Molecular Challenges and Opportunities in Climate Change-Induced Kidney Diseases.

As temperatures continue to modify due to weather changes, more regions are being exposed to extreme heat and cold. Physiological distress due to low and high temperatures can affect the heart, blood vessels, liver, and especially, the kidneys. Dehydration causes impaired cell function and heat itself triggers cellular stress. The decline in circulating plasma volume by sweat, which stresses the renal and cardiovascular systems, has been related to some molecules that are crucial players in preventing or provoking cellular damage. Hypovolemia and blood redistribution to cutaneous blood vessels reduce perfusion to the kidney triggering the activation of the renin-angiotensin-aldosterone system. In this review, we expose a deeper understanding of the modulation of molecules that interact with other proteins in humans to provide significant findings in the context of extreme heat and cold environments and renal damage reversal. We focus on the molecular changes exerted by temperature and dehydration in the renal system as both parameters are heavily implicated by weather change (e.g., vasopressin-induced fructose uptake, fructogenesis, and hypertension). We also discuss the compensatory mechanisms activated under extreme temperatures that can exert further kidney injury. To finalize, we place special emphasis on the renal mechanisms of protection against temperature extremes, focusing on two important protein groups: heat shock proteins and sirtuins.

Unveiling Mixed Cryoglobulinemia in Suspected Sepsis Without a Source.

Cryoglobulinemia is an uncommon condition characterized by the presence of cryoprecipitable immune complexes in circulation, leading to clinical symptoms like purpura, muscle weakness, and joint pain. Specifically, mixed cryoglobulinemia involves the formation of these complexes due to rheumatoid factors, mainly IgM, occasionally IgG or IgA. Previously, Hepatitis C (HCV) was a common cause of mixed cryoglobulinemia, as the chronic HCV infection triggered immune responses that resulted in cryoglobulin formation. However, the emergence of direct-acting antivirals (DAAs) for HCV treatment has shifted the landscape, with autoimmune and lymphoproliferative disorders becoming more prominent etiological factors for mixed cryoglobulinemia. This case report features a 67-year-old woman with a history of Hepatitis C-related cirrhosis. She presented at the emergency department with signs of septic shock and widespread joint pain, particularly in the knees, shoulders, and neck. Effective sepsis management was achieved using antibiotics, albumin infusion, and midodrine. Nonetheless, significant cervical and bilateral knee pain persisted. Further examination uncovered hypocomplementemia and positive results for rheumatoid factors (IgA, IgM, IgG) and cryoglobulin agglutination, confirming the diagnosis of mixed cryoglobulinemia. This case emphasizes the importance of considering mixed cryoglobulinemia in chronic Hepatitis C patients displaying fatigue and joint pain, even in the absence of the traditional clinical manifestations. Moreover, the case underscores the dual benefits of DAA treatment for Hepatitis C in individuals with mixed cryoglobulinemia by achieving viral eradication and alleviating cryoglobulinemia-related symptoms, thus preventing further organ damage.