Lecture 10.1: Acute Kidney Injury Flashcards
What is AKI long-form?
Acute Kidney Injury
What are the Categories of AKIs? (3)
- Pre-Renal
- Renal
- Post-Renal
What happens to Urea & Creatinine in AKI?
Increases
When do AKIs occur (generally)?
- Usually a complication of serious illness
What is the definition of an AKI? (at least one of 3 criteria)
- Increase in Serum Creatinine by 26.5 μmol/l within 48
hours - Increase in Serum Creatinine to ≥ 1.5x baseline, known
/presumed to have occurred within the prior 7 days - Urine volume < 0.5 ml/kg/h for 6 hours (oliguria less
than 400ml per day)
Risk Factors for AKI
- Polypharmacy
- Elderly
- Multiple Co-Morbidities
- Diabetes
- Heart Failure
- Liver Cirrhosis
- Dehydration
- Infection/Sepsis
- CKD
- Renal Stones
- BPH
Classification of AKI (KDIGOL): Stage 1
- Serum Creatinine: 1.5–1.9 times baseline
OR ≥0.3 mg/dl ( ≥26.5 mmol/l) increase - Urine Output: <0.5 ml/kg/h for 6–12 hours
Classification of AKI (KDIGOL): Stage 2
- Serum Creatinine: 2.0–2.9 times baseline
- Urine Output: <0.5 ml/kg/h for ≥12 hours
Classification of AKI (KDIGOL): Stage 3
- Serum Creatinine: 3.0 times baseline OR
Increase in serum creatinine to ≥4.0 mg/dl
( ≥353.6 mmol/l) - Urine Output: <0.3 ml/kg/h for ≥24 hours
OR Anuria for ≥12 hours
Rifle and Akin AKI Classification
Causes of Pre-Renal AKI (6)
- CHF
- Liver Failure
- NSAIDs
- ARBs
- ACE Inhibitors
- Cyclosporine
How do CHF and Liver Failure cause AKI? (3)
- Hypovolemia
- Decreased Cardiac Output
- Decreased Effective Circulating Volume
How do NSAIDs, ARBs, ACE Inhibitors & Cyclosporine cause AKI? (1)
Impaired Renal Autoregulation
Causes of Renal/Intrinsic AKI (6)
- Ischaemia
- Sepsis
- Nephrotoxins
- Vasculitis
- TTP/HUS (Thrombotic Thrombocytopenic
Purpura, Hemolytic Uremic Syndrome) - Malignant Hypertension
- Acute Glomerulonephritis
How do Ischaemia, Sepsis & Nephrotoxins cause AKI? (1)
Tubular Damage
How do Vasculitis, TTP/HUS & Malignant Hypertension cause AKI? (1)
Vascular Damage
Types of Post-Renal AKI (2)
- Bilateral Ureteropelvic Obstruction
- Bladder Outlet Obstruction
Nephrotic Syndrome
- Nephrotic syndrome is a condition
involving the loss of significant volumes of
protein via the kidneys (proteinuria) which
results in hypoalbuminaemia - Massive proteinuria (≥3.5 g/day) * Hypoalbuminaemia (serum albumin ≤30
g/L)
Nephritic Syndrome
- Haematuria
- Mild to Moderate Proteinuria (typically less
than 3.5g/L/day) - Hypertension
- Oliguria
- Red Cell Casts in the Urine
Nephrotic Syndrome Mechanism
- Injury to Podocytes
- Scarring
- Deposition of matrix or other elements
Nephritic Syndrome Mechanism
- Inflammation
- Reactive Cell Proliferation
- Breaks in GBM (Glomerular Basement
Membrane) - Crescent Formation
What are some other Nephrotoxins? (3)
- Aminoglycosides Diuretics (gentamicin,
amikacin) - Bacterial endotoxins e.g. E.coli
- IV contrast (sometimes)
What happens in Tumour Lysis Syndrome?
- Cancer cells die rapidly → hyperuricaemia → Hyperphsophataemia
What are the Effects of Hyperuricaemia? (5)
- Precipitation in the renal tubules
- Renal Vasoconstriction
- Impaired Autoregulation
- Decreased Renal Blood Flow
- Inflammation
What are the Effects of Hyperphsophataemia?
- Calcium phosphate deposits in renal
tubules - Seizures/Muscle Cramps
Luminal Causes of Post-Renal AKI (3)
- Renal Stones
- Blood Clots
- Sloughed Tissue
Mural Causes of Post-Renal AKI (2)
- Strictures due to infection or post
TURP/TURBT - Cancer
Extrinsic Compression Causes of Post-Renal AKI (4)
- Benign Prostatic Hyperplasia
- Cancer
- Pregnancy
- Retroperitoneal Fibrosis
Signs and Symptoms of AKI (8)
- Nausea
- Lethargy
- Decreased Urine Output
- Haematuria
- Dysuria
- Fluid Overload (Oedema, Orthopnoea)
- Electrolyte Abnormalities
- Acid-Base Disturbance
