Acute Renal Failure Essay

Injury to the glomerulus and the tubules presents the onset of Intra-renal failure (Matzke, 2011). Some of the frequent causes for Intra-renal failure are glomerulonephritis; pyelonephritis; and tubular injury. Post-renal failure develops from things like ureteroliths, tumors, or anatomic impediments. Opposite of the acute form, the chronic form has a slow onset that has no early stage symptoms. It is important to know that following an acute episode a chronic renal episode often follows, and at this juncture the damage is irreversible. Glomerulonephritis and pyelonephritis combined, has been reported to be the forerunner in as much as half the cases from acute to chronic renal failure. Diabetes mellitus, renal vascular disease, such as atherosclerosis, hypertension, polycystic kidney disease, drug damage, and nephrolith are all examples of other causes of CKD (Pradeep, 2014). Biopsies of kidneys that suffered with CKD reveal smaller kidneys with scarring on the tubules.

Acute renal failure occurs quickly over a period of days or weeks with a reduction in GFR and elevation of BUN, plasma creatinine and crystatin C levels. Oliguria (urine output of < 30ml/hr or < 400 ml/day) is usually associated with ARF, although urine output may be normal or increased as well. Fluid is still filtered at the glomerulus but there is an alteration in tubular secretion or reabsorption. Most types of ARF are reversible if diagnosed and treated early (Perrin, 2009).

Systemic and can quickly become life-threatening with organ failure, including reduced blood pressure and heart failure 1 2

Acute renal failure condition is diagnosed and retitled as acute kidney injury. The purpose of the change of terminology was to encompass the full spectrum of the clinical manifestations associated with the syndrome. This includes a range from a small decline in kidney function to a severe impairment. Furthermore, the acute condition is characterized by a rapid loss of kidney function. In addition, associated manifestation(s) may be displayed as a rise in serum creatinine or a reduction in urine output. As a result of increase of serum creatinine or decline in urine output may developed and aggress to the clinical manifestation azotemia.

This is sudden injury to the kidneys which stops them working instantly or nearly instantly, AKI can range from the kidneys only to stop functioning slightly or to completely stop working. Due to the name of it some people think that it is physical injury or blow to the kidneys however it is a result in complications of other conditions. It is usually seen in older people who are very unwell and get admitted to hospital, it’s vital that AKI is detected quickly as if AKI

Lily was a 65 year old lady with stage 5 CKD, she had recently begun hemodialysis treatment three times a week as an inpatient and had been responding well to treatment. During dialysis treatment on the morning of the first day, Lily’s observations showed that she was: tachycardic, hypotensive, tachypnoeaic, had an oxygen saturation level of 88% and was becoming confused and drowsy. It became apparent that Lily had become hypovolaemic. The hypovolaemic shock seen in this patient was of a particular critical nature due to the fact that her dialysis treatment had moved her rapidly through the first two stages of shock with her compensatory mechanisms failing very quickly (Tait, 2012). It was also much harder to identify the early signs of

Chronic Kidney Disease (CKD) is a disease that is described as a loss of kidney function gradually over time. As kidney function decreases, the waste collection in the body’s blood becomes high and makes the individual feel sick. This disease can lead to other complications in the body such as anemia, poor nutritional health, high blood pressure, and nerve damage. These complications will begin to progress and show as CKD progresses to advanced stages. Early detection of this disease is essential when it comes to treatment. If CKD is diagnosed early enough the disease progression can be slowed down and managed. This disease will eventually lead to failure of the kidneys

Acute renal failure, also known as acute kidney injury is described to be a rapid loss of

Parenchymal echogenicity is the most frequently used marker for evaluating the presence of renal parenchymal disease. It is evaluated by comparing the echogenicity of the renal cortex, medulla and pyelic sinus with that of the adjacent liver and spleen (assuming that the liver and spleen present normal echogenicity). Echogenicity is divided into four different grades from 0 to III.9 However, the grading of parenchymal echogenicity does not differentiate between different histopathological conditions, and a normal renal echogenicity does not exclude that the patient’s kidney is damaged. In the evaluation of renal pathologies, sensitivity and specificity of echogenicity in grades I are 62% and 58%, respectively, whereas sensitivity and specificity of echogenicity in grade III are 20% and 96%, respectively.10 Parenchymal echogenicity varies also with the patient’s age (it is increased in newborn babies due to elevated cellularity and in elderly patients due to fibrosis). Increased cortical echogenicity has proved to correlate significantly with the prevalence of glomerular sclerosis, tubular atrophy, focal leukocyte infiltration, fluid retention, arteriosclerosis and with the presence of hyaline cylinders.11 These lesions are generally tubulointerstitial since the glomerular component accounts only for 8% of the renal parenchyma. Also the presence of diffused calcifications or precipitation of the calcium salts can increase the cortical echogenicity. The renal medulla can also appear hyperechoic, correlating histopathologically with the grade of medullary nephrocalcinosis, medullary tubular ectasia, medullary fibrosis, vascular congestion, and urate or protein deposits. The

In patients with heart failure, hypovolemia, cirrhosis, nephrotic syndrome, or hypoalbuminemia, renal function may be further compromised. BUN, creatinine clearance, and urine output should be monitored closely (Lexi-Comp, 2016).

Chronic kidney disease (CKD) is an irreversible condition that progresses causing kidney dysfunction and then to kidney failure. It is classified by a GFR of <60mL/min for longer than 3 months. There are five stages of CKD: Stage 1 has kidney damage but has a GFR ≥ 90. Stage 2 has mild damage and a GFR of 60-89. Stage 3 has moderate damage and a GFR of 30-59. Stage 4 has severe damage and a GFR of 15-29. Stage 5 is also known as end stage renal disease (ESRD), this is kidney failure with a GFR of ≤ 15 and theses patients are typically on dialysis or in need of an immediate transplant. The leading cause of CKD is diabetes. Hypertension is also a major cause. Since most DM patients have HTN,

Mr. Armstrong has a history of renal insufficiency and uncontrolled hypertension, along with symptoms of fatigue, pedal edema, and occasional shortness of breath. He does not have a history of trauma or obstruction to his kidneys, but his creatinine and BUN levels are currently at 3.5 mg/dl and 40 mg/dl. Normal creatinine concentration values are 0.7 to 1.2 mg/dl and normal BUN values are 10 to 20 mg/dl; this reveals that Mr. Armstrong’s kidneys are not removing wastes properly (McCance, Huether, Brashers, & Rote, 2014).  Mr. Armstrong’s history of renal insufficiency and uncontrolled hypertension is commonly found in patients diagnosed with intrarenal (intrinsic) acute renal failure. Intrarenal acute renal failure can be categorized as

High blood pressure which is called hypertension is another common disease which can cause chronic renal failure. This

As soon as (GRF) becomes less than 15 %, the symptoms of kidney failure clearly

There are different types of renal failure such as chronic kidney disease which is a slow progression over time and it can go unnoticed for a long time. Acute renal failure occurs suddenly, happening within a few hours or a few days, if not caught in time