Management of Fluid Overload in Chronic Renal Failure

The second option to explore would be continuing the dialysis treatments. While considering this option with the family it is very important to stress the hardships that go along with the aggressive treatment. Making the family fully aware of the

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.

All the symptoms that were described were based on the kidney functions, so more and further

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).

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.

In this assignment I am going to be discussing dysfunction in relation to water balance and its possible treatments. Oedema which is the medical term for fluid retention in the body and it is one of the signs and symptoms of kidney dysfunction, which is caused by the imbalance of water within the body e.g. a build-up of fluid causes affected tissue to become swollen and this can occur in one particular part of our bodies and this is usually the case with Oedema that occurs as a result of Kidney failure.

Renal History: The patient learned that he had kidney disease a few years ago. He had a biopsy in October 2012 that showed IgA nephropathy per TGH records. He started dialysis in 2013. Initially, he started peritoneal dialysis for seven months. He had a lot of side effects

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

The treatment for this patient is to replace the fluid which should stop the release of angiotensin and aldersterone. This should be accomplished with normal saline. If there is hypokalemia you would need to supplement with potassium. A proton pump inhibitor would also need to be used like prilosec to prevent further losses in hydrogen ions. If she was on any diuretics they need to be discontinued and if renal failure is

The introduction of dialysis as a lifesaving treatment for kidney failure was not the result for any large scale research

Consider a fluid restriction to prevent possible fluid overloading due to his decreased renal function (Vera, 2011).

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

stage is moderate, glomerular filtration rate (GFR) in the kidney has been reduced.7Yet, kidney still