Acute kidney injury or AKI is a common cause of concern for both patients and physicians. This article explains the AKI definition, causes, symptoms, and treatment.
Acute kidney injury or AKI is a rapid or abrupt decline in kidney filtration function. When this happens, the kidney loses its ability to eliminate the byproducts of the body’s normal metabolism, like salts, waste material, and fluids from the blood. This causes waste material and electrolyte accumulation and fluid overflow, which can be life-threatening. Unresolved acute kidney injury can lead to chronic kidney disease (CKD), a permanent condition.
Acute kidney injury is a reasonably common condition among hospitalized patients. In the United States, about 1 % of patients admitted to hospitals have some degree of AKI when admitted.
Usually, AKI is an incidental finding in patients that go to the emergency room with another chief complaint. Heart failure is a good example. In the United States, 2 to 5 percent of all hospitalized patients develop acute kidney failure at some point during admission.
Besides, in intense care unit patients (ICU), that number goes up to a baffling 67%. In post-operated patients or patients after surgery, AKI incidence, or cases is up to 2%. The people who die after 90 days of acute kidney failure are 25%, and 23% progress to a higher stage of kidney problems. Acute kidney failure represents 95% of all nephrology consults in a hospital center.
Kidney function and the basics of acute kidney injury can be an overwhelming subject. I am a medical doctor. In this article, I will describe everything you need to know about acute kidney injury in a detailed and simple manner.
What is the kidney, and what does it do?
The kidneys are two coffee bean-shaped organs found in the posterior part of the abdominal cavity which name is retroperitoneum. They connect with the bladder through two thin muscle tubes called the ureters.
The kidneys’ primary function is to filter blood, remove excess fluid, electrolytes, and waste material to make urine. Urine flows from the kidneys to the bladder. Then, it goes from the bladder to the urethra and finally, from the urethra to the toilet.
The kidneys are vital in maintaining a healthy balance of electrolytes, fluids, acids, and bases in the body. They are also crucial in arterial tension regulation and are the target of important antihypertensive medications (i.e., ACE inhibitors). Kidneys also produce essential hormones that control red blood cell production.
Each kidney is made up of millions of nephrons. Each nephron has two main parts the glomerulus and the tubule. The glomerulus is the filter, it works more or less in the same way as a coffee filter does. The tubule removes and adds different elements to the original filtrate according to the body’s needs.
For example, in the dehydrated person, the tubule will absorb a lot of the fluid from the original glomerular filtrate. If a person has excess acid in the body, the tubules will excrete that acid and reabsorb bicarbonate in turn. The substances and fluid the tubules do not reabsorb become urine that flows into the bladder.
Blood flows into the kidneys through the renal arteries. This is a large artery that branches out into smaller and smaller vessels until finally, blood reaches the nephrons. The kidneys filter out about 150 quarts of blood every day. Of those 150, about 99% is reabsorbed in the tubules. Only 2 quarts of the blood of the original 150 becomes urine.
What is creatinine, and why is it so important?
Creatinine is a waste product that comes from our normal metabolic processes. What makes creatinine so special is that it is one of the few substances that is completely filtrated in the glomerulus as it is neither reabsorbed nor secreted in the renal tubules.
These characteristics make creatinine levels a great indicator of how well is the kidney filtrating the blood. If creatinine rises above normal levels, that means that for some reason, the kidney is unable to excrete it in the urine, which causes it to accumulate in the blood.
Creatinine levels measurement is one of the most important diagnostic tools in renal injury. Creatinine helps calculate the glomerular filtration rate, which is the amount of blood the kidney filtrates per minute.
Normal creatinine levels range between 0.9 to 1.3 mg/dl in men and 0.6 to 1.1 in women. Any creatinine value above that is indicative of some form of kidney damage.
How is acute kidney injury defined?
Acute kidney injury is a relatively new term that replaces the old term of acute kidney failure. Acute kidney failure is an outdated term that refers to severe acute renal dysfunction with extreme fluid and waste retention with small or absent urine output. The problem with that definition is that recent research shows that subtle increases in serum creatinine or a small decrease in urine output in a short period may also lead to severe clinical consequences.
In 2012, an organization called KDIGO (Kidney Disease: Improving Global Outcomes), published the definition. According to it, acute kidney injury is an abrupt (in hours) decrease in kidney function, which encompasses injury (structural damage) and loss of function. The current diagnostic approach focuses on an abrupt rise in serum creatinine levels and/or a sharp decrease in urinary output in a given period.
Why have a definition of acute kidney injury?
The idea behind the new definition of acute kidney injury is to enable early recognition and treatment. Earlier treatment leads to fewer complications, fewer deaths, and shorter hospital stays. AKI diagnosis requires at least one of the following three:
- A rise in creatinine over 50% of its baseline value
- A fall in the glomerular filtration rate by over 25%
- A decrease in urine output value below 5ml/kg/hour
The goal is that these changes will allow doctors to detect high-risk patients earlier to prevent future complications or death.
Who gets acute kidney injury?
Everybody can suffer from acute kidney injury in certain conditions. For example, a perfectly healthy 20-year-old person can have acute kidney injury if he or she has an accident with severe blood loss.
A 10-year-old with no previous medical condition can suffer acute kidney injury after streptococcal pharyngitis complicated with glomerulonephritis. So, nobody is totally safe from AKI.
However, some individuals have a higher risk than others. Here is a list of the most important risk factors for AKI:
- Preexisting chronic kidney disease probably the most important risk factor
- History of heart failure
- History of diabetes
- The old age of 65 and over
- Septic patients
- Chronic infection
- Post-surgery. Particularly after cardiac surgery
- Nephrotoxic drug ingestion, for example, NSAIDs, aminoglycosides, amphotericin B, and vancomycin.
- Exposure to iodine contrast in the last week
- Blood loss or transfusion
- History of liver disease
- History of autoimmune disease
- Multiple myeloma patients
What are the three types of AKI?
There are many causes of AKI, including infections, heart disease, liver disease, autoimmune diseases, cancer, hypertension, and traumatisms. In short, causes are uncountable.
Having this many causes for a single condition can be overwhelming, even for experienced physicians. That is why the medical community divides AKI causes into three main categories prerenal AKI, intrinsic AKI, and post-renal AKI.
Every time a doctor faces an acute kidney injury, the first thing he will do is classified as prerenal, intrinsic, or extrinsic. Some AKI patients have mixed conditions with both an intrinsic and post-renal component.
Many times untreated AKI evolves to intrinsic AKI. Patients with chronic kidney disease (CKD) can present a sudden worsening in their condition. This situation also classifies as AKI. Acute kidney injury often speeds up CKD.
What is Prerenal AKI?
Prerenal AKI is the result of decreased renal perfusion (blood flow). Prerenal AKI represents around 70% of all cases of acute kidney injury.
In most cases, the kidney is perfectly capable of filtrating blood, secreting and excreting products in the tubular system, and producing urine according to the body’s needs.
There is nothing wrong with the kidney itself, the problem is that there isn’t enough blood reaching the glomeruli.
Suppose decreased blood flow persists for a long time. In that case, the kidney itself can suffer damage, and the injury evolves from prerenal to renal. Prerenal AKI has many causes, here is a list of the most frequent ones:
- Volume depletion: Like in severe diarrhea or severe vomiting. Individuals in extreme age groups (elders and infants) are more vulnerable to AKI due to vomiting and diarrhea.
- Hemorrhage: As in accidents, gunshots, and GI bleeds
- Certain medications: Angiotensin-converting enzyme inhibitors (ACE inhibitors) like Captopril, Enalapril, and Ramipril. Angiotensin receptor blockers (ARBs) like Losartan and Olmesartan. Non-Steroid Anti-inflammatory drugs (NSAIDs) like Ibuprofen or Diclofenac.
- Heart Failure: In which the heart is unable to pump enough blood to the kidney.
- Atherosclerosis leads to renal artery stenosis.
What is Intrinsic AKI?
In intrinsic acute kidney injury, there is structural kidney damage that can be the consequence of primary kidney disease, a complication of another disease in a distant organ, drug toxicity, or prolonged hypo-perfusion.
The approach to intrinsic renal injury varies according to the affected part of the kidney. Intrinsic kidney diseases are broadly categorized as glomerular, tubular, or interstitial.
Glomerular causes involve the inflammation of the glomeruli and the blood vessels surrounding them. Glomerulonephritis is usually the result of an autoimmune process like Systemic Lupus Erythematosus or Goodpasture Syndrome and streptococcic glomerulonephritis.
The term interstitial nephritis refers to the inflammation of kidney tissue that is not part of the nephron. Allergic interstitial nephritis (AIN) is the most common form of acute interstitial nephritis.
Most of the time, AIN is the result of medication drugs. The most common culprits are NSAIDs and antibiotics like cephalosporins, penicillins, sulfonamides, rifampin, and ciprofloxacin.
Interstitial nephritis is often a severe condition that frequently leads to CKD.
In acute tubular necrosis, an important part of the tubular system is destroyed. It causes the kidney to lose its ability to reabsorb and secrete elements to maintain body homeostasis.
The most common cause of acute tubular necrosis is prerenal AKI, followed by drug toxicity. Drugs like amphotericin b, some NSAIDs, some anesthetics, aminoglycoside antibiotics, sulfa drugs, contrast agents, are some of the most common culprits.
Sepsis (a potentially life-threatening response to infection) is another cause to take into consideration.
What is post-renal AKI?
Post-renal AKI is the result of a blockage in urine outflow outside the kidney. It is due to a blockage in any part of the urine outflow system, including the renal pelvis, the ureters, the bladder, and the urethra.
The blockage causes increased backward pressure, which leads to increased intratubular pressure and a decreased glomerular filtration rate. In some cases, obstruction causes the kidneys to fill up with liquid (hydronephrosis). Some common causes include the following:
- Kidney stone disease
- Tumors that compress the ureters
- Abdominal hematoma that compresses the urinary outflow system.
- Benign prostatic hypertrophy
- Renal vein thrombosis
- Obstructed Foley catheter
- Bladder stone
How does infection cause AKI?
Many types of infection can cause acute kidney injury. The same infection can cause AKI by different individuals’ mechanisms.
Infections can cause kidney injury by direct invasion or by inducing autoimmune mechanisms. Viruses, bacteria, parasites, and fungi can cause AKI.
Examples of an infection that cause acute kidney injury due to direct damage to kidney tissue include:
- Leptospirosis: Mainly by interstitial nephritis.
- Acute pyelonephritis: E. coli is the most frequent microorganism. However, other microorganisms like Klebsiella spp., Enterobacter spp., Pseudomonas aeruginosa, Staphylococcus aureus, and Enterococci can also cause acute pyelonephritis.
- Nematode infections
- Fungal infections: Fungal infections are particularly frequent in hospitalized patients, infections from microorganisms like Candida, Aspergillus, and Mucor can present as fungal balls, micro-abscesses in the renal vasculature that causes microinfarctions.
Examples of infections that cause immune-mediated kidney injury include:
- Streptococcal pharyngitis and erysipelas: Weeks after the primary infection resolves, immune complexes deposits in the kidney’s basal membrane cause glomerulonephritis.
- Hepatitis B infection: Hepatitis B infections can produce glomerulonephritis by similar mechanisms as streptococcus.
- Hepatitis C virus
- Epstein Barr virus
- Human immunodeficiency virus
- Hanta Virus
Sepsis is a dysregulated immune response to infection that leads to organ damage far from the original site of infection. The setting of acute kidney injury during sepsis is one of the most important predictors of death or mortality.
This situation has a significant effect on other organs’ functions. Also, it leads to more complications as a lengthy stay in the intensive care unit.
The mechanisms that produce septic AKI are more complex than direct invasion and immunocomplex deposition. In fact, the exact mechanism is not yet fully understood.
However, researchers believe septic AKI is the result of merging multiple factors, including hypotension, vascular dysfunction, immune cell infiltration in the renal tissue, thrombosis, and tubular obstruction.
What does AKI stage 1 mean?
The staging system proposed by KDIGO grades AKI severity based on serum creatinine levels and urine output (or quantity of urine produced throughout the day):
- Firstly: In AKI stage 1, there is an increase of 1.5 to 1.9 times over the baseline serum creatinine level in the last 48 hours or a urine output of fewer than 0.5 ml per kg per hour for 6 consecutive hours.
- Secondly: In AKI stage 2, there is an increase of 2 to 2.9 times over the baseline serum creatinine level or a urine output of fewer than 0.5 ml per kg per hour for 12 consecutive hours.
- Thirdly: In AKI stage 3, there is an increase of 3 times over the original serum creatinine level, the need to begin renal replacement therapy, or a urine output of 0.3 per ml per kg per hour for over 12 hours or anuria over 24 hours.
What are the symptoms of acute kidney injury?
The symptoms of acute kidney injury can vary greatly from patient to patient, and the clinical picture depends mostly on the underlying cause of AKI as well as on the severity of it.
Most of the time, patients will not present symptoms of AKI itself. Still, they have symptoms of the underlying cause, such as swelling of the extremities and difficulty breathing in acute decompensated heart failure, for example.
Most patients with mild or moderate acute renal injury are identified through laboratory testing rather than by symptoms.
However, patients with severe AKI and high creatinine levels can present with uremia (waste accumulation) and the symptoms that come with it.
Some of these symptoms include lightheadedness, confusion, decreased consciousness, decreased appetite, nausea, vomiting, and swelling in the eyes due to edema.
Moderate to severe patients can also present a decreased urine output. A decrease in urine output can be either oliguria ( urine output less than 400ml per day) or anuria (urine output of less than 100ml per day).
Other symptoms seen in severe cases include anemia, bleeding caused by uremic platelet dysfunction, and coma.
What are the signs and symptoms of prerenal AKI?
Some signs and symptoms can point towards specific pathologies. Prerenal AKI usually presents with other symptoms of hypovolemia like tachycardia, low blood pressure, dizziness, and decreased urine output.
Patients usually have a history of hemorrhage, diarrhea, vomiting, or heart failure symptoms.
What are the signs and symptoms of intrinsic AKI?
Intrinsic renal failure presents with different symptoms depending on the location of the injury. Glomerular pathologies usually present with macroscopic or microscopic blood in the urine (hematuria), swelling (edema), and hypertension.
The triad of hematuria, hypertension, and edema is the hallmark of nephritic syndrome. Acute tubular necrosis occurs in the context of sepsis, hypotension, or exposure to nephrotoxic agents. Clinical findings are unremarkable, and diagnosis is made based on laboratory findings.
In tubular necrosis, there is polyuria instead of oliguria. That is to say, that instead of urinating too little, these patients will be urinating a lot.
With no tubular function, the kidneys lose their ability to reabsorb water from the urine. Allergic interstitial nephritis has a history of antibiotic therapy, and patients usually present with fever, rash, and eosinophilia (high levels of a specific white blood cell-eosinophil).
What are the signs and symptoms of postrenal AKI?
Postrenal AKI presents itself with symptoms of urine retention or prostatic disease. Including post urinary drip, increased urine frequency, or a dilated bladder.
In the case of kidney stones, symptoms may include severe low back pain, tenderness in a point between the ribs and the spinal column, and fever. Also, patients with an obstructive tumor may have a history of unexplained weight loss in the last months.
What pee color is bad?
In acute kidney injury, urine tends to turn very strong and dark. It can look very yellow, brown, or reddish. However, this does not occur in all cases of acute kidney injury.
Hematuria (bloody urine) can also present as brown urine. It should not be mistaken for dark urine due to any of the causes, as mentioned earlier.
What tests are done to find out if you have acute kidney injury?
Acute kidney injury diagnosis in made whenever a patient meets one of the diagnostic criteria outlined in AKI definition. The most basic testing includes creatinine level determination, determining the glomerular filtration rate, and monitoring urine output.
However, once a diagnosis is made, your physician may require other tests to determine the cause of AKI, monitor its progress, and prevent complications.
What are laboratory tests useful in AKI?
Laboratory workup for AKI includes:
- Urine analysis with microscopy: This is possible, the most useful test in determining the cause of AKI. The test’s performance increases when a seasoned nephrologist examines the urine sample under the microscope. The finding of muddy brown casts with or without tubular cells is practically diagnostic acute tubular necrosis. In contrast, the presence of dysmorphic red blood cells or red blood cell casts indicates glomerular disease. White blood cells or white blood cell casts suggest interstitial nephritis or pyelonephritis. Hyaline casts point towards prerenal AKI.
- Kidney function tests: Increased blood urea nitrogen (BUN) and creatinine are the hallmarks of AKI diagnosis. However, BUN can also be elevated in patients with gastrointestinal bleeding, steroid treatment, and protein loading. A BUN- creatinine ratio that exceeds 20:1 is suggestive of prerenal AKI.
- Urine electrolytes: The fractional excretion of sodium FENa is a useful and common indicator. However, it is only valuable in the context of oliguria (the patient is urinating between 100 and 400ml in a day). In oliguric patients with FENa equal to or less than 1%, the cause is probably prerenal. A FENa value of more than 1% is a sign the renal tubules have lost their capacity to reabsorb sodium. However, acute tubular secondary to rhabdomyolysis, severe burns, radiocontrast nephropathy, and acute glomerulonephritis can have FENa values of less than 1%.
Are imaging studies necessary?
A renal ultrasound is a quick, uncomplicated, and cheap test. It is quite useful for detecting obstructions in the urinary collecting system.
What cases require a renal biopsy?
A renal biopsy is a procedure to take a piece of kidney tissue for microscopic examination in a pathology lab, usually through a needle or other surgical equipment. It is a complex procedure that involves general anesthesia and has important complications in a minority of cases.
The most common complication of a kidney biopsy is bleeding. Bleeding can occur in the collective urinary system causing blood in the urine (hematuria), pain, and obstruction.
Suppose the bleeding occurs inside the renal capsule, which is the outer portion of the kidney. In that case, it can have a compressive effect on the kidney and produce systemic hypertension. The kidney can undergo fibrosis, which ultimately leads to chronic hypertension.
So, in general, physicians prefer to avoid it unless there is an absolute necessity. Some indications for renal biopsy include the following:
- The renal function that does not return to normal values after a prolonged period.
- Unexplained renal failure
- Connective tissue diseases, like Systemic Lupus Erythematosus
- Renal masses
- Renal transplant rejection
How can you prevent acute kidney injury?
There are many ways to develop acute kidney injury. Most of them are unpredictable and, therefore, not preventable (like hemorrhage, infection, abdominal tumor).
Some cases of AKI are just a consequence of another disease like heart disease, which is complicated with heart failure or liver diseases. Each of these diseases is preventable in their own way (exercising, avoiding excess alcohol consumption, avoiding smoking, etc.).
AKI secondary to drug toxicity is probably the most preventable form of acute kidney injury. Patients with normal kidney function who take certain medications are at greater risk of developing acute kidney injury, including hypovolemia and hypotension. The mnemonic DAMN is quite helpful to remember these medications:
- D for diuretics (i.e furosemide)
- A for ACE inhibitors (i.e., captopril) and ARBs (losartan)
- M for metformin
- N for NSAIDS (i.e Ibuprofen, Ketoprofen)
In Northern Ireland, the Health and Social Health System recommends patients that take these drugs to suspend them when they have severe diarrhea and vomiting for longer than 12 hours and are unable to drink any fluid.
Acute kidney injury secondary to iodine contrast media is also preventable in most cases. Before performing a contrast imaging study in a non-emergency setting, the patient’s creatinine levels and glomerular filtration rate should be obtained to discard undiagnosed chronic kidney disease that could turn acute iodine-based contrast.
Extensive oral hydration in the hours before the procedure has been shown to reduce the risk of acute kidney injury. Patients with risk factors for AKI should receive intravenous hydration with 0.9 sodium chloride before the procedure.
In a hospital setting, the close monitoring of urine output and the frequent measurement of creatinine and electrolytes in patients with risk factors for AKI (see the section above) help prevent AKI.
How do we treat acute kidney injury?
As you might imagine by now, therapy of acute kidney injury depends on the underlying cause and the degree of kidney function loss.
Treatment is mostly supportive. Maintenance of adequate liquid volume and the correction of biochemical anomalies (like electrolyte imbalance) are the two cornerstones of care.
In patients with post-renal AKI, consulting urology to resolve the blockage is the most important step.
Patients with AKI represent a fluid management challenge. Renal hypoperfusion or kidney’s lack of oxygen due to hypovolemia (low amount of blood) or hypotension (low blood pressure) is the most frequent cause of AKI.
An early reversal of hypovolemia with rapid fluid infusion is often sufficient to treat the majority of cases. However, giving too much fluid too fast can lead to life-threatening volume overload. So, hemodynamic monitoring is vital. Fluid overload usually responds to treatment with furosemide.
Cases of severe AKI that doesn’t respond to treatment might require renal replacement therapy (dialysis). Indications for renal replacement therapy include the following:
- Severe volume overload resistant to diuretic treatment: Volume overload can lead to complications such as acute heart failure with pulmonary edema.
- Severe metabolic acidosis: The proteins and enzymes inside the body need a neuter Ph to work properly.
- Hyperkalemia (potassium greater than 6.5 and rising): Potassium abnormalities cause life-threatening arrhythmias and sudden death.
- Uremia (typically with BUN over 100): Accumulation of metabolic waste causes serious symptoms like confusion, decrease in consciousness that can evolve into coma, pericarditis, anemia, platelet destruction
How do you detox your kidneys?
In the last few decades, kidney detoxing and kidney cleansing programs have gained a lot of popularity. However, so far, there isn’t any convincing scientific evidence that cleansing programs do anything.
If there where toxins that are accumulating in your kidneys, that would mean you have uremia, and the only effective “detox” therapy, in that case, is dialysis.
Just remember drinking water every day and having a healthy diet. That is all the help your kidneys require from you.
What is the prognosis for acute kidney failure?
The prognosis or possible outcomes in acute kidney failure is directly related to the cause, the presence of a previous CKD, and how much kidney function was lost. Those that develop stage 3 AKI have a mortality rate of 50% compared to 3% in patients with stage 1 AKI.
One study shows that survivors of AKI stage 3 had the worst quality of life than the general population. Several factors affect the prognosis or possible outcomes. Factors that increase the risk of the worst outcome include:
- Older age
- Multi-organ Failure
- Several transfusion
- Vasopressor support: The patient requires medication to maintain stable blood pressure.
- Postoperative AKI
Are you having symptoms of Acute Kidney Injury?
This tool is an acute kidney injury symptoms checker. It gathers the most important signs, symptoms, and risk factors for having this condition. Therefore, it will help anybody who uses it to determine the likelihood of having this disorder. The most important feature of this tool is that it is free and would only take you a few minutes.