Acute renal failure (ARF) in burn disease results in a range of phenomena important not only from theoretical, but also from practical point of views, whose causes are manifold. ARF is generally defined as a rapid renal failure resulting in accumulation of protein metabolism degradation products (catabolism). It has been known, for some time, that thermal agents do not produce only local skin damages, but also disturb the integrity of the whole organism producing major functional damages of all organs and systems. Most frequently organs affected by burn disease are the following: the lungs, the heart, the kidney, the liver and blood coagulation systems. There are many factors influencing the renal function during the burns. The most important are: decreased cardiac output, respiratory failure with hypoxia and acidosis, toxaemia and sepsis [1, 4, 6 7, 8-10, 12, 19]. ARF in burn disease may be early due to hypovolaemia and hypoperfusion of the kidneys or late, occurring after a week as a consequence of infection and endotoxaemia. Development of ARF in burn disease is a very unfavorable prognostic sign necessitating a complex evaluation. Anuria in an early phase of burn disease may indicate the development of ARF, particularly if urine findings are positive to haemoglobin, proteins, myoglobin, which is of the utmost importance in deep burns inflicted by high voltage current. The immediate cause of anuria in burn disease may be a reflex transfer and penetration of the large quantities of toxic materials into the circulation form the region affected by burns leading to the spasm of afferent glomerular arteriolae producing sudden discontinuation of glomerular filtration. After burns, sudden increase in the osmotic activity ensues in the affected tissue. Some low molecular links may result, and such particles tend to change the osmotic balance and stimulate the development of oedema, and if not excreted, they increase osmolarity. In 20-30% of the patients with burn disease anuria is absent [2, 5, 11, 14, 18, 20]. The genesis of burn disease-associated anaemias is therefore multifactorial. These factors are the following: haemorrhage, haemolysis and etrythropoiesis level decrease. In massive burns, large amounts of non-specific inflammatory components are produced as well: prostaglandins, histamine, quinines leukocyte phenomena, bacterial toxins, etc. [1, 6, 13-16]. The study based on a years-long treatment of our patients with burn disease included on 100 patients. The youngest of the patients was 14 years old, and the oldest 65 years. The percent of burns-affected body surface ranged from 25% to 75%. In 3/4 of the patients the picture of an early renal failure developed, with oliguria immediately after infliction of the burns with rapid increase of serum urea and creatinine levels, while in 1/4 of the patients ARF occurred on the eighth day following the infliction of the burns. "late form of acute renal failure". Among our series with burn disease, anuria was present in 34.0% of patients and oliguria in 25.0%. ARF (early phase) occurred in 59 patients, 38 patients had no sing of ARF, while late ARF developed only in 3 patients. ARF-associated mortality rate was high among these patients (23%), being 6% among anuric patients with ARF and 17% in patients with ARF with anuria. Seventy-seven percent of the patients survived, and their serum and urine analyses performed upon subsequent out-patient follow-up examinations ranged within normal values. Such high percentage of survival among our patients included in the study is based on an early diagnosis of ARF, understanding of pathophysiology of shock associated with burn disease, adequate therapeutic approaches, including both medicamentous treatment and extracorporeal haemodialysis along with early surgical management (Shema 1, 2). For the time being, haemodialysis is the most effective therapeutical procedure in the treatment of ARF, although the mortality rate of dialyzable patients