View of the Hemolytic Anemia Can Cause AKI by Promoting Reported Symptoms

Clinical Images in Nephrology and Dialysis

AKI in a Patient with Hemolytic Anemia

Jose´ Antonio Tesser Poloni 1,2 and Fernanda Hermes Hickmann3 KIDNEY360 1: 72–73, 2020. doi: https://doi.org/10.34067/KID.0000082019

Clinical Images in Nephrology and Dialysis erythrocyte destruction leads to excessive release of Case Answer hemoglobin/heme into the circulation, with subsequent A 15-year-old woman presented to a hospital with filtration of some of this protein into the renal tubules. malaise and visible pallor that had lasted for 2 weeks. The heme group present in the molecules of hemoglobin The patient was treated with ferrous iron and dis- causes cell injury and death. Cell death by regulated charged home. Following discharge, the patient’s necrosis causes tremendous tissue damage in a wide symptoms did not improve and she subsequently variety of diseases, including myocardial infarction, developed dark urine. As a result, the family decided stroke, sepsis, and ischemia-reperfusion injury upon solid to seek care at a larger center. When the patient arrived organ transplantation (3). to our center, urinalysis was obtained in view of the Hemolytic anemia can cause AKI by promoting reported symptoms. Dipstick urinalysis revealed pH heme pigment–related cellular injury and cell death. 7.0, specific gravity 1.015, protein 31, hemoglobin 31, Basic tests such as urinalysis and complete blood cell urobilinogen excess, and bilirubin 11. Examination of count supplemented with urine-sediment examination the spun urine sediment revealed numerous renal can lead to the correct diagnosis and treatment. tubular epithelial cells (RTECs) (.50/high power field), red blood cells (1–2/high power field), granular Teaching Points casts (5–6/lower power field) and RTEC casts (1–2/lower c Dark urine can be a sign of urinary pigment due to power field). On admission, serum chemistry revealed a rhabdomyolysis, hyperbilirubinuria, or hemolytic ane- serum creatinine of 1.31 mg/dl and the complete blood mia (as described in this case). count was notable for hemoglobin 7.4g/dl, hematocrit c These clinical conditions can lead to acute tubular 25%, and platelets 252,000/ml. Review of the patient’s injury due to the toxicity of myoglobin (rhabdo- medication list uncovered recent use of cephalexin myolysis), direct bilirubin (hyperbilirubinuria) and for the past 4 weeks to treat a finger infection. The hemoglobin (hemolytic anemia) or their metabolites spun urine sediment was prepared and stained with to tubular epithelial cells. May–Grünwald–Giemsa stain. Numerous iron deposits c Urine sediment will provide the clue to suspect acute (hemosiderin granules) were clearly seen within the tubular injury with increased numbers of RTECs, casts (Figure 1, A and C) and RTECs (Figure 1B), which pigmented granular casts, and RTEC casts. was diagnostic of heme pigment–related kidney injury. c Acute tubular injury that develops in patients with Due to concern for drug-induced hemolytic anemia hemolytic anemia can be mediated by iron deposits with pigment-related AKI, prednisone 40 mg (morning) within RTECs. and 20 mg (afternoon) was prescribed. Over the next 12 days, the patient’s symptoms improved and the serum creatinine returned to baseline (0.69 mg/dl). Author Contributions In this case, hemolytic anemia was caused by cepha- J. Poloni wrote the original draft; F. Hickmann reviewed lexin. This drug has been described to cause both hemo- and edited the writing; and J. Poloni and F. Hickmann con- lytic anemia and acute tubular injury (1,2). Intravascular ceptualized the study.

Figure 1. | Urine sediment. Original magnification, 3400. (A) Urinary cast with iron deposits within the matrix (unstained, bright- field microscopy). (B) Renal tubular epithelial cell with iron deposits (May–Gru¨nwald–Giemsa stain, bright-field microscopy). (C) Urinary cast with iron deposits within the matrix (May–Gru¨nwald–Giemsa stain, bright-field microscopy).

1Health School, Universidade do Vale do Rio dos Sinos (UNISINOS), Sa˜o Leopoldo, Brazil; 2Controllab, Rio de Janeiro, Brazil; and 3Carlos Franco Voegeli Clinical Analysis Laboratory, Santa Casa de Miserico´rdia de Porto Alegre, Porto Alegre, Brazil

Correspondence: Dr. Jose´ A.T. Poloni, Health School, Universidade do Vale do Rio dos Sinos (UNISINOS), Sa˜o Leopoldo, Brazil 93022-750. Email: [email protected]

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