Today, we’ve got some interesting case of a 14-year-old male with some malaise and abdominal pain.
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A 14-year-old male is evaluated for malaise and abdominal pain. He reports passing dark urine this morning. His past medical history is significant for Streptococcal pharyngitis ten days ago, for which he received Amoxicillin.
Today, his vital signs are within normal limits, except for an elevated blood pressure of 145/95 mmHg. Examination reveals spatial edema with pronounced periorbital swelling. He has 1+ pedal edema bilaterally. Abdominal exam reveals mild, diffuse tenderness without rebound or guarding.
Laboratory studies are unremarkable except for a serum creatinine of 2 mg/dL. What is the common finding associated with the patient's condition?
(A) Hypovolemia
(B) Polyuria
(C) Red blood cell cast
(D) Hypokalemia
The correct answer here is C. Basically, the patient has glomerulonephritis. This is characterized by red blood cell casts that are almost pathognomonic for glomerulonephritis.
Poststreptococcal glomerulonephritis is not common but also not unusual. The history of streptococcal pharyngitis should lead to that conclusion.
Other symptoms of glomerulonephritis include white blood cell casts, hematuria, and proteinuria. But for this question, you have to hone in on the glomerulonephritis.
Other findings in the urine sediment include granular casts. Dysmorphic red blood cells are strongly associated with glomerulonephritis and proteinuria. This is clinically manifested by a slow and progressive rise in serum creatinine and fluid hypertension, peripheral or periorbital edema, and sometimes, hypercoagulability.
Rhabdomyolysis may come to mind but it wasn't really an option among the choices. This could happen on the boards.
There might be systemic manifestations of some underlying disease process associated with glomerulonephritis. There's a group of immunologically triggered disorders that result primarily or characterized by glomerular inflammation. It can also manifest the proliferation of glomerular tissues that damage that basement membrane, mesangium, or the capillary endothelium.
Glomerulonephritis is associated with hypervolemia. In this case, you have the proteinuria. But with the edema, you should immediately be able to figure out that it wasn't associated with hypovolemia. The patient had pedal edema and periorbital edema.
It is also important to mention that there are three primary mechanisms of glomerular inflammation. And what distinguishes a nephrotic syndrome from glomerulonephritis is the inflammation as a mechanism of damaging the glomerular apparatus.
This might come in the boards that the mechanisms are either immune complex deposition as in this case. Anti-glomerular basement disease is associated with Wegener's granulomatosis, eosinophilic granulomatosis with polyangiitis, or microscopic polyangiitis.
The other mechanism is the antineutrophil cytoplasmic autoantibody (ANCA) or small vessel vasculitis. It causes damage to the glomerular filtration barrier. This...