Acute Kidney Injury (Acute Renal Failure)

Acute kidney injury (acute renal
failure)
FAITH
Introduction
• A clinical syndrome where the kidney fails in
its excretory function and is hence unable to
maintain fluid and electrolyte homeostasis.
• Defined as sudden potentially reversible
reduction in renal functions.
• It is an abrupt reduction in glomerular
filtration rate characterised by increased blood
urea nitrogen.
• It usually lasts days to weeks and may be
reversible.
• ARF may have oliguria or anuria.
• Oliguria is urine output <0.5mls/kg/hr.
• In older children it is <400mls/day.Neonates
and infants it is < 1mls/kg/hr.
Effects of ARF
• The kidneys are unable to perform their major
functions of:
Fluid and electrolyte balance
Blood pressure control
Regulation of acid-base balance
Hormonal control
Excretion of toxic products of metabolism
Causes of ARF
• It is classified into I) prerenal= this is due to
renal hypo perfusion
• ii) intrinsic renal= due to parenchyma kidney
damage and
• iii) post renal which is due to bilateral
obstruction of urinary tract
Pre-renal causes
• It is due to inadequate perfusion to the kidney.
• It is the commonest cause of ARF in children.
• Causes include:
Dehydration
Hemorrhage
 Sepsis
 Hypoalbuminemia
 Cardiac failure
• If the underlying cause of the renal hypoperfusion
is reversed promptly, renal functions returns to
normal. If hypoperfusion is sustained intrinsic
renal parencymal damage can develop.
Treatment
Restore circulation by giving 20mls/kg over 30 min-
1 hour
In hemorrhage use volume expanders e.g dextran
fluids and whole blood.
Renal(intrinsic causes)
• Acute Glomerulonephritis
• Hemolytic-uremic syndrome
• Acute tubular necrosis Cortical necrosis
• Renal vein thrombosis
• Rhabdomyolysis
• Acute interstitial nephritis
• Tumor infiltration
• Tumor lysis syndrome
Post renal causes
 Posterior urethral valves
 Ureteropelvic junction obstruction(blockage at the
junction where the ureter attaches to the kidney)
 Ureterocele (swelling at the bottom of ureters)
 Malignancy
 Urolithiasis(minerals and acid salts)
 Hemorrhagic cystitis(urinary bladder lining becomes
inflamed and bleeds)
 Neurogenic bladder(lack bladder control due to a brain
,spinal cord or nerve problem)
Clinical manifestations
• A careful history and examination helps reveal
the cause of ARF
• Physical exam done : evaluation of volume
status is important e.g. prerenal renal failure is
initially associated with poor peripheral
perfusion while initial volume overload
suggests renal disease. Abdominal masses
may suggest obstruction
Laboratory findings
• Haemogram: may show anemia, leukopenia
(SLE), thrombocytopenia (HUS)
• Serum electrolytes: hyponatremia , raised
urea, creatinine, uric acid, K, phosphate
Laboratory
• Urine tests: hematuria, proteinuria, RBC casts
and granular casts suggest intrinsic renal
failure
• In pre-renal failure the specific gravity is raised
( > 1.020), urine osmolality is raised ( >500
mOsm/kg), low urine sodium (< 20 mEq/l) and
a fractional excretion of sodium –FENA < 1%
(2.5% in newborns)
Labs
• Intrinsic failure: specific gravity low (<1.010),
low urine osm (< 350 mOsm/kg), high urine
Na ( > 40mEq/l) and FENA > 2% (10% in
neonates)
• Chest xray: cardiomegaly and fluid overload,
• Renal ultrasound may reveal renal disease or
obstruction
• Renal biopsy may be required
Treatment
• Catheterisation may be needed to monitor
output and may relieve an obstruction
• Monitor fluid input/output, weight .
• If no volume overload then expand volume
with isotonic saline at 20 ml/kg in 30 min,
correct hypovolemia
• Hypovolemic patient will void in 2 hrs after
correction and failure suggests intrinsic/post
renal failure
Treatment
• Diuretics: only after correcting circulating
volume usually frusemide at 2-4mg/kg stat
(options – mannitol, bumetanide)
• If urine output not improved then continuous
diuretic infusion considered
• If diuretic challenge fails stop them and begin
fluid restriction- if normovolemic use urine
output for the day + insensible loss
(400ml/m2/d), restrict more if hypervolemic
Treatment
• Hyper kalemia develops in ARF so ECG monitoring is
useful, monitor these and levels and correct. Avoid
external K .
• Restrict salt and water-hypertension
• In severe anaemia transfuse packed cells 10mls/kg.
• Nutrition-sodium,potassium and phosphorus should
be restricted.
• Protein intake should be restricted moderately while
maximising carolic intake to minimise the
accumulation of nitrogenous waste.
• ARF patients prone to GIT bleed and may be
given H2 receptor blockers
• Hypertension is corrected by diuretics, salt
and water restriction,
• Long acting agents eg amlodipine, propranolol
and labetalol used
• Severe hypertension corrected with IV
labetalol, esmolol or nitroprussiden infusions
Indications of dialysis
• Volume overload with evidence of
hypertension/pulmonary oedema
• Persistence hyperkalemia
• Severe metabolic acidosis unresponsive to
medical management.
• Neurologic symptoms(altered mental
status,seizures)
• Blood urea nitrogen>100-150mgldl.
• Calcium-phosphorus imbalance with
hypocalcemic tetany.
Types of dialysis
• Intermittent haemodialysis-stable
hemodynamic status patients.
• Peritoneal dialysis-uses the lining of the
abdomen to filter blood inside the body done
in neonates and infants with ARF.
• Continuous renal replacement therapy-useful
in patients with unstable haemodynamic
status
Prognosis
• Depends on the underlying condition rather than ARF
itself
• If renal limited condition eg PSGN mortality is < 1%
while multiorgan failure >90%
• Complete recovery expected in prerenal failure, HUS,
ATN TSS(toxic shock syndrome) but not in
RPGN(rapidly progressive glomerulonephritis),
bilateral renal vein thrombosis,
• Long term sequelae include CRF, htn, RTA(renal
tubular acidosis) and urinary concentrating defect

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