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.

Two small kidneys on ultrasound indicate chronicity.

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%

Post renal causes Obstruction Stones Tumor Enlarged prostate

Reversible pre renal acute renal failure

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

Metabolic acidosis Hypocalcaemia

Reduced renal production of 1,25 dihydroxychlocalciferol

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.

Renal replacement therapy This may be required as supportive

management in ARF.

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 %.

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