CHRONIC GLOMERULONEPHRITIS
Chronic Glomerulonephritis may have its onset as Acute Glomerulonephritis or may represent a milder type of Ag - Ab reaction. After repeated occurrences of these reactions, the kidneys are reduced to 1/5th of their normal size, consisting largely of fibrous tissue. The cortex shrinks to a layer of 1-2 mm in thickness or less. Bands of scar tissue distort the remaining cortex, making the surface of the kidney rough and irregular. Many glomeruli and their tubules become scarred, and the branches of the renal artery are thickened. The result is severe glomerular damage which results in Chronic Glomerulonephritis.
Clinical Manifestation
1. Patients with severe disease no symptoms at all for a long time. Sudden, severe nosebleed, a stroke, or a convulsion 1 indication of disease.
2. Feet are slightly swollen at night.
3. Loss of weight and strength increasing irritability and nocturia. Headaches, dizziness and digestive disturbances.
4. Anaemia
5. As CG progresses Neck veins are distended, cardiomegaly. Gallop rhythm, signs of CHF, crackles (Lungs) peripheral neuropathy with deep tendon reflexes and neuro sensory changes) frank uraemia, pericarditis with cardiac friction rub and pulsus poradoxus
Diagnostic Evaluation
1. Physical examination poorly nourished Patient with a yellow grey pigmentation of the skin and periorbital and peripheral (dependent) edema.
2. BP normal or severely elevated
3. Retinal findings haemorrhage, exudate, narrowed tortuous arterioles and papilledema
4. Urinalysis reveals a fixed sp: Gravity of 1.010, variable proteinuria and urine sediment changes,
5. Blood studies hyperkalaemia Ved serum bicarbonate (metabolic acidosis), hypermagnesemia (may dev. if magnesium containing antacids are given to Pts with renal failure). Anaemia (2° to Med erythropoiesis and shortened red cell survival time), hypoalbuminemia with edema (2º to protein loss through the damaged renal glomeruli) depressed serum Calcium and increased serum phosphorus.
6. Nerve conduction velocity impaired (when glomerular filtration rate Des below 50 ml/min) [as a result a increasing levels of waste products in the tissues a nervous system and electrolyte abnormalities].
7. X-ray chest cardiac. Enlargement and pulmonary. Edema, ECG. May be normal but may reflect HT [with LVH and electrolyte disturbances, such as] hyperkalaemia [and spiked T waves). Left ventricular hypertrophy.
Medical Management
1. Symptomatic Treatment.
If HT-Treatment readjusting the diet and fluid intake [to maintain as normal a metabolic state as possible].
Protein intake is adjusted according to the response of the Patient C adequate calories to prevent protein from being used for energy.
If UTI diagnosis and treat it.
Sev. Edema bed rest, head of the bed is elevated to promote comfort and diuresis. Monitor weight daily and diuretics are administered to reduce fluid overload. Na and fluid intake is adjusted according to the ability of the Patients kidneys to excrete H.0 and Na.
2. Dialysis [extreme cases of chronic glomerulonephritis]- keeps the Pt in optimal physical. Condition prevent fluid and electrolyte imbalances and minimizes the risk of complication of renal failure.
Nursing Management
1. Provide adequate explanation to the Pt and family regarding the disease.
2. Provide Emotional support throughout the course of disease. and treat encourage question. Patient and family to verbalize their concerns and answer
3. Observe Pt for changes in fluid and electrolyte status and for signs of deterioration of renal function.
4. Report changes in fld. and electrolyte status and cardiac neurologic status promptly.
5. If dialysis is initiated, the Pt and family request [ considerable assistance and support in dealing with the need for this therapy and its long-term implications].
