Acute Renal Failure


This chapter will cover acute renal failure. The learning objectives for this lecture are as follows, we will define acute renal failure. After defining acute renal failure, we will describe the causes of acute renal failure. Our next objective will be to familiarize ourselves with the symptoms of acute renal failure. And finally, we will look at the evaluation and the treatment of acute renal failure. The outline is a reflection of the learning objectives. We will define acute renal failure, identify causes, discuss key aspects of the physical exam and laboratory evaluation, and decide when treatment is necessary, for example, regional replacement therapy. Acute renal failure is defined as the rapid reduction of glomerular filtration rate that occurs over a period of hours to days. When this happens is the rate of production of certain waste products exceed the rate in which the kidney can excrete these products. If this is the case, these products will build up and you will see an increase in serum blood urea nitrogen also known as BUN or serum creatinine. This is called azotemia. Any significant rise in the serium requiring renal replacement therapy or a reduction of urine output to less than 0.5 milligrams per kilogram per day can also be defined as acute renal failure. Continuing with the theme of decreased urine output, when discussing acute renal failure it is important to determine the quality of the urine output. Oliguria is defined as less than 400 mils of urine in 24 hours. Non-oliguric renal failure is defined as urine output of greater than 400 mils in 24 hours. Anuric renal failure is less than 200 mils in 24 hours. There are three categories of acute renal failure. The first is prerenal acute renal failure or prerenal azotemia. This results from decreased renal blood flow or renal perfusion pressure. Prerenal acute renal failure along with acute tubular necrosis account for more than half of the cases of acute renal failure in patients who are hospitalized. Causes of poor or decreased renal blood flow include, but are not limited to, hypovolemia, volume depletion or hemorrhage, cardiogenic shock, sepsis, medications– for example, NSAIDS– and structural irregularities of the vessel, such as renal artery stenosis, The second category is intrinsic or intrarenal acute renal failure, which results from injury within the nephron unit or the renal parenchyma itself. There are several causes of intrinsic renal failure. And they include Acute Tubular Necrosis or ATN, Acute Interstitial Nephritis, AIN, glomerulonephritis, and thromboembolism. The third category is post renal acute renal failure. This usually results from any condition that is causing urinary outflow obstruction, such as prostate disease, kidney stones, pelvic tumors, recent pelvic surgeries, or medications that may cause urinary retention. Since we have identified the categories of acute renal failure, let’s turn our focus to the history and physical examination of a patient with acute renal failure. We want to identify key parts of the history and physical examination that will help us both make the diagnosis and possibly help us identify a cause. It is always important to perform a thorough history. Ask the patient about any new medications both prescribed an over the counter. Ask about any symptoms that may result in volume depletion or increased insensible losses, such as nausea, vomiting, fever, and decreased oral intake of fluids. Review the vital signs carefully. Orthostatic hypotension may suggest hypovolemia. Look in the mouth of the patient to determine if the mucous membranes are moist. Dry mucous membranes also reflect if the patient is volume depleted. Moving down from the head, assist neck veins to aid in determining volume status. Elevated neck vein suggest that the patient is volume overloaded. Listen for an S3 sound or a pericardial friction rub. A friction rub could be a sign of uremic pericarditis and further studies are indicated as well as possibly renal replacement therapy. Examine the abdomen for bladder fullness as this can clue you in about obstruction of urine flow. Check for lower extremity edema, as well as skin turgor, which also weigh in assessing the volume status of the patient. After performing a thorough history and physical examination, you should order laboratory tests that will aid in you making the diagnosis. If urine is available, obtain an analysis and review the urine sediments under a microscope. The urine sediment can be helpful in many ways, such as identifying red blood cells, white blood cells, crystals from medications, for example, a acyclovir or indinavir. You can also look for cellular cast, which suggest infection or glomerulonephritis. Granular casts suggest tubular ischemia and injury. Urine electrolytes are helpful as well. Low urinary sodium, for instance, suggest prerenal azotemia. It is important to place a Foley catheter to monitor urine output and relieve a potential obstruction. Urinary retention can be evaluated by a bladder scan or post-void residual. Obtaining an ultrasound of the kidneys is also helpful. It will not only is just the size of the kidney, but it can also identify hydronephrosis or obstruction. If hydronephrosis is identified, percutaneous nephrostomy tubes to alleviate the obstruction may be indicated. Going back to the urine sodium, you can use it to calculate the fractional excretion of sodium along with urine creatinine, plasma sodium, and plasma creatinine. A result of less than 1% suggest prerenal acute renal failure. The urine sediment as mentioned earlier in this presentation is very helpful. Hyaline cast may frequently be in prerenal azotemia, but are generally physiologic. Cellular cast are usually associated with inflammation of the nephron or parenchyma. Deeply grain related or muddy brown cast are often seen in acute tubular necrosis, Indications for regional replacement therapy, most often hemodialysis, are remembered by the acronym AEIOU. A is for Acidosis. A for Acidosis is a reason to provide replacement therapy as an acidic pH can call serious detriment to the human body. E is for Electrolyte abnormalities, such as hyperkalemia, hypercalcemia, and hyperphosphatemia are all reasons to consider renal replacement therapy. Hyperkalemia can cause cardiac arrest and must be corrected. I is for Injections of toxins or medications that might require dialysis as this would aid in the clearance in patients with and without renal failure. O is for volume overload that is compromising the respiratory status and is also an indication for regional replacement therapy. And lastly, U for for Uremic Symptoms, such as uremic pericarditis, anorexia, and uremic encephalitis are reasons to perform renal replacement therapy, In summary, acute renal failure is defined as a rapid decrease in GFR, which will be noted by a rise in serum creatinine or BUN. There are prerenal intrinsic and post renal causes. History and physical examination are key to making the diagnosis. Be sure to check urine analysis, urine electrolytes, serum electrolytes, and then urine ultrasound. Always remember used dialysis when indicated. We recommend the Primer on Kidney Diseases for further reading.

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