Acute Kidney Injury II: Pathophysiology

Prerenal acute kidney injury occurs when reduced blood flow to the kidneys decreases filtration capacity without directly damaging kidney tissue. Common causes include hypovolemia from bleeding or dehydration, decreased cardiac output from heart failure, and systemic vasodilation from sepsis. If blood flow is not restored promptly, prolonged reduced perfusion can lead to ischemia and intrinsic kidney damage.

Intrarenal acute kidney injury results from direct damage to kidney structures like glomeruli, tubules, or blood vessels. Acute tubular necrosis causes epithelial cell death and obstruction, reducing glomerular filtration rate. Acute interstitial nephritis causes inflammation and edema impairing tubular function. Glomerulonephritis damages glomeruli through immune-mediated inflammation, resulting in reduced filtration and proteinuria.

Postrenal acute kidney injury occurs when urinary tract obstruction prevents urine flow, increasing pressure in renal tubules and reducing glomerular filtration rate. Common causes include kidney stones, strictures, tumors, benign prostatic hyperplasia, and urethral injury. Prolonged obstruction leads to renal ischemia, hydronephrosis, and tubular atrophy, potentially causing irreversible kidney damage without timely intervention.

In prerenal acute kidney injury, kidneys activate autoregulatory mechanisms to preserve glomerular filtration rate despite low blood flow. Prostaglandin-mediated dilation of the afferent arteriole and angiotensin II-mediated constriction of the efferent arteriole help maintain filtration. The kidneys also enhance sodium and water reabsorption to maintain fluid balance during reduced perfusion.

Acute tubular necrosis involves ischemia or nephrotoxin damage to renal tubular epithelial cells, causing cell death and tubular obstruction with decreased glomerular filtration rate. Acute interstitial nephritis involves an immune response to medications or infections causing inflammation and edema in the renal interstitium, impairing tubular function. Both are forms of intrarenal acute kidney injury with distinct pathophysiologic mechanisms.

Early intervention for postrenal obstruction is critical because prolonged blockage causes progressive renal damage. Sustained pressure in renal tubules leads to renal ischemia, hydronephrosis, and tubular atrophy. Without timely relief, this damage becomes irreversible, resulting in permanent loss of kidney function. Early removal of obstruction can prevent these complications.

Acute tubular necrosis occurs when ischemia or nephrotoxins damage renal tubular epithelial cells, causing cell death and sloughing into the tubular lumen. This results in obstruction, filtrate back-leak, and reduced urine output. While acute kidney injury iii clinical manifestations often shows reversibility with prompt treatment, severe or prolonged acute tubular necrosis can lead to permanent kidney damage.