What are complications of altered fluid and electrolyte balance in acute tubular necrosis (ATN)?

Updated: Mar 15, 2021
  • Author: Sangeeta Mutnuri, MBBS; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Specific fluid imbalances vary with the phase of illness. During oliguria, salt and water retention often leads to hypertension, edema, and heart failure. The polyuric phase of ATN may lead to hypovolemia and create a setting for prerenal azotemia and perpetuation of ATN.

Clearly, the maintenance of fluid and electrolyte balance is critical. ATN may lead to dangerous electrolyte imbalances, especially hyperkalemia and hyponatremia. 

Hyperkalemia can be associated with life-threatening cardiac arrhythmias (eg, ventricular tachycardia or fibrillation, complete heart block, bradycardia, asystole). Arrhythmias have been reported in up to 30% of patients. On electrocardiography (ECG), hyperkalemia manifests as peaked T waves, prolonged PR interval, P wave flattening, and a widened QRS complex. In addition to these worrisome cardiac effects, hyperkalemia can also lead to neuromuscular dysfunction and, potentially, respiratory failure. Hyperkalemia can be treated with glucose and insulin, binding resins, or, if necessary, dialysis.

Hyponatremia is cause for concern because of its effects on the central nervous system. In general, correction of hyponatremia should be of sufficient rapidity and magnitude to reverse the manifestations of hypotonicity, but not be so rapid or large as to potentiate the risk of osmotic demyelination. The most recent published guidelines on treatment of hyponatremia recommend rates of correction of serum sodium ranging from 8 to 12 mmol/L per 24 h. [30]  Go to Hyponatremia for complete information on this topic.

Other electrolyte disturbances include hyperphosphatemia, hypocalcemia, and hypermagnesemia. Hypocalcemia may be secondary to both deposition of calcium phosphate and reduced levels of 1,25-dihydroxyvitamin D. It is usually asymptomatic, but hypocalcemia may result in nonspecific ECG changes, muscle cramps, or seizures.

In rhabdomyolysis, hypocalcemia results from deposition of calcium in the injured muscle. The deposited calcium is eventually released back into the circulation during the recovery phase, thereby accounting for transient hypercalcemia. For this reason, calcium administration is generally not recommended for hypocalcemia during the acute phase of rhabdomyolysis, unless the patient is symptomatic.

The 2011 UK Renal Association guidelines recommend administering 0.9% sodium chloride and sodium bicarbonate for intravenous volume expansion in patients at risk of developing AKI secondary to rhabdomyolysis. [7]  Metabolic acidosis may occur. It may be treated with bicarbonate or dialysis as well.

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