ACUTE KIDNEY INJURY –
Acute Kidney Injury (AKI) is currently recognized as the preferred nomenclature for the clinical disorder formerly called Acute Renal Failure(ARF).This transition in terminology was meant to emphasize that the spectrum of the disease is much broader than a subset of patients who experience failure and require dialysis support .This nomenclature explains that renal failure occur as a continuum 1. AKIN recently defined AKI as “ functional or structural abnormalities or markers of kidney damage including abnormality in blood, urine or tissue tests or imaging studies present for < 3 months.”2
A large trial by Uchino et al.3, on the epidemiology and outcome of AKI in critically ill adult patients reported an overall mortality …show more content…
Increased extracellular fluid losses: hemorrhage B. Gastrointestinal fluid loss: vomiting, diarrhea, enterocutaneous fistula C. Renal fluid loss: diuretics, osmotic diuresis, hypoadrenalism, nephrogenic diabetes insipidus D. Extravascular sequestration: burns, pancreatitis, severe hypoalbuminemia (hypoproteinemia) E. Decreased intake: dehydration, altered mental status
II. Altered renal hemodynamics resulting in hypoperfusion A. Low cardiac output state: diseases of the myocardium, valves, and pericardium (including tamponade); pulmonary hypertension or massive pulmonary embolism leading to right and left heart failure; impaired venous return (e.g., abdominal compartment syndrome or positive pressure ventilation) B. Systemic vasodilation: sepsis, antihypertensives, afterload reducers, anaphylaxis C. Renal vasoconstriction: hypercalcemia, catecholamines, calcineurin inhibitors, amphotericin B D. Impairment of renal autoregulatory responses: cyclooxygenase inhibitors (e.g., nonsteroidal anti-inflammatory drugs), angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers E. Hepatorenal syndrome
In cases of hypovolemia, there occurs a fall in mean arterial pressure.This results in the activation of an array of compensatory mechanisms to preserve renalblood flow. This …show more content…
Autoregulatory mechanisms in the kidney is activated, Stretch receptors in the afferent arterioles trigger vasodialation through a local myogenic reflex
Release of Angiotensin II results in the release of prostaglandins (PG E2 and PGI2) that results in afferent arteriolar vasodialation and efferent arteriolar vasoconstriction which in turn increases the fraction of plasma filtered, maintains the intraglomerular pressures and increases gfr.
Also since the amount of solutes delivered to the DCT declines due to hypovolemia,macula densa senses the change and results in afferent arteriolar dialatation through Tubulogomerular Feedback.
But in some cases these regulatory mechanisms fail like severe hypovolemia, old age, pre existing diseases like atherosclerosis, long standing hypertension, chronic kidney disease and drugs that blunt these compensatory mechanisms like NSAIDS, ACE inhibitors and Angiotensin Receptor
Acute Kidney Injury (AKI) is currently recognized as the preferred nomenclature for the clinical disorder formerly called Acute Renal Failure(ARF).This transition in terminology was meant to emphasize that the spectrum of the disease is much broader than a subset of patients who experience failure and require dialysis support .This nomenclature explains that renal failure occur as a continuum 1. AKIN recently defined AKI as “ functional or structural abnormalities or markers of kidney damage including abnormality in blood, urine or tissue tests or imaging studies present for < 3 months.”2
A large trial by Uchino et al.3, on the epidemiology and outcome of AKI in critically ill adult patients reported an overall mortality …show more content…
Increased extracellular fluid losses: hemorrhage B. Gastrointestinal fluid loss: vomiting, diarrhea, enterocutaneous fistula C. Renal fluid loss: diuretics, osmotic diuresis, hypoadrenalism, nephrogenic diabetes insipidus D. Extravascular sequestration: burns, pancreatitis, severe hypoalbuminemia (hypoproteinemia) E. Decreased intake: dehydration, altered mental status
II. Altered renal hemodynamics resulting in hypoperfusion A. Low cardiac output state: diseases of the myocardium, valves, and pericardium (including tamponade); pulmonary hypertension or massive pulmonary embolism leading to right and left heart failure; impaired venous return (e.g., abdominal compartment syndrome or positive pressure ventilation) B. Systemic vasodilation: sepsis, antihypertensives, afterload reducers, anaphylaxis C. Renal vasoconstriction: hypercalcemia, catecholamines, calcineurin inhibitors, amphotericin B D. Impairment of renal autoregulatory responses: cyclooxygenase inhibitors (e.g., nonsteroidal anti-inflammatory drugs), angiotensin-converting enzyme inhibitors, or angiotensin II receptor blockers E. Hepatorenal syndrome
In cases of hypovolemia, there occurs a fall in mean arterial pressure.This results in the activation of an array of compensatory mechanisms to preserve renalblood flow. This …show more content…
Autoregulatory mechanisms in the kidney is activated, Stretch receptors in the afferent arterioles trigger vasodialation through a local myogenic reflex
Release of Angiotensin II results in the release of prostaglandins (PG E2 and PGI2) that results in afferent arteriolar vasodialation and efferent arteriolar vasoconstriction which in turn increases the fraction of plasma filtered, maintains the intraglomerular pressures and increases gfr.
Also since the amount of solutes delivered to the DCT declines due to hypovolemia,macula densa senses the change and results in afferent arteriolar dialatation through Tubulogomerular Feedback.
But in some cases these regulatory mechanisms fail like severe hypovolemia, old age, pre existing diseases like atherosclerosis, long standing hypertension, chronic kidney disease and drugs that blunt these compensatory mechanisms like NSAIDS, ACE inhibitors and Angiotensin Receptor