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In prerenal ARF, the is a insufficient circulation of blood to the kidneys, resulting in the blood not being cleaned. This then results in a built up of wanted waste and substances in the blood. The kidney has a high tolerance, even at low blood pressure it is still able to function , when the blood flow reduces, when the rate continues to decrease the urinary output decreases and stop once the rate reaches zero. The oxygen consumed also decrease, this oxygen is used to keep the renal tubular cells alive. The early signs of prerenal failure is a decreased urinary output and a low concentration of sodium in the urine.
This type of involves damage to both kidneys, 40% of acute renal failures are intrinsic ARF. 90% of the intrinsic renal failure causes are caused by toxins, which then causes acute tubular necrosis (ATN). Intrinsic acute renal failure is classified in 3 types; Intrinsic ARF could be caused by vascular disease, examples of this include low blood platelet and red blood cell counts and inflammation of the blood vessels. The second type is it could be caused by accumulation of proteins in the kidney tissues which can then lead to an allergy or infection in these tissues in the kidney. The remaining type is caused by the by ishchemia, this is when the blood flow is reduced to the kidneys and also can be caused by the accumulation of toxins in the tissues in the kidneys. Treatment of intrinsic ARF is to restore the blood flow to the kidneys, drugs maybe used to restore the blood flow.
3. Postrenal -
Postrenal ARF is caused by a blockage which causes the flow of urine to be restricted and thus causing the pressure to build to in all of the renal nephrons. This leads to the nephrons shutting down due to the excessive pressure. The extent of the renal failure is directly related with the extent of the obstruction. The main aim of the treatment is to reduce the obstruction, to allow urine to flow freely and reduce the pressure build up.
A young adult was admitted to A&E after being knocked down by a car. Upon examination he was severely shocked with swelling and tenderness in his abdomen. IV fluid was given, in theatre a splenectomy was performed, for a ruptured spleen and mesenteric damage and a tear in the duodenum was noted. 3 days later he was taken back to theatre for pyrexia and hypotension. Gangrenous segment of the small intestine was noted and removed. Following this the patient became oliguric despite adequate hydration.
The table above shows the results obtained when then the patient's blood and urine were analysed.
Using this table i will now analyse the results-
The patients serum sodium level is 128mmol/L, the reference range states that the normal range should be between 135-145mmol/L, when compared to the reference range the patient has a low level of serum sodium ,
The level of serum potassium is above the normal range. Potassium is generally excreted through urine, this patient has the process of metabolic acidosis occurring, this produces more serum potassium, which in turn causes hyperalaemia. This can then lead to acute renal failure as the level of potassium becomes excessive.
The level of serum bicarbonate in the patient's blood is below the normal range. The kidney normally removes bicarbonate and allows hydrogen ions to be excreted into the urine and removed. The level of bicarbonate is lower than normal, possibly due to the excessive loss of fluids. The kidneys continued to remove bicarbonate at normal rate, even though there is less bicarbonate in the fluids. Also the level of bicarbonate would have decreased from the loss of fluids through the tear in the duodenum and the ruptured spleen.
The level of urea in the patient's blood is significantly higher than the reference range. The reference range states that the level of serum urea is normally between 3.3-6.7, this patient has a level of 22 mol/L, which very high. The cause of this maybe due to, excessive fluid loss and gastrointestinal bleeding from the tear in the duodenum.
The level of creatinine in the patient's blood and urine is much higher than the reference range, the reference range states that the normal level is between 60-110 mmol/L, the level in the patient is 225 mmol/L. Creatinine is produced by muscles, this is a sign of reduced kidney function. The kidney cant remove the excess creatinine due to the ruptured spleen and also shock experienced by the patient, this can lead to obstruction of the urinary tract in the kidney, thus reducing the urinary output, allowing the creatinine to accumulate in the kidneys.
The level of calcium in the patient is lower than the reference range, the reference range suggest the level of serum calcium is about 2.20-2.55 mmol/L, the level in the patient is 1.72 mmol/L. The cause of this is the gangrenous segment of the the small intestine which was removed, this could have ment less absorption of nutrients initially.
The patients level of serum phosphate shows that the patient has a very high level compared with the reference ranage. The reference range states that the 0.8-1.4 mmol/L, the patient has a level of 2.96 mmol/L. This maybe due to the ruptureed spleen the patient suffered whcih in turn would have decreased the urinary output, allow the level of serum phosphate to build up.
The level of albumin in this patient are below the reference range, the patients level is 28 g/L. The reference range is 35-50 g/L. This lowered level may have been caused by gastrointestinal bleeding from the tear in the duodenum, shock and from the ruptured spleen, which would have ment a loss of blood and fluids.
The urine levels of the patient were 16 mmol/L, the reference range suggests it should be between 0.4-1.8 mmol/L. Shock and swealing would have caused the restriction in the tract which would lead to the urinary output decresing and thus more urine being held in the kidneys.
The two graphs above shows the effect of the admission and onset of oliguria. From the first graph we can see that when the onset of oliguria occured, the level of serum creatinine also gradually increased but then after sometime, the level of oliguria decreased which eventually lead to the level of serum creatinine decreasing. The level of serum urea also increased when oliguria was administered and onset. The concentration of urea, creatinine and potassium increased, this means that even though the patient was hydrated, the urinary output remained low, below 400 ml per day. This shows that the patient has renal failure.
There are there phases of renal failure-
Oliguria phase- this phase lasts for upto 8-10 days, but can last for longer. In this phase the urine output decreases for upto 1-8 days, the urine output decreases below 400 ml per day.
Diuretic phase- In this phase, the urine output volume increases, this is because the glomerular filtration rate increases. In this phase the urine output can exceed above 5L per day, which causes a high risk of dehydration. This phase lasts between 5-9 days.
Recovery phase- In this phase this phase lasts between 10-14 days. In this phase the kidneys are slowly returning to there normal funstions and levels. The levels of urea, creatininie and potassium decrease. The tubular cells regenerate and normal function is restored.
When renal acute renal failure is in the intrinsic renal failure phase, the failure is preventable if the patient is diagnosed early and the progress is halted. In this case, ARF couldn't have been treated early because it was an accident and a sudden shock to the body causing not only acute renal failure but other damage, a ruptured spleen, a tear in the duodenum and shock. Within 14 days, this patient was able to recover from acute renal failure. This means that this patient didn't have cornic renal failure which is very serious and can have effects on the other parts of the body, even if the patient fully recovers. In this case the patient had prerenal failure; this is due to an insufficient supply of blood to the kidney, resulting in a reduced amount of filtration of the blood. Treatments for acute renal failure include dialysis, haemofiltration and renal replacement treatment.
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