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GLOMERULAR DISEASES:
ACUTE NEPHRITIC SYNDROME
Post-infectious glomerulonephritis, rapidly progressive glomerulonephritis, and
membranous glomerulonephritis
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Manifestations: hematuria, edema, azotemia, proteinuria, and hypertension
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May be mild or may progress to AKD or death
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Medical Management: supportive care and dietary modifications (protein and
sodium restricted): treat cause if appropriate – antibiotics, corticosteroids, and
immunosuppressants.
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Nursing management: patient assessment, fluid balance, dietary and fluid
restrictions, patient education, and follow-up care.
GLOMERULONEPHRITIS
Inflammation of the glomeruli; 3rd leading cause of renal failure in the US; is
classified to describe the extent of damage (diffuse, focal), the initial cause of the
disorder (systemic lupus erythematous, systemic sclerosis [scleroderma],
streptococcal infection), or extent of changes (minimal, widespread). Non-infectious
inflammation of the glomerular leads to renal failure. KIDNEYS BECOME LARGE,
EDMATOUS, AND CONGESTED.
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Treatment = Restrict fluids, change diet, give meds, restrict proteins, if the
cause is strep, give strep meds
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S&S = hypertension, edema, oliguria, hematuria RBC’s WBC’s and proteinuria,
abdominal and flank pain
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Management: Fluid retention because of decreased GFR. Give antibiotics,
(restrict protein because that glomerulus isn’t functioning), monitor fluids, and
the goal is to resolve edema, which can lead to CHF and several other
problems. Glomerulonephritis can lead to renal failure and can lead to a strep
throat infection.
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Labs: ↓ GFR, increased BUN, and creatinine. Urine with fixed specific gravity
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1.010, casts, proteinuria, electrolyte imbalances, and hypoalbuminemia.
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Assess exposure to drugs, immunizations, and microbial infections, viral
infections;
evaluate PT for generalized immune disorders. Cardiac status.
NEPHROTIC SYNDROME
Glomerulus is excessively permeable to plasma protein = proteinuria = ↓plasma
protein & tissue edema
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Causes: chronic glomerulonephritis, diabetes w intercapillary
glomerulosclerosis, amyloidosis, lupus erythematous,
-Increased glomerular permeability to protein, resulting in protein loss
-Protein in the urine (proteinuria), albumin ↓, anasarca (generalized edema), ascites
-Renal damage (HTN, edema)
-Risk for blood clots
Proteins monitor’ fluid exchange with the oncotic pressure
Treat symptoms; goal: cure/control primary disease & relieve edema (use cautiously:
ACE- inhibitors, NSAIDs, low Na+, low- to moderate-protein diet; sometimes loop or
thiazide diuretics are needed); assess edema; PT is usually anorexic, so give small
frequent meals
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POLYCYSTIC KIDNEY DISEASE
-Kidney tissue replaced with cysts
-Genetic recessive gene, starts in childhood, grows & causes pain. Use Tylenol not
NSAIDs
-Hematuria b/c of cysts & they have several cysts in their kidneys and they will have a
problem with tenderness and flank pain.
Nursing Management:
There is no specific treatment. A major aim of treatment is to prevent infections of the
urinary tract &/or to treat them w/ appropriate antibiotics if they occur. Nephrectomy
may be necessary if pain, bleeding, or infection becomes a chronic, serious problem.
Dialysis & kidney transplant may be needed to treat ESRD. When the PT begins to
experience progressive renal failure, the interventions are determined by the
remaining renal fx
RENAL CANCER:
Renal cell carcinoma accounts for more than 85% of all kidney tumors. The tumors
may metastasize to the lung, bone, liver, brain, and kidney.
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Many tumors produce no symptoms and are discovered on a routine exam.
Signs and symptoms that only occur in 10% include hematuria, pain, and mass
in the flank. Colicky pain occurs if a clot or mass of tumor cells passes down
the ureter.
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Assessment: diagnosis of a renal tumor may require IV urography or CT.
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Goal is to detect the tumor early and to eradicate the tumors before they
metastasize.
RENAL FAILURE:
ACUTE KIDNEY INJURY (AKI)
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Characterized by a rapid loss of kidney function demonstrated by a rise in serum
creatinine and/or a reduction in urine output or even the development of azotemia
(an accumulation of nitrogenous waste products [urea nitrogen, creatinine, BUN] in
the blood) severe enough to warrant renal replacement therapy (RRT). ARF will have
an abrupt onset and may be reversible
-Definition: a rapid decline in renal function usually due to a complication of another
disorder
-Risk factors: diabetes, major surgery or trauma, elderly, uncontrolled HTN, liver
disease, infection, lower UTIs, IV contrast, nephrotoxic drug use (Vancomycin and
gentamycin) if not regulated can send you into renal failure, severe blood loss.
-Labs: renal sonogram or a CT/MRI, BUN INCREASED, ↓GFR, anemia, ↓ RBC
lifespan.
-Assessment: urine output scanty to normal, hematuria, ↓specific gravity,
PHASES OF AKI:
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Initiation period: begins with an initial insult and ends when oliguria develops.
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Oliguria period: increase in serum concentration [urea, creatinine, uric acid,
organic acids, K, and magnesium]. Uremic symptoms first appear and
hyperkalemia
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develops. Some PTs have ↓a renal function with increasing nitrogen retention, but
still, excrete normal amounts of urine (1 to 2 L/day). Which occurs usually after
exposure to nephrotoxic agents and traumatic injury.
3.
Diuresis period: Gradual increase in urine output, which shows GFR has
started to recover. Lab values stabilize and eventually ↓. Even though the
urinary output may reach normal or elevated levels, renal function may still be
marked abnormal. PT must be observed closely for dehydration during this
phase.
4.
Recovery period: improvement of renal function and may take 3 to 12 months.
Lab values return to normal.
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