Acute Kidney Injury

Página 1

Definition

sudden, often reversible loss of renal function which develops over days to weeks and is usually accompanied with a reduction in urine volume.

Página 2

Causes

1. Pre-renal

Impaired perfusion --> such as in cardiac failure, sepsis, blood loss, dehydration, vascular occlusion

Signs and symptoms: tachycardiac, poor peripheral perfusion, delayed CR, postural hypotension (> 20/10 from lying to standing);

In sepsis --> still lead to ATN

Metabolic acidosis and hyperkalaemia

can also occur in patients taking NSAIDs and ACE-I without hypotension.

Remember concealed blood loss e.g. GI tract, trauma in femur or pelvis, pregnant, crush injuries, burns, inflammatory skin diseases or sepsis

2. Renal

Glomerulonephrititis, small vessel vasculitis, acute tubular necrosis --> Drugs, toxins, prolonged hypotension

Interstitial nephritis --> Drugs, toxins, inflammatory disease, infection

Signs and symptoms

Glomerulonephritis --> haematuria and proteinuria (SLE or vasculitis)

Drug hx

3. Post Renal - damage arises due to back pressure

Urinary calculi, retroperitoneal fibrosis, BPH, prostate cancer, cervical cancer, urethral stricture/ valves, meatal stenosis/ phimosis

Signs and symptoms

Look for bladder enlargement; imaging with ultrasound; hydronephrosis;

loin pain, haematuria, renal colic, difficult in micturition,

Renal ultrasound will exclude.

Prompt relief restores renal function

Pathophysiology

Many causes often multifactorial.

Classified as pre-renal, renal and post -renal

Hypoperfusion --> ATN (inflammatory changes, focal breaks in the basement membrane and interstitial oedema).

Dead tubular cells --> shed into tubular lumen --> lead to tubular obstruction

Clinical features

If patient has high serum creatinine --> need to determine if acute or acute on chronic or a sign of CKD (therefore need baseline results).

Diagnosis

1. RIFLE criteria

2. KDIGO criteria

Página 3

Complications

Anaemia --> due to blood loss, decrease in EPO, haemolysis

increased risk of bleeding, spontaneous haemorhage --> due to uraemia

Página 4

Investigations

1. UEC --> compare to previous results, K > 6 treat urgently

2. Calcium, Mg, Phosphate --> low calcium, high phosphate (CKD); calcium low in rhabdo, measure CK, hypercalcaemia in (MM)

3. Albumin (low in nephrotic syndrome and sepsis (take blood cultures)

4. FBC --> Anaemia (CKD, low platelets and abnormal coag in DIC and sepsis --> take blood cultures)

5. CRP ( sepsis or inflammatory disease)

6. U/A --> haematuria --> glomeruloneprhritis; leucocytes (infection or intersitital nephritiis) crystals

7. Renal u/s --> hydronephrosis +/- large bladder in obstruction; small (CKD); asymmetrical (renovascular or developmental disease --> renal artery imaging)

8. Cultures

9. C X-ray: pulmonary oedema in fluid overload globular heart in uraemic effusion (perform echo); Bat wing appearance; fibrotic hcanges

10. Serology; HIV, Hepatitis if dialsysis

11. ECG: if electrolyte abnormalities

Página 5

Management:

1. Haemodynamic status --> central venous pressure

2. Hyperkalaemia and acidosis --> tx > 6.5 with insulin and glucose; acidosis (bicarbonate 100 mmol if ph <7.0)

3. Discontinue nephrotoxic drugs

4. Avoid fluid overload (match intake to output + 500mL)

5. Electrolyte distubrances (dilute hyponatraemia

6. Dietary measures (avoid high protein)

7. Infection --> monitor

8. Medications --> cease nephrotixic agents; Consider PPI

9. Immunosupression --> glomerulonephritis

10. Renal replacement therapy (decision driven by hyperkalaemia, fluid overload and acidosis)

1. Haemodialysis or haemofiltration (high volume)

2. Peritoneal dialysis

11. Renal tract obstruction --> catherisation, stent, percutaneous nephrostomy

recovery

1. return of urine output and improvement in plasma biochemistry

2. Diuretic phase --> urine output increases rapidly before it returns to normal

3. Support NaCl, Na bicarbonate, K, phospahte