Key facts:
Authors: Stephanie Horne and Andrew Stein
Top Tip: Rehydrate, exclude obstruction (ultrasound), stop nephrotoxic drugs
Key Differential Diagnoses
- Chronic renal failure
- Raised creatinine, with another cause of metabolic acidosis
Key Investigations
- Urinalysis (heavy proteinuria = glomerular disease)
- U+E, LFT, Bone, Glucose, CK
- FBC, ESR, CRP, INR, VBG/ABG
- ECG, CXR
- Renal US
Key Treatment
- Rx underlying cause (especially sepsis, stop drugs)
- IV + FLUIDS (dry), or
- ± PO/IV FUROSEMIDE 80-250 mg od/bd (wet)
- ± IV INSULIN 10 units in 50 mls 50% DEXTROSE over 30 mins (if hyperkalaemic, and regime below)
- ± Urinary catheter
Key Management Decisions
- IV fluids or diuretics
- Dialysis
Background
Think about infection, dehydration and drugs; with underlying renovascular disease, myeloma or obstruction. Rapidly progressive intrinsic renal disease (glomerulonephritis or interstitial nephritis) is rare
'The Beautiful Glomerulus' (rarely the problem in AKI)
- There may be no symptoms or signs, but oliguria (urine output <400 mls/24 hrs) is common. But AKI (new name for ARF) can also be polyuric. Ie, urine output is not part of the definition of AKI. The K and creatinine should be ascertained immediately, with urinalysis organised in the first 1h, and a renal US within 12 hrs
- If indicated, a renal screen should be known in first 24 hrs (not just performed). Oligo-anuria means a urine output <100 mls/24 hrs. Rapid anuria is very rare and suggests: 1. acute obstruction; 2. acute/severe glomerulonephritis; or 3. acute renal artery occlusion. All require urgent senior review
- The main objectives of initial management. are: (1) to prevent cardiovascular collapse and death; and, (2) to call for specialist advice
- 95% of hospital-acquired and 75% of community-acquired AKI is pre-renal (mainly hypovolaemia)
- The hallmark of prerenal failure is that it is quickly reversible with appropriate therapy. Thus, it can be thought of as 'a good kidney looking at a bad world.' (Joseph V Nally, 2004)
- If not reversed, a 10-14 day period of Acute Tubular Necrosis (ATN) typically ensues, when dialysis is required. Renal function then almost always recovers, to the baseline creatinine
- The decision to dialyse is multifactorial; but fluid overload, a potassium of > 6 mcmol/L, a creatinine of >400 and urea >30 should make you think about it. Serum urea is a better marker of 'uraemia' (ie symptoms/severity) than creatinine, which is a better marker of renal function
- If urea > 50 mmol/L, you should have a good reason not to dialyse
Definition
- Rapid loss of renal function, associated with rapidly rising creatinine
Note: no agreed definition exists; this is debated in the RIFLE paper (2004) in 'prognosis' (below)
Epidemiology
- AKI not requiring dialysis is very common: >15% acute admissions have a creatinine > 120 mcmol/L
[Ref] - In one very large study, 7.2% developed a raised creatinine, whilst in hospital. This carried a poor prognosis, with a mortality of 19.4% (ie AKI that does not require dialysis also carries a high mortality): [Ref]
- But AKI, requiring dialysis is quite rare, approximately 200 patients/million/yr (about 2x the incidence of new ESRF); and has a very high mortality (>50%): [Ref]
Causes
- Pre (75%); often caused by the 'surgical triad' (= hypovolaemia, infection and drugs), or bleeding; recent angiography (or vascular surgery) can cause cholesterol emboli (rarely spontaneous). Angiography can also cause contrast nephropathy
Cholesterol emboli: Feet can reflect what is happening in kidneys: [Ref] - Renal (20%): two important groups:
- Drugs: NSAIDs; ACEi/ARB; diuretics (K sparing?); antibiotics (aminoglycosides nephrotoxic; penicillins (and others) can cause interstitial nephritis)
- Steroid-responsive nephritis: eg interstitial (antibiotics?) + glomerulo-nephritis
Note: Goodpastures Syndrome is rare, extremely. A regional renal unit might see 1-2 a year; this could be today of course. Henoch schonlein purpura (below) is more common, but still rare
- Henoch schonlein purpura (rare; rash typically on lower legs and buttocks)
Post (5%) = obstructive nephropathy (ON): prostatic hypertrophy (benign/malignant) in man, pelvic carcinoma in woman
Note: ON should always be actively excluded as it it usually reversible; and prompt treatment can prevent permanent renal damge; a 'normal' Renal US does not absolutely exclude obstruction (ie non-dilated obstruction can occur, eg retroperitoneal fibrosis)
Risk factors
- Age
- Atheroma
- Surgery/angiography
- DM
- Myeloma
- Previous CRF
Symptoms
- There may be no symptoms
- Of dehydration/fluid overload
- Uraemia (anorexia, nausea)
- Of underlying cause; eg, back pain suggests myeloma or anuerysm
- Oliguria (= < 400 mls/day)
Note: anuria is a medical emergency and suggests obstruction, vascular catastrophe or severe glomerulonephritis (or a blocked catheter)
Key question
- "Has anyone changed your tablets in the last 4-6 weeks?"
Signs
- Of dehydration/fluid overload
- Of underlying disease; eg vasculitis lesions; lower leg livedo reticularis rash suggests cholesterol emboli; epigastric or femoral bruits suggest renovascular disease; feel for aneurysm
- Palpable bladder (examine for); do a PR
Investigation
The K+ and creatinine should be ascertained within the first 1h, with urinalysis and a renal US (to exclude obstruction) within 12 hrs
Urine
- Urinalysis (heavy (proteinuria++) is hallmark of glomerular disease, until otherwise proven
- MSU (look for casts if ?glomerular disease)
- Urinary Na: <10 mmol/L suggests dehydration (or hepatorenal syndrome); unreliable test, if patient on/had diuretics
Blood
- FBC (severe = myeloma, haemolysis or bleeding?; low platelets = HUS/TTP?)
- CRP (sepsis?), ESR (myeloma?), INR
- U+E (K?), Bone (Ca? myeloma?), LFTs (high protein-albumin gap ?myeloma; low albumin ?nephrotic syndrome), Glucose, CK (rhabdomyolysis), PSA (if have good reason to believe obstructive nephropathy; false +ves in retention)
- VBG/ABG (acidosis? lactate?),
- BC (if pyrexial)
Other
- ECG
- CXR (pulmonary oedema?; pulmonary haemorrhage in pulmonary-renal syndrome eg ANCA+ve vasculitis or Goodpasture's Syndrome)
Pulmonary haemorrhage; looks just like pulmonary oedema (this patient had SLE)
Key investigations
- Urinalysis
- K+/Creatinine
- US
Specialist investigations
Blood
- 'Renal screen' =C3/4, Igs,ANA/dsDNA, ANCA, AGBM, PEP, Hep B/C/HIV
- If ?post-infectious GN, ASOT
- If ?haemolysis, LDH (high)/haptoglobin (low)
Other
- Renal US; the primary reason for doing an US is to exclude obstruction. But it has two other functions:
- find out whether patient has one or two kidneys (preparing for renal biopsy); and,
- looking for small kidneys (indicating CRF)
- renal biopsy/angiogram?
Note: when performed, biopsy affects management in 70%; AKI dogma: 'patient with AKI, normal sized kidneys, with no obvious cause = biopsy' And soon
Differential diagnoses
- Chronic renal failure
- Raised creatinine, and other causes metabolic acidosis
Treatment
The only two absolute indications for dialysis are hyperkalaemia (> 6.5 mcmol/L) and fluid overload, resistant to medical therapy. If urea is > 50 mmol/L, you have to have a good reason not to dialyse
Treatment - first line
Rx the underlying cause:
- Eg antibiotics if infected, unblock a catheter
Drugs (depends on fluid state)
- IV + FLUIDS, or
- PO/IV FUROSEMIDE 80-250 mg od/bd (80 mg if creat <200; 120 mg if 200-400; 250 mg, if 400+)
Note: furosemide increases UO, and treats hyperkalaemia and fluid overload but does not affect dialysis need or death; the main dangers of too much frusemide in ARF are seizures, deafness and bullous rashes
[Ref]
If hyperkalaemic
- IV INSULIN 10 units in 50 mls 50% DEXTROSE over 30 mins, if hyperkalaemic; watch for hypoglycaemia
- ± PO CALCIUM RESONIUM, 15 g qds, if hyperkalaemic
- ± IV 10% CALCIUM GLUCONATE 10 mls, if life-threatening hyperkalaemia, or cardiac instability
- ± Nebulised SALBUTAMOL 5 mg, if hyperkalaemic (brief action)
If hypercalcaemic
- ± IV DISODIUM PAMIDRONATE 15-60 mg over 30 mins via wide bore cannula in large vein (rate < 20 mg/hr in renal failure), if hypercalcaemic
Procedures
- IV
- If unsure re palpable bladder, catheterise
- If fluid overloaded and hypoxic, sit up and give OXYGEN (28-60% via Venturi Mask, or <100% via non-rebreathe Bag)
- If unwell, urinary catheter, CVP line + arterial line (if clotting/platelets OK)[Ref]
Key management decision
- Dialysis/not
Treatment - second line
- Dialysis
Note: no one type of acute dialysis has been shown to be superior to any other; though if patient is hypotensive, continuous forms (usually on ITU) are generally preferred; in extremis, venesection can be lifesaving, whilst waiting for dialysis - Indications for dialysis:
- Absolute (only 2)
K > 6.5, not responding to medial Rx
Fluid overload, not responding to medical Rx - Relative
Urea > 50 mmol/L (have to have a good reason not to dialyse)
Acidosis
Anaemia
Pericarditis
Reduced conscious level
- Absolute (only 2)
Treatment - third line (of 5 diseases to look out for)
-
Acute renal artery thrombosis/embolism (of a single functioning kidney): may be treated surgically, or by angioplasty and stenting
-
Rhabdomyolysis: alkaline diuresis may prevent the development of severe renal failure, but must be undertaken with care in oliguric patients
-
Acute tubulointerstitial nephritis: may respond to a short course of high-dose corticosteroids, though no controlled trials have been undertaken to support this approach
-
Crescentic glomerulonephritis: may respond to treatment with IV methylprednisolone and cyclophosphamide ± plasma exchange
-
HUS/TTP, if it has an immune basis: may respond to plasma exchange with fresh frozen plasma
Prescribing issues
- Take careful drug history; ring GP if necessary
Immunosuppression? = senior renal decision
- If suspect interstitial nephritis, consider PO PREDNSIOLONE 60 mg od
- If suspect glomerulonephritis, consider IV METHYLPREDNISOLONE 500 mg od
Stop
- Nephrotoxic drugs (aminoglycosides, NSAIDs)
- HMG CoA reductase inhibitor ('statin'), if CK raised
- ACEi/ARB, K sparing diuretic, if K raised
- Metformin, if creatinine >200 mcmol/L
Admit?
- Yes
Bed plan
- Medical admission ward
- ± Renal
- ± ITU
Referrals
Medical
- Renal (ring your nearest unit, if renal team not on site)
Other
- Pharmacist (drugs)
The Rest
Despite advances in dialysis technology, AKI still has a 50% mortality. Why is not clear. It may be 'a good kidney looking at a bad world'
Maxim
- "The first three cause of SOB in a patient with AKI or ACKI are pulmonary oedema, pulmonary oedema and pulmonary oedema"
Complications
- If dehydration is not treated promptly, Acute Tubular Necrosis (ATN) often follows; ie kidneys continue to be perfused but make little urine
- They usually restart working 10-14 days later. There may be an evolutionary advantage to this mechanism
- Dialysis may be necessary during this time
- ESRF rare (3%), except in cortical necrosis (pregnancy)
- Patients normally either die, or return to baseline creatinine
Follow-up
- Renal
Prognosis
- 50% overall mortality; 30% if on renal ward; 70% if on ITU
[Ref] - Poor prognosis: multisystems failure, oliguria, ventilation, burns, jaundice (especially if hyponatraemic), male, sepsis, MI/CVA; if on dialysis, worse prognosis if elderly, CNS depression, inotrope after 1st wk
- The 2004 RIFLE paper proposed a prognostically important scoring system:
RIFLE-R (>1.5x rise creatinine), RIFLE-I (>2x rise), RIFLE-F (>3x rise)[Ref] [Ref]
RIFLE criteria
Prognosis (by RIFLE criteria):
Crude hospital mortality for septic and non-septic AKI stratified by RIFLE category. Bagshaw et al. Critical Care 2008 12:R47 doi:10.1186/cc6863
2° Prevention + Health Promotion
- Avoid ACEi/ARBs in future, if thought to be factor in ARF
- Hydrate peri and post-operatively/angiogram (prevents contrast nephropathy)
Don't forget
- Renal US in first 12 hrs
- If performed, chase renal screen within 24 hrs
- Accurate drug history vital
- To examine for a bladder (if in doubt, catheterise)
- Rapid anuria suggests: 1. acute obstruction; 2. acute/severe glomerulonephritis; or 3. acute renal artery occlusion
Red flags
- K+ >6.4
- Fluid overload
- Acidosis, pH < 7.25