Acute Kidney Injury Flashcards
What tests are done to determine if there is a problem with the kidneys?
-Bloods
=Serum creatinine-reference range 60-110 micromole/L
=Calculates estimated glomerular filtration rate- reference range >60 mL/min
-Urine
=Urine output
=Urinalysis- blood and/or protein in urine
What is acute kidney injury?
-An abrupt decrease in kidney function
=Retention of waste products
=Impaired fluid balance
=Abnormal electrolyte balance (potassium)
-Staging system to stratify in studies (based in serum creatinine and urine output)
AKI is defined as any of the following:
- Increase in serum creatinine by > 26.5 μmols/L in 48 hours or,
- Increase in serum creatinine by > 1.5x baseline creatinine within last 7 days or
- Urine volume < 0.5ml/kg/hr for 6 hours
Describe diagnosis of AKI
- Diagnosis relies on assessment of renal function/ urine output
- Many patients will have pre-existing CKD
- Review of clinical events will normally identify cause
Describe Stage 1 AKI
Serum creatinine:
=1.5-1.9 times baseline/ >/26.5 micromoles/L increase
Urine Output:
=<0.5ml/kg/hour for 6-12 hours
Describe Stage 2 AKI
-SC:
=2.0-2.9 times baseline
-UO:
=<0.5ml/kg/hour for >/12 hours
Describe Stage 3 AKI
-SC: =3.0 times baseline/ increase in serum creatinine to >/353.6 micromoles/L / Initiation of renal replacement therapy -UO: =<0.3ml/kg/hour for >/24 hours OR =Anuria for >/12 hours
What are the causes of AKI?
-Pre-renal
=Reduced perfusion
=Blood supply problem
=Cardiac failure, sepsis, blood loss, dehydration, vascular occlusion
-Renal
=Within kidney
=Glomerulonephritis, small-vessel vasculitis, acute tubular necrosis, interstitial nephritis
-Post-renal
=Obstruction
=Stones, prostatic enlargement, prostatic cancer, retroperitoneal fibrosis, ureteral valve stenosis
Describe pre-renal causes of AKI
-Volume depletion/ Hypovolaemia
=Diarrhoea, bleeding, third space loss (ascites), diuresis, sepsis
-Hypotension
=Heart failure, sepsis, oedematous states, drugs, liver failure
-Renal ischaemia
=Hepatorenal syndrome, arterial occlusions, dissection of abdominal aorta, severe renovascular disease, renal artery stenosis
-Drugs
=NSAIDs, calcineurin inhibitors, ACE/ARBs
What mechanisms lead to AKI?
- Reduced glomerular perfusion
- Glomerular filtration rate is reduced
- Constriction of efferent arteriole
What mechanisms are activated in hypovolaemia?
-Sympathetic NS =Tachycardia, vasoconstriction -Renin-aldosterone axis =vasoconstriction =aldosterone stimulates salt and water retention -Neuroendocrine axis =increased antidiuretic hormone (ADH) =Reduced urine output
What is the hypovolaemia-initial fluid resuscitation?
-IV fluid challenge
=500mL 0.9% sodium chloride or plasmalyte over 15 minutes
=Reasonable to repeat if no response
=Do not give more than 2000mL as resuscitation fluid without senior input
What are the drugs that make AKI worse?
- ACE inhibitors and Angiotensin receptor blockers
- Blood pressure lowering drugs (beta blockers, amlodipine/ calcium channel blockers)
- Diuretics
- Non-steroidal anti-inflammatory drugs
- Radiocontrast agents
What is the initial treatment of AKI?
- IV fluids
- Stop nephrotoxins (withhold lisinopril and other blood pressure lowering treatments, NSAIDs)
- Physiological monitoring (pulse, bp, fluid input and output)
Why is hyperkalaemia life-threatening?
-Can lead to abnormalities in electrical conduction system of the heart (main intracellular cation)
=cardiac arrest
=asystole/ ventricular fibrillation
- Broad QRS complexes
- Tenting of T wave
- Loss of p wave
- Abnormal rhythms
- Sine wave
What is the most appropriate initial treatment for hyperkalaemia?
-Intravenous calcium chloride/ gluconate
=protects heart from hyperkalaemia effects
=stabilises myocardium for 20-30 minutes
What is the treatment for hyperkalaemia?
-IV calcium salts if ECG abnormal (lasts 30 mins)
-Insulin/ glucose and nebulized salbutamol
=Pushes potassium into cells, lasts 4-6 hours
-Treat underlying cause
=Need to get kidneys working to excrete potassium
What does acute tubular injury cause?
-Ischaemia (even less oxygen to hypoxic medulla so disrupts cellular energetics)
-Tubular injury and cell death
=Back leak of glomerular filtration
=Tubular obstruction by cellular casts (sloughed cells block)
=Inflammation (neutrophils and macrophages)
=REDUCED GLOMERULAR FILTRATION
Describe acute tubular injury
-Diagnosis of exclusion
=Is there is a treatable cause of renal failure?
-Follows many different causes of AKI (most common cause)
=Currently no preventative strategies
-Recovery is normal outcome with support but long-term consequences
What suggests a glomerular cause of AKI?
-Urinalysis of protein and blood (active urinary sediment)
-Creatinine raised
=Glomerular nephritis (inflammatory crescent= mass of inflammatory cells)
How is systemic vasculitis diagnosed?
-Dipstick urinalysis (protein and blood)
-Serum anti-neutrophil cytoplasmic antibodies (ANCA)
-Often present with coincident infection
-Tissue diagnosis
=Kidney most common
=Lung
=Nerve
What is the treatment for systemic vasculitis?
-Glucocorticoids
=Oral prednisolone
-Plasma exchange
=Significant renal disease and/or pulmonary haemorrhage
-Cyclophosphamide (kill lymphocytes)/ Rituximab (monoclonal antibodies aimed at B cells)
What are the common intrarenal causes of AKI in a ITU setting?
- Acute tubular injury (may follow severe hypotension)
- Rhabdomyolysis (crush injury/ long lie on floor after fall- myoglobin released from damaged muscles and taken up by tubular cells but cant be removed)
- Contrast nephropathy
- Interstitial nephritis (drugs- penicillin, NSAIDs)
- Systemic vasculitis
- Myeloma (tumour of plasma cells)
- Haemolytic uraemia syndrome (E Coli 0157 infection)
How can post-renal causes be diagnosed?
-Ultrasound renal tract (shows hydronephrotic kidney)/ bladder scan (estimate volume in bladder)
=renal pelvis seems larger and darker, causes kidney to be dilated
Describe hydronephrosis
- Renal pelvis seems larger and darker, causes kidney to be dilated (pressure of fluid)
- Pressure over time built up= persists so damage to kidney cortex
What are the lower urinary tract symptoms?
- Urgency
- Frequency
- Nocturia
- Incontinence
- Hesitancy
- Poor stream
- Terminal dribbling
What are the sphincters of the bladder?
-Internal urethral sphincter (involuntary)
=under control of alpha-1 adrenoceptor
-External urethral sphincter (voluntary)
*prostatic between
What are the treatments for hydronephrosis?
-Insert a urinary catheter
=allow decompression of renal tract
=may become polyuric (cant concentrate as well)
-Start an alpha-blocker (Tamsulosin)
=sphincter more capable of relax (less retention)
=trial without catheter (TWOC)
-May need transurethral prostatic resection (TURP) surgery due to renal impairment
What are causes of post-renal AKI?
- Pelvis cancer= cervical, ovarian
- Bladder lesions/ tumours can occlude ureteric orifice
- Blood clot in bladder
- needs to block both kidneys
- Prostate hypertrophy, cancer
- Ureter= calculi, tumour, extrinsic compression (retroperitoneal fibrosis, tumour)
Describe normal renal structure
- Glomeruli (filtering units)
- Tubules (reabsorption)
- Interstitium (bit in between tubules)= mainly comprises microvascular capillaries in health
- Mesangium (structural support)
Why is AKI important?
AKI is COMMON (affects 7% of hospital inpatients) and has adverse consequences:
- Increased length of stay in hospital
- Increased morbidity
- Increased hospital & post-discharge mortality
- Very costly (~£500 million/annum)
What adverse renal outcomes in severe AKI independently associated with?
- Increased incidence of chronic kidney disease
- Increased incidence of end-stage renal disease
How does myeloma lead to intrarenal obstruction?
-Lumen of nephron tubules obstruction
-Bone marrow tumour
-Proliferation of B cells= many single antibodies (paraproteins)
=precipitates in nephron- casts cause complete obstruction
What are the tubulointerstitial causes of AKI?
-Acute allergic interstitial nephritis (AIN)
=DRUG-RELATED e.g. PPIs, (omeprazole) antibiotics, diuretics, NSAIDs
=May have an eosinophilia (no rash)
=Often respond well to steroids
What are the causes of cesentric RPGN (rapidly progressing Glomerular nephritis)?
-Goodpasture’s syndrome: anti-GBM Ab (collagen in glomerular basement membrane)
-Wegener’s granulomatosis: PR3 Ab
-Microscopic polyarteritis (MPA): MPO Ab
=both have auto-antibodies to proteins in neutrophils
=vasculitis
-SLE: Anti-nuclear Ab (ANA), anti-dsDNA Abs (young women)
What is a disease of the vasculature of the kidney?
-Haemolytic uraemic syndrome (HUS)
=E coli related (E coli O157)
=Familial cases (genetic aetiology, complement)
=Glomerular microvascular thrombosis
Describe a clinical history in AKI
- Renal history – pre-existing renal disease, diabetes, family history
- Urine volume - ?acute oliguria
- Drug history – ? New drugs, nephrotoxic drugs (NSAIDs, ACEI, antibiotics)
- Systemic symptoms – diarrhoea, rashes etc
- Fluid status (JVP, postural BP) ?dehydrated
- ?evidence of infection
- ?rash, joint pathology
- Arterial bruits ?underlying renovascular disease
- Palpable bladder (obstruction)
- Check drug chart!
What investigations are down in suspected AKI?
- Urine dipstick – simple BUT important (blood, protein)
- Urine culture
- Renal Ultrasound - if obstructed then decompress
- Renal biopsy (AKI and normal sized kidneys)
- Angiography ± intervention
What blood tests are don is suspected AKI?
- FBC, blood film, clotting screen
- Biochemistry including Ca2+, PO42- LFTs and albumin
- Creatinine kinase (rhabdomyolysis)- statins, long lie
- Blood cultures
- Virology and serology e.g Hep B, ASOT
What immunological tests are done in AKI?
-IgGs and serum electrophoresis (myeloma)
-Complement levels (SLE, post strep GN)
-Autoantibodies e.g.
=Anti-nuclear factor (ANA) - SLE
=Anti-neutrophil Ab (ANCA) - vasculitis
=Anti-GBM Ab - Goodpasture’s syndrome,
What are the other tests that can be done in suspected AKI?
- Urine: Bence Jones protein = light chains (myeloma)
- Chest X ray (cardiac size, pulmonary oedema or haemorrhage)
- ECG especially if hyperkalaemia
Describe the general treatment for AKI
- Optimise fluid balance and circulation
- Stop exacerbating factors e.g. nephrotoxic drugs (check drug charts)
- Appropriate prescribing (check BNF, discuss with pharmacist) e.g. opiates accumulate in AKI
- Supportive treatment e.g. dialysis, nutrition
Describe the specific treatment of AKI
- Obstruction - drain renal tract
- Sepsis - effective antibiotics
- RPGN e.g. SLE - immunosuppression
- Goodpasture’s syndrome - Plasma exchange
- Compartment syndrome - fasciotomy
When do we start dialysis
-Severe Uraemia
=no prospect of immediate improvement
=uraemic encephalopathy or seizures
=uraemic pericarditis
-Hyperkalaemia unresponsive to medical treatment (>6.5)
=ECG changes
-Fluid overload, especially pulmonary oedema, resistant to treatment with diuretics/fluid restriction
-Severe acidosis (results in myocardial depression and hypotension)
What are the risks associated with haemodialysis?
-Vascular access related complications -
=Pneumothorax
=Infection
=Bleeding
- Anticoagulation required which may be problematic in patients with bleeding.
- Hypotension may be troublesome in some patients (sepsis, IHD, diabetes)
