Diagnostic Evaluation And Assessment Of Anemia in A Patient With Chronic Kidney Disease And Gastrointestinal Angioectasias Undergoing Hemodialysis

Abstract Anemia in patients with chronic kidney disease may have underlying causes that require a broad approach. Here, we present a clinical case of anemia in a patient with chronic kidney disease and gastrointestinal angioectasias undergoing hemodialysis. 

KEYWORDS anemia, angioectasias, blood transfusions, chronic kidney disease, erythropoiesis-stimulating agents, hemodialysis

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1 | INTRODUCTION 

Management of anemia in chronic kidney disease (CKD) patients in hemodialysis must be tailored. Keeping hemoglobin levels within adequate ranges depends on nutritional, inflammatory, mechanical, and immunological factors unique for each patient and on their response to erythropoiesis-stimulating agents. Hence, each patient requires a personalized approach and treatment.

2 | CASE PRESENTATION 

This is a 68-year-old male patient with a long history of type 2 diabetes mellitus (20 years) treated with low-dose intermediate insulin, hypertension controlled with calcium channel blockers and angiotensin-converting enzyme inhibitors (ACE inhibitors), pulmonary emphysema secondary to smoking, and stage 5 chronic kidney disease, receiving hemodialysis three times per week since 2017. In February 2018, he received an arteriovenous dialysis graft for vascular access. He was hospitalized in June 2018 to treat an ulcer in his left foot associated with his underlying diabetes, which required debridement and specialized wound care, with good evolution and discharged after 10 days with an oral antiplatelet agent.

In August 2018, he presents a sudden episode of pallor and weakness at home, and he is taken to the Emergency Department, where he is hospitalized with a diagnosis of lower gastrointestinal (GI) tract bleeding, with a digital rectal examination revealing hemorrhoids and blood-stained feces. His first laboratory results showed hemoglobin at 4.8  g/ dl (2.98mmol/L) and a mean corpuscular volume (MCV) of 95fl. His hemoglobin 1 month prior was 12.3  g/dl (7.63mmol/L), so he received 3 units of packed red blood cells (PRBC), and a gastroenterologist is brought in for a consultation. During his hospitalization, he remained stable, without new bleeding episodes and he was discharged with hemoglobin at 8.9 g/dl (5.52mmol/L), with an appointment for a colonoscopy and antiplatelet suspension. He continued his hemodialysis as an outpatient without heparin, increasing his erythropoietin (EPO) beta to 10,000 intravenous (IV) Units (U) (400U/kg·week) every hemodialysis session.

In September 2018, 2weeks after he was discharged, he was taken to the Emergency Department with a new episode of haematochezia and hemoglobin at 7.0  g/dl (4.34mmol/L), MCV at 92 fl, and a red blood cell distribution width (RDW) below 2. An urgent colonoscopy was performed, finding two angioectasias (angiodysplasias) in the ascending colon, without any other findings in the mucosa. Unfortunately, angioectasias were left untreated because, at the time of colonoscopy, thermo-coagulation with either argon plasma or heat probe options was not available at the hospital. He received one unit of PRBC and was scheduled for future thermo-coagulation of the angioectasias once argon plasma was functional.

His hemoglobin levels were monitored monthly, as well as platelets and coagulation studies remain normal. The patient received PRBCs as needed until thermo-coagulation could be performed in April 2019. Colonoscopy was performed, and four vascular malformations, compatible with angioectasias, were observed in the ascending colon (Figure 1) and treated with argon plasma thermo-coagulation, without complications.

He continued with IV Iron supplements during hemodialysis and Epo, though beta Epo had to be changed to alpha Epo at an equivalent dose, because of unavailability at that time

During the follow-up of his anemia, an upper endoscopy was done in August 2019 that showed only gastric erosions. Since he remained with hemoglobin levels below 10 g/dl, and had episodes of scant but active bleeding in the caecum, a video capsule endoscopy was ordered. In September 2019, he underwent another colonoscopy for follow-up, but no evidence of angioectasias was found; only a single isolated diverticulum in the ascending colon with the rest of the mucosa was reported as normal. Hematology was then consulted for assessment since there was no evidence of major gastrointestinal bleeding and the patient persisted with anemia. Bone marrow and peripheral blood analyses were conducted to complete the diagnostic assessment.

Figure 2 presents a graphical depiction of the case timeline and the transfusions and endoscopies conducted and the hemoglobin response.

FIGURE 1 Angiodysplasia found in the mucosa of the ascending colon, during the April 2019 colonoscopy

3 | INVESTIGATIONS

We collected as much information related to the multiple causes of anemia to work through the differential diagnosis. Several laboratory studies are used in the evaluation in hemodialysis patients to adjust the use of hematopoietic agents. The patient's hematology work up included a bone marrow aspiration that showed normocellular content, medullar hyperplasia, and no evidence of parvovirus B19. Iron kinetics showed normal low iron levels (59mcg/ dl), low saturation (18%), normal folic acid and B12 levels. Parathyroid hormone (PTH) values remain at 385pg/ mL average and protein electrophoresis ruled out multiple myeloma. With the aim of identifying lesions in the gastrointestinal tract, the patient also underwent various endoscopic procedures (Figure 2).

To define the causes of persistent anemia in this patient, it is key to keep the target hemoglobin values proposed in treatment guidelines.1 In this particular case, it was difficult to raise hemoglobin values above 9.0  g/ dl (5.59mmol/L) with transfusions only (Figure 2), since his blood type was O negative and it was difficult to find compatible units to transfuse. Our hospital has only one gastroenterologist, which also limits the possibility to schedule follow-up appointments and procedures in a short period of time.

4 | DIFFERENTIAL DIAGNOSIS 

Anemia in CKD hemodialysis patients is multifactorial, and the variability in the values of hemoglobin depends on blood losses (e.g., gastrointestinal bleeding or coagulation in the hemodialysis system), infections (e.g., catheter infections or diabetic foot), chronic disease inflammatory processes (e.g., diabetic foot, hyperparathyroidism, malignancies), nutritional deficit (e.g., decreased levels of iron and cofactors, such as B12 vitamin and folic acid), metabolic causes (e.g., hypo- or hyperthyroidism), certain drugs (e.g., angiotensin-converting enzyme inhibitors), and frequent changes in plasma volume due to accumulation of interdialytic liquids.2

FIGURE 2 Timeline of the case, with transfusions ( ) and upper ( ) and lower ( ) endoscopies conducted and the hemoglobin response

Active gastrointestinal bleeding must be ruled out: Hemodialysis patients may present gastrointestinal anemia, with lesions in the gastric or duodenal mucosa and between 4% and 13% may present with angioectasias.3 In about 45% of the cases, there may be a co-infection with Helicobacter pylori,4 and as a predisposing factor to bleeding, with a mucosal lesion after exposure to anticoagulants three times per week.

Among hematological causes of anemia, multiple myeloma must be ruled out, looking for abnormal proliferation of plasma cells, with plasmocytes in the bone marrow and production of monoclonal proteins.5 Pure secondary red blood cell aplasia presents as normocytic, normochromic, sudden, progressive, and severe anemia mediated by antibodies. It is characterized by the complete absence of the red blood cell precursors in the bone marrow and may be due to malignancies, immune or viral causes, or secondary to certain drugs, such as Epo.6 In some patients, resistance to Epo may be present and causes, such as hyperparathyroidism, nutritional deficits, infections, and drug–drug interactions, must be explored in order to correct it.1

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