Essay On Renal Failure

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.

Intrarenal acute renal failure- accounts for 30% to 40% of the cases of ARF- generally results from acute tubular necrosis due to disturbances within the glomerulus or renal tubules. ATN most often occurs after surgery but is also associated with sepsis, severe trauma, including severe burns,

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.

Hypertension. His blood pressure is great here in the office. I will have him continue with his same medication and I will continue to follow along and he was asked also monitor for signs of hypotension and I did review with him what to be monitoring for.

“The patient is Adam Rudd, a 78 y/o white male with a history of hypertension. He has been diagnosed with hypertension past 15 years and is on anti-hypertensive medications and aspirin. He is very weak and short of breath. He is accompanied with his longtime friend Jennifer, who reports that Rudd was looking very weak and was complaining of severe headache and blurred vision before coming to the hospital. He is 5’9” and weighs 270 lb. Vital signs recorded were: oral temperature 98.20 F, BP 224/120 mm Hg with a heart rate of 102 beats/minute and respiration of 24 breaths per minute. The pulse oximetry reading was 94% on room air. He is complaining of severe headache and blurred vision. Rudd said that he did not take his antihypertensive medication or aspirin since he ran out of pills. He has not been taking his medication for past 15 days. He reports no known allergies to any medications or other substances.”

the renal issues began. One of the function of the kidneys is to regulate blood volume and pressure.

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

CKD will cause the body to retain many excess fluids and waste that are normally filtered out to prevent internal harm throughout the body. With kidney disease there will be a rise in blood pressure due to the amount of extra fluid that is retained in the blood vessels. This fluid retention will cause the passageways to become narrow and make blood passage through the vessels increasingly difficult, in turn causing an increase in blood pressure. There will also be an increase in protein and blood found in the urine because it is not filtered out properly by the kidneys. Swelling will occur in the extremities and around the eyes because of the fluid retention as well. The longer the urine goes unfiltered the harder it may become to urinate due to pain or blockage or there may be more frequent night time urination (The National Kidney Foundation, 12).

Ms. S.M. was a patient admitted for the management of renal failure. During morning rounds, we noticed her potassium levels to be elevated. She was asymptomatic and her EKG did not show any abnormal changes. As a team, we coordinated with each other and successfully managed her potassium levels. The hours spent to manage this patient helped me to understand the importance of clear communication and the dynamics of team work in a hospital setting. Though we managed her hyperkalemia, the patient was still facing an uncertain prognosis with her kidney disease. Her family members were worried about providing financial support for her care, which is a major problem in India. It made me wonder if there was anything more we could do for her. However, along with providing clinical care, establishing a relationship with her and her son gave me a sense of satisfaction. It made me realize the potential of developing long term relations with my patients in this field.

The pathophysiology of acute renal failure is still uncertain though it is thought to be

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).

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

Hemodialysis (HD) is one of several renal replacement therapies used for the treatment of end stage kidney disease (ESKD) and kidney failure. Dialysis removes excess fluids and waste products and restores chemical and electrolyte balance. HD involves passing the patient’s blood through an artificial semipermeable membrane to perform the filtering and excretion functions of the kidney. One important step before starting regular hemodialysis sessions is preparing the vascular access; ideally, a vascular access should be placed weeks or months before you start dialysis. The

research paper, is to provide a general overview of the causes of kidney failure, shedding light on it

Glomerulonephritis (GN), or the inflammation of glomeruli, is a leading cause of renal failure worldwide. Inflammation is characterized by vascular fragility, infiltration of leukocytes, and edema. Glomerular disease may manifest by three major syndromes: nephritic syndrome, nephrotic syndrome, and rapidly progressive glomerulonephritis (RPGN). Nephritic syndrome consists of sudden onset of hematuria, non-nephrotic range proteinuria (1.5 g/24 h), active sediment with red blood cell (RBC) casts or dysmorphic RBCs, acute renal failure, and hypertension. Nephrotic syndrome is characterized by heavy proteinuria (>3.5 g/24 h), edema, hypoalbuminemia, and hyperlipidemia. RPGN is characterized by active sediment (RBC casts and dysmorphic RBCs) and rapid development of acute renal failure usually over a period of weeks to months. Glomerulonephritis accounts for the majority of progressive renal disease in many parts of the world.