AKCUTE

KIDNEY
INJURE
 Definition
• Acute renal failure is a syndrome in which
acute and rapidly progressive (for days and
hours) violation of excretory renal function
with development of oliguria/anuria and
azotemia suddenly occurs with healthy or
slightly damaged kidneys
• The process can be reversed
 Ethiology
1. Prerenal causes

• Circulatory shock due to trauma, surgical intervention,

hemorrhage, etc.
• Hypovolemia due to dehydration or redistribution of
fluids (pancreatitis, burning).
• Decreased cardiac output in cardiogenic shock,
congestive heart failure, cardiac tamponade, acute
massive pulmonary embolism.
• Medicaments inhibiting vasodilating prostaglandins -
ACE inhibitors, non-steroidal anti-inflammatory drugs.
 Ethiology
2. Renal causes

• Glomerulopathies: acute glomerulonephritis, rapidly-

progressive glomerulonephritis, nephropathy of
pregnancy, hemolytic uremic syndrome.
• Tubulo-interstitial lesions: acute interstitial nephritis in
the use of nephrotoxic drugs (aminoglucosides,
analgine, amidophen, phenobarbital, radiofrequency
substances -urrograph, iodamide etc.), heavy metals,
industrial poisons (ethylene glycol) , mushroom
poisoning
 Ethiology
3. Post renal causes
Obstruction in urine output from the renal pelvis to
the urethra:
- bilateral or unilateral (in a single kidney)
obstruction of ureters from stones, clots, tumors,
etc.
- sub-physical obstruction - bladder sclerosis,
prostate adenoma and carcinoma, neurogenic
bladder.
 Pathogenesis

Pre-renal etiologic factors lead to a

reduction in circulating blood volume and a
decrease in renal blood supply (renal
hypoperfusion). As a result, renal ischemia
occurs and reduces glomerular filtration.
Functional renal failure develops, which is
reversible.
 Pathogenesis

In Renal acute renal failure results

in toxic damage to the renal
tubules from exogenous
(medications) or endogenous
nephrotoxins.
 Pathogenesis
Post renal etiologic factors result in acute
urinary obstruction, intrauterine pressure rise,
blockage of glomerular filtration and
discontinuation of diuresis.
 Clinical course
The syndrome occurs in 4 stages
1. Stage of latent renal damage
It is masked by poor general state of shock,
trauma or operation
 Clinical course
2. Oligo-anuria stage.
As a result of stopping production or irradiation
of the urine, the diuresis decreases below 500
ml / 24h (oliguria) and less than 150 ml / 24h
(anuria). There is azotemia - a progressive
increase in nitrogen-containing products (urea,
creatinine, uric acid). Azotemia causes
gastrointestinal disturbances - gastritis, colitis.
Occur easy fatigue, dizziness, nausea, vomiting,
somnolence. The tongue is enamelled, the breathing
is deep, loud, the heartbeat is fast. There are changes
in hydroelectrolyte exchange. Due to reduced diuresis
fluid is retained in the body. Hyperhydration occurs,
body swellings, body fluids, pulmonary edema and
cerebral edema occur. Of the electrolyte disturbances,
hyperpotasium is the most important one, leading to
disturbances in heart rhythm, AV block and heart
arrest.
 Clinical course
3. Stage of polyuria – continues for 2-3 weeks
• Increased diuresis
• Decreased azotemia
4. Stage of recovery – continues for a few
months. There is complete or defective healing
and 10 % of patients remain permanently on
hemodialysis
 Complications of acute renal failure

1. Pulmonary edema
2. Pericardial effusion
3. Brain edema
4. Erosive gastroduodenitis
 Prophylaxis
• Adult patients
• Patients with diabetes, high blood pressure,
myeloma
• Contrast induced nephropathy
 Treatment
I. Conservatively
1. Furosemide – amp. i.v. (100-400 mg/ 24 h)
2. Dopamin – with low blood pressure
3. Sodium bicarbonate – amp. i.v.
4. Treatment of hyperkalemia:
• Ca gluconici – 1 amp. 10 ml i.v.
• Ser. Glucosae 250 ml + 4E
Ins. Actrapid HM
• Furosemide