Renal Flashcards
Pre-renal causes of AKI
Hypovolaemia
Low BP
Renal artery stenosis
Intrinsic causes of AKI
Acute tubular necrosis
Nephrotoxic meds
Glomerulonephritis
Interstitial nephritis
Post-renal causes of AKI
BPH
Bladder cancer
Calculi
Any cause of obstruction
What are the three phases of AKI
Oliguric/anuric phase
Polyuric/maintenance phase
Recovery phase
Complications of AKI
Hyperkalaemia Pulmonary oedema/fluid overload Metabolic acidosis Uraemic encephalopathy/pericarditis Low Ca, high PO4
ECG changes in hyperkalaemia
Small/absent P waves
Prolonged PR interval
Peaked T waves
Slurring into ST
Which treatments of hyperkalaemia increase K excretion
IV NaCl
Diuretics
Which treatments of hyperkalaemia move K into cells
Beta-agonists
Bicarbonate
IV insulin
What happens to BUN:Creatinine ratio in pre-renal AKI Vs intrinsic AKI
- In pre-renal AKI as normal all Cr is excreted, tubules are still working and reabsorbing urea so serum urea is higher. So BUN:Cr >20:1
- In intrinsic AKI as normal all Cr is excreted, tubules aren’t working though so more urea being excreted than normal so less serum urea compared to pre-reanl. So BUN:Cr <20:1 (closer to 1)
What happens to urine Na and osmolality in pre-renal AKI
Decreased renal blood flow but tubules still working. RAAS activated causing Na and H2O retention. Concentrated urine - high osmolality >500 but looking at just urine Na concentration this is low <20 because Na is being reabsorbed by the still-functioning tubules
What happens to urine Na and osmolality in intrinsic AKI
Tubules damaged so can’t function and cant reabsorb Na. So Na and H2O lost in urine - dilute urine with a high Na concentration. Low urine osmolality <350, high urinary Na concentration >40
Management of AKI
Treat underlying cause
Stop nephrotoxic drugs
Monitor pH, fluid balance and electrolytes
Involve renal team
How long does disease need to be present to classify as chronic kidney disease
3 months
Causes of CKD
HTN DM Renal artery stenosis Glomerulonephritis Reflux nephropathy Pyelonephritis PCKD
Clinical features of CKD
Polyuria Oedema Anaemia Low Ca, High PO4 Metabolic acidosis Hyperkalaemia Uraemia Mineral and bone disorder
Three main types of renal replacement therapy
Dialysis
Haemofiltration
Transplant
How long does it take before a fistula can be used for dialysis
4 weeks
When would you use haemofiltration rather than dialysis
When a patient is really haemodynamically unstable
What’s the difference between haemodialysis and haemofiltration
Dialysis uses a diffusion gradient whereas filtration uses a hydrostatic pressure gradient
Possible complications of an AV fistula
Thrombosis Stenosis Steal syndrome Infection Heart failure
Haemodialysis is performed roughly how often and for how long each time?
Three times a week
4 hours
What are the two types of peritoneal dialysis
Continuous ambulatory PD (4-6 exchanges/day) Assisted PD (fill in morning, exchange overnight)
6 features of nephrotic syndrome
Proteinuria Increased risk of infection Oedema Hypoalbuminuria Hyperlipidaemia Hypercoagulable state
2 most common causes of nephrotic syndrome in adults
FSGS (black population) Membranous nephropathy (white population)
Most common cause of nephrotic syndrome in children
Minimal change disease
Secondary causes of nephrotic syndrome
SLE Hep B Hep C HIV DM Malignancy
4 primary causes of nephrotic syndrome
Minimal change disease
FSGS
Membranous nephropathy
Membranoproliferative glomerulonephritis
Management of nephrotic syndrome
Low Na and protein diet Fluid restriction Loop diuretics ACEi/ARB VTE prophylaxis Statins Renal biopsy
8 features of nephritic syndrome
Haematuria Hypertension Oliguria Uraemia RBC casts Sterile pyuria Mild proteinuria Mild oedema
5 causes of nephritic syndrome
IgA nephropathy Post-strep glomerulonephritis Rapidly progressive glomerulonephritis (Anti-GBM, GPA, MPA, EGPA_ Membranoproliferative glomerulonephritis HSP
Management of nephritic syndrome
Low Na diet
Fluid restriction
ACEi/ARB
Consider immunosuppression
cANCA positive vasculitis
Granulomatosis with polyangitis (Wegeners)