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Management of patients with renal disorders
•Primary glomerular disease
•Renal failure
Pathophysiology
• Primary glomerular disease: Inflammation of glomerular
capillaries
• Antigen-antibody complexes—Deposition of these complexes
in glomerular capillaries (IgG)—inducing inflammatory
response
• Major indicators of Glomerular Injury—proteinuria, hematuria,
decreased GFR, hypertension, edema, decreased excretion of
Na
• Acute Nephritic Syndrome: clinical manifestations of
glomerular inflammation
• Glomerulonephritis: inflammation of glomerular capillaries that
occurs in acute or chronic form
Health assessment
clinical manifestations
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Main manifestations of AGI:
Hematuria, edema, azotemia, proteinuria,
Hematuria could be microscopic or macroscopic
Cola-colored urine because of RBCs
Edema & hypertension
Proteinuria due to increased permeability of glomerular
membrane; with pitting edema
• Headache, malaise, flank pain
• In elderly, circulatory overload, with dyspnea, pulmonary
edema
AGI Clinical manifestations
• In acute nephritic syndrome: the kidneys become large &
edematous, congested
• Elevated serum IgA
• As urine out put decreases, BUN and creatinine in the blood
increases
• Kidney biopsy may be needed
• If improvement: amount of urine increases; urinary protein
diminish
• Some may develop uremia and require dialysis for survival
Complications
• Hypertensive encephalopathy: emergency management of
hypertension
• Glomerulonephritis, without treatment, progresses to ESRD: S
& S—hematuria, proteinuria
• Heart failure & pulmonary edema
Nursing management
• Treat symptoms, preserve kidney function & treat
complications:
 Antibiotic, Penicillin; if the cause is infection
 Corticosteriods; managing HTN; controlling proteinuria
 protein restriction, when renal insufficiency and increased BUN
 Na restriction, when HTN, edema & HF
 Liberal intake of CHOs, to provide energy & reduce catabolism
of protein; Intake and output, daily weight,
 Fluid based on I & O
 Patient education
Chronic glomerulonephritis
• Secondary to repeated acute nephritic syndrome & other health
conditions; hyperlipidemia
• Kidneys are reduced to one-fifth of normal size—fibrous
tissues; cortex shrinks to 1-2 mm in thickness
• Glomeruli become scarred; renal artery branches are thickened
• The result is sever glomeruli damage– ESRD
• May discovered accidentally, when HTN, elevated BUN &
Creatinine are detected
• May report general symptoms: weight loss, increasing
irritability, increased need to urinate at night, headache,
digestive disturbances
Chronic glomerulonephritis
• As progresses, develop signs of chronic renal diseases or
renal failure:
 poorly nourished with yellow-gray pigmentation of the skin
 Periorbital and peripheral edema
 Normal blood pressure or severe HTN
 retinal hemorrhage and exudates
 Anemia-pale mucous membrane
 Cardiomegaly, gallop rhythm, distended neck veins
 peripheral neuropathy & neurosensory changes
 Development of pericarditis; friction rub, pulsus paradoxus
Assessment / diagnostic findings
 Urine, fixed specific gravity 1.010, variable proteinuria, urinary
casts
 When GFR is below 50ml/min
• Hyperkalemia, decreased K excretion
• Metabolic acidosis, because of decreased acid secretion
• Anemia, decreased production of erythropoiesis
• Hypoalbuminemia – secondary to protein loss
• Increased serum phosphorous level
• Decreased calcium, the Ca binds with phosphorus
• mental changes; and impaired nerve conduction due to
electrolyte imbalances & uremia
Management: symptoms management
• Reduce hypertension: Na & water restrictions,
antihypertensives; monitor Wt. daily, diuretics,
• Protein of high biologic value—dairy products, eggs, meat to
promote good nutritional status
• Adequate calories—spare protein for tissue growth
• Manage UTI
• Initiation of dialysis may be required; in the early period of the
disease process.
• Nursing management
 Monitor fluid & electrolytes imbalances
 Report system changes
 reduce anxiety; Emotional support
Nephrotic syndrome
• A type of renal failure-increased glomerular permeability; is
manifested by
 Massive proteinuria; Hypoalbuminemia; Diffuse edema
 Hyperlipidemia, increased serum cholesterol & LDL
 Caused by intrinsic renal disease or systemic diseases that
cause glomerular damage
 Major manifestations
 Edema, pitting in dependent areas (periorbital), ascites
 Irritability, headache,-- malaise
Nephrotic syndrome
management
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Treat underlying disease; slowing progression to CKD
Typical treatment include:
Diuretics for edema
ACE inhibitors to reduce proteinuria
Lipid lowering agents
• Nursing management:
• Instruct to follow medications & dietary regimen
• Aware about and communicate health changes
Renal Failure
Acute Renal Failure
• A rapid loss of renal functions related to kidney damage
• A life-threatening metabolic complications can occur—
metabolic acidosis, fluid & electrolyte imbalances
• Accepted criterion for ARF: 50% or greater increase in serum
creatinine; The normal is less than 1 mg/dL
• Increased BUN
• Changes in urine volume may occurs
 Oliguria, less than 500 ml/day
 Anuria, less than 50 ml/day
 Non-oliguria, greater than 800 ml/day
ACUTE RENAL FAILURE
• There is a specific underlying problem
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Some of these factors—reduce blood flow to the kidney
Hypovolemia; hypotension; reduced cardiac output
Obstruction by tumor, blood clot, or renal stone
Bilateral obstruction of renal arteries or veins
• Should be treated before permanent damage occur
Categories of ARF
• Pre renal ARF; is the result of impaired blood flow, causing
hypoperfusion and decreasing GFR
• Intra renal ARF: is the result of actual parenchymal damage to
glomeruli or tubules—abnormal reabsorption & decreased
urine flow; leading to acute tubular necrosis; intra-tubular
obstruction
• Post renal ARF: obstruction distal to the kidney:
 pressure rises in the kidney, decreased GFR
Read chart 44-4, P. 1321.
Phases of ARF
 The initiation period: begins with insult and ends when oliguria
develops
 The oliguria period:
 increase serum concentrations of substances that kidneys
excretes
 Uremic symptoms appear and life-threatening condition,
hyperkalemia, develops
 Some patients have decreased renal function but excrete
2L/day, non-oliguria renal failure; Occurs after exposure to
nephrrotoxic agents, burn, trumatic injury
Phases of ARF
 The diuresis period:
 gradual increase in urine—glomerular filtration starts to
recover
 renal function may still abnormal; because
 uremic symptoms present—thus, needs expert attention
 Observe for dehydration
 The recovery period:
 Signals improvement of kidney function; may need 3-12
months; lab values return to normal
 Leave 1-3% reduction in the GFR—not clinically significant
Assessment
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Appears critically ill & lethargic; dry skin; dehydration
CNS symptoms: drowsiness, headache, seizures
Urine output: scant to normal; hematuria may be present
Low specific gravity indicating inability to concentrate, a sign
of tubular damage; an early sign
Pre renal azotemia—decreased urinary Na to less than 20
mEq/L; Intra renal azotemia—urinary Na more the 40 mEq/L
Increased BUN and creatinine
Hyperkalemia with oliguria or anuria; metabolic acidosis, can
not excrete acid metabolites
phosphate high and calcium low—decreased absorption from
GIT; Anemia;
CT, MRI or ultrasonography
Prevention of ARF
• Careful history to identify exposure to nephrotoxic agents,
medications:
 Blood tests for BUN & creatinine, 24 hours after initiation of
nephrotoxic medications and 2 times a week
• Adequate hydration for those at risk for dehydration
• Prevent & treat shock promptly
• For critically ill patients; monitor CVP, arterial pressure, urine
output
• Treat hypotension promptly
• Prevent & treat infections
• READ CHART 44-5, P 1322
Management
principles
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Treat the underlying cause:
pre renal azotemia by optimizing renal perfusion,
post renal failure with removing obstruction,
intra renal azotemia with supportive therapy; with
Removal of causative agents,
Aggressive management of pre and post-renal failure
Avoidance of associated risk factors
Prompt treatment of shock and infection