Acute Kidney Injury Case Study

A condition where kidney function rapidly declines over hours to days.

AKI caused by decreased blood flow to the kidneys.

AKI caused by damage to the kidney tissue (tubules).

AKI caused by a blockage in the urine flow pathway.

Recovery from AKI within 48 hours of injury.

AKI that persists beyond 48 hours.

A blood test that measures the level of urea nitrogen in the blood.

A blood test that measures the level of creatinine in the blood; a marker of kidney function.

Kidney dysfunction that develops over a short period, usually within a few hours or days. It's marked by sudden changes in kidney function, urine output, or blood creatinine levels.

Progressive loss of kidney function over many months or years. It often leads to end-stage renal disease (ESRD) if not managed.

Decreased urine output compared to normal.

Classification system for AKI severity, usually based on serum creatinine and urine output.

Kidney Disease: Improving Global Outcomes guidelines, a set of recommendations for managing kidney disease.

Fluid-filled sacs that can develop on the kidneys.

Kidney disease that develops suddenly or acutely, lasting for up to 7 days.

A treatment for severe kidney failure, often dialysis, that helps remove waste products when the kidneys cannot do this adequately by themselves.

AKI can be caused by reduced blood flow to the kidneys (prerenal), damage to the kidney tissue itself (intrinsic), or a blockage in the urine flow pathway (postrenal).

Acute Kidney Injury (AKI) is a sudden decline in kidney function that occurs over hours or days. It can be caused by various factors.

A primary concern is the potential progression of AKI into Chronic Kidney Disease (CKD).

AKI involves various pathophysiological changes including: reduced renal perfusion, tubular dysfunction and cell death, intraluminal tubular obstruction, and metabolic alterations affecting tubuloglomerular balance.

Chronic Kidney Disease (CKD) is a long-term, progressive loss of kidney function that can develop over months or years.

AKI, if not properly treated, can lead to long-term damage and progressive deterioration of kidney function, eventually resulting in CKD.

AKI can involve a build-up of cell debris in the kidney tubules, leading to obstruction and backleak of filtrate.

Early diagnosis and treatment are critical for preventing long-term kidney damage and improving patient outcomes.

Excess fluid in the body, commonly seen in AKI due to reduced kidney function.

A common symptom of fluid overload in AKI, due to fluid accumulating in the lungs.

Swelling in the legs and feet, often caused by fluid retention in AKI.

Can be caused by fluid buildup in the lungs (pulmonary edema), a common finding in AKI.

A high level of creatinine in the blood, indicating impaired kidney function. It suggests a potential problem with the kidneys' ability to filter waste products.

An increase in the thickness of the bladder wall detected on ultrasound, often a sign of cystitis or other bladder conditions.

A smaller than normal capacity of the bladder, indicating potential difficulty in storing urine effectively.

A blockage in the urinary tract that prevents the flow of urine from the bladder, potentially contributing to AKI if not addressed.

The mechanism of how kidney function declines rapidly in AKI. It involves inflammatory mediators, vasoconstriction, and ischemia that lead to cell death.

Inflammatory mediators like cytokines and chemokines are released, leading to interstitial inflammation and vascular congestion, which obstructs small blood vessels and limits blood flow to the kidneys.

Vasoconstriction, the narrowing of blood vessels, further reduces blood flow to the kidneys, leading to ischemia and cell death.

Ischemia refers to reduced blood flow to the kidneys, depriving cells of oxygen and nutrients, ultimately leading to cell death.

A type of AKI where the cause is reduced blood flow to the kidneys, often due to dehydration or low blood pressure.

Hypovolemia (low blood volume), severe blood loss, dehydration, and heart failure can all reduce blood flow to the kidneys.

The body compensates by dilating the afferent arterioles (blood vessels leading to the glomerulus) and constricting the efferent arterioles (blood vessels leaving the glomerulus) to maintain filtration pressure.

The body's adaptive mechanisms fail due to already high levels of angiotensin II, leading to a decline in glomerular filtration rate (GFR).

The initiation phase involves the onset of ischemic injury in the proximal tubule and thick ascending limb of the loop of Henle, leading to cell damage and inflammation.

Continuous ischemic injury and inflammation lead to vascular congestion, further reducing blood flow and causing worsening kidney damage.

This phase is characterized by stable, low GFR and urine output, with persistent intrarenal vasoconstriction and medullary ischemia.

Repair and regeneration of renal parenchymal cells, particularly tubular epithelial cells, occur, potentially leading to improved kidney function.

Contrast agents used in imaging procedures can directly damage kidney cells and cause acute renal failure, often reversible.

Certain antibiotics like aminoglycosides and anti-cancer drugs like cisplatin can damage the kidneys.

Substances produced by the body, such as myoglobin, hemoglobin, and myeloma light chains, can overwhelm the kidneys and lead to AKI.