Practical Management of Acute Glomerulonephritis in Children
This column was originally published in the May 1961 issue of Consultant.
Author:
Lewis A. Barness, MD
University of Pennsylvania
Citation:
Barness LA. Practical management of acute glomerulonephritis in children. 1961;1:34-37.
Acute glomerulonephritis is fairly common in children, accounting for about 5% of all pediatric hospital admissions. It is a serious illness and deserves serious attention. Too often, however, the attention it gets is excessive and complicates the child’s life with restrictions that have no proven value. Except in the acute phase, no particular therapeutic regimen seems to produce better results than any other. It seems wise, therefore, to choose a method that causes the child the least possible hardship—not one which, by prolonged confinement to bed and undue concern for diet, hinders recovery and involves too long an absence from school. Here is the method I find satisfactory; it features, whenever possible, a minimum of bed rest, a free diet, and normal physical activity.
Diagnosing acute glomerulonephritis is usually not difficult. Typically, the child will have been brought for treatment because of gross hematuria, headache, and edema—usually 2 or 3 weeks after a sore throat, skin infection, or other infection. (In rare cases, no history of infection can be elicited.) Urinalysis shows many red blood cells, a 2+ or 3+ protein, and occasional granular or hyaline casts. The blood urea nitrogen is usually elevated, varying from 20 mg% to 150 mg% (values over 100 mg% suggest a chronic process). The erythrocyte sedimentation rate is almost invariably elevated; the serum cholesterol, slightly elevated; and the serum albumin, slightly low. Nasopharynx cultures frequently reveal B-hemolytic group A streptococci, perhaps residuum from the preceding infection (antigenantibody reaction to this organism is thought to be the cause of acute glomerulonephritis).
If Hypertension Is Present
The most important factor to consider when planning treatment is hypertension. If it is present, we restrict the patient to bed, give phenobarbital, 3 mg/lb of body weight, and offer fluids ad lib. If the blood pressure does not return to nearly normal limits within 4 hours, we place the patient on a low-sodium diet and give reserpine, 0.1 mg/kg, and apresoline, 0.15 mg/kg, intramuscularly. This usually lowers the blood pressure promptly. The blood pressure tends to gradually rise again, in which case the doses of reserpine and apresoline are repeated every 12 hours, or as often as every 8 hours if necessary.
Almost all patients respond to this regimen, but in rare instances, there is no blood pressure response. If there is not, we use still another measure: magnesium sulfate, 0.1 gm/kg in a 50% solution, intramuscularly. This may be repeated every 4 hours for a total of not more than 3 doses. Incidentally, we have not found chlorothiazide helpful in hypertension from acute nephritis.
If the heart is enlarging or if the blood pressure drops suddenly without drug therapy, we begin rapid digitalization. If the patient is convulsing, we repeat the phenobarbital and may give 3 cc of paraldehyde intramuscularly. On rare occasions, in the child with hypertensive encephalopathy due to acute nephritis, we have carefully performed a lumbar puncture, removing only 1 or 2 drops of spinal fluid; this measure dramatically stops the seizures and immediately lowers the blood pressure.
Once the blood pressure has returned to normal—or if the patient begins treatment with normal blood pressure—we adopt a more relaxed attitude. We give the child procaine penicillin, 300,000 units intramuscularly daily, because almost all children still harbor streptococci in the acute phase of the disease. We place the child on a free diet, without restriction of salt, protein, or fluid, because we feel that it is more important that he eat, rather than be concerned with what he eats. If he is oliguric, on the first day, we urge fluids up to 1000 cc over his output, and if he is vomiting, we give these fluids intravenously. If oliguria persists, after the first day we restrict fluids to 300 cc over the measured output.
The Question of Bed Rest
The next point about treatment is a controversial one—when to allow the patient out of bed. We do not want tooearly ambulation to impair healing of the diseased kidneys, but at the same time, how useful (and how practical) is prolonged bed rest? Our policy is a liberal one, perhaps because we have seen patients with glomerulonephritis who had been kept in bed needlessly long—with no beneficial effects, and some harmful ones. As soon as the patient’s appetite returns and he says he’s hungry, we obtain an erythrocyte sedimentation rate and an Addis count. On the next day, we allow him out of bed. If his sedimentation rate does not increase more than 10% of what it was on the previous day, or if his Addis count does not rise more than 20%, we send him home on limited activity for one week. At the end of the week, we re-examine him for general well-being, blood pressure, appetite, absence of vomiting, tiredness, and sedimentation rate. If his general health is satisfactory, and the sedimentation rate has not increased since discharge, he is then allowed to go back to school for half days. If, after a week, he is not tired in school, he is allowed back to full school activity, restricted only from strenuous activities such as gym class, bicycle riding, and football.
During the recovery period, we compare physical examinations and urinalyses at monthly intervals. At the same time, we give injections of long-acting intramuscular penicillin through one complete respiratory-infection season, to safeguard against exacerbation. It is customary, and not a warning of exacerbation, for white cells to appear in the urine for a short time, as the hematuria disappears during the first or second month of disease. Proteinuria, hematuria, casts, and white cells generally disappear in a month or 2, and the sedimentation rate may become normal in this time. However, full recovery may take longer, and we do not become concerned about progress as long as the laboratory findings return to normal within 2 years after onset of the disease.
With the above regimen, we have been able to release most of our patients from the hospital within 10 days or 2 weeks. Normally, they can return to full activity within a month or 6 weeks after onset of the disease. We have rarely seen a recurrence.
Prognosis for acute glomerulonephritis in children is almost always good. About 90% to 95% go on to complete remission without residua. Another 3% to 8% develop chronic glomerulonephritis, which may persist for 2 to 20 years or longer, with eventual death in renal failure. In the acute phase, 1% to 2% die, but usually as a result of hypertensive complications such as cardiac failure and hypertensive encephalopathy; only rarely does a child die of renal failure with the usual signs of uremia. The disease, of course, should not be treated casually. But on the other hand, treatment that is too restrictive—too concerned with diet and bed rest—does not decrease mortality and only imposes needless hardships on the patient.
Lewis A. Barness, MD, is Associate Professor of Pediatrics at the University of Pennsylvania School of Medicine, and Acting Chief of Service at the Hospital of the University of Pennsylvania. He serves as Chief of Pediatrics at Philadelphia General Hospital and as Associate Physician at the Children's Hospital of Philadelphia. For last month's issue of CONSULTANT, Dr. Barness wrote on the problem of hypernatremia in infants; in this issue, he turns his attention to the treatment of glomerulonephritis