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Case 6 Glomerulonephropathy Rev'd
Case 6 Glomerulonephropathy Rev'd
The urinalysis may also be suggestive of a urinary tract infection with pyuria,
bacteriuria, and positive nitrites or leukocyte esterase along with mild
proteinuria. Proteinuria in such children typically resolves with
successful treatment of the infection. If the proteinuria persists after
eradication of the infection, further work-up is indicated.
Among children with persistent proteinuria, a complete history and physical
examination should be reviewed, including measurement of the blood
pressure. Initial laboratory evaluation includes renal function tests (blood
urea nitrogen and creatinine), serum electrolytes, cholesterol,
albumin, and total protein. Other tests such as renal ultrasound,
serum complement levels (C3 and C4), ANA, streptozyme testing,
hepatitis B and C serology, and HIV testing should be considered if
appropriate. A voiding cystourethrogram should be considered if there is an
abnormal ultrasound with scarring or a history of febrile urinary tract
infections.
If this initial evaluation is normal, the urine dipstick should be repeated on at
least two additional specimens. If these subsequent tests are negative for
protein, the diagnosis is transient proteinuria.
If the proteinuria persists or if any of the studies are abnormal, the patient
should be referred to a pediatric nephrologist. At this point, urinary
protein excretion should be quantified by a timed collection, if obtainable.
Indications for renal biopsy The role of renal biopsy in a child with isolated
asymptomatic persistent proteinuria is controversial. Many nephrologists
recommend close monitoring for those children with urinary protein excretion
below 500 mg/m2 per day before considering a biopsy. Monitoring should
include assessment of blood pressure, protein excretion, and renal function.
If any of these parameters shows evidence of progressive disease, a renal
biopsy should be performed to establish a diagnosis.
membrane with absence of proliferation. The main thing that can be seen by
electron microscoy is in the visceral epithelial cells which show a
uniform and diffuse effacement of foot processes. Clinical
presentation will see massive proteinuria while renal function remains
good. The proteinuria is highly selective w/ most of the protein being
albumin. As stated before there is usually a dramatic response to
corticosteroids. Long term prognosis is excellent.
Focal Semental Glomerulosclerosis (BAD PROGNOSIS & seen in
morbidly obese pts.) is characterized by sclerosis of some, but not all,
glomeruli (focal) and in the affected glomeruli only a portion of the
capillary tuft is involved (segmental). Nephrotic syndrome is often seen
with it. It is the MCC of nephrotic syndrome in adults (esp. Hispanic
and African Americans), and HIV pts (HIV-associated neuropathy).
The clinical signs differ from minimal change disease in the flowing
ways:
interstitium.
Acute renal failure Acute renal failure can develop in some patients with
the nephrotic syndrome, particularly minimal change disease. The
mechanism is not understood; several factors including hypovolemia,
interstitial edema, ischemic tubular injury, and the use of NSAIDs have been
suggested. (See "Acute kidney injury (acute renal failure) in minimal change
disease and other forms of nephrotic syndrome"). Two other major settings
are collapsing FGS, focal glomerulosclerosis, in which the tubular injury is
thought to play an important role, and crescentic glomerulonephritis
superimposed upon membranous nephropathy, in which the urine sediment
becomes active. (See "Causes and diagnosis of membranous nephropathy").
Thromboembolism Patients with the nephrotic syndrome have an
increased incidence (10 to 40 percent of patients) of arterial and venous
thromboemboli, particularly deep vein and renal vein thrombosis [20,21].
Cerebral vein thrombosis has also been rarely reported [22]. The mechanism
of the hypercoagulability is not completely understood. (See "Renal vein
thrombosis and hypercoagulable state in nephrotic syndrome").
Renal vein thrombosis is found disproportionately in patients with
membranous nephropathy, particularly those excreting more than 10 g of
protein per day. It can present acutely or, much more commonly, in an
indolent manner. The acute presentation includes flank pain, gross
hematuria, and a decline in renal function. Most patients are asymptomatic,
and the diagnosis of renal vein thrombosis is suspected only when
pulmonary thromboembolism develops.
Infection Patients with the nephrotic syndrome are susceptible to
infection, which was the leading cause of death in children with the nephrotic
syndrome before antibiotics became available. Pneumococcal infections,
especially peritonitis, were particularly common. The mechanism of the
impairment of normal defense mechanisms is not well understood; low levels
of immunoglobulin G may play a role.
Miscellaneous Proximal tubular dysfunction has been noted in some
patients with the nephrotic syndrome, often in association with advanced
disease. This can result in glucosuria, aminoaciduria, phosphaturia, renal
tubular acidosis, and vitamin D deficiency. A decrease in thyroxine-binding
globulins can cause marked changes in various thyroid function tests,
although patients are clinically euthyroid. (See "Endocrine dysfunction in the
nephrotic syndrome"). Anemia, perhaps due to the urinary loss or impaired
synthesis of erythropoietin, has also been described in a few patients [2325].
9. List Indications for renal biopsy or nephrology referral
skin. Increase unsaturated fat intake, including olive oil, canola oil, peanut
butter, avocadoes, fish and nuts. Eat low-fat desserts. Increase intake of
fruits and vegetables. There is no potassium or phosphorus restriction
necessary.
Monitor fluid intake, which includes all fluids and foods that are liquid at
room temperature. Fluid management in nephrotic syndrome is tenuous,
especially during an acute flare.