Complications
A late complication usually arising several days after glomerular filtration falls.
Treatment includes dietary restriction and the administration of phosphate binders, such as calcium acetate, calcium carbonate, sevelamer, or lanthanum carbonate.
Hemodialysis is effective in phosphorus reduction. In patients in whom intense renal replacement is undertaken, such as those on continuous renal replacement therapies or daily dialysis regimens, phosphorus replacement may be required.
Uremic toxins accumulate with severe and untreated renal failure, resulting in lethargy, confusion, and obtundation.
Dialysis is required for management of uremia.
Impaired volume regulation is common in AKI not occurring from prerenal azotemia.[160]
Volume intake is limited and diuresis maximized with agents such as furosemide.
Response to diuretics is variable.
Ultrafiltration (volume removal by renal replacement therapy) may be required.
Results from impaired excretion of potassium, cell lysis, or tissue breakdown.
Severe hyperkalemia may result in classic ECG findings of peaked T waves, increased PR interval, widened QRS, atrial arrest, and deterioration to a sine wave pattern.
Restrictions on dietary potassium intake should be imposed on all patients and may be sufficient for mild hyperkalemia.
Sodium polystyrene sulfonate may be used for moderate to severe cases of hyperkalemia. However, its effects are not immediate and serum potassium must be rapidly lowered.
If these initial steps are not sufficient or if hyperkalemia is severe, medical intervention is mandated and includes cardiac evaluation by ECG.
If classic changes are present, treatment with intravenous calcium is required immediately in addition to rapid lowering of serum potassium with insulin, glucose, and beta-agonists. Care should be taken to prevent extravasation when giving calcium salts intravenously, because they are highly toxic to tissues.
If hyperkalemia is refractory to medical treatment or if cardiac manifestations are present, hemodialysis is indicated for rapid potassium normalization.
Results from accumulation of nonvolatile acids. Oral or intravenous bicarbonate preparations such as sodium bicarbonate or sodium citrate/citric acid may be used to manage metabolic acidosis.
Management often requires dialysis if severe and if respiratory compensation is unable to maintain pH.
AKI may leave the patient with prolonged renal damage, and functional recovery may not return to the baseline.
Recovery is dependent on the mechanism and severity of the injury and the underlying comorbid medical conditions.
AKI in children may be associated with chronic renal disease that may progress to end-stage renal disease.[161][162]
Patients with partial or no recovery from AKI are at increased risk for congestive heart failure and acute myocardial infarction.[160][163]
Some patients may not recover from severe kidney injury, especially those with underlying kidney disease or other comorbid medical conditions. Chronic renal replacement therapy may be required.[155]
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