This week in the office I had a patient who developed acute tubular necrosis, the most common type of acute kidney injury, apparently as a result of dehydration. I see a lot of patients in the office with illnesses that put them at risk to develop dehydration. Often I sense that they simply tolerate my emphasis on avoiding severe dehydration without realizing why it’s so important. Acute tubular necrosis is the serious complication of severe dehydration that we try to avoid by maintaining good hydration. That is why I try really hard to encourage patients to find a way to stay adequately hydrated especially when they have illnesses or conditions that make it difficult.
It had been a long time since I’d seen a case of acute tubular necrosis in an outpatient with what appeared to be nothing more than a viral gastroenteritis, but this case reminded that it pays to have a high index of suspicion of this complication of dehydration. Our kidneys are incredibly good at coping with the wide variations of water intake, water loss, and need to conserve or excrete water, sodium, potassium and other things we ingest. Most of the time even when we challenge the capacity of our kidneys to remain functional despite not taking in as much water as is needed to maintain our blood pressure and tissue needs optimally our kidneys manage to keep all of these needs balanced. In extreme situations if we become so dehydrated that our kidneys just cannot keep functioning properly a condition called acute tubular necrosis can occur. The renal tubules function deep in the part of the kidney where oxygen supply is lowest, and are the part of the kidney that is most severely injured when the kidney faces extremely poor circulation. This leads to “necrosis” (cell death) of the cells lining these tubules, hence the name acute tubular necrosis. When this happens kidney function can go from normal or near normal to severe malfunction over a period of just a few days. The kidneys stop filtering the blood of wastes, stop making urine or become unable to properly regulate the production of urine. This can lead to toxic buildup of wastes and little of no urine production, or the kidneys may fail to properly reabsorb properly the filtrate from the tubules and may excrete too much water and or electrolytes causing life-threatening metabolic imbalances.
Treatment to allow the patient to survive and the kidneys to have a chance to recover can require at least rapid fluid resuscitation with subsequent careful fluid and electrolyte management, and sometimes even renal dialysis to maintain some degree of homeostasis. Most of the time if fluid and electrolyte status is maintained, dialysis if used if needed, and other complications are avoided the kidneys recover and start to function again. Still, especially in older patients or those with other major health problems acute tubular necrosis can have high mortality rates. Occasionally permanent kidney failure can result and long term dialysis or renal transplantation is needed.
Most experts look at acute tubular necrosis as having three stages or phases. First is the initiation phase, where the kidney suffers the causative insult, the renal tubules are injured and the lining cells die, slough off blocking the tubules and the patient develops the rapid onset of loss of kidney function. Lab values including serum creatinine and blood urea nitrogen (BUN) rise rapidly. Next is the maintenance phase, where the blood filtration rate remains very low, leading to continued rise in the BUN and creatinine, and where continued intensive support is often required. This phase often lasts 1-2 weeks, though can be extremely variable. Last is the recovery phase where the lining cells of the renal tubules regenerate and the kidney recovers its ability to function to filter the blood. In many cases the serum markers of kidney function return to their pre-ATN levels.
Usually acute tubular necrosis is caused by one of several conditions associated with severe extremely low circulation to the kidney. These can include most of the causes of shock like severe infections with septic shock, in the setting of major acute myocardial infarction, or drug overdose. Another common cause of acute renal failure similar to ATN is with the use of large volumes of iodine based contrast agents for radiologic testing. Other causes can include numerous medications and other toxins.
ATN is more likely to happen to older adults, in persons with underlying diabetes or other chronic conditions like hypertension, or those on concomitant drugs that can be nephrotoxic like the non-steroidal anti-inflammatory drugs or aminoglycoside antibiotics.
Prevention of acute tubular necrosis is key, with avoiding dehydration, avoidance of nephrotoxic drugs when possible, and by recognizing patients at risk for acute tubular necrosis complicating IV contrast studies so they can be avoided or have special measures used to minimize their risk.