acute kidney injury is character deterioration in kidney function and manifested by an increase in serum creatinine level with or without reduced urine output so here we have the left and right kidney the renal artery supplies the kidneys the renal artery branches and supplies the functional units of the kidneys called the nephrons now the branches of the renal artery's form what's called the glomerulus which filters the filtrate into the many nephron tubules substances in the filtrate can be reabsorbed and many things secreted into the tubules along its way the end product is urine if we zoom into the area here where the glomerulus is and the tubules the girl merliss is where filtration occurs the afferent arteriole brings blood into the glomerulus filtration occurs and then leaves via the efferent arterioles the efferent arteriole continues to form the Vasa recta between the two Buell and the Vasa recta is the interstitial using this diagram we can appreciate the nephrons for functions for making urine the first is filtration the glomerulus filters your blood reabsorption and then secretion where the two Buell returns needed substances into your blood and removes waste along the tubules and the fourth one is excretion the final product really being urine acute kidney injury is a rapid decrease in glomerular filtration that result in abnormal fluid and electrolyte balance and hazard tamiya as a team you are being an increase in the wastes nitrogen as well as creatinine essentially acute kidney injury can be thought of disruption in the four functions of the nephrons we just talked about clinically acute kidney injury is diagnosed when there is an abrupt increase in serum creatinine Crowden comes from the metabolism of creatine in skeletal muscle and dietary meat intake creatinine is freely filtered across the glomerular and not reabsorbed from the tubules creatinine however can be secreted into the tubules the screening levels are maintained in serum when you have acute kidney injury the four functions of making urine are disrupted and so you have an increase in the waste that is creatinine the main fact is affecting the actual glomerular filtration our hydrostatic pressure which is your blood pressure essentially and the colloid osmotic pressure and the fluid pressure which are going the other way the net filtration pressure favors going into the tubules in acute kidney injury you have reduced glomerular filtration which can be due to a number of things firstly a reduced hydrostatic pressure which is your blood pressure or cumulative increase in the colloid osmotic pressure or fluid pressure from whatever cause as a result of these changes you have a accumulation of creatinine in serum creatinine does not get filtered by the glomerulus or secreted into the tubules resulting in elevated serum creatinine to make it simple the causes of acute renal injury or kidney injury can be classified into three types these are pre rino which is as a result of decreased perfusion to the normal kidney in torino acute kidney injury and post renal also called post obstructive acute kidney injury pree renal acute kidney injury is also known as pre renal azerty mia pre renal causes include hypovolemia reduced cardiac output like in cardiogenic shock for example or reduced effective circulatory volume such as in congestive heart failure or liver failure essentially these causes lead to reduced blood flow to the kidneys and so you have a reduced hydrostatic pressure thus you get reduced glomerular filtration another cause of pre renal acute kidney injury is impaired renal autoregulation due to our the use of neurotoxins such as non-steroidal anti-inflammatory drugs now non-steroidal anti-inflammatory drugs they actually cause vasoconstriction to the afferent arterioles and so this will result in reduced hydrostatic pressure resulting in reduced glomerular filtration ACE inhibitors or angiotensin receptor blockers causes vasodilation of the efferent arterioles which is useful at times but in renal injury it actually amplifies the renal injury because it reduces the hydrostatic pressure and reduces glomerular filtration rate finally cyclosporine also causes acute kidney injury now my definition the pre renal acute kidney injury we talked about doesn't actually involve the parenchyma doesn't involve the in actual nephrons really so pre rino acute kidney injury is usually reversible however prolonged pre renal can lead to ischemic injury causing injury no acute kidney injury and we'll talk about intra renal acute kidney injury later but first let's talk about post renal causes of acute kidney injury post renal acute kidney injury is also known as post obstructive acute kidney injury and it's essentially obstruction anywhere along the urinary tract from the renal pelvis ureter bladder to the urethra it can be caused by renal stones which can cause obstruction along the ureter this leads to Dalit ation of the ureter proximally termed hydronephrosis other causes of post renal include prostate enlargement prostate cancer cervical cancer bladder cancer which causes all obstruction and finally here I wrote a lower urinary tract infection which is kind of controversial because technically it doesn't but if it goes up to your kidneys it can and so post renal causes can lead to internal causes of acute kidney injury because as obstruction or infection occurs it can be pushed up the urine can be pushed up the waist pushed up causing injury to the nephrons increasing serum creatinine you intra renal causes of acute kidney injury are probably the most important to understand but essentially it can be divided to four types intra renal causes include glomerular nephritis tubular disease interstitial disease and vascular disease so for glomerulonephritis it is essentially inflammation of the glomerulus the proper term for this is nephrotic syndrome and there are many causes of it the second group of intra renal causes is tubular disease the most important is acute tubular necrosis which is a result of prolonged ischemia from pre renal acute kidney injury and is probably the most common renal injury in hospitals other tubular disease can be from infection injuring the tubular cells or from nephrotoxic the third group of intra renal causes are the interstitial disease these include acute interstitial nephritis and acute interstitial nephritis can also be from a number of things ischemia infection connective tissue diseases as well as the use of nephrotoxic or nefra toxins the last group of internal causes as vascular which includes vasculitis and microangiopathic hemolytic anemia causes such as TTP and hates us now we can appreciate the pathophysiology which occurs in intra renal acute kidney injury by focusing on the changes that occur in this diagram with prolonged pre renal acute kidney injury or Aki for short this can lead to ischemia which leads to tubular disease with tubular injury the injured tubular cells form epithelial castes epithelial castes occurs from damaged tubules and can be seen on urine microscopy this will result in an inflammatory reaction whereby there is an increase in adhesion molecules and leukocyte activation neutrophils are recruited to the area and further perpetuate the inflammatory response injuring the tubules this causes further damage to the tubules and surrounding areas including the interstitial leukocytes form white cell casts which can be seen in urine microscopy and signifies inflammation or infection inflamed interstitial from whatever cause including infection or Nefer toxins also result in an inflammatory response leading to leukocyte recruitment tubular injury and white cell casts in glomerulonephritis there is inflammation of the glomerulus this is special because with damaged glomerulus the red blood cells can actually pass through as filtrate and the red blood cells can form casts again these red blood cell casts can be seen in urine microscopy and signifies glomerular injury lamella information as well as vascular inflammation promotes the inflammatory response as we discussed earlier in in Torino Aki the inflammatory response results in the release of many peptides involved in vasoconstriction this is why in Torino Aki usually coexists with pre reno aki due to vasoconstriction when the kidneys are in this period of reduced blood flow they are vulnerable to further insult with Nefer toxins such as non-steroidal anti-inflammatory drugs or amino glycosides some Nefer toxins can also directly actually injure the tubules or the interstitial important effort options to know about include non-steroidal anti-inflammatory drugs I donated contrast amino glycosides myoglobin crystals formed in those in your body as well as in myeloma where you have power proteins four investigations in acute kidney injury baseline blood tests are important and this includes full blood count Electra la urea creatinine you will have an elevation of creatinine which is diagnostic for Aki you may have an elevation in urea as well as nitrogen for pre renal the fractional excretion of sodium and urea can be calculated and is helpful in diagnosing or differentiating pre renal to acute tubular necrosis for example also with pre renal it's important to investigate or look out look out for the fluid state of the patient if there are hypovolemic or hypervolemic intra renal investigations of acute kidney injury include urinalysis urine MCs microscopic culture sensitivity urine casts which we talked about the different types of casts renal ultrasound urine protein creatine ratio and albumin ratio for post renal causes it's again important to do a urinalysis and urine MCs but here fundamentally doing a bladder scan is easy to check for essentially urine retention you can check it the catheter if the patient has one see if it's blocked or kinked because this can cause post renal Aki also imaging is actually very important so Ct KUB or even a renal tract ultrasound is useful to check for any obstruction signs management of Aki will depend on the course but essentially give someone fluids if it's a pre renal cause and they're hypovolemic or diuretics if they're fluid overloaded to help clear the fluid stop never toxins we talked about earlier treat the underlying cause again if it's an infection use antibiotics if it's renal stone treat the pain but also try to remove the stone if it's big if it's an obstructed catheter try flushing it treat underlying complications of acute kidney injury mainly electrolyte imbalances some of these complications can get out of hand and so some patients will require dialysis so indications for acute dialysis in scenario where someone has acute kidney injury you can easily remember with the acronym AEIOU so a is for acidosis which is refractory it doesn't change is for electrolyte imbalance specifically refractory severe hyperkalemia intoxication or ingestion you can remember what as the acronym slime so these toxins include silicic acid too much lithium isopropanol magnesium laxatives ethylene glycol oh is for overload so fluid overload just as persistent and you is for uremic complications because with acute kidney injury as well as chronic and injury urea can be so high and can lead to complications such as pericarditis as well as platelet dysfunction leading to bleeding and these are some indications for acute dialysis to remove all this waste from the blood thank you for watching I hope you enjoyed this video you