Acute kidney failure, acute renal failure and acute kidney injury are all synonymous terms. But their use is not always precise. Their use at times refers to grey areas that are just points along a spectrum. A focus on the pathogenesis and pathophysiology of the disorder will shed some light on the matter.
In the strictest sense of the definition, acute renal failure (ARF) is an abrupt decline in kidney function due to injury to the organ. Proper synonyms for it are acute kidney failure (AKF) and acute kidney injury (AKI). It usually occurs within hours to a few days of the insult. It results in either an increase in the serum creatinine of 0.3 mg/dL or more; an increase in the serum creatinine of more than 50%; a reduction in the volume of urine output of less than 5 mL/kg/h for more than 6 hours; or any combination of these changes.
Most of the time acute kidney failure is reversible (kidney function returns to normal or near normal). But a high number of patients die from it if they have certain coexisting disease(s). The mortality is especially high if the coexisting disease is one that triggered the AKF.
Some patients with it require dialysis (artificial kidney function treatment). But the need is usually short-term until renal function returns to normal or near normal. The deciding factors are the speed with which the kidneys recover and if there are related complications, one of the most common of which is fluid overload. When AKF is not reversible though, permanent dialysis is required.
The development of ARF can be due to prerenal, intrarenal or postrenal factors. Prerenal factors have to do with reduced blood flow to the kidneys. They result in a reduced GFR. Intrarenal refers to disease or damage to the internal structures of the kidney. Postrenal has to do with the blockage of urine outflow from the urinary tract.
Prerenal acute renal failure
The term prerenal ARF as it is commonly used refers to a state of decreased filtering of blood by the kidneys due to reduced perfusion of them. In many cases it is the resultant drop of blood pressure in afferent arterioles that causes the reduction in GFR but there is no actual injury to the kidneys. In these cases volume repletion promptly restores GFR to normal. Since injury does not occur in these cases the term AKI or either of its synonyms is a misnomer. Thus, their use in this setting is imprecise.
The equating of prerenal azotemia with ARF is also at times not exact. The elevation of BUN that occurs when there is inadequate blood flow to the kidneys is not due to just reduced filtering of it by the glomeruli. To compensate for a drop in blood pressure the kidneys increase their reabsorption of BUN in the proximal tubules and collecting ducts. One of the factors indirectly leading to that response is activation of the RAAS. When there is no damage to the kidneys though, fluid replacement promptly lowers the blood urea level.
Intrarenal acute renal failure
When intrarenal factors are involved the renal tubules are the most common sites injured. The most common cause is more severely reduced blood flow to the kidneys to a degree further along the prerenal spectrum. The type of injury it leads to is ischemia. The pattern of the injury is necrosis. Thus, the most common form of ARF is acute tubular necrosis (ATN). When ischemia is most severe it leads to renal cortical necrosis, which if it involves both kidneys, can result in renal failure which is not reversible.
There are other mechanisms of internal injury to the kidneys and other structures that can suffer injury leading to ARF. But ischemia is the most common means and ATN is the most common form. Therefore, ATN and ARF are well-deserved synonyms.
Postrenal acute renal failure
Postrenal acute kidney injury occurs when there is blockage of the outflow of urine from one or both kidneys. The blockage can be anywhere in the urinary tract from the renal pelvis to the urethral meatus. If there are two kidneys though, the blockage must involve both in order for acute kidney failure to be apparent. The reason is one well-functioning kidney can shoulder the load of what the body needs in terms of renal function.
Early on, with so-called postrenal acute renal failure, GFR might fall before any damage to the kidneys occurs. The reason is the downstream blockage causes hydrostatic pressure to rise in the renal tubules as well as Bowman’s capsules. This causes a decrease in the net filtration pressure which is pressure within the glomerulus minus pressure within Bowman’s capsule. Because of the decrease in the pressure gradient less fluid filters from the glomeruli into the capsules.
The drop in GFR, azotemia and decreased urine volume which occur in this setting are signs of acute renal failure. But a more precise term for this state is probably renal insufficiency. It might be difficult to confirm though unless there is evidence that kidney injury has not occurred and kidney function promptly returns to normal when the obstruction is relieved.
With longer standing or more complete obstruction there is actual injury to the kidney tubules from the pressure buildup within them. In addition, after 3 – 4 hours, arteries supplying the kidneys tend to constrict. When the decrease in blood flow reaches a certain point, ischemic injury to the kidneys also occurs. At this stage acute renal failure is not a misnomer nor is it a point along the way. Chronic renal failure can also develop from postrenal obstruction if this process is more gradual.