Heart, Lung, Kidney Interaction Following Urosepsis and Acute Viral Interstitial Pneumonia
-
Fatemeh Afra
,
Mojtaba Mojtahedzadeh
,
Leila Sadat Hosseini
,
Khashayar Shahverdi
,
Maryam Albaji
,
Atabak Najafi
,
Seyed Hamidreza Sharifnia
,
Parisa Kianpour
,
Amirmohammad Shabani
,
Amirmahdi Mojtahedzadeh
Abstract
Organ-organ interactions play a crucial role in the progression and severity of critical illnesses such as sepsis. Dysregulated interaction among the heart, lungs, and kidneys (mediated by inflammatory, neurohormonal, and metabolic processes) can exacerbate organ dysfunction, contributing to the development of multi-organ failure. We report the case of a 70-year-old woman with significant comorbidities, including type 2 diabetes mellitus (DM-II), chronic kidney disease (CKD), heart failure (HF), nephrolithiasis, and morbid obesity, who was admitted with severe urosepsis caused by extended-spectrum β-lactamase (ESBL)-producing Escherichia coli. Her clinical course was further complicated by acute viral interstitial pneumonia progressing to ARDS. During the ICU admission, the patient experienced a complicated clinical course characterized by mixed septic and cardiogenic shock, right ventricular dysfunction, hypoxemic respiratory failure, and acute-on-chronic kidney injury. Treatment included lung-protective mechanical ventilation, hemodynamic support with inodilator therapy, insulin-dextrose-potassium administration, adjunctive therapies targeting inflammation and endothelial dysfunction, and judicious fluid management. Over the course of hospitalization, cardiac, respiratory, and renal function progressively improved, allowing discharge in a stable condition. This case highlights the clinically important role of organ-organ cross-talk in the development of multi-organ dysfunction during severe sepsis complicated by viral pneumonia. Hemodynamic instability, inflammation-related capillary leakage, and increased pressure within encapsulated organs may interact to perpetuate a cycle of organ injury, particularly in patients with underlying conditions such as heart failure, CKD, or obesity. Patient-specific management strategies may support organ recovery and improve clinical outcomes by disrupting this cycle.
[1] Joannidis M, Forni LG, Klein SJ, Honore PM, Kashani K, Ostermann M, et al. Lung-kidney interactions in critically ill patients: consensus report of the Acute Disease Quality Initiative (ADQI) 21 Workgroup. Intensive Care Med. 2020; 46(4):654-72.
[2] Husain-Syed F, McCullough PA, Birk HW, Renker M, Brocca A, Seeger W, et al. Cardio-Pulmonary-Renal Interactions: A Multidisciplinary Approach. J Am Coll Cardiol. 2015; 65(22):2433-48.
[3] Battaglini D, Rocco PRM. Editorial: Crosstalk between lung and brain, heart, kidney and vascular system in critical illness. Front Physiol. 2024; 15:1516682.
[4] De Pasquale CG, Arnolda LF, Doyle IR, Grant RL, Aylward PE, Bersten AD. Prolonged alveolocapillary barrier damage after acute cardiogenic pulmonary edema. Crit Care Med. 2003; 31(4):1060-7.
[5] Pappas LK, Giannopoulos G, Loukides S, Gavrielatos G, Athanasopoulou E, Alexanian IP, et al. Exhaled breath condensate in acute and chronic heart failure: new insights into the role of lung injury and barrier dysfunction. Am J Respir Crit Care Med. 2014; 190(3):342-5.
[6] Wagenlehner FM, Lichtenstern C, Rolfes C, Mayer K, Uhle F, Weidner W, et al. Diagnosis and management for urosepsis. Int J Urol. 2013; 20(10):963-70.
[7] Rosser CJ, Bare RL, Meredith JW. Urinary tract infections in the critically ill patient with a urinary catheter. Am J Surg. 1999; 177(4):287-90.
[8] Albaramki JH, Abdelghani T, Dalaeen A, Khdair Ahmad F, Alassaf A, Odeh R, et al. Urinary tract infection caused by extended-spectrum β-lactamase-producing bacteria: Risk factors and antibiotic resistance. Pediatr Int. 2019; 61(11):1127-32.
[9] Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet. 1967; 2(7511):319-23.
[10] Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012; 307(23):2526-33.
[11] Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, et al. Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination. J Crit Care. 1994; 9(1):72-81.
[12] Torres A, Serra-Batlles J, Ferrer A, Jiménez P, Celis R, Cobo E, et al. Severe community-acquired pneumonia. Epidemiology and prognostic factors. Am Rev Respir Dis. 1991; 144(2):312-8.
[13] Choi SH, Hong SB, Ko GB, Lee Y, Park HJ, Park SY, et al. Viral infection in patients with severe pneumonia requiring intensive care unit admission. Am J Respir Crit Care Med. 2012; 186(4):325-32.
[14] Nguyen C, Kaku S, Tutera D, Kuschner WG, Barr J. Viral Respiratory Infections of Adults in the Intensive Care Unit. J Intensive Care Med. 2016; 31(7):427-41.
[15] Borges A, Bento L. Organ crosstalk and dysfunction in sepsis. Ann Intensive Care. 2024; 14(1):147.
[16] Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016; 315(8):801-10.
[17] de Zoete MR, Palm NW, Zhu S, Flavell RA. Inflammasomes. Cold Spring Harb Perspect Biol. 2014; 6(12):a016287.
[18] Rocha NN, Silva PL, Battaglini D, Rocco PRM. Heart-lung crosstalk in acute respiratory distress syndrome. Front Physiol. 2024; 15:1478514.
[19] Balkrishna A, Sinha S, Kumar A, Arya V, Gautam AK, Valis M, et al. Sepsis-mediated renal dysfunction: Pathophysiology, biomarkers and role of phytoconstituents in its management. Biomed Pharmacother. 2023; 165:115183.
[20] Archer SL, Sharp WW, Weir EK. Differentiating COVID-19 Pneumonia From Acute Respiratory Distress Syndrome and High Altitude Pulmonary Edema: Therapeutic Implications. Circulation. 2020; 142(2):101-4.
[21] Gower WA, Nogee LM. Surfactant dysfunction. Paediatr Respir Rev. 2011; 12(4):223-9.
[22] Taenaka H, Matthay MA. Mechanisms of impaired alveolar fluid clearance. Anat Rec (Hoboken). 2025; 308(4):1026-39.
[23] Corrin B. Diffuse Alveolar Damage. In: Evans TW, Haslett C, editors. ARDS Acute Respiratory Distress in Adults. Boston, MA: Springer US; 1996. p. 37-46.
[24] Archer SL, Dunham-Snary KJ, Bentley R, Alizadeh E, Weir EK. Hypoxic Pulmonary Vasoconstriction: An Important Component of the Homeostatic Oxygen Sensing System. Physiol Res. 2024; 73(S2):S493-S510.
[25] Johnson DW, Roy TK, Secomb TW. Analysis of flow resistance in the pulmonary arterial circulation: implications for hypoxic pulmonary vasoconstriction. J Appl Physiol (1985). 2021; 131(4):1211-8.
[26] Dunham-Snary KJ, Wu D, Sykes EA, Thakrar A, Parlow LRG, Mewburn JD, et al. Hypoxic Pulmonary Vasoconstriction: From Molecular Mechanisms to Medicine. Chest. 2017; 151(1):181-92.
[27] Schumacker PT. Lung cell hypoxia: role of mitochondrial reactive oxygen species signaling in triggering responses. Proc Am Thorac Soc. 2011; 8(6):477-84.
[28] Mahmood SS, Pinsky MR. Heart-lung interactions during mechanical ventilation: the basics. Ann Transl Med. 2018; 6(18):349.
[29] Corp A, Thomas C, Adlam M. The cardiovascular effects of positive pressure ventilation. BJA Educ. 2021; 21(6):202-9.
[30] Kakihana Y, Ito T, Nakahara M, Yamaguchi K, Yasuda T. Sepsis-induced myocardial dysfunction: pathophysiology and management. J Intensive Care. 2016; 4:22.
[31] Aissaoui N, Boissier F, Chew M, Singer M, Vignon P. Sepsis-induced cardiomyopathy. Eur Heart J. 2025; 46(34):3339-53.
[32] Aissaoui N. Sepsis-induced cardiomyopathy: Time to bring the heart back to the forefront. Arch Cardiovasc Dis. 2025; 118(12):634-5.
[33] Messmer AS, Moser M, Zuercher P, Schefold JC, Müller M, Pfortmueller CA. Fluid Overload Phenotypes in Critical Illness-A Machine Learning Approach. J Clin Med. 2022; 11(2):336.
[34] Messmer AS, Dill T, Müller M, Pfortmueller CA. Active fluid de-resuscitation in critically ill patients with septic shock: A systematic review and meta-analysis. Eur J Intern Med. 2023; 109:89-96.
[35] Hippensteel JA, Uchimido R, Tyler PD, Burke RC, Han X, Zhang F, et al. Intravenous fluid resuscitation is associated with septic endothelial glycocalyx degradation. Crit Care. 2019; 23(1):259.
[36] Pfortmueller CA, Dabrowski W, Wise R, van Regenmortel N, Malbrain MLNG. Fluid accumulation syndrome in sepsis and septic shock: pathophysiology, relevance and treatment-a comprehensive review. Ann Intensive Care. 2024; 14(1):115.
[37] Harsoor VR, Reddy K, Anjum N. Restrictive v/s liberal fluid strategies in management of sepsis. Eur J Cardiovasc Med. 2024; 14:912-6.
[38] Lintz VC, Vieira RA, Carioca FL, Ferraz IS, Silva HM, Ventura AMC, et al. Fluid accumulation in critically ill children: a systematic review and meta-analysis. EClinicalMedicine. 2024; 74:102714.
[39] Kelm DJ, Perrin JT, Cartin-Ceba R, Gajic O, Schenck L, Kennedy CC. Fluid overload in patients with severe sepsis and septic shock treated with early goal-directed therapy is associated with increased acute need for fluid-related medical interventions and hospital death. Shock. 2015; 43(1):68-73.
[40] Verbrugge FH, Dupont M, Steels P, Grieten L, Malbrain M, Tang WH, et al. Abdominal contributions to cardiorenal dysfunction in congestive heart failure. J Am Coll Cardiol. 2013; 62(6):485-95.
[41] Chelazzi C, Villa G, De Gaudio AR. Cardiorenal syndromes and sepsis. Int J Nephrol. 2011; 2011:652967.
[42] Zhou ZK, Yu MM, Shou ST, Chai YF, Liu YC. Interaction between gut-heart axis in sepsis-induced cardiomyopathy. Pharmacol Res. 2025; 217:107806.
[43] Pan S, Lv Z, Wang R, Shu H, Yuan S, Yu Y, et al. Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment. Oxid Med Cell Longev. 2022; 2022:1328729.
[44] Suphatheerawatr N, Jaturapisanukul S, Prommool S, Kurathong S, Pongsittisak W. Intra-abdominal hypertension among medical septic patients associated with worsening kidney outcomes (IAH-WK study). Medicine (Baltimore). 2023; 102(4):e32807.
[45] Regueira T, Bruhn A, Hasbun P, Aguirre M, Romero C, Llanos O, et al. Intra-abdominal hypertension: incidence and association with organ dysfunction during early septic shock. J Crit Care. 2008; 23(4):461-7.
[46] Plantefeve G, Hellmann R, Pajot O, Thirion M, Bleichner G, Mentec H. Abdominal compartment syndrome and intraabdominal sepsis: two of the same kind? Acta Clin Belg. 2007; 62 Suppl 1:162-7.
[47] Manion S, Tobias JD. Abdominal compartment syndrome after sepsis in an infant with congenital heart disease. J Cardiothorac Vasc Anesth. 2006; 20(1):71-5.
[48] Grant RW, Dixit VD. Adipose tissue as an immunological organ. Obesity (Silver Spring). 2015; 23(3):512-8.
[49] Zhao P, Saltiel AR. Interaction of Adipocyte Metabolic and Immune Functions Through TBK1. Front Immunol. 2020; 11:592949.
[50] Wrba L, Halbgebauer R, Roos J, Huber-Lang M, Fischer-Posovszky P. Adipose tissue: a neglected organ in the response to severe trauma? Cell Mol Life Sci. 2022; 79(4):207.
[51] Ripa F, Pietropaolo A, Montanari E, Hameed BMZ, Gauhar V, Somani BK. Association of Kidney Stones and Recurrent UTIs: the Chicken and Egg situation. A Systematic Review of Literature. Curr Urol Rep. 2022; 23(9):165-74.
[52] Fayssoil A, Pousset F, Carlier R, Joussain C, Wahbi K, Mansencal N, et al. Recurrent urosepsis on nephrolithiasis in a patient with sarcoglycanopathy treated with dapagliflozin for heart failure. Heliyon. 2023.
[53] Karki N, Leslie SW. Struvite and Triple Phosphate Renal Calculi. 2023. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025.
[54] Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014; 10(1):37-47.
[55] Aguilar MG, AlHussen HA, Gandhi PD, Kaur P, Pothacamuri MA, Talikoti MAH, et al. Sepsis-Associated Acute Kidney Injury: Pathophysiology and Treatment Modalities. Cureus. 2024; 16(12):e75992.
[56] Muğlu H, İnan Kahraman E, Sünger E, Murt A, Bilici A, Görgülü N. Acute Kidney Injury Secondary to Abdominal Compartment Syndrome: Biomarkers, Pressure Variability, and Clinical Outcomes. Medicina (Kaunas). 2025; 61(3):383.
[57] Mirza SA, Mohammed NS, Ali ZQ, Mohamed AS. The effects of methamphetamine intoxication on acute kidney injury in Iraqi male addicts. Toxicol Rep. 2025; 14:102065.
[58] Bouglé A, Duranteau J. Pathophysiology of sepsis-induced acute kidney injury: the role of global renal blood flow and renal vascular resistance. Contrib Nephrol. 2011; 174:89-97.
[59] Nørgård MØ, Svenningsen P. Acute Kidney Injury by Ischemia/Reperfusion and Extracellular Vesicles. Int J Mol Sci. 2023; 24(20):15312.
[60] Liu C, Peng Z, Gao X, Gajic O, Dong Y, Prokop LJ, et al. Simultaneous Use of Hypertonic Saline and IV Furosemide for Fluid Overload: A Systematic Review and Meta-Analysis. Crit Care Med. 2021; 49(11):e1163-75.
[61] Zhou Y, Jin X, Lv Y, Wang P, Yang Y, Liang G, et al. Early application of airway pressure release ventilation may reduce the duration of mechanical ventilation in acute respiratory distress syndrome. Intensive Care Med. 2017; 43(11):1648-59.
[62] Carsetti A, Damiani E, Domizi R, Scorcella C, Pantanetti S, Falcetta S, et al. Airway pressure release ventilation during acute hypoxemic respiratory failure: a systematic review and meta-analysis of randomized controlled trials. Ann Intensive Care. 2019; 9(1):44.
[63] Evans L, Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med. 2021; 47(11):1181-247.
[64] Amin A, Maleki M. Positive inotropes in heart failure: a review article. Heart Asia. 2012; 4(1):16-22.
[65] Yin J, Chi Y, Liu D, Li X, Li X. Unfractionated heparin attenuated histone-induced pulmonary endothelial glycocalyx injury through Ang/Tie2 pathway. J Inflamm (Lond). 2025; 22(1):9.
[66] Allison SP, Morley CJ, Burns-Cox CJ. Insulin, glucose, and potassium in the treatment of congestive heart failure. Br Med J. 1972; 3(5828):675-8.
[67] Mousavi S, Moradi M, Khorshidahmad T, Motamedi M. Anti-Inflammatory Effects of Heparin and Its Derivatives: A Systematic Review. Adv Pharmacol Sci. 2015; 2015:507151.
[68] Shute JK, Calzetta L, Cardaci V, di Toro S, Page CP, Cazzola M. Inhaled nebulised unfractionated heparin improves lung function in moderate to very severe COPD: A pilot study. Pulm Pharmacol Ther. 2018; 48:88-96.
[69] Shute JK, Puxeddu E, Calzetta L. Therapeutic use of heparin and derivatives beyond anticoagulation in patients with bronchial asthma or COPD. Curr Opin Pharmacol. 2018; 40:39-45.
[70] von Ehr A, Steenbuck ID, Häfele C, Remmersmann F, Vico TA, Ehlert C, et al. Experimental evidence on colchicine's mode of action in human carotid artery plaques. Atherosclerosis. 2025; 406:119239.
[71] Li Y, Zhang Y, Lu J, Yin Y, Xie J, Xu B. Anti-inflammatory mechanisms and research progress of colchicine in atherosclerotic therapy. J Cell Mol Med. 2021; 25(17):8087-94.
[72] Tang Taylor L, Long C, Pandhair O. Hydroxocobalamin in Septic Shock Management - Should It Be Introduced Sooner? Am J Respir Crit Care Med. 2025; 211(Abstracts):A5790-A.
[73] Spiess BD. Vasoplegia and cardiopulmonary bypass: role of oxidation-reduction dysregulation as a mechanism and therapeutic target. Br J Anaesth. 2026; 136(1):20-3.
[74] Ge Y, Li M, Wang B, Zhang Y, Zhou X, Zhang Y, et al. Melatonin ameliorates sepsis-induced myocardial dysfunction by promoting autophagy via SIRT1-mediated TFEB deacetylation. Int Immunopharmacol. 2026; 170:116098.
[75] Xu J, Liang C, Yao S, Wang F. Melatonin Exerts Positive Effects on Sepsis Through Various Beneficial Mechanisms. Drug Des Devel Ther. 2025; 19:1333-45.
[2] Husain-Syed F, McCullough PA, Birk HW, Renker M, Brocca A, Seeger W, et al. Cardio-Pulmonary-Renal Interactions: A Multidisciplinary Approach. J Am Coll Cardiol. 2015; 65(22):2433-48.
[3] Battaglini D, Rocco PRM. Editorial: Crosstalk between lung and brain, heart, kidney and vascular system in critical illness. Front Physiol. 2024; 15:1516682.
[4] De Pasquale CG, Arnolda LF, Doyle IR, Grant RL, Aylward PE, Bersten AD. Prolonged alveolocapillary barrier damage after acute cardiogenic pulmonary edema. Crit Care Med. 2003; 31(4):1060-7.
[5] Pappas LK, Giannopoulos G, Loukides S, Gavrielatos G, Athanasopoulou E, Alexanian IP, et al. Exhaled breath condensate in acute and chronic heart failure: new insights into the role of lung injury and barrier dysfunction. Am J Respir Crit Care Med. 2014; 190(3):342-5.
[6] Wagenlehner FM, Lichtenstern C, Rolfes C, Mayer K, Uhle F, Weidner W, et al. Diagnosis and management for urosepsis. Int J Urol. 2013; 20(10):963-70.
[7] Rosser CJ, Bare RL, Meredith JW. Urinary tract infections in the critically ill patient with a urinary catheter. Am J Surg. 1999; 177(4):287-90.
[8] Albaramki JH, Abdelghani T, Dalaeen A, Khdair Ahmad F, Alassaf A, Odeh R, et al. Urinary tract infection caused by extended-spectrum β-lactamase-producing bacteria: Risk factors and antibiotic resistance. Pediatr Int. 2019; 61(11):1127-32.
[9] Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet. 1967; 2(7511):319-23.
[10] Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, et al. Acute respiratory distress syndrome: the Berlin Definition. JAMA. 2012; 307(23):2526-33.
[11] Bernard GR, Artigas A, Brigham KL, Carlet J, Falke K, Hudson L, et al. Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination. J Crit Care. 1994; 9(1):72-81.
[12] Torres A, Serra-Batlles J, Ferrer A, Jiménez P, Celis R, Cobo E, et al. Severe community-acquired pneumonia. Epidemiology and prognostic factors. Am Rev Respir Dis. 1991; 144(2):312-8.
[13] Choi SH, Hong SB, Ko GB, Lee Y, Park HJ, Park SY, et al. Viral infection in patients with severe pneumonia requiring intensive care unit admission. Am J Respir Crit Care Med. 2012; 186(4):325-32.
[14] Nguyen C, Kaku S, Tutera D, Kuschner WG, Barr J. Viral Respiratory Infections of Adults in the Intensive Care Unit. J Intensive Care Med. 2016; 31(7):427-41.
[15] Borges A, Bento L. Organ crosstalk and dysfunction in sepsis. Ann Intensive Care. 2024; 14(1):147.
[16] Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016; 315(8):801-10.
[17] de Zoete MR, Palm NW, Zhu S, Flavell RA. Inflammasomes. Cold Spring Harb Perspect Biol. 2014; 6(12):a016287.
[18] Rocha NN, Silva PL, Battaglini D, Rocco PRM. Heart-lung crosstalk in acute respiratory distress syndrome. Front Physiol. 2024; 15:1478514.
[19] Balkrishna A, Sinha S, Kumar A, Arya V, Gautam AK, Valis M, et al. Sepsis-mediated renal dysfunction: Pathophysiology, biomarkers and role of phytoconstituents in its management. Biomed Pharmacother. 2023; 165:115183.
[20] Archer SL, Sharp WW, Weir EK. Differentiating COVID-19 Pneumonia From Acute Respiratory Distress Syndrome and High Altitude Pulmonary Edema: Therapeutic Implications. Circulation. 2020; 142(2):101-4.
[21] Gower WA, Nogee LM. Surfactant dysfunction. Paediatr Respir Rev. 2011; 12(4):223-9.
[22] Taenaka H, Matthay MA. Mechanisms of impaired alveolar fluid clearance. Anat Rec (Hoboken). 2025; 308(4):1026-39.
[23] Corrin B. Diffuse Alveolar Damage. In: Evans TW, Haslett C, editors. ARDS Acute Respiratory Distress in Adults. Boston, MA: Springer US; 1996. p. 37-46.
[24] Archer SL, Dunham-Snary KJ, Bentley R, Alizadeh E, Weir EK. Hypoxic Pulmonary Vasoconstriction: An Important Component of the Homeostatic Oxygen Sensing System. Physiol Res. 2024; 73(S2):S493-S510.
[25] Johnson DW, Roy TK, Secomb TW. Analysis of flow resistance in the pulmonary arterial circulation: implications for hypoxic pulmonary vasoconstriction. J Appl Physiol (1985). 2021; 131(4):1211-8.
[26] Dunham-Snary KJ, Wu D, Sykes EA, Thakrar A, Parlow LRG, Mewburn JD, et al. Hypoxic Pulmonary Vasoconstriction: From Molecular Mechanisms to Medicine. Chest. 2017; 151(1):181-92.
[27] Schumacker PT. Lung cell hypoxia: role of mitochondrial reactive oxygen species signaling in triggering responses. Proc Am Thorac Soc. 2011; 8(6):477-84.
[28] Mahmood SS, Pinsky MR. Heart-lung interactions during mechanical ventilation: the basics. Ann Transl Med. 2018; 6(18):349.
[29] Corp A, Thomas C, Adlam M. The cardiovascular effects of positive pressure ventilation. BJA Educ. 2021; 21(6):202-9.
[30] Kakihana Y, Ito T, Nakahara M, Yamaguchi K, Yasuda T. Sepsis-induced myocardial dysfunction: pathophysiology and management. J Intensive Care. 2016; 4:22.
[31] Aissaoui N, Boissier F, Chew M, Singer M, Vignon P. Sepsis-induced cardiomyopathy. Eur Heart J. 2025; 46(34):3339-53.
[32] Aissaoui N. Sepsis-induced cardiomyopathy: Time to bring the heart back to the forefront. Arch Cardiovasc Dis. 2025; 118(12):634-5.
[33] Messmer AS, Moser M, Zuercher P, Schefold JC, Müller M, Pfortmueller CA. Fluid Overload Phenotypes in Critical Illness-A Machine Learning Approach. J Clin Med. 2022; 11(2):336.
[34] Messmer AS, Dill T, Müller M, Pfortmueller CA. Active fluid de-resuscitation in critically ill patients with septic shock: A systematic review and meta-analysis. Eur J Intern Med. 2023; 109:89-96.
[35] Hippensteel JA, Uchimido R, Tyler PD, Burke RC, Han X, Zhang F, et al. Intravenous fluid resuscitation is associated with septic endothelial glycocalyx degradation. Crit Care. 2019; 23(1):259.
[36] Pfortmueller CA, Dabrowski W, Wise R, van Regenmortel N, Malbrain MLNG. Fluid accumulation syndrome in sepsis and septic shock: pathophysiology, relevance and treatment-a comprehensive review. Ann Intensive Care. 2024; 14(1):115.
[37] Harsoor VR, Reddy K, Anjum N. Restrictive v/s liberal fluid strategies in management of sepsis. Eur J Cardiovasc Med. 2024; 14:912-6.
[38] Lintz VC, Vieira RA, Carioca FL, Ferraz IS, Silva HM, Ventura AMC, et al. Fluid accumulation in critically ill children: a systematic review and meta-analysis. EClinicalMedicine. 2024; 74:102714.
[39] Kelm DJ, Perrin JT, Cartin-Ceba R, Gajic O, Schenck L, Kennedy CC. Fluid overload in patients with severe sepsis and septic shock treated with early goal-directed therapy is associated with increased acute need for fluid-related medical interventions and hospital death. Shock. 2015; 43(1):68-73.
[40] Verbrugge FH, Dupont M, Steels P, Grieten L, Malbrain M, Tang WH, et al. Abdominal contributions to cardiorenal dysfunction in congestive heart failure. J Am Coll Cardiol. 2013; 62(6):485-95.
[41] Chelazzi C, Villa G, De Gaudio AR. Cardiorenal syndromes and sepsis. Int J Nephrol. 2011; 2011:652967.
[42] Zhou ZK, Yu MM, Shou ST, Chai YF, Liu YC. Interaction between gut-heart axis in sepsis-induced cardiomyopathy. Pharmacol Res. 2025; 217:107806.
[43] Pan S, Lv Z, Wang R, Shu H, Yuan S, Yu Y, et al. Sepsis-Induced Brain Dysfunction: Pathogenesis, Diagnosis, and Treatment. Oxid Med Cell Longev. 2022; 2022:1328729.
[44] Suphatheerawatr N, Jaturapisanukul S, Prommool S, Kurathong S, Pongsittisak W. Intra-abdominal hypertension among medical septic patients associated with worsening kidney outcomes (IAH-WK study). Medicine (Baltimore). 2023; 102(4):e32807.
[45] Regueira T, Bruhn A, Hasbun P, Aguirre M, Romero C, Llanos O, et al. Intra-abdominal hypertension: incidence and association with organ dysfunction during early septic shock. J Crit Care. 2008; 23(4):461-7.
[46] Plantefeve G, Hellmann R, Pajot O, Thirion M, Bleichner G, Mentec H. Abdominal compartment syndrome and intraabdominal sepsis: two of the same kind? Acta Clin Belg. 2007; 62 Suppl 1:162-7.
[47] Manion S, Tobias JD. Abdominal compartment syndrome after sepsis in an infant with congenital heart disease. J Cardiothorac Vasc Anesth. 2006; 20(1):71-5.
[48] Grant RW, Dixit VD. Adipose tissue as an immunological organ. Obesity (Silver Spring). 2015; 23(3):512-8.
[49] Zhao P, Saltiel AR. Interaction of Adipocyte Metabolic and Immune Functions Through TBK1. Front Immunol. 2020; 11:592949.
[50] Wrba L, Halbgebauer R, Roos J, Huber-Lang M, Fischer-Posovszky P. Adipose tissue: a neglected organ in the response to severe trauma? Cell Mol Life Sci. 2022; 79(4):207.
[51] Ripa F, Pietropaolo A, Montanari E, Hameed BMZ, Gauhar V, Somani BK. Association of Kidney Stones and Recurrent UTIs: the Chicken and Egg situation. A Systematic Review of Literature. Curr Urol Rep. 2022; 23(9):165-74.
[52] Fayssoil A, Pousset F, Carlier R, Joussain C, Wahbi K, Mansencal N, et al. Recurrent urosepsis on nephrolithiasis in a patient with sarcoglycanopathy treated with dapagliflozin for heart failure. Heliyon. 2023.
[53] Karki N, Leslie SW. Struvite and Triple Phosphate Renal Calculi. 2023. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025.
[54] Prowle JR, Kirwan CJ, Bellomo R. Fluid management for the prevention and attenuation of acute kidney injury. Nat Rev Nephrol. 2014; 10(1):37-47.
[55] Aguilar MG, AlHussen HA, Gandhi PD, Kaur P, Pothacamuri MA, Talikoti MAH, et al. Sepsis-Associated Acute Kidney Injury: Pathophysiology and Treatment Modalities. Cureus. 2024; 16(12):e75992.
[56] Muğlu H, İnan Kahraman E, Sünger E, Murt A, Bilici A, Görgülü N. Acute Kidney Injury Secondary to Abdominal Compartment Syndrome: Biomarkers, Pressure Variability, and Clinical Outcomes. Medicina (Kaunas). 2025; 61(3):383.
[57] Mirza SA, Mohammed NS, Ali ZQ, Mohamed AS. The effects of methamphetamine intoxication on acute kidney injury in Iraqi male addicts. Toxicol Rep. 2025; 14:102065.
[58] Bouglé A, Duranteau J. Pathophysiology of sepsis-induced acute kidney injury: the role of global renal blood flow and renal vascular resistance. Contrib Nephrol. 2011; 174:89-97.
[59] Nørgård MØ, Svenningsen P. Acute Kidney Injury by Ischemia/Reperfusion and Extracellular Vesicles. Int J Mol Sci. 2023; 24(20):15312.
[60] Liu C, Peng Z, Gao X, Gajic O, Dong Y, Prokop LJ, et al. Simultaneous Use of Hypertonic Saline and IV Furosemide for Fluid Overload: A Systematic Review and Meta-Analysis. Crit Care Med. 2021; 49(11):e1163-75.
[61] Zhou Y, Jin X, Lv Y, Wang P, Yang Y, Liang G, et al. Early application of airway pressure release ventilation may reduce the duration of mechanical ventilation in acute respiratory distress syndrome. Intensive Care Med. 2017; 43(11):1648-59.
[62] Carsetti A, Damiani E, Domizi R, Scorcella C, Pantanetti S, Falcetta S, et al. Airway pressure release ventilation during acute hypoxemic respiratory failure: a systematic review and meta-analysis of randomized controlled trials. Ann Intensive Care. 2019; 9(1):44.
[63] Evans L, Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med. 2021; 47(11):1181-247.
[64] Amin A, Maleki M. Positive inotropes in heart failure: a review article. Heart Asia. 2012; 4(1):16-22.
[65] Yin J, Chi Y, Liu D, Li X, Li X. Unfractionated heparin attenuated histone-induced pulmonary endothelial glycocalyx injury through Ang/Tie2 pathway. J Inflamm (Lond). 2025; 22(1):9.
[66] Allison SP, Morley CJ, Burns-Cox CJ. Insulin, glucose, and potassium in the treatment of congestive heart failure. Br Med J. 1972; 3(5828):675-8.
[67] Mousavi S, Moradi M, Khorshidahmad T, Motamedi M. Anti-Inflammatory Effects of Heparin and Its Derivatives: A Systematic Review. Adv Pharmacol Sci. 2015; 2015:507151.
[68] Shute JK, Calzetta L, Cardaci V, di Toro S, Page CP, Cazzola M. Inhaled nebulised unfractionated heparin improves lung function in moderate to very severe COPD: A pilot study. Pulm Pharmacol Ther. 2018; 48:88-96.
[69] Shute JK, Puxeddu E, Calzetta L. Therapeutic use of heparin and derivatives beyond anticoagulation in patients with bronchial asthma or COPD. Curr Opin Pharmacol. 2018; 40:39-45.
[70] von Ehr A, Steenbuck ID, Häfele C, Remmersmann F, Vico TA, Ehlert C, et al. Experimental evidence on colchicine's mode of action in human carotid artery plaques. Atherosclerosis. 2025; 406:119239.
[71] Li Y, Zhang Y, Lu J, Yin Y, Xie J, Xu B. Anti-inflammatory mechanisms and research progress of colchicine in atherosclerotic therapy. J Cell Mol Med. 2021; 25(17):8087-94.
[72] Tang Taylor L, Long C, Pandhair O. Hydroxocobalamin in Septic Shock Management - Should It Be Introduced Sooner? Am J Respir Crit Care Med. 2025; 211(Abstracts):A5790-A.
[73] Spiess BD. Vasoplegia and cardiopulmonary bypass: role of oxidation-reduction dysregulation as a mechanism and therapeutic target. Br J Anaesth. 2026; 136(1):20-3.
[74] Ge Y, Li M, Wang B, Zhang Y, Zhou X, Zhang Y, et al. Melatonin ameliorates sepsis-induced myocardial dysfunction by promoting autophagy via SIRT1-mediated TFEB deacetylation. Int Immunopharmacol. 2026; 170:116098.
[75] Xu J, Liang C, Yao S, Wang F. Melatonin Exerts Positive Effects on Sepsis Through Various Beneficial Mechanisms. Drug Des Devel Ther. 2025; 19:1333-45.
| Files | ||
| Issue | Article in Press |
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| Section | Case Report(s) | |
| Keywords | ||
| Organ crosstalk Sepsis Heart-Lung–Kidney Interaction Cardiorenal-Cardiopulmonary syndrome | ||
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How to Cite
1.
Afra F, Mojtahedzadeh M, Hosseini LS, Shahverdi K, Albaji M, Najafi A, Sharifnia SH, Kianpour P, Shabani A, Mojtahedzadeh A. Heart, Lung, Kidney Interaction Following Urosepsis and Acute Viral Interstitial Pneumonia. Arch Anesth & Crit Care. 2026;.
