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Acute kidney injury : dr. Haidar Alamri

In other words AKI can be defined as an abrupt elevation in the serum creatinine
concentration or a decrease in urine output.

Why this sudden loss occur? For a kidney to function there should be sufficient amount of
blood reaching it , the internal structures in kidneys must function well , and lastly , the
passages the urine pass through to the exterior must be patent .

So if the blood reaching the kidney is not enough , the kidney will not works properly and
this is because of pre renal causes as the kidney itself is not damaged nor the passages of
urine is obstructed .

If the problem in renal parenchyma , the cause is said to be renal causes.

If there is an obstruction of urinary passages , the cause is said to be post renal causes.

when managed properly , pre renal and post renal causes are rapidly reversible.

Remember in definition we mentioned decreased urine output , AKI can be divided into
oliguric ( urine output less than 400 ml \24h) or non oliguric ( urine output more than 400 ml
\24h).

Clinical features :

The kidney is essential in filtering the blood removing nitrogenous waste products and
maintaining water and electrolytes balance so whatever the cause( pre renal , renal or post
renal ), when the kidneys is not functioning , the patient will suffers from signs and
symptoms of uremia ( accumulation of urea in blood ) and these includes :

Anorexia ( loss of appetite ) , nausea , vomiting followed by drowsiness, apathy, confusion,

Water and H ions will not be excreted properly so pulmonary odema or acidosis may
develops , so the patient may suffer from tachypnea ( increase respiratory rate ).

Anemia (decrease erythropoietin secretion ) bleeding ( abnormal platelets function ) or

Now there is a specific features for each of the three causes ( pre renal , renal and post renal
).

For pre renal AKI , the causes usually is either systemic ( hypotension so we look for postural
hypotension or signs of sepsis ) or local ( vasoconstriction of afferent renal vessels so we
should look for drugs ' ACE inhibitors , NSAID ..etc )
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For post renal causes: here there is an obstruction in urinary passages , as you know people
has two kidneys , two ureters and single bladder and urethra , and for AKI to develops , both
kidneys must be affected , so in most cases the obstruction is after bladder ( prostatic
enlargement , stone in urethra , bladder malignancy or involving both ureters for example
retroperitoneal fibrosis , or obstruction of ureter in patients with single kidney ) .

So we may expect to find symptoms and signs of distal obstruction (loin pain, haematuria,
renal colic or difficulty in micturition) .

For renal causes : kidney consists of glomeruli , tubules , interstitial tissue so parenchymal
diseases are either involving glomeruli ( acute glomerulonephritis, look for autoimmune
diseases like SLE, systemic vasculitis or goodpasture disease ) or tubules ( acute tubular
necrosis , the most common cause in hospitalized patients look for drugs e.g. paracetamol, ,
herbal medicines ,aminoglycosides, amphotericin, NSAIDs, ACE inhibitors or snake bite ) or
interstitial tissues ( acute interstitial nephritis again look for adverse drug reaction)

Investigations:

Increase blood urea and serum creatinine are the hallmark of renal failure ,

serum Electrolyte( usually shows high potassium level , hyperkalemia , low calcium and
high phosphorus usually indicate chronic kidney disease yet it may be found in some cases of
acute kidney injury such as rhabdomyolysis).

CBC looking for anemia

Fractional excretion of sodium : think of sodium as a water escort , so in pre renal AKI , the
kidney get small amount of water so it try to conserve each drop of it so it will reabsorb
water and hence sodium , so if we want to ensure that the cause of AKI is pre renal we
measure fractional excretion of sodium if it is less than 1% , the cause is pre renal .( this do
not apply if the patient is on diuretics).

GUE:

RBC Casts or dysmorphic ( abnormal shaped) RBCs suggest glomerulonephritis ,

Leucocytes suggest infection or interstitial nephritis,

MUDDY BROWN CASTS suggest ACUTE TUBULAR NECROSIS.

Renal ultrasound :

Looking for kidney size ( small kidneys indicate chronic Kidney Injury; post renal obstruction
leads to enlarged kidneys ; hydronephrosis and hydroureter)

ECG help in detecting electrolytes abnormalities and CXR helps in detecting pulmonary
edema .
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Treatment:

First thing we must do is correcting underlying causes , so if the problem is pre renal , we
give fluids , post renal causes are reversed by relieving the obstruction and renal causes
require detecting and stopping the cause ( stop nephrotoxic drugs and give
immunosuppression in case of autoimmune diseases)

Begin IV normal saline for patients with volume depletion. Stop potential nephrotoxic drugs
and look particularly for aminoglycoside antibiotics, ACE inhibitors, loop diuretics,
cyclosporine, and NSAIDs.

Select dialysis for:

• refractory hyperkalemia, acidosis , or volume overload

• signs or symptoms of uremia (altered mentation, asterixis, pericardial friction rub,

• certain drug intoxications

For urinary obstruction, choose a catheter to relieve bladder outlet obstruction. If the
obstruction is above the bladder, select retrograde or antegrade nephrostomies,