From the Guidelines
In patients with acute tubular necrosis (ATN), electrolyte abnormalities are common and can be serious, with hyperkalemia, hyperphosphatemia, hypocalcemia, and hyponatremia being frequent occurrences, as evidenced by the high prevalence of these disorders in patients with kidney failure 1.
Electrolyte Abnormalities in ATN
The kidney's compromised ability to maintain homeostasis when tubular cells are damaged leads to various electrolyte disturbances.
- Hyperkalemia develops as damaged tubular cells cannot properly excrete potassium, leading to potentially dangerous elevations in serum potassium levels.
- Metabolic acidosis often occurs simultaneously due to impaired acid excretion and bicarbonate reabsorption.
- Hyperphosphatemia develops as phosphate excretion decreases, while hypocalcemia frequently accompanies this due to decreased vitamin D activation and calcium-phosphate binding.
- Hyponatremia may occur from water retention exceeding sodium retention.
- Hypermagnesemia can develop in severe cases due to decreased magnesium excretion.
Management of Electrolyte Abnormalities
Management typically involves careful monitoring of electrolyte levels, dietary restrictions (particularly potassium), and sometimes medications like calcium resonium or dialysis in severe cases.
- The use of dialysis solutions containing potassium, phosphate, and magnesium can help prevent electrolyte disorders during kidney replacement therapy (KRT) 1.
- Preventing KRT-related electrolytes derangements by modulating KRT fluid composition may represent the most appropriate therapeutic strategy, given the possibly severe clinical implications and the risks associated with exogenous supplementation 1.
- Commercial KRT solutions enriched with phosphate, potassium, and magnesium are widely available and can be safely used as dialysis and replacement fluids, even in the setting of regional citrate anticoagulation 1.
From the Research
Electrolyte Imbalance with ATN
- Electrolyte imbalance, particularly hyperkalemia, is a common complication in patients with acute tubular necrosis (ATN) 2.
- The use of sodium polystyrene sulfonate (SPS) to treat hyperkalemia can lead to an increase in sodium levels, potentially causing hypernatremia 3, 4, 5.
- SPS can also decrease serum calcium and magnesium levels, and increase intact parathyroid hormone (iPTH) values 3.
- The treatment of hyperkalemia with SPS may be associated with harm, including bowel necrosis and fluid overload 4, 6.
- Newer potassium binders, such as patiromer and sodium zirconium cyclosilicate, have been shown to be safer and more effective in managing hyperkalemia, and may be a better option for patients with ATN 6.
Management of Electrolyte Imbalance
- Early diagnosis and treatment of electrolyte imbalance are crucial in managing ATN 2.
- Enteral rather than parenteral hyperalimentation may improve survival in severely malnourished patients with ATN 2.
- Avoidance of intravenous lines, bladder catheters, and respirators can help reduce the risk of sepsis and multiorgan failure in patients with ATN 2.
- More aggressive dialysis with biocompatible membranes may improve survival in some patients with ATN 2.