Dolipska, Joanna

Krzanowska, Katarzyna

Krzanowski, Marcin

Kuźniewski, Marek

Jagiellonian Univeristy Repository

Joanna DOLIPSKAMarcin KRZANOWSKIKatarzyna KRZANOWSKAMarek KUŻNIEWSK1Acute kidney injury caused by rhabdomiolysis secondary to influenza (AH1N1) infectionDepartment of Nephrology, Jagiellonian University Medical College, Krakow, Poland Head: Prof. Marek Kuzniewski, MD, PhDAdditional key words: acute kidney injuryhigh cut-off dialyzerslight chain deposition disease multiple myelomaDodatkowe słowa kluczowe: ostre uszkodzenie nerek dializatory typu high cut-off choroba złogów łańcucha lekkiego szpiczak mnogiIntroductionRhabdomyolysis, destruction of skele­tal muscles is one of a common cause of AKI. It can be provoked by large amount of causes. Most common is crush syndro­me, but also drug, toxins and infections can lead to muscles damage [1], As a re­sult of muscle damage, large amount of potential toxic intracellular content are released. Among them, myoglobin take an important part in pathophysiology of AKI. Excess myoglobin may damage kid­ney in three main ways: vasoconstriction, formation of intratubular casts and the di­rect toxicity [1]. Acute kidney injury (AKI) occurs in 17-35% of adult patients with rhabdomyolysis and together with DIC are the most severe complications of rhabdo­myolysis [1]. Case presentationWe present a case of a 51-year-old previously healthy white male who pre­sented with weakness and anuria. Tree days prior to admission felt musculo- sceletal pain, cough and high fever. Two days was treated ambulatory with levo- floxaxin and anty-inflammatory drugs. Negated another drugs or toxins intake, mushroom intoxication, injury, intense physical work. Lab results reveled normal morpholo­gy, elevated C reactive protein (CRP) 199 mg/l [N <5 mg/IJ), high levels of creatini­ne 556 pmol/l [N 62-106 pmol/l], eGFR 10 ml/min/1, 73m2 MDRD [N >90 ml/mi- n/1. 73m2 MDRD], urea 23 mmol/l [N 2. 76- 8. 07 mmol/l], hyperkaliemia - 6. 8 mmol/l, [N 3. 5-5. 1 mmol/l]), hyponatremia - 129 mmol/l, [N 136-145 mmol/l], hypocalca­emia - 1. 35 mmol/l [N 2. 15-2. 55 mmol/l], hyperphosphatemia - 3 mmol/l [N 0. 81- 1. 45 mmol/l] compensated metabolic aci­dosis (pH 7. 35, bicarbonate 15 mmol/l [N pH 7. 36-7. 42, bicarbonate 22-26 mmol/l]), elevated transaminase - aspartate trans­aminase (AST) 2392 U/L [5-40 U/l], ala­nine transaminase (ALT) 524 U/L [N 5-41 U/l) with extremely high lactate dehydro­genase (LDH) 16416 U/l [N 135-225 U/l] and creatinine kinase (CK) 486180 U/l [N 20-200 U/l]. He was treated with intrave-Conflict of interest not declaredReceived: 11. 08. 2019Accepted: 31. 08. 2019Address for correspondence: Joanna Dolipska, Klinika Nefrologii Uniwersytet Jagielloński, Collegium Medicum, ul. Kopernika 15c 3-332 Kraków, Poland phone: +48 696 033 774 e-mail: dolipska@gmail. com498Figure 1Bedside chest X-ray, dialysis catheter in right atrium. Przyłóżkowe zdjęcie rig, końcówka cewnika dializacyjnego w prawym przedsionku. J. Dolipska et al. Figure 2Computer tomography of the abdomen. Tomografia komputerowa jamy brzusznej. Figure 3Computer tomography, simple cysts in both kidneys - the largest in the upper pole of the left kidney. Tomografia komputerowa, torbiele proste w obu nerkach - największa w górnym biegunie lewej nerki. nous fluids, and underwent intermittent day-by-day hemodialysis. Microbiological and molecular dia­gnosis of infections confirmed influenza (AH1N1) infection (blood and urine culture were negative, HIV, HBV, HCV, CMV, EBV were negative). Oseltamivir was incorpora­ted to treatment. Chest x-ray showed no abnormalities (Fig. 1). Computer tomography of abdo­men and pelvis was performed - it showed normal-sized kidneys (Fig. 2) with simple cysts (Fig. 3, arrows) with lack of contrast excretion. After a 26-day period of anuria, spon­taneous diuresis appeared. We stopped renal replacement therapy on day 29 and observed spontaneous decline in creatini­ne and urea (on discharge: creatinine 192 pmol/l, eGFR 34 ml/min/1. 73m2 MDRD, urea 4. 7 mmol/l, CK 140 U/l with no elec­trolyte abnormalities, diuresis 2500 ml/ day). Hospitalization was complicated by Clostridium difficile infection. DiscussionInfluenza is a common seasonal in­fection on autumn-to-spring period. Can be complicated by pneumonia [2-4], car­diac [5, 6] and central nervous system involvement [7-11]. One of a potentially life-threatening complication is rhab­domyolysis, and it should be taken into consideration in patients with AKI and sings of infection [12-15]. The treatment of patient with rhabdomyolysis due to in­fluenza is the same like in other cause of rhabdomyolisis (fluid resuscitation, urinary alkalization, correction of electro­lyte, acid-base, and metabolic abnormali­ties). For now we haven't got evidence that antiviral treatment improve the out­come of patients with influenza-provoked rhabdomyolisis. We need further investi­gation in this area. References1. Torres PA, Helmstetter JA, Kaye AM, Kaye AD: Rhabdomyolysis: Pathogenesis, Diagnosis, and Treatment. Ochsner J. 2015; 15: 58-69. 2. Chertow DS, Memoli MJ: Bacterial coinfection in Influenza: A grand rounds review. JAMA. 2013; 309: 275-282. 3. Chung DR, Huh K: Novel pandemic influenza A (H1N1) and community-associated methicillin-re­sistant Staphylococcus aureus pneumonia. Expert Rev Anti Infect Ther. 2015; 13: 197-207. 4. Murray RJ, Robinson JO, White JN, Hughes F, Coombs GW. et al: Community-acquired pneumonia due to pandemic A(H1 N1 )2009 in­fluenzavirus and methicillin resistant Staphylo­coccus aureus co-infection. PLOS ONE. 2010; 5: e8705. 5. Kwong JC, Schwartz KL, Campitelli MA, Chung H, Crowcroft NS. et al: Acute myocardial infarc­tion after laboratory-confirmed influenza infection. N Engl J Med. 2018; 378: 345-353. 6. Mamas MA, Fraser D, Neyses L: Cardiovascular manifestations associated with influenza virus in­fection. Int J Cardiol. 2008; 130: 304-309. 7. Goenka A, Michael BD, Ledger E, Hart I J, Ab- soud M. et al: Neurological manifestations of influenza infection in children and adults: Results of a National British Surveillance Study. Clin Infect Dis. 2014; 58: 775-784. Przegląd Lekarski 2019 / 76 / 9 4998. Steininger C, Popow-Kraupp T, Laferl H, Seiser A, Gódl I. et al: Acute Encephalopathy associated with influenza A virus infection. Clin Infect Dis. 2003; 36: 567-574. 9. Fujimoto S, Kobayashi M, Uemura O, Iwasa M, Ando T. et al: PCR on cerebrospinal fluid to show influenza-associated acute encephalopathy or en­cephalitis. The Lancet. 1998; 352: 873-875. 10. Salonen O, Koshkiniemi M, Saari A, Myllyla V, Pyhala R. et al: Myelitis associated with influenza Avirus infection. J Neurovirol. 1997; 3: 83-85. 11. Okuno H, Yahata Y, Tanaka-Taya K, Arai S, Sa- toh H. et al: Characteristics and outcomes of in­fluenza-associated encephalopathy cases among children and adults in Japan, 2010-2015. Clin In­fect Dis. 2018; 66: 1831-1837. 12. Fadila MF, Wool KJ: Rhabdomyolysis secondary to ilnfluenza A infection: A case report and review of the literature. North Am J Med Sci. 2015; 7: 122- 124. 13. Ibrahim AM, Manthri S, Soriano PK, Bhatti V, Mamillapalli CK: Rhabdomyolysis associated with influenza A virus infection. Cureus. 2018; 10: e2786. 14. Odio CD, Mandimika C, Jabuonski TA, Mali- nis M: Severe influenza A(H1N1) virus infeclion complicated by myositis, refractory rhabdomyoly­sis, and compartment syndrome. Case Rep Med. 2019; 2019: 1540761. 15. Runnstrom M, Ebied AM, Khoury AP, Reddy R: Influenza-induced rhabdomyolysis. BMJ Case Rep CP. 2018; 11: e226610. r». «1

Acute kidney injury caused by rhabdomiolysis secondary to influenza (AH1N1) infection

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