Renal failure (acute)
D E FI N I T ION
Impairment of renal function over days or weeks, which often results in "
plasma urea/creatinine and oliguria (<400 mL/day) and is usually reversible. The term acute
kidney injury (AKI) represents the full spectrum of acute kidney dysfunction.
AE T IOLOGY Pre-renal (# renal perfusion):
Shock (hypovolaemic, septic, cardiogenic), hepatorenal syndrome (liver failure).
Renal:
Acute tubular necrosis (ATN): Ischaemia, drugs and toxins (paracetamol, aminoglycosides,
amphotericin B, NSAIDs, ACE-inhibtors, lithium).
Acute glomerulonephritis.
Acute interstitial nephritis: NSAIDs, penicillins, sulphonamides, leptospirosis.
Small or large vessel obstruction: Renal artery/vein thrombosis, cholesterol emboli, vasculitis,
haemolytic microangipathy (e.g. HUS or TTP).
Others: Light-chain (myeloma), urate (lympho- or myeloproliferative disorders, particularly
after chemotherapy/radiation induced cell lysis), pigment (haemolysis, rhabdomyolysis,
malaria) nephropathy, accelerated phase hypertension (e.g. in pre-eclampsia).
Post-renal: Stone, tumour (pelvic, prostate, bladder), blood clots, retroperitoneal fibrosis.
E P IDEMIOLOGY
A population-based study estimates an incidence of 1800 per million.
H ISTORY
Malaise, anorexia, nausea, vomiting, pruritus, drowsiness, convulsions, coma
(caused by uraemia). Symptoms of the cause or complications usually dominate (see below).
EXAMINA T I ON
Oedema, signs of the cause and complications (see below).
INVE S T I G A T IONS
Blood: ABG, FBC, U&E (urea, creatinine, Na
þ
, K
þ
), LFT, ESR/CRP,
Ca2þ
, clotting, culture, blood film: red cell fragmentation in HUS/TTP.
Other blood tests: CK (for rhabdomyolysis), urate, serum electrophoresis and autoantibodies.
Urine:Stick testing: Haematuria, proteinuria (e.g. glomerulonephritis).
Microscopy: Red cell casts (in glomerulonephritis). Culture and sensitivity. Bence-Jones
protein (exclude myeloma). Urine osmolality/Naþ
:
. Renal ARF: # Urine osmolality/specific gravity (as a result of # renal concentrating ability), "
urine Na
þ
(as a result of # reabsorptive ability), " fractional excretion of Na
þ
(PCr.UNa/
PNa.UCr): >2%.
. Pre-renal ARF: " Urine osmolality, # urine Na
þ
, # fractional excretion of Na
þ
(<1%).
CXR: To monitor for fluid overload.
ECG: Check for hyperkalaemia (tented T waves).
Renal ultrasound: To exclude an obstructive cause.
Renal biopsy (e.g. acute tubulointerstitial nephritis: tubulitis and intense interstitial cellular
infiltrate including eosinophils).
MANAGEMENT
Assess hydration and fluid balance: Pulse rate, lying and standing BP, JVP,
skin turgor, chest auscultation, ?peripheral oedema, CVP, fluid and weight charts.
Treat the complications:
Hyperkalaemia (if ECG changes or K
þ
>7 mmol/L):
. 10 mL of 10% calcium gluconate IV (protect the myocardium) and ECG monitoring.
. 50 mL 50% dextrose with 5U actrapid insulin over 15 min (drive K
þ
into cells).
. Nebulized salbutamol can also # K
þ
.
. Ca2þ
/Na
þ
resonium PO/PR (# bowel absorption).
. Contact renal team and arrange for dialysis if appropriate (see below).
Metabolic acidosis (if pH<7.2):
. 50–100 mL of 8.4% bicarbonate via central line over 15–30 min.
Pulmonary oedema:
. O2, consider CPAP.
. IV GTN 2–10 mg/h.
NEPHROLOGY
129
Renal failure (acute) (continued)
. IV furosemide: 250mg over 1 h, followed by infusion (5–10 mg/h).
. IV diamorphine (single dose of 2.5 mg) relieves anxiety and breathlessness.
Treat the cause:
. IV fluids if volume depleted: 500 mL colloid or 0.9% saline over 30 min, assess response
(i.e. urine output/CVP), continue fluids until CVP 5–10 cm. Inotropes if hypotension
persists in spite of CVP of >10 cm.
. Treatment of infection: adjust the dose of antibiotics in view of the renal impairment.
. Stop the nephrotoxic drugs (e.g. ACEI and NSAIDs) and non-essential drugs.
. Identify intrinsic renal disease and treat.
. Relieve the obstruction e.g. urinary catheter, nephrostomies.
Optimize nutritional support.
Identify and treat bleeding tendency: Prophylaxis with PPIs or H2 antagonist, transfuse if
required, avoid aspirin.
Indications for haemofiltration/dialysis (see below): Persistent hyperkalaemia (K
þ
>7 mmol/
L), fluid overload (e.g. refractory pulmonary oedema), pericarditis, acidosis (arterial
pH<7.1, bicarbonate <12 mmol/L), symptomatic uraemia (tremor, cognitive impairment,
coma, fits, urea typically >45 mmol/L).
Haemofiltration (continuous arteriovenous or venous–venous): Filtration of plasma water
across the membrane induced by the hydrostatic pressure gradient, and ‘convective’
transport of solutes in the same direction as water. Substitution fluid is required to prevent
excessive fluid removal.
Dialysis: Intermittent haemodialysis (using central venous catheters or arteriovenous fistulae)
or peritoneal dialysis (using a double cuff straight Tenckhoff catheter). Solutes passively
diffuse down their concentration gradient (urea, creatinine and potassium move from
blood to dialysate, calcium and bicarbonate, move from dialysate to blood).
Venesect 250–500 mL if delay for dialysis.
The choice of modality depends upon: availability, expertise, haemodynamic stability,
vascular access, and whether the primary need is for fluid and/or solute removal.
Haemofiltration is preferred in hypotensive or haemodynamically unstable patients since
the rate of fluid and solute removal is slow.
Treatment of pigment/light chain/urate nephropathy
Pigment nephropathy: Isotonic saline to maintain diuresis of 200–300 mL/h. Careful
monitoring for fluid overload. If a diuresis is established, switch to an alkaline solution
(bicarbonate). " Urine pH to >6.5 may # release of free iron from myoglobin and
intratubular pigment deposition and cast formation. If the desired diuresis is not
establishedwith adequate volume repletion alone: loop diuretics or mannitol (if mannitol
is used, monitor plasma osmolality).
Myeloma cast nephropathy: Thalidomide and dexamethasone to # light chain production.
Isotonic fluids (aim urine output 3 L/day), careful monitoring for fluid overload.
Urate nephropathy: Allopurinol, loop diuretic and fluids (to wash out the obstructing uric acid
crystals). Haemodialysis if diuresis cannot be induced.
COMPL I C A T IONS
Common and life-threatening: Hyperkalaemia, sepsis, metabolic acidosis,
pulmonary oedema, hypertension.
Less common: Gastric ulceration, bleeding (platelet dysfunction), muscle wasting (hypercatabolic
state), uraemic pericarditis, uraemic encephalopathy, acute cortical necrosis.
P ROGNOS I S ATN
has biphasic recovery starting with oliguria then leading to polyuria
(resulting from regeneration of the tubular cells). Prognosis depends on the number of other
organs involved, e.g. heart, lung. Many of those with ATN recover. Acute cortical necrosis
may cause hypertension and chronic renal failure
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