dextrose 5%?
0.9% NaCl = risk of hypernatraemia and hyperchloraemic metabolic acidosis
Hartmann’s = risk of hyperkalaemia
Dextrose 5% = do not use for fluid resuscitation
Maximum rate of K infusion?
No more than 10mmol/kg/hour
Features and most common cause of nephrotic vs nephritic syndrome?
Nephrotic = oedema, proteinuria (“frothy urine”), hypoalbuminaemia, hypercholesterolaemia,
→ minimal change disease (kids), FSGS (adults)
Nephritic = haematuria, hypertension, mild proteinuria, oliguria
→ IgA nephropathy
What causes hypercoagulability in nephrotic syndrome?
Antithrombin III loss via urine
Definition of AKI?
Rapid onset reduction in renal function causing oliguria and elevated serum urea + creatinine
Cause of pre-renal vs intrinsic vs post-renal causes AKI?
Pre-renal (most common) = ischaemia
Intrinsic = kidney damage
Post-renal = obstruction
Urine osmolality and urine sodium in pre-renal vs intrinsic AKI and explain?
Pre-renal = urine osmolality high, urine sodium low
→ kidneys concentrate urine and retain sodium to increase blood pressure
Intrinsic = urine osmolality low, urine sodium high
→ damaged kidneys fail to concentrate urine or retain sodium
Investigations for AKI?
U&Es
Urinalysis
Renal tract USS (if no cause found)
Biochemical features of AKI?
Hyperkalaemia
Hyperphosphataemia
Hyperuricaemia
High creatinine
Metabolic acidosis
Staging of AKI?
I = 1.5x creatinine baseline or reduction in urine output to < 0.5mL/kg/hour for ≥ 6 hours
II = 2.5x creatinine baseline or reduction in urine output to < 0.5mL/kg/hour for ≥ 12 hours
III = ≥ 3 x creatinine baseline or reduction in urine output to < 0.3mL/kg/hour for ≥ 24 hours
Management of AKI?
Stop nephrotoxic drugs!
Treat hyperkalaemia (if present)
Pre-renal = IV fluid challenge
Intrinsic = treat underlying cause, nephrology referral
Post-renal = catheterise, urology referral
Drugs which should be stopped in AKI?
NSAIDs (except aspirin at cardioprotective dose)
Aminoglycosides
ACEi/ARBs
Diuretics
Drugs which may become toxic in AKI?
Metformin
Digoxin
Lithium
Opioids
Management of hyperkalaemia?
< 6mmol/L = supportive, adjust medication
> 6mmol/L = ECG then treat if abnormal
≥ 6.5mmol/L = urgent treatment
→ IV calcium gluconate + IV insulin/dextrose or + nebulised salbutamol
Most common intrinsic AKI and causes?
Acute tubular necrosis
→ ischaemia or nephrotoxins
Urinalysis features of acute tubular necrosis?
Muddy brown casts
Renal epithelial cell casts
Most common cause of acute interstitial nephritis?
Drugs (especially antibiotics)
Features of acute interstitial nephritis?
AKI
Hypertension
Rash, fever
Eosinophilia
Most common type of glomerulonephritis?
IgA nephropathy
Outline management of glomerulonephritis?
1st line = supportive management
2nd line = ACEi/ARB
3rd line = steroid
Features of IgA nephropathy?
12-72 hours post-URTI
Nephritic syndrome (haematuria dominant)
Features of post-streptococcal glomerulonephritis?
7-14 days post-URTI
Nephritic syndrome (proteinuria dominant)
Investigation for IgA nephropathy vs post-streptococcal glomerulonephritis?
IgA nephropathy = renal biopsy
Post-strep = anti-streptolysin O titre
Biopsy features of membranous glomerulonephritis?
Thickened basement membrane
IgG and complement deposits
“Spike and dome” appearance
Biopsy feature of minimal change disease?
Fusion of podocytes
Biopsy feature of rapidly progressive glomerulonephritis?
Epithelial crescents
Biopsy features of FSGS?
Focal and segmental sclerosis
Features of Henoch-Schönlein purpura (HSP)?
Post-URTI
Vasculitis → purpuric rash
Abdominal pain
Arthralgia/Arthritis
IgA nephropathy
Monitoring of Henoch-Schönlein purpura (HSP)?
BP and urinalysis for 6-12 months
Features of rhabdomyolysis?
AKI
PMH trauma e.g. long lie
Muscle pain and swelling
Red/brown “tea coloured” urine
Biochemical features of rhabdomyolysis?
Severely raised CK
Raised LDH
Hypocalcaemia (Ca absorbed by muscle)
Hyperkalaemia/phosphataemia/uricaemia
Features of haemolytic uraemic syndrome (HUS)?
Triad of:
→ AKI
→ microangiopathic haemolytic anaemia
→ thrombocytopaenia
Blood film features of HUS?
Reticulocytes
Schistocytes
Most common causes of CKD?
Diabetes
Hypertension
Chronic glomerulonephritis
Polycystic kidney disease
Staging of CKD?
I = GFR > 90ml/min with evidence of kidney damage
II = GFR 60-90ml/min with evidence of kidney damage
III = GFR 30-59ml/min
IV = GFR 15-29ml/min
V = GFR < 15ml/min
N.B. patients are usually asymptomatic until IV or V
eGFR variables?
CAGE:
Creatinine
Age
Gender
Ethnicity
Investigation and management of CKD proteinuria?
Albumin:creatinine ratio
Management = ACEi/ARB
Complications of CKD?
Fluid overload → hypertension, oedema
Hyperkalaemia → arrhythmias
Hyperuricaemia → itch, pericarditis, encephalopathy
Low EPO → anaemia → LVH
Low vitamin D → hypocalcaemia/hyperphosphataemia → bone disease, secondary/tertiary hypoparathyroidism
Management of CKD anaemia?
1st line = correct iron deficiency (oral or IV)
2nd line = EPO injections
Management of CKD bone disease?
1st line = low phosphate diet
2nd line = phosphate-binders (sevelamer) + vitamin D analogue (alfacalcidol)
Total parathyroidectomy for tertiary hyperpathyroidism