acute renal failure (arf) acute kidney injury aki is a sudden and usually reversible loss of renal...
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Acute renal failure (ARF)
acute kidney injury AKI is a sudden and usually reversible loss of renal function which develops over days or weeks and is usually accompanied by a reduction in urine volume.
A rasied creatinine level can be due to acute, acute on chronic of chronic kidney disease.
Causes of ARF Pre renal
Systemic Heart failure Blood/ fluid loss/ shock called hypovolemia
Local Renal artery stenosis Disease affecting arterioles
Under perfusion initially causes rapidly reversible changes,. Subsequently, acute tubular necrosis that may lead to intrinsic renal failure.
Intrinsic renal disease
Toxic /septic renal failure 85% glomerular diseases 5%
Primary Component of systemic disease
Interstitial disease 10%
Pathogenesis The kidneys can regulate its own
blood flow and GFR over a wide range of perfusion pressure
When the perfusion pressure falls—as in hypovolaemia, shock, heart failure or narrowing of renal arteries—the resistance vessels in kidneys dilate. It is mediated by prostaglandins.
(this is impaired by NSAIDS)
if autoregualtion of blood is fails, the GFR can stillbe maintained by selective constriction of efferent arteriols by rennin angiotensin mechanism ( it is inhibited by ACE inhibitors)
More sever or prolonged under perfusion of kidneys may lead to failure of these compensatory responses, and acute fall in GFR. This leads to formation of low volume concentrated urine (osmolality >600mOsm/kg) but low in sodium (<20mmol/l)
Note these changes may be absent in patient with pre existing renal impairment or those who received diuretics
Clinical features:
Marked hypotension Signs of hypoperfusion such as
delayed capillary return, cool peripheries etc.
Postural hypotension is reliable sign of early hypovolemia.
The causes reduces renal hypo perfusion
The sign suggesting following may be present
Shock Blood loss Crush injuries Burns SepsisThese causes should be assessed
Management Establish and correct the under lying causes is very
important step. Treat hypovolemia with restore blood volume as soon
as possible ( with blood, plasm, isotonic saline 0.9%) Optimize systemic haemodynamics. Monitoring the
central venous pressure and pulmonary wedge pressure is necessary for fluid administration.
Note: Meta analysis trials do not support the role of low dose dopamine in ARf.
Correct the metabolic acidosis Restoring the blood volume will correct the acidosis by
restoring the kidney function. Sodium bi carbonate (50 ml of 8.4%) may be used
severe acidosis.
Prognosis
Good full recovery of renal function if early treatment is given.
In some case treatments is ineffective and renal failure becomes established.
Established acute renal failure (ARF)
Acute renal failure (ARF) may develop follwing severe and prolonged underperfusion of kidneys when the histological pattern of acute tubular necrosis is usually seen.
Acute tubular necrosis (ATN) It is necrosis of renal tubular cells may
result from ischemia of nephrotoxicity caused by chemicals, bacterial toxins or combination.
Drugs includes Aminoglycosides antibiotics like
gentamicin, the cytotoxic drugs cisplastin, anti fungal amphotericin B.
Fortunately there is good recovery because renal tubular cells can regenerate and reform basement membrane.
Features of established ARF
These show the causal conditions Urea and creatinine
Raised urea and creatinine Alterationin urine volume
Oliguria/ anuria
Disturbance in fluid, electrolytes and acid base balance
Hyperkalaemia Due massive tissue breakdown,
hemolysis, and metabolic acidosis. Dilutional hyponatraemia
Oliguric patient continue to drink of excessive fluid is given
Uremia
Uremic features: Anorexia Nausea and vomiting Drowsiness Apathy, confusion Hiccups Fits, coma and death.
Respiratory features
Inc resp. rate due to acidosis infection pulmonary edema due to excessive
fluid administration
Blood
anemia Bloold loss Hemolysis Dec.erythropoetin secretion.
Platelets and cogulation dysfunctions. Severe infection
Depressed immunity.
Management
Initial Management is targeted at following priorities: Hyperkalemia Pulmonary edema Infection Uremia itself
Hyperkalemia i.v calcium gluconate (10ml of 10%
solution) Inhaled β2 agonist e.g salbutamol i.v glucose (50ml of 50% solution) Insulin 5 U actrapid Intravenous sodium bicarbonate. Iv lasix and normal saline. Ion exchange resin ( resonium) orally or
rectally Dialysis
Immediate fluid management
Volume replacement CVP monitoring Pulmonary edema may require dialysis to
remove water and sodium from the body. Temporary respiratory support
CPEP IPPVSevere acidosis may require sodium bi carbonate if
volume status allows
Addressing the underlying causes of ARF
Remove post renal obstruction Uretric dilation Prostate surgery Percutaneous nephrostomy
No specifis treatment of ATN immuno suppressive drugs for
rapidly progressive glomerulo nephritis.
Plasma exchange in micro angiopathic disease.
FlUID AND ELECTROLYTE BALANCE
After initial resusitation, Maintain I/O chart Daily weight
Daily intake should equal the urinr out put plus 500 ml to cover insensible loss.
Protein and energy intake By dietary protein restriction ( 40g
per day), in whom dialysis is likely to be avoided.
Patients on dialysis may require more dietary proteins ( 1 g / kg proteins daily and 10-12g nitrogen).
Adequate energy is needed in hypercatabolic states like sepsis and burns.
Infection control
Treated accordingly with porper antibiotics.
dose adjustment is required. Drugs like NSAIDS and ACE inhibitors
should usually be avoided.
Prognosis
In uncomplicated ARF, due to blood loss, hypovolemia, mortality is low.
In ARF associated with serious infection/ sepsis and multi organ failure , mortality is 50 to 70 %.