We report the case of a 64-year-old man with no history of interest, who consulted for weight loss of 17 kg, asthenia, anorexia and anemia.
The patient was managed conservatively and showed nonspecific inflammatory changes in the colonic mucosa. A gastroscopy showed gastric neoplasia and antral gastropathy, with biopsy.
Histology of gastric biopsy confirmed a solid proliferation pattern suggestive of GIST, and immunohistochemistry was positive for CD117.
AA amyloid deposits were observed in biopsies of gastric mucosa, tumor and colonic mucosa.
Later, he began with edema in the lower limbs and diarrhea.
Laboratory tests revealed hemoglobin 8.7 g/dl, hematocrit 28%, mean corpuscular volume 75, serum creatinine 1.3 mg/dl; total proteins 5.9 g/dl; albumin 1.36 g/dl; cholesterol 96 mg/dl.
Proteinuria was 5.1 g/day and sediment with 4-6 seizures/field.
Given the poor situation of the patient, renal biopsy was not performed and it was assumed that the amyloidosis previously observed in gastrointestinal biopsies was responsible for nephrotic syndrome and diarrhea.
Cardiac amyloidosis was ruled out by echocardiography.
Treatment was initiated with a selective tyrosine kinase inhibitor of cKit, Imatinib (Glivec®), 100 mg daily.
Fifteen months after diagnosis, surgical excision was decided after a decrease in tumor mass was observed in the positron emission tomography/computed tomography study.
Pathology confirmed the involvement of the stomach and splenic angle of the resected colon.
In this sense, it was classified as a high-risk GIST (> 5 cm in size, > 5 mitosis per high-power field)2.
Renal function continued to deteriorate, so he finally entered the regular hemodialysis program, one year and seven months after the finding of GIST, with the diagnosis of chronic renal failure secondary to AA amyloidosis.
