Acute Kidney Injury in Adults: An Underdiagnosed Condition

Kristy Washinger; MSN; FNP-BC


Journal for Nurse Practitioners. 2017;13(10):667-674. 

In This Article


The treatment of AKI is dependent on the clinical presentation and the underlying etiology. Management focuses on preventing the progression of AKI and providing supportive care while awaiting kidney recovery. Collaboration among primary care physicians, hospitalists, nephrologists, other physicians (eg, surgeons), and advanced care providers is key to optimizing the management of AKI.

Supportive Care

Supportive care includes the maintenance of fluid, electrolyte and acid-base balance, nutritional support, prevention of infection, monitoring for hematologic manifestations, and the discontinuation of nephrotoxic agents and medications that potentially impair glomerular filtration. The treatment plan must be individualized to each patient.

Fluid Balance

The maintenance of fluid balance includes strict intake and output from all sources and early correction of hypovolemia and hypotension. The goal is to restore renal perfusion, reduce ischemic time, and prevent the development of intrinsic renal failure. This can reverse most prerenal causes of AKI and likely prevent the progression of AKI while allowing for renal recovery.

Monitoring for symptoms of fluid overload is important for the oliguric patient. Fluid overload symptoms can include pitting edema (periorbital, sacral, and peripheral), increased or bounding pulses, S3 gallop, dyspnea, jugular vein distention, weight gain, moist tongue, and hypertension.

In case of fluid overload, strict fluid restriction, antihypertensives, and diuretic therapy (loop diuretics) may be needed. Close monitoring of volume status is indicated with these interventions to maintain euvolemia and prevent hypovolemia.

Electrolyte Imbalances

Electrolyte imbalances of potassium must be monitored frequently. Early recognition and treatment of hyperkalemia is important to maintain adequate cardiac status and prevent complications. In the setting of hyperkalemia, an electrocardiogram should also be conducted to evaluate for changes that indicate a cardiac arrhythmia related to hyperkalemia. These changes can include tall T waves, ST segment depression, prolonged P-R interval, broadening of QRS complex, and ventricular tachycardia and fibrillation.[16] If hyperkalemia develops, immediate treatment is necessary. IV bicarbonate and calcium gluconate should be administered followed by IV insulin in conjunction with dextrose.[17] Potassium in the diet should also be restricted. Medications that may cause hyperkalemia such as angiotensinconverting enzyme inhibitors, angiotensin II receptor blockers, potassium-sparing diuretics, and nonsteroidal anti-inflammatory drugs should also be eliminated.

Acid-base imbalances, metabolic acidosis, and metabolic alkalosis can occur because of the inability of the nephrons in the injured kidney to secrete and expel hydrogen ions and reabsorb bicarbonate ions. Diabetic ketoacidosis and lactic acidosis can intensify metabolic acidosis in the critically ill patient.

Symptoms of metabolic acidosis include nausea, vomiting, Kussmaul respirations, tachycardia, and alterations in mental status. Oxygen saturations and arterial blood gases should be monitored frequently. In many cases, mechanical ventilation is required. RRT may be considered for severe electrolyte imbalances including hyperkalemia and acid-base balances when medication management is not sufficient.[18]


Malnutrition is commonly associated with mortality in the AKI patient.[2] Twenty to thirty kcal/kg/d maintains nitrogen balance and avoids hyperglycemia, hypertriglyceridemia, and fluid accumulation.[2] A protein intake of 0.8 to 1.0 g/kg/d in noncatabolic patients not requiring RRT is adequate.[2] For hypercatabolic patients receiving RRT, an increase of protein to a maximum of 1.7 g/kg/d is recommended.[2] Enteral nutrition is preferred (oral or enteral tube). The hospital-based dietician can be critical in managing and following nutritional status in the AKI patient.


During AKI, an impairment of the immune system can increase a patient's risk of infection. Common infections include wounds, urinary tract infection, pneumonia, and sepsis. All of these can contribute to mortality. Steps to prevent infection include hand hygiene, adequate skin and respiratory care, and limitation of invasive procedures.[19] Monitor closely for symptoms of infection and laboratory changes such as increased white blood cells, erythrocyte sedimentation rate, and/or C-reactive protein along with blood and urine cultures.

Hematologic Manifestations

Hematologic manifestations can occur in AKI because clotting factors and platelet synthesis can be reduced. This can cause patients to have an increased risk of bleeding and bruising. If symptoms of bleeding occur, prothrombin time, partial prothrombin time, international normalized ratio, and clotting factors are indicated.

A complete CBC should be monitored frequently to evaluate for anemia. Initial management focuses on the correctable causes of anemia (eg, iron deficiency, blood loss, infection, and so on). Additional laboratory tests include iron studies, B12, and folate levels. In many cases, packed red blood cells and/or erythropoietin-stimulating agents are indicated.

Medication Considerations

Medication considerations include the discontinuation of medications that impair eGFR (nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, and angiotensin II receptor blockers) while avoiding the addition of medications that cause nephrotoxicity (Table 3). Renal dosing of medications may prevent drug toxicity. Collaboration with a pharmacist is needed to calculate renal dosing because of laboratory fluctuations during the AKI episode. eGFR renal dosing, as listed in the package insert mandated by the US Food and Drug Administration, requires a stable rate, and the AKI patient is not considered as such.