Clinical assessment in AKI

How to investigate and treat a patient with acute kidney injury

Treat the imminent threat to life

Adopt an ABCDE approach
What is the potassium?
What is their fluid status?
Once these two urgent issues are addressed focus on the systemic history and examination looking for reversibility wherever possible

History
- Any obvious causes of decrease volume (Haemorrhage/haematoma, GI loss – D+V, renal loss, skin loss (burns/erythema), third spacing (pancreatitis), dehydration)
- Cardiac failure (recent echo? recent ischaemic insult to heart? etc.)
- Sepsis (and if so what is the source?)
Examination
- Cool peripheries = shut down
- Warm to touch = sepsis?
- Capillary refill time – greater than 2 seconds implies volume depletion or poor cardiac function
- Peripheral pulses = are they bounding
- Lying and standing blood pressure – significant drop implies hypovolaemia
- JVP: may be low if volume deplete or raised if heart failure or AKI causing significant volume overload (an emergency)
- Face – sunken eyes imply dehydration
- Reduced skin turgor
- Dry mouth and mucous membranes, dry lips – systemic hypovolaemia
- Signs of peripheral oedema – pitting oedema
- Lungs: signs of fine basal crepitations – pulmonary oedema. Signs of pneumonia – source of sepsis
- Heart: Listen for an S3 – fluid overloaded especially in CCF patients
- Abdomen: Shifting dullness, source of sepsis
- Urine output – catheterised if necessary

Hypovolemic picture: Hypotensive, peripherally shutdown with a lowered JVP
Cardiogenic picture: Hypotension, raised JVP, peripherally shutdown, early signs of fluid overload
Systemic vasodilation (Sepsis): Hypotension with wide pulse pressure, warm peripheries and low JVP.

History
- Cardiovascular history (smoking, DM, cholesterol, hypertension, PVD/IHD/CCF/stoke, AF, prosthetic valves)
- Known nephrotic syndrome (renal vein thrombosis)
- Recent infection – skin/throat
- “B type” symptoms – night sweats, weight loss and fevers
- Rashes, joint swellings
- Known autoimmune disease
- Easy bruising (myeloma)
Examination
- As for pre-renal but be wary of rashes, skin changes, arthropathy, uveitis, oral ulceration, epistaxis, new neurology including hearing loss, stigmata of endocarditis

History
- Lower urinary tract symptoms (LUTS) – frequency, urgency, dysuria, nocturia, poor stream, hesitancy, terminal dribbling, strangury
- Prostate disease
- Malignancy
- Haematuria (visible and non-visible)
- Loin pain
Examination
- As for pre-renal AKI but examine for palpable abdominal masses, palpable bladder, visible haematuria, rectal examination for prostate in males

Urine dip – always send for microscopy
- Sodium of <20 helpful is thinking pre-renal AKI
- Blood: vasculitits, acute GN, TMA, myoglobinaemia (send for centriguation)
- White cells: Infection, obstruction and AIN
- Protein: Acute GN, myeloma, TIN
- Can be normal in any aetiology of AKI
Bloods
- Routine FBC, CRP, U+Es, LFTs, Clotting, Bone profile (calcium and phosphate), CK and G+S
- Venous blood gas – rapid analysis of potassium, acidaemia and lactate
- Blood cultures is suspicion of sepsis
- If Renal AKI is suspected or history is suggestive of unusual pathology: ANA, ANCA, anti-GBM, ASOT, protein electrophoresis (urine and serum), immunoglobulins, Rheumatoid factor, viral serology, cryoglobulins, antiphosphplipid antibodies , blood film/LDH/reticulocyte count
Imaging
- CXR – urgent is signs of pulmonary oedema or haemoptysis
- USS renal tract as soon as possible – this must be urgent if infected hydroneprhosis is suspected
Renal biopsy
- In a rare number of cases
- Where a renal course is suspected and the biopsy will change management
- Indications include: Unexplained AKI, ?glomerular disease, prolonged AKI, suspected TIN and many more
Early involvement of nephrology is paramount when a complex cause of AKI is suspected or the patient is developing fluid overload, refractory hyperkalaemia, refractory acidaemia, and refractory uraemia or has an indication of dialysis. Early involvement of nephrology reduced mortality.