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Acute Renal Failure Essay

Acute renal failure (ARF), also know as Acute Kidney Injury/Impairment (AKI) is described as a condition where there is a rapid decline in kidney function which results in an increase in accumulation of waste materials in the body and decreased urine output, usually over hours to weeks, occurring in a person with or without a previous pre-existing renal disease (Van Biesen, W. , Vanholder, R. , & Lameire, N. , 2006).

Acute loss of renal function can be due to poor perfusion to the kidneys, called prerenal failure, from an obstruction of urine flow from the kidneys, called postrenal failure, or from complications from within the kidneys called intrinsic renal failure (Rahman, M. , Shad, F. , & Smith, M. C. , 2012). Prerenal acute failure can occur if the person sustains injuries such as: a decrease in in circulating volume like with hemorrhages, dehydration, burns, shock, or edema. It can also present with decreases in cardiac output, occlusion of arteries to the kidneys and with complications due to drug or medication use (Copstead, L. -E. C. & Bannisk, J. L. , 2010).

This type of failure is responsible for 70% of reported cases of ARF from within the community and 40% of those diagnosed within hospitals (Copstead, L. -E. C. , & Bannisk, J. L. , 2010). This disruption in the circulating volume impairs cardiac output which then reduces the amount available to the kidneys resulting in kidney injury/impairment (Copstead, L. -E. C. , & Bannisk, J. L. , 2010). Postrenal failure occurs from an obstruction to the outflow of urine from the kidneys in conditions resulting from: benign prostatic hyperplasia, obstructed catheters, abdominal tumors, strictures, or renal calculi.

This type of failure is the least common of the three and is most times, responsive to treatment(s) (Copstead, L. -E. C. , & Bannisk, J. L. , 2010). If left untreated, the damage to the kidneys progresses and develops into acute tubular necrosis or intrinsic acute renal failure and eventual irreversible kidney damage (Copstead, L. -E. C. , & Bannisk, J. L. , 2010). Intrinsic failure is the last classification of renal failure and develops in instances specific to the area of the body affected; this can be interstitial, glomerular, vascular or tubular (Rahman, M. , Shad, F. , & Smith, M. C. , 2012).

Interstitial renal damage can occur from, infections, viruses, bacteria, fungi, or secondary conditions such as: sarcoidosis or lupus. But in most cases, use of medications is the most common cause (Rahman, M. , Shad, F. , & Smith, M. C. , 2012). Glomerular causes of renal damage occur from inflammation within the kidney related to a systemic illness or pulmonary renal complication. Acute vascular renal damage occurs from injury to renal arteries or veins such as in, thrombosis, hypertension, scleroderma renal crisis, infarction and atheroembolic disease (Rahman, M. Shad, F. , & Smith, M. C. , 2012).

The most common type of intrinsic renal damage occurs from acute tubular necrosis and is the most common diagnosis related to hospitalized patients; cause of which is ischemia or from a toxic substance to the kidneys. This renal injury is more serious in that it does not improve when treatment has commenced with reperfusion of intravascular volume and blood flow and may require temporary renal replacement therapy (Rahman, M. , Shad, F. , & Smith, M. C. , 2012). Diagnosis, Signs and Symptoms, Complications and Managment

Until recently, there had not been a concise agreement of standard definable criteria for ARF in the scientific community; it has been noted that there have been 35 different definitions for this condition (Kidney Disease: Improving Global Outcomes (KDIGO), 2012). In 2004, the Acute Dialysis Quality Initiative (ADQI) developed a standardized classification system, named RIFLE, which included a broader classification system to allow for measurement of minor decline in kidney function to patients who require renal replacement therapy.

Due to this new classification, ARF is now known more commonly as Acute Kidney Injury/Impairment (AKI) and has also lead to increases in the number of reported cases of AKI (Kidney Disease: Improving Global Outcomes (KDIGO), 2012). A study examining reports from hospitals of patients discharged with the diagnosis of AKI within the US, found that between 1992 and 2001 an increase of incidence of AKI in patients rose 11% per year, culminating in a rate of approximately 35 patients per 1000 in 2001 (Siew, E. D. & Davenport, A. , 2015).

Diagnosis of AKI results from patient history (medication use or illness), physical examination assessing for signs of volume depletion (burns, bleeding) or rashes indicating systemic illness or infection, and laboratory results based on RIFLE criteria (Rahman, M. , Shad, F. , & Smith, M. C. , 2012). RIFLE stands for “the increasing severity classes Risk, Injury, and Failure; and the two outcome classes, Loss and End-Stage Renal Disease (ESRD)” (Singbartl, K. , & Kellum, J. A. , 2012).

There are three severity grades for RIFLE and are defined by changes in serum creatinine levels or urine output where the worst of each is measured; the two outcome criteria, Loss and ESRD, are measured by the duration of loss of kidney function (KDIGO, 2012). Stage 1 is a measurement of serum creatinine (SCr) level of 1. 5-1. 9 x above normal levels within a 48-hour period and <0. 5ml/kg/h rate of urine output per 6-12 hours indicates an acute process.

Stage 2, with an elevated SCr of 2. 0-2. 9 x above than normal and urine output less than 0. ml/kg/h per 12 hours indicates injury to the kidneys, whereas a rise over weeks to months represents kidney failure in Stage 3, when SCr reaches or rises above levels of 3. 0-4. 0 x above the baseline renal function and urine output has decreased to less than . 03ml/kg/h for 24 hours or more, or the failure of the kidneys to produce any urine for 12 hours or more (KDIGO, 2012) (See Appendix A for RIFLE Figure).

A complete blood count may also be tested for signs of hemolytic anemia and can be indicative of hemolytic uremic syndrome or thrombotic thrombocytopenic purpura (Rahman, M. , Shad, F. , & Smith, M. C. 2012). Urinalysis measurement of fractional excretion of sodium can also indicate where anatomically the renal dysfunction has occurred such as in a prerenal region or intrinsic; using the calculation of FENA=100 x (urinary sodium x SCr)/ (serum Na+ x urinary creatinine). Values less than 1% show a prerenal cause and values above 2% shows an intrinsic cause (Rahman, M. , Shad, F. , & Smith, M. C. (2012). Other diagnostic tests include renal ultrasonography to discount possible obstructions, and renal biopsy when the cause of the kidney injury cannot be defined (Rahman, M. , Shad, F. , & Smith, M. C. (2012).

Signs and symptoms deriving from prerenal AKI can include: vomiting, diarrhea, poor skin turgor, weight loss, dilated neck veins, peripheral edema, ascites and an S3 heart sound. Intrinsic renal kidney injury can present with: muscle tenderness, compartment syndrome, edema, rash, oral or nasal ulcers and a fever. Postrenal AKI can present with: bladder distention, a pelvic mass or prostate enlargement (Rahman, M. , Shad, F. , & Smith, M. C. (2012). Some potential complications resultant of AKI can include symptoms such as fluid buildup due to the loss of function from the kidneys; this results in difficulty breathing.

The pericardium surrounding the heart can also become inflamed, causing the client to have complaints of chest pain. The client may also present with muscle weakness due to the imbalance of fluids and electrolytes in the circulatory system, such as with increases in serum potassium levels. If kidney injury progression cannot be successfully treated, slowed or reversed, permanent kidney damage can occur resulting in permanent loss of kidney function, or end-stage kidney disease requiring dialysis treatment or eventual death (Mayo Clinic, 2015).

Treatment and management of AKI requires hospitalization and length of stay is dependent on the underlying cause of the disease and how quickly the problem(s) can be resolved. If a circulatory volume issue is related to the AKI, intravenous therapy may be used to replenish the loss of bodily fluids, as in the case of burns or hemorrhages (Mayo Clinic, 2015). If fluid volume is overloaded and edema is present, treatment could include medication intervention such as the use of diuretics and possible catheterization (Mayo Clinic, 2015).

AKI caused by a potassium imbalance due to renal filtration insufficiency can also be treated with medications; calcium, glucose, or sodium polystyrene are such drugs that prevent the accumulation of potassium in the circulatory system (Mayo Clinic, 2015). Hemodialysis may also be initiated to remove toxins, waste and excess fluids from the body; dialysis may be required for a short period until kidney function recovers or perhaps long-term if chronic kidney failure develops (Mayo Clinic, 2015).

Management of AKI after discharge from the hospital may require the client to make changes in their diet like avoiding foods high in potassium (bananas oranges, spinach, etc. ), reducing the amount of sodium (frozen foods, canned goods, fast food, processed meats and cheeses) and phosphorus intake (nuts, dried beans, milk, cheese, peanut butter). Clients will also need to be cautious when using over-the-counter medications like aspirin, Tylenol and ibuprofen because over-ingestion of these products can increase risk of AKI (Mayo Clinic, 2015).

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