AKI - CKD Flashcards
Define AKI
• An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.
o NOTE: this can occur in patients with previously normal kidneys or in patients with pre-existing renal disease (acute-on-chronic)
What is used to determine AKI (3)
KDIGO
o Increase in serum creatinine > 26 umol/L within 48 hrs
o Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
o Urine volume < 0.5 ml/kg/hr for >6 hours
Commonest causes of AKI (3)
sepsis, ischaemia, nephrotoxins (SIN)
Pre-renal causes of AKI (10)
• Pre-Renal (40-70%) – INADEQUATE PERFUSION
o Anything causing renal hypoperfusion
Hypotension (e.g. shock, sepsis, anaphylaxis)
Hypovolaemia (e.g. haemorrhage, severe vomiting)
Renal artery stenosis, ACEi, NSAIDs, ARBs
o Heart failure – cardiorenal syndrome
o Cirrhosis – hepatorenal syndrome
Intrinsic renal causes of AKI (13)
o Glomerular - glomerulonephritis, haemolytic uraemic syndrome, autoimmune such as SLE, drugs
o Tubular - acute tubular necrosis (ATN) is commonest intrinsic renal cause; often occurs as a result of pre-renal damage or nephrotoxins (e.g. aminoglycosides)
o Interstitial - acute interstitial nephritis (e.g. NSAIDs, autoimmune), drugs, infiltration with lymphoma/infection/tumour lysis syndrome following chemotherapy
o Vascular - vasculitides (e.g. Wegener’s granulomatosis), large vessel occlusion
o Eclampsia
Intrinsic AKI classifications (5)
Glomerular Tubular Interstiitial Vascular Eclampsia
Pre-renal AKI mechanisms (5)
Hypotension Hypovolaemia Renal artery stenosis Heart failure Cirrhosis
Post-renal AKI classification (3)
Luminal
Mural
Extrinsic compression
Post-renal causes of AKI (11)
o Luminal: stones, clots, sloughed papillae
o Mural: malignancy (ureteric, bladder, prostate), BPH, urethral strictures
o Extrinsic compression: malignancy (esp pelvic), retroperitoneal fibrosis, prostatic hypertrophy
RF of AKI (18)
Age over 75
CKD
Comorbidities (heart failure, peripheral vascular disease, chronic liver disease, DM)
Malignant hypertension
Connective tissue disease (SLE, scleroderma…)
Myeloproliferative disorders (multiple myeloma)
Sepsis
Hypovolaemia
Use of nephrotoxic medications (aminoglycosides, vancomycin, ACEi if overused, NSAIDs)
Poor fluid intake/increased losses
History of urinary symptoms
Nephrotoxic drugs? (4)
Vancomycin, NSAIDs, aminoglycosides, ACEi if overused
Epidemiology of AKI
- 18% of adults admitted to hospital will develop an AKI
* Most common in the ELDERLY
S/s of AKI (17)
• Depends on underlying CAUSE • Oliguria/anuria o NOTE: abrupt anuria suggests post-renal obstruction • Nausea/vomiting • Dehydration • Confusion
- Hypertension or hypotension
- Distended bladder – palpable
- May have palpable kidneys (suggests polycystic disease)
- May have renal bruit (sign of renovascular disease)
- Dehydration - postural hypotension
- Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
- Pallor, rash, bruising (vascular disease)
Ix for AKI (metabolic 3, urinalysis 5, bloods 6, immunology 5, virology 2, imaging 3)
Basal metabolic profile (hyperkalaemia, high creatinine, metabolic acidosis)
• Urinalysis
o Blood - suggests nephritic cause
o Leucocyte esterase and nitrites - UTI
o Glucose
o Protein – suggests glomerular disease
o Urine osmolality
• Bloods
o FBC
o Blood film
o U&Es
o Clotting
o LFTs
o CRP
o Immunology
• Serum immunoglobulins and protein electrophoresis - for multiple myeloma
Also check for Bence-Jones proteins in the urine
• ANA - associated with SLE
Also check anti-dsDNA antibodies (high in active lupus)
• Complement levels - low in active lupus
• Anti-GBM antibodies - Goodpasture’s syndrome
• Antistreptolysin-O antibodies - high after Streptococcal infection
o Virology - check for hepatitis and HIV
• Renal Ultrasound
o Check for post-renal cause
o Can help distinguish obstruction and hydronephrosis
o Shows cysts, small kidneys, masses
• Other Imaging
o CXR - pulmonary oedema
o AXR - renal stones
Urine culture if suspicion of infection
What is urgent to check in AKI
K+ and ECG for hyperkalaemia
What do patients with glomerular disease show in a urine dip/exam
Patients with glomerular disease typically present with proteinuria and microscopic haematuria with hypertension and oedema.
What happens in prerenal azotemia
decreased renal flow stimulates salt and water retention to restore volume and pressure.
Mx of AKI (including for 3 types of KI)
• Begin with ABCDE approach along side checking for hyperkalaemia and treating if needed (10 ml 10% calcium gluconate, then 10 units actrapid in 50ml 20% glucose)
• Assess volume status – BP, JVP, skin turgor, capillary refill, urine output
• Aim for euvolaemia
• Stop nephrotoxic drugs such as ACEi, NSAIDs, ARBs, gentamicin, amphotericin, metformin
• Monitor – fluid status, daily U&Es
• Nutrition is vital in critically unwell patient – aim for normal calorie intake and protein.
• Treat the underlying cause
o Pre-renal: correct volume depletion with appropriate fluids/sepsis with antibiotics
o Post-renal: catheterise and consider CT of renal tract and urology referral if obstruction likely cause – requires urgent relief
o Intrinsic renal: refer to nephrology, check for signs of systemic disease
• Renal replacement therapy - dialysis
When is renal replacement therapy considered (4)
o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management
o Severe metabolic acidaemia
o Uraemic complications
Complications of AKI (5)
- Pulmonary oedema
- Acidaemia
- Uraemia
- Hyperkalaemia
- Bleeding
Indicators of poor prognosis for patients with AKI (5)
o Age o Multiple organ failure o Oliguria o Hypotension o CKD
Define CKD
- Progressive loss of kidney function over a period of months or years
- Defined as impaired renal function for >3 months with or without evidence of kidney damage i.e. GFR <60ml/min
Classifications of CKD
• Classification of CKD o Stage 1: Normal • eGFR > 90 ml/min per 1.73 m2 with other evidence of CKD (microalbuminuria, proteinuria, haematuria, structural abnormalities, biopsy showing glomerulonephritis) o Stage 2: Mild Impairment • eGFR 60-89 ml/min per 1.73 m2 with other evidence of CKD o Stage 3a: Moderate Impairment • eGFR 45-59 ml/min per 1.73 m2 o Stage 3b: Moderate Impairment • eGFR 30-44 ml/min per 1.73 m2 o Stage 4: Severe Impairment • eGFR 15-29 ml/min per 1.73 m2 o Stage 5: Established Renal Failure • eGFR < 15 ml/min per 1.73 m2 or on dialysis
