22 Year male, Jawad, resident of Karachi, B.com part 1 student, admitted on 17 jan 2012 in suit throught emergency with following complaints:
Fever for one week
On further questioning he admitted having cola colour urine soon after having fever but does not complained significantly sore throat. He denied rashes, joint pain, photosensitivity, oral ulcers, frothy urine. He did complaint low grade headache but no history of fits or unconsciousness.
PAST HiSTORY: He mentioned intermittent self limiting spontaneous nasal bleeding since childhood.
There is no history of hospitalization for any reason in past. There is no history of blood transfusion and there is no history of jaundice.
In Family , he has another sister elder than him, and she is quite well. His mother and father are healthy too.
Investigated :
GI team performed endoscopy and found grade 11 varices. his Hepatic profile found normal. his liver enzymes were mildly elevated.
Impression was modified and wilson disease and his serum ceruloplasmin came out to be decreased.
DISCUSSION
Acute poststreptococcal glomerulonephritis (APSGN) results from an antecedent infection of the skin or throat caused by nephritogenic strains of group A beta-hemolytic streptococci.The concept of nephritogenic streptococci was initially advanced by Seegal and Earl in 1941, who noted that rheumatic fever and acute poststreptococcal glomerulonephritis (both nonsuppurative complications of streptococcal infections) did not simultaneously occur in the same patient and differ in geographic location. Acute poststreptococcal glomerulonephritis occurs predominantly in males and often completely heals, whereas patients with rheumatic fever often experience relapsing attacks.
The M and T proteins in the bacterial wall have been used for characterizing streptococci. Nephritogenicity is mainly restricted to certain M protein serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60) that have shown nephritogenic potential. These may cause skin or throat infections, but specific M types, such as 49, 55, 57, and 60, are most commonly associated with skin infections. However, not all strains of a nephritis-associated M protein serotype are nephritogenic. In addition, many M protein serotypes do not confer lifetime immunity. Group C streptococci have been responsible for recent epidemics of APSGN (eg, Streptococcus zooepidemicus). Thus, it is possible that nephritogenic antigens are present and possibly shared by streptococci from several groups.
In addition, nontypeable group A streptococci are frequently isolated from the skin or throat of patients with glomerulonephritis, representing presumably unclassified nephritogenic strains. The overall risk of developing acute poststreptococcal glomerulonephritis after infection by these nephritogenic strains is about 15%. The risk of nephritis may also be related to the M type and the site of infection. The risk of developing nephritis infection by M type 49 is 5% if it is present in the throat. This risk increases to 25% if infection by the same organism in the skin is present.
An immune complex–mediated mechanism is the most widely proposed mechanism leading to the development of APSGN. Nephritogenic streptococci produce proteins with unique antigenic determinants. These antigenic determinants have a particular affinity for sites within the normal glomerulus. Following release into the circulation, the antigens bind to these sites within the glomerulus. Once bound to the glomerulus, they activate complement directly by interaction with properdin.
Glomerular-bound streptococcal antibodies also serve as fixed antigens and bind to circulating antistreptococcal antibodies, forming immune complexes. Complement fixation via the classic pathway leads to the generation of additional inflammatory mediators and recruitment of inflammatory cells.
Other nonimmune complex mediated mechanisms have been proposed for the development of APSGN, such as delayed-type hypersensitivity, superantigens, and autoimmune phenomena.
A role for delayed-type hypersensitivity has been implicated in the pathogenesis of this disease. Early in the course of APSGN, resident endothelial and mesangial cells are predominantly proliferated, and this is accompanied by infiltration with polymorphonuclear leukocytes and monocytes. Macrophages are effector cells that cause resident cellular proliferation. The infiltration of macrophages in the glomeruli is mediated by complement-induced chemotaxis and, most likely, by an antigen-specific event related to delayed-type hypersensitivity mediated by helper/inducer T cells.
Streptococcal M proteins and pyrogenic exotoxins can act as superantigens. These cause a marked expansion of T cells expressing specific T-cell receptor B-chain variable gene segments. Massive T-cell activation occurs, with release of T-cell–derived lymphokines such as IL-1 and IL-6.
Autologous IgG in APSGN becomes antigenic and elicits an anti-IgG rheumatoid factor response, leading to formation of cryoglobulins. Cryoglobulins, rheumatoid factors, and other autoimmune phenomena occur in APSGN and are thought to play a role in the pathogenesis of the disease together with streptococcal superantigens.
Epidemic poststreptococcal acute glomerulonephritis appears to end in virtually complete resolution and healing in all patients, and the prognosis is favorable for 95% of children with acute sporadic poststreptococcal glomerulonephritis. The prognosis for persons with acute glomerulonephritis secondary to other causes is less certain.
Edema usually resolves within 5-10 days, and the blood pressure usually returns to normal after 2-3 weeks, even though persistence of elevated pressures for as many as 6 weeks is compatible with complete resolution.
Urinary abnormalities resolve at various times after onset. Proteinuria may disappear within the first 2-3 months or may slowly decrease over 6 months. Intermittent or postural proteinuria has been noted for 1-2 years after onset.
Gross hematuria usually disappears within 1-3 weeks but may be exacerbated by physical activity. C3 concentration returns to normal in more than 95% of patients by the end of 8-10 weeks. Microscopic hematuria usually disappears after 6 months, but its presence for as long as 1 year should not cause undue concern, and even more prolonged hematuria (1-3 y) has been observed in some patients who ultimately have demonstrated complete resolution of their renal disease. Strongly consider the possibility of chronic renal disease when both hematuria and proteinuria persist longer than 12 months.
In a few hospitalized patients, the initial injury is so severe that either persistent renal failure or progressive renal failure ensues. However, histologic regression of the disease in most patients is predictable, and the ultimate prognosis is good.
Although clinical resolution occurs in most patients, several authors report time-related reduction in precise measurements of renal function, as well as diminished renal functional reserve. These studies further support the thesis that any significant loss of nephrons leads to hyperfiltration of the remaining units. Studies that have followed up children with APSGN for 10-20 years have shown that approximately 20% of the patients have abnormal urine analyses, with less than 1% having azotemia.
Clinical manifestations of the disease rarely recur after the first 3 months, and second episodes of acute glomerulonephritis are rare.
The most common acute complication is hypertension with or without central nervous system (CNS) manifestations.
Anemia is common early in the disease and is primarily due to dilution, although in 2 instances, autoimmune hemolytic anaemia was documented in the early stages of APSGN.Anemia tends to resolve with diuresis. A few patients may have diminished erythropoiesis in the recovery phase and have some persisting anemia.
An occasional patient develops pulmonary edema because of the marked increase in vascular volume that is present in the early phase of the disease.
Congestive heart failure is rare but has been reported. Definite myocarditis has also been documented.
In most patients with moderate to severe APSGN, a measurable reduction in volume of glomerular filtrate (GF) is present, and the capacity to excrete salt and water is usually diminished, leading to expansion of the extracellular fluid (ECF) volume. The expanded ECF volume is responsible for edema and, in part, for hypertension, anemia, circulatory congestion, and encephalopathy. Persistence or worsening of azotemia is always troubling and may suggest acute kidney injury. The presence of acute kidney injury may suggest an alternate diagnosis (eg, membranoproliferative glomerulonephritis [MPGN], Henoch-Schönlein purpura [HSP], systemic lupus erythematosus [SLE]) or a severe or worsening APSGN, such as observed in those with crescentic glomerulonephritis or rapidly progressive glomerulonephritis.
Clearly outline a follow-up plan and discuss the plan with the family. Blood pressure measurements and urine examinations for protein and blood constitute the basis of the follow-up plan. Perform examinations at 4- to 6-week intervals for the first 6 months and at 3- to 6-month intervals thereafter, until both hematuria and proteinuria have been absent and the blood pressure has been normal for 1 year. Documenting that the low C3 has returned to normal after 8-10 weeks may be useful.
Almost characteristic by their absence are arthralgia, arthritis, carditis, hepatic involvement, and gastrointestinal bleeding. Pallor is common at onset and is not explained entirely by the presence of anemia.
The median age of presentation in childhood is age 6-8 years, with the condition being extremely rare prior to age 2 years. In very young children, it is postulated that APSGN is rare because of the low rate of streptococcal pharyngitis in this age group and an immature immune response.[48] Males are 2 times more likely to have this condition compared with females; the reason this difference in sex prevalence is not known. However, the site of streptococcal infection (pyoderma or pharyngitis) does not influence the sex difference.
Edema and/or hematuria
Edema and/or gross hematuria represent the most common clinical presentation resulting in patients seeking medical attention. One or both findings usually appear abruptly and may be associated with various degrees of malaise, lethargy, anorexia, fever, abdominal pain, and headache. The classic description of tea- or cola-colored urine occurs in approximately 25-60% of patients.
Edema is the most frequent and sometimes the only clinical finding. According to some investigators, edema is found in approximately 85% of patients. Edema usually appears abruptly and first involves the periorbital area, but it may be generalized. The degree of edema widely varies and depends on a number of factors, including the severity of glomerular involvement, the fluid intake, and the degree of hypoalbuminemia. The triad of edema, hematuria, and hypertension is classic for APSGN. Three phases of the disease can be identified: the latent phase, the acute phase, and the recovery phase.
Gross hematuria occurs at onset in 30-50% of children with poststreptococcal acute glomerulonephritis who require hospitalization. The urine is usually described as being smoky, cola colored, tea colored, or rusty. The color is usually dependent on the amount of blood present and the pH of the urine. Observant parents may note oliguria. Clots are exceedingly rare in persons with acute glomerulonephritis.
Proteinuria
Varying degrees of proteinuria are also typically present, but nephrotic syndrome is rare, occurring in 2-4% of cases.
Hypertension
Hypertension is the third cardinal feature of poststreptococcal acute glomerulonephritis and is reported in 50-90% of children who are hospitalized with acute glomerulonephritis. The magnitude of the increase in blood pressure widely varies; however, systolic pressures greater than 200 mm Hg and diastolic pressures greater than 120 mm Hg are not unusual. Hypertension usually resolves in 1-2 weeks and rarely requires long-term treatment.
Hypertensive encephalopathy
Hypertensive encephalopathy can be the presenting feature of postinfectious glomerulonephritis. This condition has been reported in approximately 5% of hospitalized children and is the most serious early complication of this disease. In these patients, hypertension is usually severe and is accompanied by signs of central nervous system (CNS) dysfunction such as headache, vomiting, depressed sensorium, confusion, visual disturbances, aphasia, memory loss, coma, and convulsions. The mechanism of hypertension is most likely retention of sodium and water with resulting expansion of the extracellular space.
Hypertensive encephalopathy has been reported in the occasional individual with minimal or no edema and with minimal urinary abnormalities. Since the urinalysis in such patients exhibits minimal abnormalities, the underlying cause may not be readily apparent. A high index of suspicion is required to make an appropriate diagnosis.
Circulatory congestion
Circulatory congestion is apparent in most children admitted to the hospital but is responsible only rarely for significant early symptoms. Dyspnea, orthopnea, and cough may be present. Both systolic and diastolic hypertension may be present to a varying degree. Either bradycardia or tachycardia may be observed.
Pulmonary rales are often audible. At times, the only evidence of congestion is detected on chest radiograph. A prominent cardiac shadow may be present until the onset of diuresis. In the patient with an otherwise normal cardiovascular system, cardiac failure is unusual.
An insidious onset of edema is more indicative of other forms of renal disease.
An occasional child may have a scarlatiniform rash or evidence of a viral exanthema, but petechial or purpuric rashes suggest other conditions.
Fever for one week
Abdominal discomfort for 5 days
Nausea and voming for 4 days
Decrease urine out put for 2 days and
Short ness of breath for one day.
According to the patient, He was alright 1 week ago before presenting to suit, then he experience fever which was followed by mailase and diffuse abdominal discomfort. Fever was maximally documented upto 101 F with no specific diurnal variation and temporarily relieved with antipyretics. He visited nearby doctor who prescribed some medication whose names are not known by patient. He got temporary relieve but soon he appeared with feeling of nausea associated with vomiting. Later on he gradually decreased urine out put and in the end he was short of breath. Before coming to suit he was investigated by another doctor who guided them to suit as he has renal impairment.
On further questioning he admitted having cola colour urine soon after having fever but does not complained significantly sore throat. He denied rashes, joint pain, photosensitivity, oral ulcers, frothy urine. He did complaint low grade headache but no history of fits or unconsciousness.
PAST HiSTORY: He mentioned intermittent self limiting spontaneous nasal bleeding since childhood.
He also complaint of mild dyspepsia and intermittent generalized itching for which he took sometimes Hakemi medication , but for very short period for time. He didn’t complaint of abdominal distention or leg edema, hemetemesis, short of breath in past.
There is no history of hospitalization for any reason in past. There is no history of blood transfusion and there is no history of jaundice.
In Family , he has another sister elder than him, and she is quite well. His mother and father are healthy too.
Personally he is student and hs got no addiction .
Investigated :
Advanced uraemia with normal size unobstructed kidneys.
Low C3 and C4 with raised ASOT.
Treated on impression Post sreptococcal GN.
Renal function did not improve after 2 wk of admission and he still required dialysis.
Renal biopsy was planned but INR was persistently high despite of Injection vit K and FFP.
Patient was reevaluated and found to have mild aschitis and altered echotexture of liver with mild enlaged liver.
GI team performed endoscopy and found grade 11 varices. his Hepatic profile found normal. his liver enzymes were mildly elevated.
Impression was modified and wilson disease and his serum ceruloplasmin came out to be decreased.
Eye examination for kyeser Fleissure ring was planned but patient became inpatient for new appearances of disease and became LAMA.
DISCUSSION
Acute glomerulonephritis is a disease characterized by the sudden appearance of edema, hematuria, proteinuria, and hypertension. It is a representative disease of acute nephritic syndrome in which inflammation of the glomerulus is manifested by proliferation of cellular elements secondary to an immunologic mechanism
The M and T proteins in the bacterial wall have been used for characterizing streptococci. Nephritogenicity is mainly restricted to certain M protein serotypes (ie, 1, 2, 4, 12, 18, 25, 49, 55, 57, and 60) that have shown nephritogenic potential. These may cause skin or throat infections, but specific M types, such as 49, 55, 57, and 60, are most commonly associated with skin infections. However, not all strains of a nephritis-associated M protein serotype are nephritogenic. In addition, many M protein serotypes do not confer lifetime immunity. Group C streptococci have been responsible for recent epidemics of APSGN (eg, Streptococcus zooepidemicus). Thus, it is possible that nephritogenic antigens are present and possibly shared by streptococci from several groups.
In addition, nontypeable group A streptococci are frequently isolated from the skin or throat of patients with glomerulonephritis, representing presumably unclassified nephritogenic strains. The overall risk of developing acute poststreptococcal glomerulonephritis after infection by these nephritogenic strains is about 15%. The risk of nephritis may also be related to the M type and the site of infection. The risk of developing nephritis infection by M type 49 is 5% if it is present in the throat. This risk increases to 25% if infection by the same organism in the skin is present.
An immune complex–mediated mechanism is the most widely proposed mechanism leading to the development of APSGN. Nephritogenic streptococci produce proteins with unique antigenic determinants. These antigenic determinants have a particular affinity for sites within the normal glomerulus. Following release into the circulation, the antigens bind to these sites within the glomerulus. Once bound to the glomerulus, they activate complement directly by interaction with properdin.
Glomerular-bound streptococcal antibodies also serve as fixed antigens and bind to circulating antistreptococcal antibodies, forming immune complexes. Complement fixation via the classic pathway leads to the generation of additional inflammatory mediators and recruitment of inflammatory cells.
Other nonimmune complex mediated mechanisms have been proposed for the development of APSGN, such as delayed-type hypersensitivity, superantigens, and autoimmune phenomena.
A role for delayed-type hypersensitivity has been implicated in the pathogenesis of this disease. Early in the course of APSGN, resident endothelial and mesangial cells are predominantly proliferated, and this is accompanied by infiltration with polymorphonuclear leukocytes and monocytes. Macrophages are effector cells that cause resident cellular proliferation. The infiltration of macrophages in the glomeruli is mediated by complement-induced chemotaxis and, most likely, by an antigen-specific event related to delayed-type hypersensitivity mediated by helper/inducer T cells.
Streptococcal M proteins and pyrogenic exotoxins can act as superantigens. These cause a marked expansion of T cells expressing specific T-cell receptor B-chain variable gene segments. Massive T-cell activation occurs, with release of T-cell–derived lymphokines such as IL-1 and IL-6.
Autologous IgG in APSGN becomes antigenic and elicits an anti-IgG rheumatoid factor response, leading to formation of cryoglobulins. Cryoglobulins, rheumatoid factors, and other autoimmune phenomena occur in APSGN and are thought to play a role in the pathogenesis of the disease together with streptococcal superantigens.
Epidemic poststreptococcal acute glomerulonephritis appears to end in virtually complete resolution and healing in all patients, and the prognosis is favorable for 95% of children with acute sporadic poststreptococcal glomerulonephritis. The prognosis for persons with acute glomerulonephritis secondary to other causes is less certain.
Edema usually resolves within 5-10 days, and the blood pressure usually returns to normal after 2-3 weeks, even though persistence of elevated pressures for as many as 6 weeks is compatible with complete resolution.
Urinary abnormalities resolve at various times after onset. Proteinuria may disappear within the first 2-3 months or may slowly decrease over 6 months. Intermittent or postural proteinuria has been noted for 1-2 years after onset.
Gross hematuria usually disappears within 1-3 weeks but may be exacerbated by physical activity. C3 concentration returns to normal in more than 95% of patients by the end of 8-10 weeks. Microscopic hematuria usually disappears after 6 months, but its presence for as long as 1 year should not cause undue concern, and even more prolonged hematuria (1-3 y) has been observed in some patients who ultimately have demonstrated complete resolution of their renal disease. Strongly consider the possibility of chronic renal disease when both hematuria and proteinuria persist longer than 12 months.
In a few hospitalized patients, the initial injury is so severe that either persistent renal failure or progressive renal failure ensues. However, histologic regression of the disease in most patients is predictable, and the ultimate prognosis is good.
Although clinical resolution occurs in most patients, several authors report time-related reduction in precise measurements of renal function, as well as diminished renal functional reserve. These studies further support the thesis that any significant loss of nephrons leads to hyperfiltration of the remaining units. Studies that have followed up children with APSGN for 10-20 years have shown that approximately 20% of the patients have abnormal urine analyses, with less than 1% having azotemia.
Clinical manifestations of the disease rarely recur after the first 3 months, and second episodes of acute glomerulonephritis are rare.
The most common acute complication is hypertension with or without central nervous system (CNS) manifestations.
Anemia is common early in the disease and is primarily due to dilution, although in 2 instances, autoimmune hemolytic anaemia was documented in the early stages of APSGN.Anemia tends to resolve with diuresis. A few patients may have diminished erythropoiesis in the recovery phase and have some persisting anemia.
An occasional patient develops pulmonary edema because of the marked increase in vascular volume that is present in the early phase of the disease.
Congestive heart failure is rare but has been reported. Definite myocarditis has also been documented.
In most patients with moderate to severe APSGN, a measurable reduction in volume of glomerular filtrate (GF) is present, and the capacity to excrete salt and water is usually diminished, leading to expansion of the extracellular fluid (ECF) volume. The expanded ECF volume is responsible for edema and, in part, for hypertension, anemia, circulatory congestion, and encephalopathy. Persistence or worsening of azotemia is always troubling and may suggest acute kidney injury. The presence of acute kidney injury may suggest an alternate diagnosis (eg, membranoproliferative glomerulonephritis [MPGN], Henoch-Schönlein purpura [HSP], systemic lupus erythematosus [SLE]) or a severe or worsening APSGN, such as observed in those with crescentic glomerulonephritis or rapidly progressive glomerulonephritis.
Patient Education
Clearly and specifically explain the nature of the disease, its course, and the eventual prognosis of the condition to the child (if old enough to understand) and the parents and/or caregivers. They need to understand that, although complete resolution is expected, a small possibility exists for persistent disease, and that an even smaller possibility exists for progression. This information is necessary for some patients to ensure that compliance with the follow-up program occurs.Clearly outline a follow-up plan and discuss the plan with the family. Blood pressure measurements and urine examinations for protein and blood constitute the basis of the follow-up plan. Perform examinations at 4- to 6-week intervals for the first 6 months and at 3- to 6-month intervals thereafter, until both hematuria and proteinuria have been absent and the blood pressure has been normal for 1 year. Documenting that the low C3 has returned to normal after 8-10 weeks may be useful.
Typical postinfectious presentation
In those patients whose acute glomerulonephritis is the result of a postinfectious cause (ie, poststreptococcal acute glomerulonephritis being the most common), a latent period of 7-21 days between onset of the streptococcal infection and development of clinical glomerulonephritis is characteristic. This latent period, more clearly defined after pharyngeal infections than after pyoderma, averages approximately 10 days.Almost characteristic by their absence are arthralgia, arthritis, carditis, hepatic involvement, and gastrointestinal bleeding. Pallor is common at onset and is not explained entirely by the presence of anemia.
The median age of presentation in childhood is age 6-8 years, with the condition being extremely rare prior to age 2 years. In very young children, it is postulated that APSGN is rare because of the low rate of streptococcal pharyngitis in this age group and an immature immune response.[48] Males are 2 times more likely to have this condition compared with females; the reason this difference in sex prevalence is not known. However, the site of streptococcal infection (pyoderma or pharyngitis) does not influence the sex difference.
Edema and/or hematuria
Edema and/or gross hematuria represent the most common clinical presentation resulting in patients seeking medical attention. One or both findings usually appear abruptly and may be associated with various degrees of malaise, lethargy, anorexia, fever, abdominal pain, and headache. The classic description of tea- or cola-colored urine occurs in approximately 25-60% of patients.
Edema is the most frequent and sometimes the only clinical finding. According to some investigators, edema is found in approximately 85% of patients. Edema usually appears abruptly and first involves the periorbital area, but it may be generalized. The degree of edema widely varies and depends on a number of factors, including the severity of glomerular involvement, the fluid intake, and the degree of hypoalbuminemia. The triad of edema, hematuria, and hypertension is classic for APSGN. Three phases of the disease can be identified: the latent phase, the acute phase, and the recovery phase.
Gross hematuria occurs at onset in 30-50% of children with poststreptococcal acute glomerulonephritis who require hospitalization. The urine is usually described as being smoky, cola colored, tea colored, or rusty. The color is usually dependent on the amount of blood present and the pH of the urine. Observant parents may note oliguria. Clots are exceedingly rare in persons with acute glomerulonephritis.
Proteinuria
Varying degrees of proteinuria are also typically present, but nephrotic syndrome is rare, occurring in 2-4% of cases.
Hypertension
Hypertension is the third cardinal feature of poststreptococcal acute glomerulonephritis and is reported in 50-90% of children who are hospitalized with acute glomerulonephritis. The magnitude of the increase in blood pressure widely varies; however, systolic pressures greater than 200 mm Hg and diastolic pressures greater than 120 mm Hg are not unusual. Hypertension usually resolves in 1-2 weeks and rarely requires long-term treatment.
Hypertensive encephalopathy
Hypertensive encephalopathy can be the presenting feature of postinfectious glomerulonephritis. This condition has been reported in approximately 5% of hospitalized children and is the most serious early complication of this disease. In these patients, hypertension is usually severe and is accompanied by signs of central nervous system (CNS) dysfunction such as headache, vomiting, depressed sensorium, confusion, visual disturbances, aphasia, memory loss, coma, and convulsions. The mechanism of hypertension is most likely retention of sodium and water with resulting expansion of the extracellular space.
Hypertensive encephalopathy has been reported in the occasional individual with minimal or no edema and with minimal urinary abnormalities. Since the urinalysis in such patients exhibits minimal abnormalities, the underlying cause may not be readily apparent. A high index of suspicion is required to make an appropriate diagnosis.
Circulatory congestion
Circulatory congestion is apparent in most children admitted to the hospital but is responsible only rarely for significant early symptoms. Dyspnea, orthopnea, and cough may be present. Both systolic and diastolic hypertension may be present to a varying degree. Either bradycardia or tachycardia may be observed.
Pulmonary rales are often audible. At times, the only evidence of congestion is detected on chest radiograph. A prominent cardiac shadow may be present until the onset of diuresis. In the patient with an otherwise normal cardiovascular system, cardiac failure is unusual.
Uncommon/atypical presentation suggesting alternative diagnosis
The development of clinical nephritis (ie, hematuria and/or edema) either during or within 2-5 days after the onset of a respiratory tract infection is atypical and suggests the possibility of some other form of glomerulonephritis. Subclinical cases may be missed and are sometimes identified based on knowledge of the affected family or contacts. One report found APSGN in 20% of asymptomatic family members with the condition. Numerous case reports describe children who present with extreme manifestations, usually hypertensive encephalopathy, who do not display the typical urinary findings at presentation.Serial examination of the urine after presentation may eventually confirm the suspicion of acute glomerulonephritis.An insidious onset of edema is more indicative of other forms of renal disease.
An occasional child may have a scarlatiniform rash or evidence of a viral exanthema, but petechial or purpuric rashes suggest other conditions.
