Expected Signs and Symptoms
Acute Kidney Injury (AKI) is characterized by high levels of creatinine, urea, and accumulation of waste products due to decreased kidney function. The patient might report fatigue, oliguria, anuria, nephrotoxic insult, and nocturia. A full history and physical examination will be ordered to determine the etiology of the condition. A history examination will help to differentiate between chronic kidney injury and AKI. It will also help to identify events that may have triggered volume loss (Workeneh, 2019). For example, oliguria might suggest AKI, while sudden anuria may suggest acute obstruction of the urinary tract or vascular catastrophe. A physical examination of vital orthostatic signs will help hypovolemia, which indicates fluid losses (Workeneh, 2019). Lab tests, including complete blood count, urine electrolytes, serum biochemistries, and urine analysis with microscopy, can help identify the etiology. Urine electrolytes might help diagnose kidney perfusion, while urinary microscopy can diagnose acute tubular necrosis, which is the leading cause of AKI. Urine sedimentary examination can help to identify tubular injury biomarkers.
Treatment and Management
The treatment of the condition is mainly supportive; the efficacies of available therapeutic modalities have not been established. Treatment goals include maintaining the homeostasis volume and improving the biochemical abnormalities. Furosemides can be used to correct fluid overload, while bicarbonate administration severe acidosis. The use of transfusions or desmopressin can correct hematologic abnormalities, while dialysis will correct hyperkalemia. Medication doses should be adjusted to avoid further damage to the kidneys. The patients should also limit the ingestion of potassium and phosphorus.
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