acute kidney injury & chronic kidney disease patrick elder & rob wise

Acute Kidney Injury & Chronic Kidney Disease

Patrick Elder & Rob Wise

Which 3 things does normal kidney function require?

Normal urine output requires:1. Adequate blood supply to

the kidneys2. Functioning kidneys3. Unobstructed flow of

urine from kidneys, down the ureters, into the bladder and out via the urethra.

What is the easiest way to classify kidney damage?

• Pre-renal

• Intrinsic (renal)

• Post-renal

Define Acute Kidney Injury (3 marks)

Kidney Damage (AKI)

•Exam AKI Definition:

•a sudden (over hours to days), significant deterioration in renal function that is potentially reversible

Clinical definition:

• An abrupt (within 48h) absolute increase in the SCr of ≥ 0.3 mg/dL (26.4 micromol/L) from baseline or

• A percentage increase in the SCr of ≥ 50% or

• Oliguria of < 0.5 mL/kg/h for > 6h

AKI: KDIGO Classification

Stage SCr criteria UOP criteria (duration of oliguria)

Stage 1 increase ≥ 26 μmol/L within 48hrs or increase ≥ 1.5 - 1.9 BL

<0.5 mL/kg/hr for > 6 consecutive hrs

Stage 2 increase ≥ 2 - 2.9 BL <0.5 mL/kg/ hr for > 12 hrs

Stage 3 Increase ≥3 BL or increase ≥ 354 μmol/L or commenced on RRT

<0.3 mL/kg/ hr for > 24 hrs or anuria for 12 hrs

SCr (serum creatinine) and UOP (urine output) remain the best biomarkers for AKI (RA, AKI Guidelines 03.2011)

Stage 1 = AKIN/ (KDIGO) definition of AKI

Just for Reference!

Pre-renal causesRenal hypoperfusion

Systemic hypotension- Hypovolaemia, hypotension (bleeding, dehydration)

- Sepsis- Anaphylatic shock

Local = hypoperfusion of the glomerulus- Renal artery stenosis (reduced glomerular pressure)- Drugs: ACE inhibitors, NSAIDs

Renal (intrinsic) causesMany causes

1. Tubular Acute Tubular Necrosis – often a result of pre-renal damage, nephrotoxins such as drugs, radiological contrast and myoglobinuria from rhabdomyolysis

2. Glomerular Glomerulonephritis – infection, drugs, autoimmune conditions such as SLE

3. Interstitial Interstitial nephritis (usually drug induced e.g NSAIDs, ABX)

4. Vascular Vasculitis, emboli, Malignant HTN, DIC...5. Complex mechanism (!) Multiple Myeloma

Post-renal causes

ObstructionIntrinsic- Urinary tumours e.g. RCC- Renal calculi

Extrinsic- Pelvic tumours (prostate, cervix, ovaries)- Strictures- Retroperitoneal tumours & fibrosis

Causes: summary

Pre-renal failure 85%– Hypoperfusion

Intrinsic renal failure 5%– Many causes– ATN

Post-renal failure 10%– Obstruction

Treatment of AKI• Treat underlying cause• Generic AKI management

– Pre-renal: IV fluids– Intrinsic: Treat medically (refer to nephrologist)– Post-renal: Relieve obstruction

• Percutaneous nephrostomy (drain pus/urine from kidneys)• Stents: antegrade (kidneys to bladder) vs retrograde (bladder to kidneys)

• Close observation:– BP, pulse– Daily weight– Fluid balance assessment– Resp function (Sats, RR, O2 requirement)

• Daily U&E• Review medications (nephrotoxins/dose adjustment)

Just for Reference!

• Define chronic kidney disease (3 marks)

Kidney Damage (CKD)

•Exam CKD Definition:

•a progressive, irreversible decline in renal function that takes place over months to years

•there must be impaired renal function for > 3 months.

Clinical definition:

• Impaired renal function for > 3 months based on abnormal structure or function or

• GFR < 60mL/min/1.73^2 for > 3 months with or without evidence of kidney damage

How many stages of CKD?

Causes

1. Endocrine: Diabetes – the most common cause (intrinsic)

2. Immunological: Glomerulonephritis – commonly autoimmune (intrinsic)

3. Unknown4. Cardiovascular: Hypertension or renovascular

disease (pre-renal)5. Infectious: UTI - Pyelonephritis and reflux

nephropathy (post-renal/intrinsic)6. Congenital: Polycystic kidney disease

Just for Reference!

Clinical features

• Pallor and malaise – due to anaemia• Pruritis – accumulation of urea + other

metabolites• Polyuria, nocturia • Bone pain – metabolic bone disease• Sleep reversal, restless legs

Treatment• Aim is to:

• Identify and treat reversible causes e.g. high blood pressure• Treat symptoms e.g. anaemia ,oedema, acidosis, restless

legs• ? Prevent progression to end stage renal disease

• Treatment of end-stage renal disease (ESRD):• Haemodialysis• Peritoneal dialysis• Kidney transplant• Conservative

Acute Kidney Injury(acute renal failure)

Hours - weeks

Chronic Kidney Disease

recovery

End stage renal disease (failure)

Months - years

Kidney Disease and Renal Failure

Kidney Disease and Renal Failure

Acute Kidney Injury(acute renal failure)

Hours - weeks

Chronic Kidney Disease

recovery

End stage renal disease (failure)

Months - years

Renal replacement therapy (RRT)

Dialysis Transplantation

Conservative therapy

+Clinical Case

• A 28 year old male body builder presents to A&E with terrible pain in his right sided abdominal pain. He has:

• Loin to groin pain (renal colic)– Can’t get comfortable– Radiates to testicle– Obstruction/extravasaion

• Haematuria – visible• Vomiting• Irritative voiding symptoms

What are the four most common types of renal stone?

• Calcium Oxalate (80%)• Calcium Phosphate (20%)• Uric acid (urate) (7%)• Struvite (infection/triple phosphate stones

(7%)

Where are the most common places a stone can get stuck?

• Any narrowings of junctions

• Pelvic ureteric junction• Pelvic brim• Ureterovesical junction• Bladder urethra outlet

X-ray landmarks

• Approximately 70-90% of renal stones are visible on a KUB X-ray

• How would we go about spotting one?

They lie at the level of T12-L3 and lateral to the psoas muscles. The right kidney is usually slightly lower than the left due to the position of the liver.