Glomerular injury and resultant nephrotic syndrome is the most likely explanation for this patients clinical deterioration. Hypoalbuminemia results in reduced serum oncotic pressure and subsequent fluid shifts into the extravascular space with associated orthostatic symptoms. Right-sided cardiac failure, if severe enough to cause this degree of edema, would likely be associated with jugular venous distention. A 24-hour urine collection to assess the degree of proteinuria and an echocardiogram should provide enough diagnostic information to distinguish between renal and cardiac causes of this patients symptoms. Loop diuretics and midodrine can be used cautiously to treat symptoms related to edema and orthostatic hypotension, respectively. Because each of these medications has the potential to exacerbate symptoms being treated with the other drug, careful clinical monitoring is essential. Hepatic enlargement is likely to be caused by amyloid deposition rather than vascular congestion. Hepatic amyloidosis rarely causes portal hypertension, as patients typically succumb to other complications of their disease prior to reaching that point. Splenic amyloidosis typically results in splenomegaly but rarely capsular rupture (which would not explain the lower extremity edema). Amyloid deposition in the vasculature typically results in minor bleeding and bruising rather than thrombotic complications.
- Renal amyloid deposition with resultant nephrotic syndrome.
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Seminars in Medical Practice
Hospital Physician Board Review Manuals
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