Chronic Kidney Disease

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CHRONIC KIDNEY

DISEASE

SHIELA D. PADILLA
When the patient has sustained enough kidney damage to require renal
replacement therapy on a permanent basis, the patient has moved into the fifth or
final stage of CKD, also referred to as chronic renal failure.
● Chronic renal failure (CRF) is the end result of a gradual, progressive
loss of kidney function.

● Causes include chronic infections (glomerulonephritis, pyelonephritis),


vascular diseases (hypertension, nephrosclerosis), obstructive processes
(renal calculi), collagen diseases (systemic lupus), nephrotoxic agents
(drugs, such as aminoglycosides), and endocrine diseases (diabetes,
hyperparathyroidism).
● This syndrome is generally progressive and produces major changes in
all body systems.
● The final stage of renal dysfunction, end-stage renal disease (ESRD), is
demonstrated by a glomerular filtration rate (GFR) of 15%–20% of normal
or less.
● Renal failure results when the kidneys cannot remove the body’s metabolic
wastes or perform their regulatory functions.

● The substances normally eliminated in the urine accumulate in the body fluids as
a result of impaired renal excretion, affecting endocrine and metabolic functions
as well as fluid, electrolyte, and acid-base disturbances.
● Renal failure is a systemic disease and is a final common pathway of many
different kidney and urinary tract diseases.
● Accumulation. As renal function declines, the end products of protein
metabolism (normally excreted in urine) accumulate in the blood.
● Adverse effects. Uremia develops and adversely affects every system in the
body.
● Progression. The disease tends to progress more rapidly in patients who
excrete significant amounts of protein or have elevated blood pressure than
those without these conditions
Pathophysiology
There are many diseases that cause chronic renal disease; each has its own pathophysiology.
However, there are common mechanisms for disease progression.

1. Pathologic features include fibrosis, loss of renal cells, and infiltration of renal tissue
by monocytes and macrophages.

2. Proteinuria, hypoxia, and extensive angiotensin II production all contribute to the


pathophysiology. In an attempt to maintain GFR, the glomerular hyperfiltration; this
results in endothelial injury.
3. Proteinuria results from increased glomerular permeability and increased capillary
pressure.
4. Hypoxia also contributes to disease progression. Angiotensin II increases glomerular
hypertension, which further damages the kidney.
Predisposing Factors

● Diabetes, which is the most common risk factor for chronic kidney failure in
the United States
● Age 60 or older
● Kidney disease present at birth (congenital)
● Family history of kidney disease
● Autoimmune Disorder (Lupus erythematosus)
● Bladder outlet obstruction (BPH and Prostatitis)
● Race (Sickle cell disease)

Precipitating Factors

● Occupational Hazard (overexposure to toxins and to some medications)


● Sedentary Lifestyle (hypertension, atherosclerosis)
● Diet (High residue diet)
Clinical Manifestations
Because virtually every body system is affected in ESRD, patients
exhibit a number of signs and symptoms.

● Peripheral neuropathy. Peripheral neuropathy, a disorder of the


peripheral nervous system, is present in some patients.

● Severe pain. Patients complain of severe pain and discomfort.


● Restless leg syndrome. Restless leg syndrome and burning
feet can occur in the early stage of uremic peripheral
neuropathy.
Complications
Potential complications of chronic renal failure that concern the nurse and necessitate a
collaborative approach to care include the following:

● Hyperkalemia. Hyperkalemia due to decreased excretion, metabolic acidosis,


catabolism, and excessive intake (diet, medications, fluids).

● Pericarditis. Pericarditis due to retention of uremic waste products and inadequate


dialysis.
● Hypertension. Hypertension due to sodium and water retention and the malfunction of
the renin-angiotensin-aldosterone system.
● Anemia. Anemia due to decreased erythropoietin production decreased RBC lifespan,
bleeding in the GI tract from irritating toxins and ulcer formation, and blood loss during
hemodialysis.
● Bone disease. Bone disease and metastatic and vascular calcifications due to retention
of phosphorus, low serum calcium levels, abnormal vitamin D metabolism, and elevated
aluminum levels.
Assessment and Diagnostic Findings

Laboratory studies required to establish the diagnosis of CRF include:

● Glomerular filtration rate. GFR and creatinine clearance decrease while


serum creatinine (more sensitive indicator of renal function) and BUN
levels increase.
● Sodium and water retention. Some patients retain sodium and water,
increasing the risk for edema, heart failure, and hypertension.
● Acidosis. Metabolic acidosis occurs in ESRD because the kidneys are
unable to excrete increased loads of acid.
● Anemia. In ESRD, erythropoietin production decreases and profound
anemia results, producing fatigue, angina, and shortness of breath.
● Blood
● BUN/Cr: Elevated, usually in proportion. A creatinine level of 12 mg/dL suggests
ESRD. A BUN of >25 mg/dL is indicative of renal damage.
● CBC: Hb decreased because of anemia, usually less than 7–8 g/dL.
● RBCs: Life span decreased because of erythropoietin deficiency, and azotemia.
● ABGs: pH decreased. Metabolic acidosis (less than 7.2) occurs because of the
loss of renal ability to excrete hydrogen and ammonia or end products of protein
catabolism. Bicarbonate and PCO2 Decreased.
● Serum sodium: May be low (if the kidney “wastes sodium”) or normal
(reflecting the dilutional state of hypernatremia).
● Potassium: Elevated related to retention and cellular shifts (acidosis) or tissue
release (RBC hemolysis). In ESRD, ECG changes may not occur until
potassium is 6.5 mEq or higher. Potassium may also be decreased if the patient
is on potassium-wasting diuretics or when the patient is receiving dialysis
treatment.
● Magnesium, phosphorus: Elevated.
● Calcium/phosphorus: Decreased.
● Proteins (especially albumin): Decreased serum level may reflect protein loss
via urine, fluid shifts, decreased intake, or decreased synthesis because of a lack
of essential amino acids.
● Serum osmolality: Higher than 285 mOsm/kg; often equal to urine.
● KUB x-rays: Demonstrates size of kidneys/ureters/bladder and presence of
obstruction (stones).
● Retrograde pyelogram: Outlines abnormalities of the renal pelvis and ureters.
● Renal arteriogram: Assesses renal circulation and identifies extravascularities,
and masses.
● Voiding cystourethrogram: Shows bladder size, reflux into ureters, and retention.
● Renal ultrasound: Determines kidney size and presence of masses, cysts, and
obstruction in the upper urinary tract.
● Renal biopsy: May be done endoscopically to examine tissue cells for histological
diagnosis.
● Renal endoscopy, nephroscopy: Done to examine renal pelvis; flush out calculi,
and hematuria; and remove selected tumors.
● ECG: This may be abnormal, reflecting electrolyte and acid-base imbalances.
● X-rays of feet, skull, spinal column, and hands: May reveal
demineralization/calcifications resulting from electrolyte shifts associated with CRF.
Medical Management

The goal of management is to maintain kidney function and homeostasis for as long as
possible.

● Pharmacologic therapy:
● Calcium and phosphorus binders treat hyperphosphatemia and
hypocalcemia;
● Antihypertensive and cardiovascular agents (digoxin and
dobutamine) manage hypertension;
● Anti-seizure agents (IV diazepam or phenytoin) are used for seizures,
and;
● Erythropoietin (Epogen) is used to treat anemia-associated ESRD.
● Nutritional therapy. Dietary intervention includes careful regulation of protein
intake, fluid intake to balance fluid losses, sodium intake to balance sodium
losses, and some restriction of potassium.
● Dialysis. Dialysis is usually initiated if the patient cannot maintain a reasonable
lifestyle with conservative treatment.
Nursing Management

The patient with ESRD requires astute nursing care to avoid the complications of reduced
renal function and the stresses and anxieties of dealing with a life-threatening illness.

Nursing Assessment

Assessment of a patient with ESRD includes the following:

● Assess fluid status (daily weight, intake and output, skin turgor, distention of neck
veins, vital signs, and respiratory effort).
● Assess nutritional dietary patterns (diet history, food preference, and calorie
counts).
● Assess nutritional status (weight changes, laboratory values).
● Assess understanding of the cause of renal failure, its consequences, and its
treatment.
● Assess patient’s and family’s responses and reactions to illness and treatment.
● Assess for signs of hyperkalemia.
Nursing Priorities

1. Maintain homeostasis.
2. Prevent complications.
3. Provide information about disease process/prognosis and
treatment needs.
4. Support adjustment to lifestyle changes.
Nursing Interventions

Nursing care is directed toward the following:

● Fluid status. Assess fluid status and identify potential sources of imbalance.
● Nutritional intake. Implement a dietary program to ensure proper nutritional intake
within the limits of the treatment regimen.
● Independence. Promote positive feelings by encouraging increased self-care and
greater independence.
● Protein. Promote intake of high–biologic–value protein foods: eggs, dairy products,
and meats.
● Medications. Alter the schedule of medications so that they are not given
immediately before meals.
● Rest. Encourage alternating activity with rest.
Discharge and Home Care Guidelines
● Vascular access care. The patient should be taught how to check the
vascular access device for patency and appropriate precautions, such as
avoiding venipuncture and blood pressure measurements on the arm with
the access device.
● Problems to report. The patient and the family need to know what
problems to report: nausea, vomiting, change in usual urine output,
ammonia odor on breath, muscle weakness, diarrhea, abdominal cramps,
clotted fistula or graft, and signs of infection.
● Follow-up. The importance of follow-up examinations and treatment is
stressed to the patient and family because of changing physical status,
renal function, and dialysis requirements.
● Home care referral. Referral for home care gives the nurse an
opportunity to assess the patient’s environment and emotional status and
the coping strategies used by the patient and family.
● Urine
● Volume: Usually less than 400 mL/24 hr (oliguria) or urine is
absent (anuria).
● Color: Abnormally cloudy urine may be caused by pus, bacteria,
fat, colloidal particles, phosphates, or urates. Dirty, brown
sediment indicates presence of RBCs, hemoglobin, myoglobin,
porphyrins.
● Specific gravity: Less than 1.015 (fixed at 1.010 reflects severe
renal damage).
● Osmolality: Less than 350 mOsm/kg is indicative of tubular
damage, and urine/serum ratio is often 1:1.
● Creatinine clearance: May be significantly decreased (less than
80 mL/min in early failure; less than 10 mL/min in ESRD).
● Sodium: More than 40 mEq/L because the kidney is not able to
reabsorb sodium.
● Protein: High-grade proteinuria (3–4+) strongly indicates
glomerular damage when RBCs and casts are also present.

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