Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis

Sepsis is resulted from a systemic inflammatory response to bacterial, viral, or fungal agents. The induced inflammatory response by these microorganisms can lead to multiple organ system failure with devastating consequences. Recent studies have shown altered expressions of several non-coding RNAs such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and circular RNAs (circRNAs) during sepsis. These transcripts have also been found to participate in the pathogenesis of multiple organ system failure through different mechanisms. NEAT1, MALAT1, THRIL, XIST, MIAT and TUG1 are among lncRNAs that participate in the pathoetiology of sepsis-related complications. miR-21, miR-155, miR-15a-5p, miR-494-3p, miR-218, miR-122, miR-208a-5p, miR-328 and miR-218 are examples of miRNAs participating in these complications. Finally, tens of circRNAs such as circC3P1, hsa_circRNA_104484, hsa_circRNA_104670 and circVMA21 and circ-PRKCI have been found to affect pathogenesis of sepsis. In the current review, we describe the role of these three classes of noncoding RNAs in the pathoetiology of sepsis-related complications.

Renal Function in Critically Ill Patients

Renal function serves as a window into the homeostasis of internal organs, and multiple organ system failure can occur in critically ill patients irrespective of the initial site of insult. Therefore, essential knowledge of renal pathophysiology is crucial in the diagnostic approach and management of critically ill patients. Close interaction between the kidney and other vital organs such as the heart, lungs, and brain is primarily responsible for the morbidity and mortality among critically ill patients. Pathologic renal changes can manifest in various conditions, such as acute kidney injury (AKI), chronic kidney disease, glomerulonephritis, fluid-electrolyte imbalances, and nephrotic syndrome.

Pathophysiology and management of hyperthermia

Hyperthermia is a state of elevated core temperature that rises rapidly above 40°C, secondary to failure of thermoregulation. Hyperthermia has many causes, but it is the hallmark of three conditions—heatstroke, malignant hyperthermia, and neuroleptic malignant syndrome. The clinical and metabolic alterations of hyperthermia, if left untreated, can culminate in multiple organ system failure and death. High temperature causes direct cellular death and tissue damage. The extent of tissue injury is a function of the degree and duration of hyperthermia. Heat-induced ischaemia-reperfusion injury, and exacerbated activation of inflammation and coagulation are also contributory. Hyperthermia is a true medical emergency with rapid progression to multiple organ system failure and death. The primary therapeutic goal is to reduce body temperature as quickly as possible using physical cooling methods, and if indicated, the use of pharmacological treatment to accelerate cooling. There is no evidence of the superiority of one cooling technique over another. Non-invasive techniques that are easy to use and well-tolerated are preferred. Pharmacological cooling with Dantrolene sodium is crucial in the treatment of malignant hyperthermia.

HFRS with Severe Heart Liver and Renal Failure: a Case Report

Hemorrhagic fever with renal syndrome (HFRS) is caused by hantavirus infection, which was characterized by abrupt high fever, systemic hemorrhage, hypotension and renal damage. Although multiple system organ damage was not uncommon, but multiple organ system failure were rare. Hereafter we report one case with simultaneous renal, heart and liver failure. In this case, we received some experience and lessons.