Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI) and Chronic Kidney Disease

• Chapter 28 focuses on Acute Kidney Injury and Chronic Kidney Disease, covering only AKI.
• Objectives include explaining the causes of AKI, identifying interventions for contrast-induced nephropathy, differentiating AKI types, and discussing clinical manifestations and management.

Causes of Acute Kidney Injury

• Reduced blood flow can cause AKI, examples include dehydration, hypotension, bleeding, vomiting, diarrhea, or hypovolemia.
• Blocked urine flow which include clotting, kidney stones, enlarged prostate or any obstruction blocking the flow like tumors can cause AKI.
• Direct kidney damage caused by infections, toxins, medications, and autoimmune diseases is a main cause of AKI.

Dynamics of AKI

• AKI is a clinical syndrome with a sudden reduction of renal function.
• AKI results in fluid and electrolyte imbalance, acid-base homeostasis disturbance, calcium, phosphate metabolism issues, blood pressure regulation problems, and erythropoiesis.
• Decreased glomerular filtration rate (GFR) is a determining factor for AKI, and is reflected by elevated BUN (blood urea nitrogen) and serum creatinine levels, called azotemia.

Acute Kidney Injury Prevalence

• AKI occurs in 10% to 15% of hospitalized patients, a prevalence of over 50% in ICU patients.
• AKI is associated with increased in-hospital morbidity, mortality, and costs.
• Survivors of AKI face an increased risk of developing chronic kidney disease (CKD).

Nephron Units

• Nephrons are the functional units of the kidneys that filter blood.
• Nephrons remove waste, regulate water control, and secrete waste products to create urine.

Common Nephrotoxins

• Aminoglycosides cause AKI in 10% to 25% of patients, with an onset delayed by 5 to 10 days after treatment begins.
• Contrast-induced nephropathy (CIN) occurs within 24 to 48 hours, peaks within 3 to 7 days; incidence is up to 50% in high-risk patients.
• High risk patients include those with diabetes and renal impairment.
• Aminoglycosides include Tobramycin, Amikacin, Neomycin, Gentamicin, and Streptomycin (TANGS).
• Aminoglycosides act against aerobic gram-negative bacteria, are mainly bactericidal, and inhibit protein synthesis at the 30s subunit, they are nephrotoxic and ototoxic (AMINO).
• The side effects of Aminoglycosides include neurotoxicity, allergic reactions, nephrotoxicity, and ototoxicity (NANO).

Reducing Risk of Contrast-Induced Nephropathy (CIN)

• Aggressive volume expansion with isotonic crystalloids (normal saline solution) should be done before and after contrast administration.
• Administer low or iso-osmolar nonionic contrast media.
• Alkalinize urine with sodium bicarbonate.
• A minimal contrast media dose is necessary.
• Stop nephrotoxic drugs 24 hours before contrast media injection like Metformin, ACE, ARBS, and NSAIDs.
• Avoid short intervals between contrast procedures.

Prerenal AKI

• Prerenal AKI is caused by any physiologic event that results in renal hypoperfusion.
• Examples include hypovolemia, cardiovascular failure, decreased renal perfusion, shock, prolonged hypotension
• Gastrointestinal bleeds, severe dehydration, diarrhea, and vomiting.

Intrarenal AKI

• Intrarenal AKI is categorized according to anatomical compartment, including glomerular, vascular, interstitial, and tubular.
• Tubular necrosis, renal ischemia, sepsis, and nephrotoxins are the most common causes of intrarenal AKI.
• AKI begins to show up within 3 to 5 days of contrast exposure.
• Tubular Necrosis are tiny ducts that filter the blood which are usually caused by heart attack, prolonged hypotension, shock and nephrotoxic medications.

Post Renal AKI

• Postrenal AKI is caused by any obstruction in the flow of urine from the collecting ducts in the kidneys to the external urethral orifice.
• Etiologies include ureteral obstruction (stones), urethral blockage (strictures or BPH), or extrinsic source (tumor or fibrosis).
• Older males (benign or malignant prostatic hypertrophy) and young patients (congenital) are most susceptible.

Management of Kidney Injury

• Includes managing fluid balance changes by treating hypovolemia and preventing hypervolemia.
• Utilize diuretics (Furosemide, mannitol, thiazide diuretics) and dopamine.
• Consider dialysis or ultrafiltration.
• Manage acid-base alterations like metabolic acidosis with IV sodium bicarbonate for severe cases.
• Manage cardiovascular alterations like hypertension, hyperkalemia, pericarditis, and CVD in CKD.
• Management also includes pulmonary alterations (pulmonary edema and pleural effusions/pulmonary infections) and gastrointestinal alterations (GI bleeding, gastritis, ulcerative esophagitis, duodenitis, anorexia, nausea/vomiting, diarrhea, GERD, uremic fetor, stomatitis, and constipation).
• Manage neuromuscular alterations (sleep disturbances, muscle irritability, restless leg/burning feet syndromes, peripheral neuropathies, and seizures).
• Address hematologic alterations like increased bleeding tendency, impaired immune syndrome, and anemia.

Anemia Management

• Anemia can be caused by erythropoietin deficiency, decreased RBC survival time, blood loss and other factors.
• Management includes administering iron and human erythropoietin and blood products.

AKI and CKD: Impact on Immune System

• Uremic toxins impair the immune system by inhibiting immune cell activation, promoting leukocyte apoptosis, and increasing oxidative stress.
• CKD can impair immune cells like natural killer cells, dendritic cells, and macrophages; patients with CKD have fewer/less reactive NK cells.

Management of Kidney Injury (Integumentary and Psychosocial Aspects)

• Manage integumentary alterations (dryness, pruritus, uremic frost, ecchymosis, purpura) with meticulous skin care/prevention of skin breakdown.
• Manage alterations in dietary intake by restricting fluid, sodium, potassium and phosphorus & providing high-calorie, moderate-protein diet.
• Manage alterations in psychosocial functioning.

Management of Kidney Injury (Drug Elimination and Skeletal Alterations)

• Manage alterations in drug elimination by adjusting dosages according to GFR.
• Management of skeletal alterations includes regulating phosphate, maintaining calcium levels, treating vitamin D deficiency, and controlling metabolic acidosis.

Preventing CKD Progression

• Secondary insults accelerate the loss of nephrons.
• Insults include hypovolemia, nephrotoxic agents, urinary obstruction/infections, NSAIDs, hyperglycemia, hypertension, and hyperlipidemia.
• Diabetes and hypertension are the number one cause of CKD.