A nephrotic syndrome is normally associated with 3 to 4+ proteinuria, fatty casts, oval fat

bodies, free fat droplets, and nonproliferative glomerulonephritis.

Typically, hematuria and red blood cell casts indicate a nephritic syndrome and
proliferative glomerulonephritis.
Chronic glomerulonephritis is characterized by proteinuria, variable hematuria, broad
waxy casts, and granular casts.
the patient's neuromuscular dysfunction is most likely the result of hypokalemia, the most
important and most serious side effect listed. Hypokalemia is produced because the
diuretics cause a large amount of Na+ to collect in the distal tubules, which leads to Na+
reabsorption (sodium avidity) and a concomitant depletion of K+. This Na+/K+ exchange
site is a primary mechanism for renal control of K+ homeostasis.
Poststreptococcal glomerulonephritis is a relatively common complication of pharyngitis
in children 6 to 10 years of age. Most cases are caused by group A -hemolytic
streptococci with specific types of M antigen.
The child's puffiness is due to dramatically decreased glomerular filtration and the
resultant oliguria with salt and water retention. As with all cases of nephritis, there is
significant hematuria and proteinuria. The loss of protein combined with the salt and
water retention produces the characteristic edema, and the increased blood volume is
sufficient to explain her modest hypertension.
Although systemic lupus erythematosus can be associated with glomerulonephritis, renal
symptoms characteristic of the nephrotic syndrome are more common in the early stages,
and it would be unusual for an 8-year-old to have lupus.
Acute tubular necrosis can be associated with water retention, edema, and high blood
pressure, but hematuria is not common in these patients. Furthermore, most cases of acute
tubular necrosis are preceded by an identifiable ingestion of some acutely nephrotoxic
agent or ischemic damage secondary to shock.
Juvenile-onset diabetes frequently causes renal symptoms, but these changes are usually
nephrotic rather than nephritic in nature (i.e., lack of hematuria and more substantial
proteinuria). The onset of diabetes is generally more gradual, and significant edema
would probably evolve over a longer period. Finally, all cases of diabetes manifest with
polyuria, and salt and fluid retention are rarely seen prior to the onset of chronic renal
failure late in the disease. Isolated hyperaldosteronism is rare and not associated with
hematuria.
Almost 75% of Na+ is reabsorbed in the proximal tubular epithelium by several
processes, including active transport at the basolateral surface and cotransport of Na+ at
the luminal surface with glucose or amino acids. An additional 22% is reabsorbed by the
active transport process in the ascending thick limb of the loop of Henle. The remaining

small percentage of Na+ that reaches the distal tubular epithelium is reabsorbed by a
highly regulated, aldosterone-sensitive process involving exchange with K+.
Membranous glomerulonephropathy (MGN) is depicted via hematoxylin, eosin, and
methenamine silver stains and is characterized by the deposition of subepithelial immune
complex deposits (ICDs). Subepithelial ICDs may reduce the negative charge in the
glomerular basement membrane (GBM) and injure podocytes, resulting in glomerular
protein loss and nephrotic syndrome (i.e., proteinuria, lipiduria, hypoalbuminemia,
hyperlipidemia, and edema). In the early stage of the disease, glomeruli have a normal
appearance by light microscopy; they reflect the paucity and small size of the ICDs and
the absence of the GBM reaction. When the disease progresses, the ICDs become more
numerous and larger, leading to diffuse thickening of the GBM. The glomerular reaction
to subepithelial ICDs (i.e., by production of a new basement membrane around individual
ICDs) is represented on a silver stain (which stains the basement membrane) by spikes
and later by domes and "train tracks."
There are primary (80%) and secondary (20%) forms of MGN. Primary (renallimited) MGN is caused by GBM/podocyte autoantibodies and is associated with
exclusive subepithelial ICDs that contain IgG and complement system protein, C3. In
secondary forms of MGN, the glomerular disorder occurs in association with an
extrarenal disease (e.g., lupus, malignant neoplasm, chronic viral hepatitis B, and drug
reactions). Affected glomeruli have a predominance of subepithelial ICDs but may also
have smaller numbers of mesangial or subendothelial ICDs; the ICDs may contain
immunoglobulin classes other than IgG as well as both early classical (C1q, C4) and
alternative pathway (properdin) complement proteins ("full house" pattern by
immunofluorescence microscopy).
The kidneys are especially sensitive to hypovolemic shock that lasts 30 minutes to 1 hour.
Acute tubular necrosis is the most common kidney lesion seen in patients recovering
from hypovolemic shock, and hyperalkemia quickly ensues, primarily as a result of
oliguria. In the absence of a substantial external potassium load, most patients have only
modest potassium accumulation, with rises in serum potassium of about 0.4 mM in a 24hour period. As with all causes of kidney failure, serum BUN and creatinine are markedly
elevated (creatinine as high as 8 to 12; normal = 0.8 to 1.5).
A positive ASO titer is generally adequate evidence to demonstrate a recent streptococcal
infection and is especially useful in diagnosing acute rheumatic fever as well as
poststreptococcal glomerulonephritis.
A complete blood count provides information that may be important in diagnosing
infection, anemia, or neoplasia.
The glomerular filtration rate (GFR) is kept within a narrow range despite changes in
arterial blood pressure by a specialized tubuloglomerular feedback mechanism. This
mechanism is implemented by a special anatomic structure called the juxtaglomerular
apparatus, which consists of the macula densa cells in the initial portion of the distal

tubule and juxtaglomerular cells in the walls of afferent and efferent arterioles.
Tubuloglomerular feedback has two components: regulation of afferent arteriolar
resistance and regulation of efferent arteriolar resistance. A drop in arterial blood pressure
decreases hydrostatic pressure in the glomerulus, thus leading to a decrease in GFR.
Macula densa cells move to correct a drop in GFR in two ways. First, they decrease
resistance in the afferent arteriole, which increases blood flow to the glomerulus and
restores glomerular hydrostatic pressure. Second, they stimulate renin release from the
juxtaglomerular cells. Renin, in turn, leads to angiotensin II synthesis. Angiotensin II
constricts the efferent arteriole, thus also acting to restore glomerular hydrostatic pressure
and GFR.