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Understanding Chronic Renal Failure

Chronic Kidney Failure (CRF) or end stage renal disease is a chronic renal failure is progressive and irreversible. Where the ability of the body fails to maintain metabolism and fluid and electrolyte balance, leading to uremia (retention of urea and other nitrogenous waste in the blood) (KMB, Vol 2 p. 1448).

Etiology


Causes of chronic renal crow quite a lot but for clinical purposes can be divided into two groups:
1. Renal parenchymal disease
Primary renal disease: glomerulonephritis, Mielonefritis, polycystic kidney, renal tuberculosis
Secondary renal diseases: lupus nephritis, nephropathy, renal Amilordosis, Poliarteritis nodasa, progressive systemic sclerosis, gout, Dm
2. Obstructive renal disease: enlarged prostate, urinary tract stones, ureteric reflux,
Broadly speaking the cause of kidney failure can be categorized
Recurrent infections and worsening of the nephron
Urinary tract obstruction
Destruction of blood vessels caused by diabetes and hypertension that long
Scar tissue and direct trauma to the kidney


Pathophysiology


Two theoretical approaches are usually proposed to explain the renal failure in chronic renal failure:

1. Traditional viewpoint
Says that all units of the nephron have been attacked by the disease but in a different stadium, and specific parts of the nephron is associated with certain functions can only really be damaged or changed in structure, such as organic lesion in the medulla will damage the anatomic structure of the loop of Henle .
2. Bricker hypothesis approach or an intact nephron hypothesis
Believes that if the disease nephron of its units will be destroyed, but the remaining intact nephrons continue to work normally. Uremia will rise if the number of nephrons that have been so reduced that fluid and electrolyte balance can not be maintained anymore.

Important adaptation made by the kidneys as a response to the threat of fluid and electrolyte imbalance. Time hypertrophied nephrons which have suffered in their efforts to implement the entire burden of the kidneys, increasing the acceleration of filtration, tubular reabsorption of load SoluTe and contained within each nephron in the kidney decreased dibawab normal.

This adaptation mechanism is quite successful in maintaining fluid and electrolyte balance of the body to the low level of kidney function.
But ultimately if 75% nephron mass has been destroyed, then the filtration rate and expenses for each nephron SoluTe so high that the balance glomerolus-tubules can no longer be maintained. Good flexibility and concentration on the process of excretion and water SoluTe be reduced.


Clinical course


General travel progressive renal failure can be divided into three atadium
Stage I
Decrease in reserve kidney (renal function between 40% - 75%). This is the lightest stage, in which kidney function is still good. At this stage, this patient had symptoms merasasakan symptoms and laboratory examination is still in renal physiology is still within normal limits. During this stage the level of serum creatinine and BUN (Blood Urea Nitrogen) in normal and asymptomatic patients. Impaired renal function may only be known by giving a heavy workload, sepersti urinary concentration test of time or by performing rigorous testing GFR.
Stage II
Insufiensi renal (kidney function between 20% - 50%). At this stage the patient can perform tasks as usual when the concentration of power and kidney decreased. At this stage of treatment must be quickly overcome shortages daloam things fluid, salt deficiency, heart disorders and the prevention of drug administration medications that are menggnggu kidney function. If these steps can be done as soon as possible with appropriate patient enter ketahap prevent more severe. At this stage more than 75% functioning tissue has been damaged. New BUN levels began to rise above normal limits. Increased BUN concentration is different, depending on the protein content in this stadium diit.pada serum creatinine levels began to increase beyond normal levels.

Insufiensi renal (kidney function between 20% - 50%). At this stage the patient can perform tasks as usual when the concentration of power and kidney decreased. At this stage of treatment must be quickly overcome shortages daloam things fluid, salt deficiency, heart disorders and the prevention of drug administration medications that are menggnggu kidney function. If these steps can be done as soon as possible with appropriate patient enter ketahap prevent more severe. At this stage more than 75% functioning tissue has been damaged. New BUN levels began to rise above normal limits. Increased BUN concentration is different, depending on the protein content in this stadium diit.pada serum creatinine levels began to increase beyond normal levels.

Polyuria due to renal failure is usually greater for a disease that primarily affects the tubules, although polyuria is moderate and rarely more than 3 liters / day. Usually found in anemia in renal failure with renal function between 5% - 25%. obviously decreased kidney function and symptoms of blood deficiency symptoms, blood pressure will go up, patients started disrupted activity.
Stage III
Uremi kidney failure (renal function less than 10%)
All the symptoms are clear and Diman patients included in the state can not do the job properly sebaimana hair day. Gejal gejal that arise include nausea, munta, appetite is reduced., Shortness of breath, dizziness, headache, decreased urine, lack of sleep, seizures convulsions and ultimately decreased consciousness until coma. Stadum end arising in approximately 90% of the nephron mass has been destroyed. GFR value was 10% of normal and creatinine levels may be of 50-10 ml / min or less.

In these conditions serum creatinine and BUN levels to rise very prominently as a decline. At end-stage renal failure, patients begin to experience symptoms severe enough because the kidneys can no longer maintain homeostasis caiaran and electrolytes in the body. Patients usually become oliguri (urinary spending) less than 500 per day because of the failure of glomerular disease processes first though first attack of kidney tubules,

attack complex gijal tubules, the complex biochemical changes and symptoms symptoms of the syndrome called uremik affects every system in the body. At end-stage renal failure, patients must be menggal unless he got treatment in the form of a kidney transplant or dialysis.


Clinical manifestations
Respiratory Disorders
Udema
Hypertension
Anorexia, nausea, vomitus
Gastric ulceration
Stomatitis
Proteinuria
Haematuria

Lethargy, apathy, concentration penuruna
Anemia
Bleeding
Poor skin turgor, gatak itchy skin
Renal dystrophy
Hyperkalemia
Metabolic Acidosis


Diagnostic Test


1. Urine:
Volume
Color
Sediment
Specific gravity
Creatinine
Protein

2. Blood:

Bun / Creatinine
Complete blood count
Red blood cells
Serum sodium
Potassium
Magnesium phosphate
Protein
Serum osmolarity

3. Pielografi intravenous
Showed abnormalities in renal pelvis and ureter
Retrograde Pielografi
Done when there is suspicion of a reversible obstruction
Renal Arteriogram
Assessing the renal circulation and identify ekstravaskular, mass.

4. Sistouretrogram micturition
Indicate the size of the bladder, reflux into the ureter, retention.
5. Ultrasono kidney
Indicate the size of the bladder, and the masses, cysts, obstruction at the top of the urinal tract.
6. Renal biopsy
Endoscopy may be done to determine the tissue cells for histological diagnosis

7. Endoscopic renal nefroskopi
Conducted to determine the renal pelvis; out stones, hematuria and selective tumor
8. ECG
Maybe it showed abnormal acid-base and electrolyte imbalance, arrhythmia, ventricular hypertrophy and pericarditis sign.


Treatment


1. Dialysis
Dialysis can be done to prevent complications of serious acute renal failure, such as hyperkalemia, pericarditis and seizures. Pericarditis improve biochemical abnormalities; cause caiarn, protein and sodium can be consumed freely; eliminate kecendurungan bleeding; and help the healing of wounds.

2. Handling hyperkalemia
Fluid and electrolyte balance is a major problem in acute renal failure, hyperkalemia is the most life-threatening condition in this disorder. Therefore, patients will be monitored through a series of examinations of hyperkalemia serum electrolyte levels (potassium values> 5.5 mEq / L; SI: 5.5 mmol / L), ECG changes (T wave peak height is low or very high), and changes in clinical status. Pningkatan potassium ions can be reduced by provision of a replacement resin (sodium sulfonate polistriren [kayexalatel]), administered orally or by retention enema.

3. Maintaining fluid balance
Keseimbanagan management of fluid is based on daily body weight, central venous pressure measurement, urine and serum concentrations, fluid loss, blood pressure and clinical status of patients. Enter and haluaran parentral from oral and urine, gastric drainage, feces, wound drainage and perspirasi calculated and used as a basis for penggantia fluid therapy.


CONCLUSIONS ASSESSMENT EXAMPLE
Hj client's name. H
Age 85 years.
Date admitted 30 April 2005 with a complaint can not pee and right back pain .. These complaints lasted three days at home. Initially the client can not defecate  2 days ago clients use dulcolax suppositories for two consecutive days and the client can SECTION.

A day later the client's hard to pee, although not able to push urine out, then the family took him to hospital. Arriving at Hospital mounted lancer urinary catheters and exit out the red color somewhat and then comes out a little brown color like tea water.

We review the client has been hospitalized for three days focus on data obtained:
General state of the client rather weak, lower limb weakness, not powered, wrinkled skin is not elastic. odema pretibial. Less muscle tone. always lying in bed, ativitas day, the day assisted by his son, urinary catheter inserted, such as water tea brown color, fabric pengalas wet and smelly.

BP 160/90 mmHg. Nadi 82 x / min, temperature 36.2 o C Agency, sclera was pale, secret eyes (+). Mouth / breath smelled of ammonia, talking softly sometimes less obvious,
Laboratory examination results
Date: 2 / 5 2005
U: 202.32
Creatinine: 3, 1993
AST: 19
SGPT: 30
WBC: 5.5 x 103 /  l
RBC: 3.90
HGB: 10.7
HCT: 32.5%
GDS: 161

Examination Support
USG:
Kidney: Looks both kidneys decreases with echodifferensiasi not clear (right kidney 5.9 x 3.1 cm left kidney 5.8 x 2.5 cm).
Impressions: PNC bilaterally.

MEDICAL THERAPY
Drugs - drugs:
IVFD NaCl 0.9% 20 TTS / min
Allopurinol 300mg 1-0-0
10mg Zonidip 0-0-1
300mg Fibrat 0-0-1
Inj. Neurosanbe 1 amp / day / drips

Based on the assessment, nursing diagnosis is obtained:
1. Excess fluid volume related to a decrease haluaran urine, fluid and sodium retention.
2. Difficulties associated with the accomplishment of ADL physical weakness.
3. Oral mucous membrane changes associated with chemical irritants.
4. Risk of damage to the integrity of the skin associated with decreased activity, impaired metabolic status.


Plan of action:
1. Excess fluid volume related to a decrease haluaran urine, fluid and sodium retention.
1. Assess fluid status:
Weigh daily weight
Balance of input and haluaran
Skin turgor and the presence of edema
Blood pressure, pulse and rhythm of the pulse.
2. Restrict fluid intake

3. Identify potential sources of fluid
Medications and fluids used for medical, oral and intra-venous.
Food
4. Explain rational fluid restriction
5. Assist clients in overcoming the discomfort caused by fluid restriction.
6. Enhance and encourage oral hygiene.

2. Difficulties associated with the accomplishment of ADL physical weakness.
Determine client's ability to berpartyisipasi in self care activities. (Scale 0-4).
Provide the necessary assistance with activities
Encourage families to help fulfill the ADL client in bed.
Helps families in personal care client in bed.
Encourage families to change their mats when wet buttocks.
Help and motivation of families to maintain the cleanliness of the client's body,

3. Oral mucous membrane changes associated with chemical irritants.
1. Inspection of the oral cavity note the humidity, the character of saliva, the presence of inflammation, ulceration.
2. Give fluids throughout the 24 hours within specified limits.
3. Give frequent oral care.
4. Encourage oral hygiene after meals and at bedtime.
5. Encourage clients to avoid a lemon dessert / ingredients that contain alcohol.

4. Risk of damage to the integrity of the skin associated with decreased activity, impaired metabolic status.
1. Inspection of the skin to change color, skin moisture, vascular.
2. Change position often, a client with a slow movement, give a soft cloth bearing on the bone ridge.
3. Maintain a dry linen free of wrinkles.
4. Keep nails short stay.
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