Acute Glomerulonephritis Nursing Care Planning and Management

When a school-age child shows up with smoky or bloody urine, puffy eyes, and a blood pressure that keeps climbing, think acute glomerulonephritis until proven otherwise. The glomeruli are inflamed, filtration drops, and the child starts holding salt and water. Track fluid balance hour by hour, control the blood pressure, watch for the cerebral and pulmonary fallout of overload, and protect the kidneys while the immune process burns itself out.

What is Acute Glomerulonephritis?

Acute glomerulonephritis (GN) is a set of renal diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue, damaging the basement membrane, mesangium, or capillary endothelium. It presents as the sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts in the urine, usually as an allergic-type reaction to infection, most often group A beta-hemolytic streptococcal infection.

Hippocrates described the back pain and hematuria followed by oliguria or anuria. Richard Bright (1789-1858) described acute GN clinically in 1827, which gave us the term Bright disease, and Theodor Langhans (1839-1915) later described the glomerular changes under the microscope.

Pathophysiology

Acute GN involves both structural and functional change. Cellular proliferation increases the number of endothelial, mesangial, and epithelial cells in the glomerular tuft, either endocapillary (within the capillary tufts) or extracapillary (in Bowman space). Extracapillary proliferation of parietal epithelial cells forms crescents, the hallmark of certain rapidly progressive GN. Neutrophils and monocytes accumulate within the capillary lumen, capillary walls thicken on light microscopy, and electron-dense immune-complex deposits appear in subendothelial, subepithelial, intramembranous, or mesangial locations. Hyalinization or sclerosis signals irreversible injury. These changes may be focal, diffuse, segmental, or global.

Functionally, the result is proteinuria, hematuria, a falling GFR (oliguria or anuria), and active sediment with RBCs and RBC casts. The drop in GFR plus avid distal-nephron salt and water retention expands intravascular volume, producing edema and, frequently, systemic hypertension.

Statistics and Incidences

Acute GN represents 10-15% of glomerular diseases. Peak incidence is in children 6 to 7 years of age, and it occurs twice as often in boys. In the United States, GN accounts for 25-30% of all end-stage renal disease (ESRD), and about one fourth of patients present with acute nephritic syndrome. Worldwide, IgA nephropathy (Berger disease) is the most common cause of GN. In Port Harcourt, Nigeria, the incidence in children aged 3-16 years was 15.5 cases per year with a male-to-female ratio of 1.1:1. A regional dialysis center in Ethiopia found acute GN second only to hypovolemia as a cause of acute kidney injury requiring dialysis, about 22% of cases. Postinfectious GN can occur at any age but usually develops in children: most cases occur in patients aged 5-15 years, and only 10% occur in patients older than 40 years, with a 2:1 male-to-female ratio.

Causes

The causes split into infectious and noninfectious groups. The most common infectious cause is infection by Streptococcus species (group A, beta-hemolytic). Noninfectious causes divide into primary renal diseases, systemic diseases, and miscellaneous conditions or agents.

Clinical Manifestations

Symptoms appear 1 to 3 weeks after the onset of a streptococcal infection. The presenting sign is usually grossly bloody urine that the caregiver describes as smoky or bloody. Periorbital or pedal edema may accompany or precede the hematuria. Fever may reach 103°F to 104°F at onset and settle to about 100°F within a few days. Hypertension occurs in 60% to 70% of patients during the first 4 or 5 days. Oliguria is usually present, with urine of high specific gravity containing albumin, red and white blood cells, and casts. Fluid overload shows as periorbital and pedal edema (in 75% of patients), crackles if pulmonary edema develops, elevated jugular venous pressure, and possible ascites and pleural effusion. In a few cases, cerebral symptoms (headache, drowsiness, convulsions, vomiting) accompany the hypertension.

Assessment and Diagnostic Findings

Several renal syndromes mimic acute GN, so accurate workup matters.

• Initial blood tests. A CBC may show a decreased hematocrit (dilutional anemia) and, with an infectious etiology, pleocytosis. Electrolytes (especially serum potassium), BUN, and creatinine estimate the GFR and reveal the degree of renal compromise.
• Complement levels. Low versus normal serum complement narrows the differential.
• Urinalysis. Urine is dark with specific gravity greater than 1.020; RBCs, RBC casts, and proteinuria are present.
• Streptozyme tests. These screen many streptococcal antigens (DNAase, streptokinase, streptolysin O, hyaluronidase) but are not quantitative. The antistreptolysin O (ASO) titer is increased in 60-80% of patients; rising ASO or streptozyme titers confirm recent infection.
• Blood and tissue cultures. Blood culture is indicated with fever, immunosuppression, IV drug use, indwelling shunts, or catheters. Throat and skin cultures help rule out Streptococcus species.

Medical Management

Treatment is mainly supportive, since there is no specific therapy for the renal disease. Restrict sodium and fluid to manage fluid retention (edema, pulmonary edema), and restrict protein in patients with azotemia unless they are malnourished. Maintain bed rest until glomerular inflammation and circulatory congestion subside; prolonged inactivity adds nothing to recovery. Long-term studies in children with AGN show few chronic sequelae.

Pharmacologic Management

The goals are to reduce morbidity, prevent complications, and eradicate the infection. Early antibiotics in streptococcal infection may render throat cultures negative but do not reliably prevent AGN. Loop diuretics drop plasma volume and edema through diuresis, lowering cardiac output and blood pressure. Vasodilators reduce systemic vascular resistance to improve forward flow. Calcium channel blockers inhibit calcium movement across the cell membrane, depressing automaticity and conduction velocity.

Nursing Management

The nurse's role with a child in AGN is central to safe recovery.

Nursing Assessment

• Physical examination. Obtain a complete physical assessment.
• Weight. Monitor daily weight as a measurable account of fluid elimination.
• Intake and output. Monitor fluid intake and output every 4 hours to gauge glomerular filtration.
• Vital signs. Monitor BP and PR every hour to catch progression of hypertension and guide intervention or referral.
• Breath sounds. Assess for adventitious breath sounds that signal pulmonary involvement.

Nursing Diagnoses

• Ineffective breathing pattern related to the inflammatory process.
• Altered urinary elimination related to decreased bladder capacity or irritation secondary to infection.
• Excess fluid volume related to a decrease in regulatory mechanisms (renal failure).
• Risk for infection related to decreased immunologic defense.
• Imbalanced nutrition: less than body requirements related to anorexia, nausea, vomiting.
• Risk for impaired skin integrity related to edema and pruritus.
• Hyperthermia related to ineffective thermoregulation secondary to infection.

Nursing Care Planning and Goals

• Excretion of excess fluid through urination.
• Demonstration of behaviors that help excrete excess fluid.
• Improvement of distended abdominal girth.
• Improvement of respiratory rate.
• Participation in and demonstration of ways to achieve effective tissue perfusion.

Nursing Interventions

• Activity. Maintain bed rest until acute symptoms and gross hematuria disappear.
• Prevent infection. Protect the child from chilling and from contact with people who have infections.
• Intake and output. Monitor and record fluid intake and urine output carefully, keeping intake within prescribed limits.
• Monitor BP. Use the same arm and a properly fitting cuff each time.
• Monitor urine. Test regularly for protein and hematuria with dipstick.

Evaluation

Goals are met when the child excretes excess fluid through urination, demonstrates behaviors that support fluid excretion, shows improved abdominal girth and respiratory rate, and participates in achieving effective tissue perfusion.

Documentation Guidelines

• Individual findings, including contributing factors, social exchanges, and specifics of behavior.
• Cultural and religious beliefs and expectations.
• Plan of care and teaching plan.
• Responses to interventions, teaching, and actions performed.
• Attainment of or progress toward desired outcomes.