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Paper text:
many children with acute glomerulonephritis ( agn ) are first seen in their primary physicians ' offices .
this initial contact may be crucial in determining the child 's most appropriate disposition as well as identifying any immediate threats to life .  
this paper will review the office approach to agn in children on the basis of upon a firm grounding in pathophysiology .
it will begin with an overview of the pathology and pathophysiology of glomerulonephritis and then present a practical outline of the important aspects of the history and physical examination pertinent to a child with suspected agn .
it will then provide guidance in choosing and interpreting appropriate laboratory studies for the initial evaluation .
finally , some guidance will be provided on referral of children with agn , including a discussion of some situations in which management by the primary caretaker may be appropriate .
agn is a complex of findings which is marked histologically by a generalized glomerular inflammation .
frequently , renal biopsy is not available , but agn can usually be recognized by the clinical picture of hematuria , fluid overload ( edema and hypertension ) , and some evidence of renal insufficiency ( elevation of bun and creatinine ) .   in most circumstances ,
glomerular inflammation begins with an antigen - antibody reaction , either direct antibody binding to an antigen expressed or trapped in the glomerulus , or the localization of a circulating complex in the kidney .
this incites injury by activating one or more systems of inflammatory mediators : the complement cascade , coagulation factors , cytokines , growth factors , and others .
the inflammation is marked by proliferation of resident glomerular cells and infiltration by lymphocytes or neutrophils .  
the glomerular inflammation and expansion impairs the microcirculation , reducing the glomerular filtration rate ( gfr ) and usually resulting in an increase in bun and creatinine .
this reduction in gfr , in turn , leads to the retention of salt and water , causing fluid overload .
indeed , hypertensive encephalopathy may be the presenting complaint in some children with agn .   in some situations , agn is a primary process , and virtually , all of the clinical findings are a consequence of the renal lesion .
the agn is but one manifestation of a systemic illness which has targeted multiple organs , each of which may be independently injured . in children ,
fortunately , most cases of agn in children are either self - limited or amenable to therapy although there may be devastating complications of the illness during the acute phase . less commonly , what begins as an apparent agn may presage the development of a chronic process , which ultimately may progress into irreversible end - stage renal disease ( esrd ) .
most typically , the child with agn will be seen because of the sudden development of change in urine color . on occasion , however , the presenting complaint may relate to a complication of the disease : hypertensive seizures , edema , and so forth .
true bright red blood in the urine is more likely a consequence of anatomic problems such as urolithiasis   than glomerulonephritis .
the gross hematuria of agn is virtually always painless ; dysuria accompanying gross hematuria points to acute hemorrhagic cystitis   rather than renal disease .
a history of previous such episodes would point to an exacerbation of a chronic process such as iga nephropathy .
although a history of a recent documented streptococcal infection would be consistent with poststreptococcal agn , such a history is frequently unavailable .  
these might include shortness of breath or exercise intolerance from fluid overload or headaches , visual disturbances , or alteration in mental status from hypertension .   since agn may be the presenting complaint of a multisystem illness , a complete review of systems is vital .
particular attention should be paid to rash , joint discomfort , recent weight change , fatigue , appetite changes , respiratory complaints , and recent medication exposure .
the family history should address the presence of any family members with autoimmune disorders , as children with both sle and membranoproliferative glomerulonephritis ( mpgn ) may have such relatives .
a family history of renal failure ( specifically asking about dialysis and kidney transplantation ) may be the first clue to a process such as alport syndrome , which may initially present with an agn picture .  
the physical examination begins with a careful assessment of vital signs , particularly blood pressure .
blood pressures 5  mm above the 99th percentile for the child 's age , sex , and height , especially if accompanied by any alteration in mental status , demand prompt attention . tachycardia and tachypnea point toward symptomatic fluid overload .
careful examination of the nose and throat may provide evidence of bleeding , suggesting the possibility of one of the anca - positive vasculitides such as wegner 's granulomatosis .
the cardiopulmonary examination will provide evidence of fluid overload or the pulmonary involvement characterizing the rare kidney - lung syndromes .
scrotal edema may occur in nephrotic syndrome as well , and orchitis is an occasional finding in hsp .  
the rash of hsp , while characteristic when florid , may initially be subtle and limited to the buttocks or the dorsa of the feet .
some peripheral edema from salt and water retention is seen in agn , but this tends to be a more subtle  brawny  edema than the pitting edema characteristic of nephrotic syndrome .  
small joint ( e.g. , fingers ) is more typical of sle , while or knee involvement is seen with hsp .
obviously , a good urinalysis is the first order of business in assessing a child with suspected agn .
the presence of red blood cell casts , while not invariably seen , is diagnostic of glomerulonephritis if present .
agn is an inflammatory process , so it is not at all unusual to see white blood cells in nephritic urine .
proteinuria is also nearly invariant in agn although any cause of gross hematuria can lead to some urinary protein .
if the urine is not grossly bloody , however , the combined presence of hematuria and proteinuria virtually always means glomerulonephritis .   the initial blood work required in suspected agn
is actually limited ; more sophisticated immunologic investigations , for example , are really  second tier  studies after the initial results are known . obviously , assessing renal function and electrolytes is an important first step , as is obtaining a hemogram . a mild degree of anemia is frequently seen with agn and likely is dilutional ; more significant anemia would be evidence that the process may be more chronic .
there are typically no important changes in the white blood cell count or platelet count in most causes of agn .
a normal platelet count in the presence of petechiae and purpura is the usual finding in hsp .   beyond these basic tests ,
a serum albumin is usually included ; a slight degree of hypoalbuminemia is typical of many inflammatory processes such as hsp , but values < 2.0 gm / dl are quite unusual in straightforward agn and point to a process with a nephrotic syndrome component . by far ,
the most important ( and frequently forgotten ) test to obtain initially is an assessment of the complement system .
this generally means obtaining a serum c3 and c4 ; the total hemolytic complement (  ch50  ) is generally of only historical interest .
poststreptococcal agn is characterized by a very low c3 , sometimes with minimal decreases in c4 .
the hypocomplementemia of poststreptococcal agn is evanescent , typically normalizing in six to eight weeks . on the other hand
thus , if a child with a few weeks ' of abnormal urine has not had a c3 measurement earlier , it may be impossible to make a diagnosis of poststreptococcal agn with certainty without a kidney biopsy .  
all of these tests should be easily obtained in the primary care setting and will usually identify the child for whom referral is going to be necessary .
the child with severe hypertension ( more than 5  mm above the 99th percentile ) , especially if accompanied by any neurologic complaints , must be referred immediately .
similarly , children with significant renal insufficiency should be assessed by a specialist . when agn is accompanied by a nephrotic syndrome ,
the additional diagnostic and therapeutic interventions are also beyond the typical primary care practice .   beyond these situations , however ,
many such children can be reasonably managed in the primary care setting . the child with agn in the setting of hsp , for example
, who is normotensive , has normal renal function , and who is not nephrotic requires little more than careful serial observation .
although the urinary abnormalities may persist for some time after the rest of the disease has resolved , these children have little if any risk of permanent kidney injury .  
many children with poststreptococcal agn may also be followed in the primary care setting , but this will entail a commitment to serial examination .
the major threat to such children is hypertension and its complications , and this may evolve over a few days . in otherwise typical poststreptococcal agn with minimal hypertension ( e.g. , blood pressure between the 95th and 99th percentiles ) and no renal failure ,
the urinary abnormalities in poststreptococcal agn may persist for a long time , even a year .
the best indicator of resolution of the disease is the return of the c3 level to normal .
persistent decrease in c3 by this time merits referral , as this could be an indicator that the  agn
acute glomerulonephritis ( agn ) is a common condition in childhood . 
 many children with agn can be managed in the primary care setting . 
 the diagnosis is usually made on the basis of urinary findings , especially the presence of red blood cell casts . 
 one of the most important initial investigations is determining the complement c3 level ; hypocomplementemia is most characteristic of post streptococcal agn , while normocomplementemia is most often seen with iga nephropathy . 
 children whose agn is accompanied by significant hypertension or renal insufficiency should be assessed by a specialist immediately . 
 the presence of serious extrarenal signs or symptoms also merits urgent referral . otherwise , serial followup in the primary care office is appropriate .