Acute Kidney Injury Midterm Notes PDF

6 1 URINARY AND RENAL DISORDERS – Acute Kidney Injury Acute Kidney Injury (AKI) Acute Kidney Injury (AKI) is defined as a sudden decline in kidney func5on, resul7ng in reduced glomerular filtra7on, fluid and...

6 1 URINARY AND RENAL DISORDERS – Acute Kidney Injury Acute Kidney Injury (AKI) Acute Kidney Injury (AKI) is defined as a sudden decline in kidney func5on, resul7ng in reduced glomerular filtra7on, fluid and electrolyte imbalances, and accumula7on of nitrogenous waste products in the blood. 1. Most Likely Cause The causes of AKI are classified into three major categories: 1. Prerenal Causes (most common) o Hypoperfusion of the kidneys due to condi7ons such as: § Low blood pressure (hypotension) from hemorrhage, shock, or sepsis. § Hypovolemia (severe dehydra7on or blood loss). § Heart failure or reduced cardiac output, causing inadequate blood flow to the kidneys. 2. Intrarenal Causes (damage within the kidney itself) o Direct damage to the kidney structures, including: § Acute tubular necrosis (ATN) caused by ischemia or nephrotoxins (e.g., drugs, toxins). § Glomerulonephri5s (immune-mediated injury to the glomeruli). § Acute inters55al nephri5s (inflamma7on of the kidney's inters77al space, oKen caused by allergic reac7ons to drugs). 3. Postrenal Causes (blockage of urine flow) o Obstruc5on of urinary ouLlow, which increases pressure in the nephrons, causing injury. Examples include: § Kidney stones (nephrolithiasis). § Prostate enlargement (benign prosta7c hyperplasia). § Tumors or ureteral strictures. 2. Pathophysiology The pathophysiology of AKI differs based on the type (prerenal, intrarenal, or postrenal), but generally follows a sequence of events: 1. Prerenal Pathophysiology (renal hypoperfusion) o Decreased renal blood flow reduces glomerular filtra5on rate (GFR), leading to insufficient blood flow to the nephrons. o Hypoxia in the renal 7ssue causes cell injury and ischemia, which may progress to acute tubular necrosis (ATN) if untreated. o GFR can recover quickly if blood flow is restored. 2. Intrarenal Pathophysiology (direct injury to the kidney) o Injury to renal tubules (as in ATN) results from: § Ischemia: Prolonged prerenal failure progresses to ischemic necrosis of the renal tubular cells. § Nephrotoxins (e.g., certain an7bio7cs, NSAIDs) cause damage to the proximal tubular cells, which are responsible for reabsorp7on.  2 o Damaged tubular cells form casts that block urine flow, worsening the injury by increasing intratubular pressure. o In glomerulonephri5s, immune complexes deposit in the glomerulus, triggering inflamma7on and injury, leading to proteinuria and hematuria. 3. Postrenal Pathophysiology (urinary tract obstruc7on) o Urinary obstruc5on (from kidney stones, tumors, or prostate enlargement) increases pressure in the nephrons, which opposes the normal pressure gradient required for filtra7on. o Prolonged obstruc7on leads to hydronephrosis (swelling of the kidney due to backed-up urine) and compression of the renal 7ssue, which damages nephron func7on. 3. Disease Transmission Transmission: o Not transmissible. AKI is a non-infec7ous disease. o However, certain infec5ons (e.g., sepsis) may lead to prerenal AKI due to shock and reduced perfusion. 4. Risk Factors The risk factors for AKI depend on the category (prerenal, intrarenal, or postrenal). Risk Factors for Prerenal AKI Age: Older adults have reduced renal reserve. Dehydra5on: Can result from excessive diarrhea, vomi7ng, or inadequate fluid intake. Shock: Hypotension from trauma, hemorrhage, or sep7c shock can decrease renal perfusion. Heart Failure: Reduced cardiac output decreases blood flow to the kidneys. Use of diure5cs: Excessive diuresis may result in dehydra7on and reduced blood volume. Risk Factors for Intrarenal AKI Medica5ons: Use of nephrotoxic drugs (e.g., aminoglycosides, NSAIDs, contrast agents for imaging) increases risk of ATN. Infec5ons: Infec7ons like glomerulonephri5s can cause immune-mediated injury to the kidneys. Autoimmune diseases: Condi7ons like lupus nephri5s may result in immune complexes that deposit in the kidneys. Sepsis: Sepsis-induced ischemia and endotoxins can damage renal tubules. Risk Factors for Postrenal AKI Kidney Stones (Nephrolithiasis): Stones block the ou[low of urine, leading to hydronephrosis and increased intratubular pressure. Prosta5c Hypertrophy (BPH): Enlargement of the prostate can block urine flow in men, especially older men. Urethral Strictures: May develop as a result of trauma, infec5on, or surgery, increasing the risk of postrenal AKI. Tumors: Cancers that invade or compress the urinary tract can lead to postrenal AKI.  3 Summary Table Criteria Acute Kidney Injury (AKI) Most Likely Prerenal (hypoperfusion), intrarenal (tubular injury), postrenal (obstruc7on). Cause Prerenal: Reduced blood flow → reduced GFR. Intrarenal: Tubular injury Pathophysiology (ischemia, nephrotoxins) → casts, obstruc7on, and backpressure. Postrenal: Obstruc7on increases nephron pressure, reducing filtra7on. Transmission Not transmissible. AKI is not an infec7ous disease. Prerenal: Dehydra7on, hemorrhage, shock, heart failure. Intrarenal: Risk Factors Nephrotoxins, glomerulonephri7s, sepsis. Postrenal: Kidney stones, prosta7c hypertrophy, tumors.