GLOMERULAR DISEASE

ACUTE NEPHRITIC SYNDROME

NEPHROTIC SYNDROME
CHRONIC GLOMERULONEPHRITIS
GLOMERULAR DISEASE
Glomerular
ACUTE NEPHRITIC SYNDROME
It reflects an acute inflammatory
response w/in the kidney & is
characterized in the urine sediment
by:
Hematuria
RBC casts
Other signs of acute inflammatory
renal injury:
proteinuria
peripheral edema
hypertension, or
renal insufficiency w/ or w/out oliguria
Pathophysiology
Pathophysiology
The hallmark of the acute nephritic syndrome is the finding
of RBCs and RBC (as well as other) casts in the urine
sediment
The finding of RBC casts in a patient w/ hematuria virtually
ensures that the patient has a glomerular pathologic process
The severity of these abnormalities also varies, since hematuria
can be either microscopic or grossly visible.
The urinary findings in acute glomerular disease vary,
ranging from normal (usu. seen in subclinical disease) to
signs of proteinuria, hematuria, pyuria, lipiduria, & RBC &
other casts
The degree of proteinuria can range from just above the upper
limit of normal to the nephrotic range
Pathophysiology
The manner in w/c RBCs pass into the urine in
glomerular dse probably due to focal disruptions in the
glomerular capillary wall produced by the underlying
inflammatory process

These focal disruptions along the glomerular capillary

wall may contribute to proteinuria & may allow plasma
proteins larger than albumin to escape into the urine
Pathophysiology
Renal Na & water retention resulting in generalized edema
is common because of poor renal perfusion stemming from
a decline in renal blood flow & proteinuria
Resulting hypoalbuminemia & a decline in intravascular
volume
Elevated blood pressure is an additional common clinical
component.
Both volume overload from inappropriate renal fluid
retention & enhanced renin secretion from renal injury &
resulting vasoconstrictor tone play important roles in this
process.
Pathophysiology
The GFR is often reduced resulting in a rise in blood
urea nitrogen
This reduction is a result of declines in:
glomerular blood flow, glomerular transcapillary hydraulic
pressure gradients, & the glomerular permeability coefficient,
w/c is a function of both porosity and surface area available for
filtration of the glomerular capillary.
Pathophysiology
Often in this syndrome, renal insufficiency is
transient, but it also can be progressive, leading to
chronic glomerulonephritis & renal failure.
Most patients w/ acute nephritis have a form of
proliferative glomerulonephritis &, occasionally, acute
tubulointerstitial nephritis
for this reason, renal biopsy is generally performed to
determine the final diagnosis.
Causes
Postreptococcal
NEPHROTIC SYNDROME
The manifestations of the nephrotic syndrome
include:
Massive proteinuria, w/ the daily loss of 3.5 gm or more
of protein (less in children)
Hypoalbuminemia, w/ plasma albumin levels <3 gm/dL
Generalized edema
Hyperlipidemia & lipiduria
Pathophysiology
The various components of nephrotic syndrome bear a
logical relationship to one another
The initial event is proteinuria
Proteinuria is due to an increase in glomerular
permeability of serum alb. & arises in response to
alterations in both the size & charge barriers of the
glomerular filtration apparatus
As a consequence of proteinuria, the serum alb. conc. &
therefore the plasma oncotic pressure fall.
Pathophysiology
The generalized edematous state common to the
nephrotic syndrome
Largely caused by this drop in plasma oncotic pressure &
the movement of fluid from the vascular to the
interstitial fluid compartment
producing a decline in plasma volume that signals the kidney
to retain Na & water
Pathophysiology
Most patients have:
Increased blood levels of cholesterol, TG, VLDL, LDL, Lp(a) lipoprotein,
& apoprotein
Decrease in HDL conc. in some patients.
These defects seem to be due in part to:
Increased synthesis of lipoproteins in the liver, abnormal transport of
circulating lipid particles
Decreased catabolism
Lipiduria follows the hyperlipidemia because not only albumin
molecules but also lipoproteins leak across the glomerular capillary wall.
The lipid appears in the urine either as free fat or as oval fat bodies,
representing lipoprotein resorbed by tubular epithelial cells & then shed
along w/ the degenerated cells.
Pathophysiology
These patients are particularly vulnerable to infection
Especially w/ staphylococci & pneumococci
This vulnerability could be related to loss of Igs or LMW
complement components in the urine
Thrombotic & thromboembolic complications are
common due to loss of anticoagulant factors (e.g.,
antithrombin III) & antiplasmin activity through the
leaky glomerulus
Renal vein thrombosis, once thought to be a cause of
nephrotic syndrome, is most often a consequence of this
hypercoagulable state
Causes
The relative frequencies of the several causes of the
nephrotic syndrome vary according to age and
geography
In children younger than 17 years in North America,
the nephrotic syndrome is almost always caused by a
lesion primary to the kidney
whereas among adults, it may often be associated w/ a
systemic disease
Causes

Approximate prevalence of primary disease = 95% in children, 60% in adults.

Approximate prevalence of systemic disease = 5% in children, 40% in adults
CHRONIC GLOMERULONEPHRITIS
Many forms of glomerular disease can progress to chronic
renal failure.
On morphologic examination, this progression is
characterized by scarring of most of the glomeruli.
UA results are more benign, w/ less proteinuria &
hematuria & w/ broad, waxy casts in the urine sediment
Occasionally, the urine may have characteristics of
nephritic, nephrotic, and chronic patterns.
This urinary finding has been called a telescoped sediment
and is usually seen in severe glomerulonephritis or
vasculitis.