Acute Kidney Injury

Original Editor - Boluwatife Williams Top Contributors - Boluwatife Williams

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Introduction

Acute kidney injury (AKI) is a sudden (within hours) decline in kidney function, which includes both injury (structural damage) and impairment (loss of function). It is often referred to as acute renal failure (ARF), is a sudden episode of kidney damage or failure that occurs within a few hours or days and is indicated by a sharp rise in serum creatinine, a decline in urine output, or both. AKI is known to occur in between 10% and 15% of hospitalized patients, with more than 50% of patients need intensive care. AKI is distinct from chronic kidney disease, which causes the kidneys to slowly lose function over time.

Epidemiology

There are significant disparities in the incidence and etiology of AKI between developing and industrialized nations.

In developing nations' cities, the most prevalent causes of AKI are hospital acquired (renal ischaemia, sepsis, and nephrotoxic medications), but in rural regions, it is more usually a result of community acquired illness (diarrhoea, dehydration, viral diseases, animal venoms, and so on).

The incidence of AKI is rising in industrialized nations. It is believed to occur up to 15% of the time in hospital inpatients, and it is more prevalent in critically sick patients, where it is anticipated to occur up to 60% of the time.

Etiology

The causes of acute kidney injury are majorly classified as:

1. Prerenal
2. Intrinsic renal
3. Postrenal

Prerenal AKI occurs due to inadequate blood flow to the kidney. Unless hypoperfusion is severe and/or extended, prerenal diseases do not usually result in permanent kidney injury (and hence are possibly reversible). The main causes under Prerenal AKI are:

• Extracellular fluid volume depletion (caused, for example, by insufficient fluid intake, diarrheal disease, and sepsis)
• Decompensated Liver Disease (cirrhosis)
• Cardiovascular illness (such as heart failure and cardiogenic shock)

Intrinsic Renal causes of AKI involve intrinsic kidney disease or damage. Blood arteries, glomeruli, tubules, and the interstitium can all be affected. Glomerular disease lowers  glomerular filtration rate (GFR) and increases glomerular capillary permeability to proteins and red blood cells; it can be inflammatory (glomerulonephritis) or caused by vascular damage from ischemia or vasculitis. Ischemia can also damage tubules and cause them to become clogged by cellular debris, protein or crystal deposition, and cellular or interstitial oedema. Interstitial inflammation (nephritis) is typically caused by an immunologic or allergic reaction. The most frequent reasons under Intrinsic renal causes include:

• Acute glomerulonephritis
• Acute tubular necrosis
• Nephrotoxins (including over-the-counter and prescription medications)

Postrenal AKI (obstructive nephropathy) is due to varieties of obstruction in the voiding and collecting sections of the urinary system When crystalline or proteinaceous material precipitates within the tubules, obstruction can also happen on a microscopic level. Bladder outlet blockage brought on by an enlarged prostate is a common cause of abrupt, and sometimes complete, cessation of urinary output in men.

Clinical Presentation

Depending on the underlying cause, signs and symptoms of acute kidney injury may include:

• Low urine output
• Swelling in the ankles, legs, and around the eyes
• Fatigue or exhaustion
• Breathing difficulty
• Confusion
• Nausea
• Seizures, or in severe situations, coma
• Chest pressure or discomfort

AKI can occasionally go unnoticed and only be detected by a healthcare professional through additional testing.

Diagnosis

According to the KDIGO (Kidney Disease: Improving Global Outcomes), AKI can be diagnosed if any one of the following is present:

• Increase in the serum creatinine value of ≥ 0.3 mg/dL (26.52 micromol/L) in 48 hours
• Increase in serum creatinine of ≥ 1.5 times baseline within the prior 7 days
• Urine volume < 0.5 mL/kg/hour for 6 hours.

Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. Other investigations include:

• Blood tests: complete blood count (CBC), BUN, creatinine, and electrolytes (including calcium and phosphate)

• Urine tests: sodium, urea, protein, and creatinine concentration; and microscopic analysis of sediment.
• Imaging: Renal ultrasonography, noncontrast CT.

Treatment

The therapy of AKI is dependent on identifying and treating the underlying cause.  In addition to treating the underlying illness, AKI is usually managed by avoiding nephrotoxins, or chemicals that are harmful to the kidneys. These include nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or naproxen, iodinated contrasts like those used in CT scans.

NSAIDs inhibit renal prostaglandins' compensatory vasodilation response to vasoconstrictor hormones generated by the body, inhibition of renal prostaglandins causes immediate impairment of renal function following NSAID use. Also an immune response that occurs roughly a week after NSAID exposure, can induce acute interstitial nephritis (AIN), which is characterized by an inflammatory cell infiltration in the kidney's interstitium.

The primary goals of early management are to address life-threatening problems, ideally in a critical care unit.

• Immediate treatment of pulmonary edema and hyperkalemia

• Dialysis is used when necessary to control hyperkalemia, pulmonary edema, metabolic acidosis, and uremic symptoms
• Adjustment of drug regimen for degree of renal dysfunction
• Restriction of water, sodium, phosphate, and potassium intake, but provision of adequate protein
• Possibly intestinal potassium binders for hyperkalemia and phosphate binders for hyperphosphatemia.

Physiotherapy management

An exercise rehabilitation programme for AKI patients could ultimately improve renal recovery following AKI, reduce progression to CKD and improve long term patient outcomes. See Renal Rehabilitation.

Dietary management

The optimal dietary therapy of critically ill patients with acute kidney damage (AKI) is crucial. AKI patients have significant protein catabolism, insulin resistance (abnormal carbohydrate metabolism), and an altered fat metabolism, and AKI patients on continuous renal replacement therapy (RRT) are at higher risk of protein and micronutrient losses.

The basic aims of AKI nutritional therapy are to reduce protein (muscle) catabolism and replenish micronutrient losses, notably folic acid, thiamine, and selenium, while keeping in mind the potentially detrimental consequences of excessive vitamin C and vitamin A in retinol form.

The proper dietary management of critically ill AKI patients requires a thorough understanding of the classification of AKI patients, the types of RRT used in their management, the specialized macronutrient and micronutrient requirements, and appropriate fluid management.

Prevention

Acute kidney injury (AKI) can be prevented in patients with trauma, burns, or significant bleeding, as well as those having major surgery, by maintaining normal fluid balance, blood volume, and blood pressure.

Iodinated contrast agents should be avoided, especially in high-risk patients (e.g., the elderly and those with pre-existing renal insufficiency, volume depletion, diabetes, or heart failure).