1. Acute Kidney Injury
James Finnerty

2. Gross Anatomy Paired, retroperitoneal structures
Upper Poles located between Tranverse Processes T____, lower poles descend to L____
Left typically higher
Receives ___% of cardiac output
Via Renal Artery, drains via Renal Vein

3. Microanatomy – The Nephron

5. Functions

6. Definition
Clinically AKI is characterised by a rapid reduction in kidney function resulting in a failure to maintain fluid, electrolyte and acid-base homoeostasis
One of:
Serum creatinine rises by ≥ ___µmol/L within 48 hours 
Serum creatinine rises ≥ ____ fold from the reference value, which is known presumed to have occurred within one week
urine output is < ___ml/kg/hr for >6 consecutive hours (Normal urine output range _____/kg per hour)
Renal Association
Also associated with uraemia
Usually Reversible

7. Epidemiology ___% of all inpatients develop acute renal failure.
Risk Factors:
Chronic Kidney Disease
Heart failure
Liver disease
Cardiovascular disease (previous MI, stroke, PVD)
Diabetes mellitus
Recent use of nephrotoxins, e.g. _____________________________________________________________________________________________________________

8. Pre-Renal Hypotension Shock Hypovolaemia Haemorrhage, Vomiting
Diarrhoea, Diuretics, dehydration
Renal Glomerulus Glomerularnephritis
Tubules Acute Tubular Necrosis
Interstitium Nephritis (NSAIDS, gent, ACE)
Vessels Vasculitis, coagulapathies
Post Renal Obstruction Stone
Tumour
Prostate
(Full list of Causes)

9. Signs and Symptoms Oliguria/ Anuria Fatigue Vomiting Pruritis
Confusion
SOB
Peripheral oedema
Oliguria/ Anuria
(How to Assess fluid status)

10. Hx and Ex Volume status by checking: For possible underlying causes:
Core temperature.
Peripheral perfusion.
Heart rate/blood pressure (and any postural changes).
Jugular venous pressure.
Moistness of mucous membranes, skin turgor.
For possible underlying causes:
Current symptoms, if the person is unwell (for example diarrhoea, vomiting, breathlessness).
Any recent symptoms that may suggest an underlying obstructive cause (for example lower urinary tract symptoms, bloating from a pelvic mass, renal colic).
Drug history
Social history — including exposure to tropical diseases (e.g. malaria) and exposure to rodents (e.g. leptospirosis, hantavirus).

11. Investigations ________________ CXR
Plasma sodium, potassium, urea, creatinine, glucose
Urine dipstick, microscopy, biochemistry, culture
(glomerulonephritis, acute pyelonephritis, and interstitial nephritis, tubular necrosis)
________________
“The most worrying findings are decreased or absent P-waves, PR prolongation, QRS widening, sine wave QRST, AV dissociation or asystole. It is often difficult to judge if T-waves are truly peaked and this finding on its own should not be an automatic indication for urgent therapy”
CXR
If a reference serum creatinine value is not available within 3 months (acceptable up to one year) and AKI is suspected repeat serum creatinine within 24 hours a reference serum creatinine value can be estimated from the nadir serum creatinine value if patient recovers from AKI

12. Complications
Uraemia
Fluid overload
Hyperkalaemia
Acidosis

13. Differential Diagnoses
Abdominal aneurysm
Alcohol toxicity
Alcoholic ketoacidosis
Chronic renal failure
Dehydration
Diabetic ketoacidosis
Gastrointestinal (GI) bleeding
Heart failure
Obstructive uropathy
Protein overloading
Renal calculi
Sickle cell anemia
Steroid use

14. Management
“Resuscitate patient with regards to their airway, breathing and circulation “
Get Senior help
Treat Dangerous complications:
Hyperkalaemia: _____________
Fluid Overload: _______________
Severe Acidosis: __________________
Severe Uraemia: _____________
Treat Underlying Cause:
Give Saline (cautiously)
Stop Nephrotoxic Drugs
Monitor Urine Output (hourly)
(Possibly) catheterise

15. Dialysis Indications for early dialysis:
Hyperkalaemia refractory to treatment
Pulmonary Oedema
Severe metabolic acidosis refractory to treatment
Uraemic encephalopathy
Uraemic Pericarditis

16. Management
Prevention: • Identify patients at risk (see AKI risk factors) •Optimise volume status •Treat sepsis promptly • Avoid nephrotoxins • Review medications, e.g. adjust drug doses, withhold antihypertensives if hypotensive • Reduce risk of contrast-induced AKI: • The risk of contrast-induced AKI is small in the general population • Patients at high risk are the acutely ill, with AKI/CKD, sepsis and hypovolaemia

17. Mortality
Mortality is ______% in those patients with isolated renal failure
This rises to 50-70% when ARF is precipitated by other organ failure