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Background {#Sec1} ========== Amyloidosis is a group of disorders caused by protein misfolding and aggregation. Systemic amyloidosis is a consequence of circulating amyloidogenic protein monomers which deposit in various tissues with variable affinities, causing tissue damage and multi-organ dysfunction. The term amyloid is a misnomer based on Rudolf Virchow's mistakenly identifying the material as starch (Amylin) \[[@CR1]\]. More than 40 different proteins have been identified as a precursor for amyloid formation in humans \[[@CR2]\]. The most common forms of systemic amyloid are AL amyloid seen in plasma cell dyscrasias, AA amyloid associated with inflammatory conditions, and TTR amyloidosis due to either familial gene mutation or wild type protein, formerly called senile amyloidosis. The clinical picture and prognosis of amyloidosis is dependent on organ(s) affected and whether organ dysfunction can be identified by symptoms or quantified by functional testing, particularly heart, kidney, and nervous system which are frequently involved and trigger testing. Cardiac involvement is manifest in approximately one-third to one-half of all AL patients at the time of diagnosis \[[@CR3]\]. The predominant presenting symptom is rapidly progressive heart failure with preserved ejection fraction. Unfortunately, symptoms of cardiac decompensation are also a major risk factor for mortality. Kyle et al. showed that in 168 patients with systemic amyloidosis, those who presented with congestive heart failure had a median survival of 4 months \[[@CR4]\]. Renal amyloidosis is frequently, but not necessarily always, associated with high grade proteinuria. The trigger for amyloid workup is usually nephrotic syndrome and/or decline of renal function. Renal amyloidosis is not as rare as it was once thought to be. Retrospective analysis of 17 years of renal biopsies in the Czech Republic revealed that 43% of cases of nephrotic syndrome above the age of 60 were due to amyloidosis \[[@CR5]\]. Neuropathy is another significant manifestation of neuron-avid monomers, which can be devastating leading to peripheral and/or autonomic neuropathies with crippling manifestations \[[@CR6], [@CR7]\]. The frequently observed rapid functional recovery of kidney and heart with therapies that limit or abolish monomer production is often attributed to direct monomer and/or oligomer toxicity \[[@CR8], [@CR9]\]. But, it also underscores the imperative of establishing the diagnosis of amyloid as early as possible so that effective therapy can be instituted. Unfortunately, the diagnosis of amyloid in tissue sections is challenging. Identification of fibrils by electron microscopy (EM) is highly specific but because of the patchy nature of the disease, and the magnification level of EM, the sensitivity is very poor a region of interest can be identified using another method. Thioflavin-T is very sensitive \[[@CR10], [@CR11]\] but its specificity is not trusted by some experts. Interpretation of Thioflavin-T staining is also plagued by its tendency to bleach, as well as the subjective assessment of intensity based on comparison to a very strong positive control. Congo red, despite having lower sensitivity, is the standard agent used to identify amyloid in tissues. While the apple-green birefringence seen under crossed polarized light is specific for amyloid material, staining with Congo red is technically difficult resulting in