Acute kidney failure (acute kidney injury or acute renal failure) is the abrupt loss of the kidney's capacity to remove metabolic wastes from the blood and to maintain fluid and electrolyte balance in the body for optimum health. AKF, if left untreated, is potentially fatal.
Acute kidney failure (AKF), also referred to as acute kidney injury or acute renal failure, is the sudden disruption of renal filtration function, resulting in the accumulation of metabolic wastes and electrolytes in the blood, which is life-threatening. AKF is known to occur in hospitalized patients, especially those who are in an advanced stage of illness and who are, therefore, the most vulnerable among high risk groups. AKF may develop within hours or, at most, a few days, and as such, it is treated as a medical emergency. Presumably, except in the case of a patient with severe disease or multiorgan dysfunction, it is possible to reverse the damage to the kidneys and to recover from AKF.
The organization Kidney Disease: Improving Global Outcomes (KDIGO) considers a case as acute kidney failure when :
The pathophysiology of AKF  can be classified into three subgroups:
The cause of AKF is multifactorial based on the aforementioned classification. It ranges from impairment of blood flow to the kidneys, to infections and malignancies, and obstruction of the ureters. Symptoms are oftentimes generalized or mimic other diseases. Diagnosis is based on laboratory examinations and confirmatory imaging studies of the underlying causes of AKF. The rationale of treatment is to eliminate the causes and to restore the normal functioning of the kidneys. Prevention depends on a large extent on primary health care and avoidance of the predisposing conditions.
The underlying causes of acute kidney failure by location of injury :
Acute kidney injury is an escalating problem of clinical and public health importance. Two to three cases per 1,000 persons are diagnosed each year . Seven percent of in-patients and 75% of severely ill patients develop the disease in conjunction with multiple organ disorders.
Low blood pressure or slow blood flow to the kidneys diminishes the kidney's filtration function, causing the accumulation of nitrogenous waste products in the blood (prerenal azotemia). Consequently, the kidneys respond to the decrease in glomerular filtration rate by reabsorbing sodium and water back into the blood stream to maintain electrolyte and fluid balance. Baroreceptors in the carotid artery and aortic arch likewise respond by causing vasoconstriction of the glomerular efferent arteriole and dilatation of the afferent arteriole to limit glomerular filtration. The renin/angiotensin/aldosterone system is activated, whereby, angiotensin II, another vasoconstrictor, causes aldosterone to be released and resulting in reabsorption of sodium and water at the renal tubules. Hypovolemia (low blood volume) likewise stimulates the hypothalamus to signal the release of ADH (anitdiurectic hormone or vasopressin), leading to further resorption of water in the tubules thus, concentrating the urine.
After glomerular dysfunction, direct damage to the kidneys is brought about by pathophysiological processes involving the inner wall of small blood vessels and death of epithelial cells in the renal tubules or acute tubular necrosis (ATN), secondary to ischemia (lack of oxygen) of the kidneys. Damage is most severe in the proximal part of the tubule and outer layers of the medulla. Incremental reactive oxygen species, decreased ATP, and death of cells are the results of hypoxemia . Immune-mediated reactions such as, activation of complement, participation of cytokines, chemokines, neutrophils, complement-mediated attack on membranes, and vasoactive hormones all contribute to disrupting the integrity of the renal parenchyma. Exposure to poisons, medications, and contrast dye used for x-ray studies may also cause ATN. Toxicity to cells from the dye and constriction of blood vessels were observed in animal models. These resulted in increased viscosity, low oxygen tension in the blood and poor circulation in the renal medulla .
Renal injury at the level of the ureters is associated with blocked tubules resulting from increased internal pressure causing ischemia and degeneration. Presence of monocytes and macrophages, cytokines, free radicals, proteases, and TNF-beta are linked to direct damage on the tubules and fibrosis .
The possible involvement of a genetic component in the etiology of AKI is being considered with apolipoprotein E (APO-E) genes . More genes may be anticipated in future studies.
Recovery from acute kidney failure is determined by the nature and location of the underlying cause of the disease. Prognosis is good and full recovery may be expected when the disease process does not involve direct damage to the kidney parenchyma itself. Partial recovery is possible in cases where there is residual pathology. Prognosis is poor when the patient is in the advanced stage of disease at the onset of renal failure. Mortality is high in severe cases of acute renal injury .
In a longitudinal study of 1-10 years period, about 12.5% of survivors of acute renal failure had to undergo dialysis; 19-31% of these patients had chronic kidney disease. The mortality rate in hospitalized AKF patients is 40- 50%. The mortality rate among ICU patients with acute kidney failure requiring dialysis is 70-to 80%.
The presentation depends on the etiology and the stage of the acute kidney failure. Mild forms may be asymptomatic and are identified on laboratory examination. More severe cases may present with lethargy, fatigue, confusion, anorexia, nausea, and weight gain. The patient may be anuric, oliguric, pass normal volumes of urine or may even complain of polyuria.
Most persons with AKF are asymptomatic; if at all, the symptoms are generalized and physical examination is not conclusive. Oftentimes, the disorder is detected incidentally from the results of blood and urine tests during consultation for some other medical condition or purpose.
Laboratory predictors of AKF:
Urine output per unit time or metabolic waste excreted should be measured. Proteins and useful substances are excreted when kidney tissue is damaged. In case of renal retention, urine remaining in the bladder after micturation is measured by inserting a catheter into the bladder. This is done in postrenal failure due to enlarged prostate.
Dark-colored urine is due to the presence of creatinine and other substances in concentrated form. Microscopy will reveal blood, pus cells and casts as indicators of disease. Measurement of electrolyte levels can help identify the cause of AKF.
Ultrasonography of the kidneys and bladder can confirm specific causes of kidney failure . Biopsy can be done for histological assessment, if needed.
Complicated and advanced cases of AKF are confined in the intensive care unit of the hospital and treated as a medical emergency. Catheterization, endoscopy or surgery are indicated in cases of postrenal AKF or obstruction of the renal outflow.
Uncomplicated cases of less than 5 days duration, without infection or malignancy may heal spontaneously with palliative procedures alone. Restoring normal kidney function can be attained by:
For anemia, infusion of crystalloid (normal saline or lactated Ringers) or colloid (in cases of significant hypoalbuminemia) fluids with packed RBCs is recommended . Use of semisynthetic hydroxyethyl starch has been linked to higher mortality rates . Blood transfusion is optional if only 1 unit is required. Fluid resuscitation should be managed by an expert in this procedure.
Proper diet, with protein equivalent to 0.8 to 1 grams per kilogram of body weight (0.4 to 0.5 grams per pound) may be prescribed. No foods that are high in phosphorus (e.g., liver, nuts, dairy products, legumes, and soft drinks) to lower the phosphorus concentration in the blood. Calcium salts (calcium carbonate or calcium acetate) or sevelamer may be taken orally to lower phosphate levels in the blood. To reduce potassium level in the blood, sodium polystyrene sulfonate may be given per orem or via the rectum.
Prolonged AKF leads to the accumulation of metabolic wastes and excess fluids in the blood, necessitating removal of these by hemodialysis. Dialysis is initiated as per need or in some cases repeated for several weeks until the kidneys normal function is restored.
The National Institute for Health and Care Excellence (NICE/UK) recommends eliminating the causes of acute kidney failure as the best strategy for prevention . NICE guidance of 2013 emphasizes the importance of early detection of patients at risk by monitoring their urinary output and creatinine levels. Risk factors such as nephrotoxic drugs and iodinated contrast agents should be avoided. These guidelines apply to all acutely ill patients in hospital. An alternative to the use of contrast dye is intravenous volume expansion with isotonic sodium bicarbonate or 0.9% sodium chloride .
Acute kidney failure (AKF) is the sudden inability of the kidneys to filter off excess salts, fluids, and waste materials from the blood, which, if left untreated, can lead to fatal consequences. In-patients who are severely ill, are most likely to develop AKF. Sudden onset and rapid progression of the disease characterize AKF in contrast to chronic kidney disease in which the loss of kidney function is gradual and lasts over a long period of time. The cause of AKF is diverse which ranges from infection, trauma, pathophysiological processes, autoimmunity, systemic diseases, to malignancy. AKF occurs in three stages:
Conditions that predispose to acute kidney failure are: autoimmune diseases (e.g., acute nephritic syndrome and interstitial nephritis); acute tubular necrosis (ATN); severe or sudden dehydration; urinary tract obstruction; and toxicity from poisons or certain medications.
Reduced blood flow that are associated with the following conditions can impair kidney functions. These are: hemorrhage, septic shock, dehydration, low blood pressure, burns, trauma, serious illness, and surgery.
Conditions that are associated with clotting of blood, leading to AKF include: transfusion reaction; hemolytic uremic syndrome; scleroderma; idiopathic thrombocytopenic thrombotic purpura (ITTP); and malignant hypertension.
Symptoms that can occur abruptly and progress rapidly in AKF are edema and crackling sound in the lungs (due to fluid retention), nausea and vomiting, confusion, low back pain, dehydration, abdominal pain, and high blood pressure.
Routine laboratory tests for AKF include serum creatinine, creatinine clearance time, blood urea nitrogen (BUN), serum potassium, serum sodium, urinalysis (microscopy), estimated glomerular filtration rate (eGFR) and certain blood tests (optional). Preferred imaging procedure is ultrasound, others that can be helpful in detecting postrenal dysfunction are X-ray, MRI, and CT scan.
Treatment is based on mitigating and if possible, eliminating the conditions which lead to the development of AKF. Complete recovery is not always possible, but repair of the damage to the kidneys should at least restore part of the filtration function and normal physiologic responses. Early detection and prompt intervention can reverse the threat to human life.
Dietary restriction must be observed in terms of kinds and amount of fluids, protein (low), salt (low), carbohydrates (high) and potassium (low) to prevent the accumulation of toxic substances in the kidneys.
Prescriptions of antibiotics, for infection; diuretics, to facilitate excretion of urine; calcium and insulin, to regulate blood potassium levels must be complied with.
Dialysis may be needed to facilitate removal of accumulated nitrogenous waste in the blood. It is mandatory in cases of cessation of micturation, dementia, pericarditis, and high potassium blood level.