Therapeutic strategies for individuals with acute kidney injury (AKI).


Acute kidney injury (AKI) is a sudden drop in glomerular filtration rate that is typically reversible (GFR). The serum blood urea nitrogen (BUN), creatinine, and other metabolic waste products ordinarily discharged by the kidney rise as a result of this.


The basic diagnosis of patients with AKI, as well as the management of AKI’s primary complications, are covered in this article. AKI is discussed individually in terms of its prevalence, etiology, pathophysiology, diagnosis, and prevention.

Immediate Analysis And Management

Individuals with AKI who are diagnosed during a medical encounter must be thoroughly screened for immediate dangers and consequences, as well as the severity of the condition and the removal of the cause. The Kidney Disease: Improving Global Outcomes (KDIGO) system categorizes AKI into three stages: mild, moderate, and severe (severe)


Generally, as AKI progresses, the difficulties it causes become more severe and life-threatening. All individuals with AKI, however, are at risk for consequences and the potential that milder AKI will advance to more severe AKI. Whether the patient is in a hospital or an outpatient environment determines the first actions in urgent care.


  1. Outpatient acute kidney injury triage:


In the outpatient context, the first assessment of a patient with AKI is focused on triaging the patient to the appropriate facility, such as the emergency room, for more chronic illness or life-threatening electrolyte imbalances.


  1. Patients to be sent to the emergency department — The following patients are referred to the emergency department:

  • Patients who meet the KDIGO criteria for stage 2 or 3 AKI.
  • Patients with stage 1 AKI who have an ontology that is undetermined, patients who have an uncertain duration or trajectory of increased creatinine, or patients who are concerned that the illness will not be reversible with basic therapies.
  • Patients with AKI of any stage who are encountered in a resource-constrained outpatient environment who require an emergency department referral for the first diagnostic examination (eg, renal ultrasonography to rule out urinary tract blockage) or therapies (eg, intravenous fluid administration).


  1. Individuals who do not require an emergency department referral:

  • Immediate examination after diagnosis.
  • Urgent nephrology referral indications — If initial therapies fail to significantly enhance the kidney damage, patients who do not require an emergency room referral and are handled as outpatients should be sent for outpatient nephrology evaluation.
  • In a patient with Acute kidney injury, hematuria, and proteinuria, the presence of glomerulonephritis (GN) is quite likely.
  • AKI develops as a side effect of an underlying illness, and future management is dependent on nephrology input (such as AKI occurring as a complication of chemotherapy).

The following are AKI complications that may necessitate emergency renal replacement therapy (RRT):

  • Pulmonary edema
  • Hyperkalemia >6.5 mEq/L
  • Signs of uremia, such as pericarditis, or a mental impairment that is otherwise unexplainable
  • Hypervolemia with severe metabolic acidosis (pH 7.1)
  • Acute poisoning

Subsequent Planning And Management


AKI is then managed in the following ways:


  • Determining the cause of Acute Kidney Injury
  • Recurrent factors, like volume loss, urinary tract infections and hypotension.
  • To avoid future harm, all current injuries should be removed.
  • Detecting and treating problems that might lead to the need for renal replacement therapy (RRT) at a later date (if AKI does not resolve)
  • Potential injuries are eliminated and avoided.


  1. Medications:

  • Nonsteroidal antiinflammatory medicines, Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and nephrotoxins are all examples of angiotensin-converting enzyme inhibitors.
  • Drugs that are renally cleared but can have substantial side effects with buildup in the presence of AKI should be stopped or dosed differently (eg, metformin, gabapentin, cefepime, morphine).


  1. Dosing: 

  • In patients with AKI, all drugs should be evaluated carefully for any necessary dosage modifications based on the anticipated glomerular filtration rate (GFR).


  1. Hypotension: 

  • Hypotension:  Rapid detection, examination, and treatment of hypotension is crucial in reducing the severity of renal damage.


  1. Contrast agents including iodine:

  • Intravascular iodinated contrast should not be administered after AKI has occurred unless it is necessary for an emergency or life-saving surgery, such as the treatment of (STEMI), or for a key diagnostic test.


  1. Evaluation and control of volume:

  • A physical exam should be performed on all individuals with AKI to determine their volume status. The primary goal of treatment should be to correct volume depletion or overflow.


  1. Hypovolemic patients:

  • Individuals with a medical history of fluid loss (such as vomiting and diarrhea), a medical examination compatible with hypovolemia (hypotension and tachycardia), or oliguria should get intravenous fluid treatment. Fluid treatment, on the other hand, should be avoided in patients with pulmonary edema or anuria. Colloid solutions are not used to treat hypovolemia in individuals with AKI.


  1. Hypervolemic patients:

  • Hypervolemia may be present at the time of the initial examination or develop as a result of excessive fluid administration in the presence of inadequate salt and water excretion. This is especially true in sepsis patients, who are frequently given extensive intravenous fluid resuscitation.


  1. Diuretics Function:

  • Individuals with acute kidney injury who are not anuric may benefit from diuretics to alleviate hypervolemia. Loop diuretics are recommended over thiazide diuretics because they have a higher natriuretic impact.


  1. Renal replacement therapy’s role:

  • Patients who have had anuria for more than 24 hours, who have failed to react to diuretics, or whose response to diuretics is inadequate to avoid increasing hypervolemia due to excessive obligatory consumption, are usually started on RRT for volume overload. RRT may allow doctors to optimize nutritional assistance and intravenous medicine administration without fear of creating volume overload, in addition to treating volume overload.


  1. Taking care of electrolyte imbalances: 

  • Hyperkalemia – The degree of hyperkalemia, the etiology of AKI (quickly reversible or likely to be extended), clinical symptoms (cardiac conduction abnormalities), and the efficacy of medicinal care all play a role in its treatment. A potassium-restricted diet should be followed by all patients with hyperkalemia (less than 2 g per day). In addition, in these individuals, all potassium-containing infusions and drugs should be avoided.
  • Hyperphosphatemia – In all patients with Acute kidney injury, excluding those with hypophosphatemia, we limit dietary phosphorus to 2 g per day. Phosphate binders are commonly used in patients with AKI who have a phosphate content >5.5 mg/dL (1.8 mmol/L), are getting enteral feeding (eating or receiving tube feeds), and have a predicted protracted course of AKI, despite the lack of evidence to support our strategy (ie, cause of AKI is not readily reversible)
  • Hypocalcemia – The degree, sharpness, and existence of symptoms all influence how hypocalcemia is treated. In individuals with hypocalcemia, hyperphosphatemia should also be addressed. The lowering of blood phosphate caused by oral phosphate binders is frequently enough to enhance serum calcium levels. The dosage of calcium supplementation in the situation of hyperphosphatemia-induced hypocalcemia should be controlled to alleviate symptoms rather than aiming for normal blood calcium levels, which can boost the calcium-phosphate product to levels that can encourage precipitation.
  • Hypomagnesemia and hypermagnesemia – Patients with hypomagnesemia and renal impairment should be treated with caution, using minimal dosages and monitored often. Because the kidneys play such a crucial role in magnesium removal, individuals with AKI may develop hypermagnesemia. Except in individuals receiving high doses of intravenous magnesium, such as women with severe preeclampsia, severe, symptomatic hypomagnesemia is uncommon.


  1. Handling acid-base irregularities:

  • As a consequence of AKI or as a direct effect of the underlying etiology, acid-base imbalances are frequently observed in patients. Although metabolic alkalosis can occur, metabolic acidosis is significantly more prevalent.


  1. Metabolic acidosis:

  • Unless the acidosis can be promptly corrected by treating the underlying etiology, we start RRT in patients with oliguric or anuric AKI who are volume overburdened and have serious metabolic acidosis (pH 7.1). (eg, diabetic ketoacidosis).


  1. Metabolic alkalosis:

  • AKI with metabolic alkalosis can occur in a small percentage of individuals, such as those with milk-alkali syndrome, acute vomiting, or nasogastric tube suction. The majority of these individuals are dehydrated, and the alkalosis is usually treated with an IV sodium chloride infusion. Patients with chronic pulmonary illness who suffer Acute kidney injury may develop compensatory metabolic alkalosis without alkalemia.


  1. Nutritional management: 

  • Nutritional care for critically sick patients with AKI aims to deliver enough calories, protein, and minerals. Most people with AKI need to limit their potassium, phosphorus, and salt consumption.
  • Due to the difficulty of dietary assistance in these individuals and the unique expectations of each patient, we get a nutritionist consultation in hospitalized patients with stage 3 AKI to best personalize treatment.
  • Consultation should be based on an individual needs assessment for individuals with earlier stages of AKI.
  • Patients with AKI on RRT or who are about to start RRT are given a fluid restriction of 1 to 1.5 L/day even if they don’t have volume depletion.
  • The severity of the underlying illness, prior nutritional condition, and comorbidities all influence nutritional needs.
  • Despite the fact that requirements vary based on the underlying catabolic state, some researchers suggest that patients require roughly 25 to 30 kcal/kg per day.
  • With the severity of the underlying disease and the start of RRT, the protein demand rises. Non Dialysis individuals with mild to severe sickness only need 0.8 to 1.2 g/kg per day, but critically ill patients or patients on RRT need 1.2 to 1.5 g/kg per day or higher.
  • In order to provide appropriate nutrition to patients with AKI who require RRT, parenteral or enteral feeding may be required. 
  • Most clinicians believe that enteral nutrition should be used instead of parenteral nutrition whenever possible in critically ill patients without AKI because it is less expensive, has fewer and more severe complications, has less mucosal permeability, has better wound healing, and has lower infection rates.
  • There is minimal data on the effectiveness and safety of enteral feeding in patients with AKI. In one research, the results of 247 consecutive individuals fed enterally were compared: 114 required dialysis, 68 had AKI but did not require dialysis, and 65 had normal renal function.
  • There was no difference in gastrointestinal or mechanical problems between the three groups, except for an increased incidence of nasogastric tube blockage and large gastric residual volumes among dialyzed patients.
  • Nonprotein calories and protein intake were 23.4 kcal/kg and 0.92 g/kg, respectively, for dialyzed patients, with the quantity of supplied protein calories being somewhat less than expected. This can be avoided by using parenteral amino acids during RRT on a regular basis.


  1. Detection of uremia:

  • Even if none of the aforementioned conditions apply, individuals with persistent AKI who develop uremic symptoms may benefit from non-emergency dialysis.
  • Anorexia, nausea, vomiting, metallic taste, and impaired mental state are only a few of the uremic signs and symptoms.
  • Asterixis and pericardial rub, among other physical examination findings, may be detected. Because uremic symptoms and indications are vague, it’s critical to rule out other reasons before starting RRT, especially if there’s no other indication.
  • Uremia must be checked on a daily basis until the AKI improves or the patient is on RRT. It’s frequently tough to decide to start RRT because of one of these signs.
  • This is especially true for critically sick individuals, who may have a variety of explanations for their neurologic dysfunction. As a result, while starting RRT, it’s important to keep track of whether or not presumptive uremic symptoms improve with treatment. To see if symptoms improve with RRT, you’ll need to go through numerous dialysis sessions.


Uremic bleeding prevention and treatment:


AKI can lead to platelet dysfunction, which can lead to a hemorrhagic diathesis. Cutaneous bleeding is the most common clinical sign, however gastrointestinal bleeding can also occur. Clinical symptoms, therapeutic reasons, and treatment strategies are described elsewhere.

Follow-up and Monitoring

  • In stable patients, serum creatinine, electrolytes, ionized calcium, total serum calcium, and phosphate should be monitored regularly.
  • In order to determine daily fluid balance, daily weights, fluid consumption, and urine output must be closely monitored.
  • If accessible, patients with moderate to severe AKI should undergo at least one nephrology outpatient examination to ensure appropriate care after discharge.
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