16. Renal 1

Question 1

What is an AKI?

Answer 1

Sudden rapid reduction in eGFR with or without oliguria/anuria.

Question 2

What is the KDIGO criteria for AKI?

Answer 2

AKI diagnosis.

Stage 1
Serum Cr x1.5-1.9 of baseline, > or equal 26umol/l increase
Urine output <0.5mL/kg/h for 6-12h

Stage 2
x2-2.9
Urine output >0.5mL/kg/h for 12h

Stage 3 
x3 baseline
>354umol/L
Anuria for 12hr
Renal dialysis
<0.3mL/kg/h

If have symptoms of both stage 1 and 3, always pick most severe so these patients are stage 3

Question 3

Complications (these are often the symptoms) of AKI and how to treat them?

Answer 3

1. Fluid overload e.g. peripheral or pulmonary oedema. Managed with IV furosemide/GTN infusion or haemodialysis if refractory
2. Uraemia -> uraemic encephalitis or uraemia pericarditis. Managed with haemodialysis.
3. Metabolic acidosis, sx -> confusion, tachycardia, kussmaul’s, N&V. Managed with IV/PO sodium bicarbonate, dialysis if refractory
4. Hyperkalaemia, sx -> asymptomatic, arryhthmias, muscle weakness, cramps parathesias, hypotension, bradycardia, cardiac arrect.

Question 4

What are the ECG changes with hyperkalaemia?

Answer 4

Forms a box

Loss of P wave ->  
Tented T wave ^
Prolonged PR ->
Wide QRS ^
Presence of sinusoidal wave (oscillation) (diagonal)  

Bradycardia

Question 5

How do we manage hyperkalaemia?

Answer 5

1. Cardiac monitor
2. ECG changes - calcium gluconate 10%, 30mls IV -> protect heart
3. 10 units soluble insulin
4. 50ml of 50% glucose
5. Consider, salbutamol nebs, furosemide, sodium bicarb IV
6. Stop cause and continue to monitor K
7. If refractory, haemodialysis

Question 6

How do we investigate AKI?

Answer 6

Good medication history
Fluid assessment (membranes, oedema, cap refill, BP, JVP)
ABG/VBG, pot and bicarb
Bloods esp. U&Es
Hepatitis/HIV, immune screen, myeloma screen, anti-GBM, septic screen
KUB for cause
ECG for pot

Question 7

How do we manage AKI?

Answer 7

ABCDE approach
Find and treat cause
Stop any nephrotoxic drugs
Fluid management  e.g. IV fluids or diuretics
Treat complications
Dialysis if necessary

Question 8

What causes an AKI?

Answer 8

Generally

Pre-renal - problems with blood supply
Renal - problems with the kidney
Post-renal - problems with urine outflow

Question 9

Pre-renal causes of AKI?

Answer 9

1. Hypovolaemia (excess loss) - acute haemorrhage, GI loss, diuresis, burns
2. Low volume circulating - heart failure or liver failure
3. Vascular insult - ACEi/ARBs, NSAIDs, contrast, renal artery stenosis

Question 10

Post-renal causes of AKI?

Answer 10

1. Luminal - kidney stones
2. Mural - cancers of renal tract, strictures
3. Extramural - abdominal/pelvic cancers, BPH

Question 11

Renal causes of AKI?

Answer 11

1. Tubular - ischaemic e.g. in artery stenosis, shock or HF. toxic e.g. nephrotoxic drugs e.g. uric acid from body in tumour lysis or rhabdomyolysis. or outside drugs like NSAIDs
2. Interstitial - immune mediated damage driven by tyep 4 hypersensitivity reaction due to meds (white cell casts)
3. Vascular -
   HUS - haemolytic anaemia, uraemic syndrome
   TTP -thrombotic, thrombocytopenia purpura
4. Glomerular

Question 12

What do we do in tubular AKI?

Answer 12

It’s reversible, self-managed
Strict urine in and output with fluid diary
Granular muddy brown casts on histology

Question 13

Signs of haemolytic anaemia?

Answer 13

Dark urine
Jaundice
Schistocytes on blood film
Petechiae
Prolonged bleeding

Question 14

What are the two types of glomerulonephritis?

Answer 14

Nephrotic - massive protein with low albumin, and high lipids
Nephritic - haematuria with microproteinuria, progressive renal impairment and HTN

Question 15

Types of nephrotic syndrome?

Answer 15

1. Minimal changes disease
2. Membranous GN
3. Diabetic nephropathy
4. Amyloid nephropathy
5. FSGS

Question 16

What is minimal changes disease?

Answer 16

Most common in children.

Idiopathic nephrotic syndrome often triggered by immunological insult, associated with non-hodgkins lymphoma.

Question 17

What is membranous glomerulonephritis?

Answer 17

Deposition of immune complexes on BM, seen on light microscopy as BM thickening.

Question 18

What is FSGS?

Answer 18

Focal segmental glomerulosclerosis.

Injury to podocytes

Question 19

What is diabetic nephropathy?

Answer 19

Excess urine glucose glycolates proteins that thickens the BM and efferent arteriole. Creates a high pressure state that causes mesangial expansion and glomerular damage.

Microalbuminuria and damage seen on light microscopy. Need HTN mx

Question 20

What is amyloid nephropathy?

Answer 20

Secondary damage to amyloidosis where proteins are deposited, damaging tissues.
Apple green birefringence.

Question 21

What are the two types of nephritic syndrome?

Answer 21

1. MPGN - membranoproliferative glomerulonephritis

2. RP(rapidly proliferating)GN/Crescenteric GN

Question 22

What is MPGN?

Answer 22

Subendothelial immune deposits (either immune complex or complement deposits) causing inflammation and damage to the glomerulus.
Light microscopy shows tram tracking.

Question 23

What is RPGN?

Answer 23

Proliferation of cells in bowman’s space causes a crescent shape. There are three types.

1. Goodpasture
2. Immune-complex mediated (post-strep, in SLE, henoch-schlolein purpura or IgA nephropathy)
3. Pauci-immune (ANCAs)

Question 24

What is good pasture syndrome?

Answer 24

Anti-glomerular membrane antibodies trigger type II hypersensitivity. Can damage BM in lungs too