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Acute kidney injury is an abrupt (within 48 hours) reduction in kidney function currently defined as an absolute increase in serum creatinine of more than or equal to 0.3 mg/dl (≥ 26.4 μmol/l), a percentage increase in serum creatinine of more than or equal to 50% (1.5-fold from baseline), or a reduction in urine output (documented oliguria of less than 0.5 ml/kg per hour for more than six hours) (Mehta et al, 2007).
The urine output alone is not a good parameter to predict renal function, as acute renal failure may be present with polyuria, oliguria or anuria.
30% of critically ill patients suffer of acute kidney injury. Acute kidney injury doubles the mortality on intensive care units compared to patients with similiar disease without acute kidney injury.
The failure of renal function is due to deteriorating working conditions of the kidney. The most common reason is a reduced renal blood flow. Per definition, there is no primary renal disease or postrenal failure (no disorders of urine transport).
Trauma, burns, bleeding, allergic shock, sepsis, pancreatitis, dehydration.
Acute heart diseases such as myocardial ischemia, pulmonary embolism or decreased cardiac output due to mechanical ventilation.
Medication with ACE inhibitors or NSAID, anesthesia, hepatorenal syndrome, hyperviscosity syndrome in multiple myeloma or polycythemia.
The failure of renal function is due to renal diseases.
Acute necrosis of tubular cells is caused by ischemia or toxic substances. The damage to the kidney function is aggravated by dead tubular cells, which occlude the renal tubules. After repair of the tubular cells, the renal function can recover.
Toxic substances produced the tubular damage either by ischemia (e.g. vasoconstriction by contrast agents) or cell damage (e.g. cisplatin). Further common toxic substances for acute tubular necrosis are aminoglycosides, antibiotics, antifungals, chemotherapy, chemicals (heavy metals, solvents, insecticides), drugs (heroin, amphetamines), or D-penicillamine. Endogenous toxins are free hemoglobin (hemolysis) or myoglobin (rhabdomyolysis).
Postrenal kidney failure is the deterioration of renal function due to inadequate drainage of urine. This is the least common cause of acute renal failure, since one kidney is sufficient for the detoxification function and causes of postrenal kidney failure have to affect both kidneys.
Acute kidney injury causes a reduced salt and water excretion. This leads to weight gain, shortness of breath and pulmonary edema.
Potassium increases 0.5 mmol/l/day during anuria. Hyperkalemia is particularly serious with additional cell disintegration (tumor lysis, hemolysis, rhabdomyolysis).
Metabolic acidosis is caused by the lack of elimination of acids from the protein metabolism, which cannot be eliminated by respiration. Metabolic acidosis is pronounced in acute kidney injury due to diabetic ketoacidosis, lactic acidosis, liver disease and tissue ischemia.
Hyperphosphatemia and hypocalcemia develops due to secondary hyperparathyroidism.
Acute kidney injury leads to a decreased renal erythropoietin secretion, hemodilution and decreased survival of erythrocytes. The risk of bleeding is increased due to dysfunction of thrombocytes.
Uremia resulting from acute renal failure causes non-specific complaints. The underlying disease for the acute kidney injury is crucial for most of the symptoms.
Usually, a risk situation for renal ischemia or toxic renal damage is observable.
Flank pain, abdominal pain or neurological symptoms are suspicious for a postrenal kidney failure.
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