The Coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) started in December 2019 and has affected millions of lives worldwide, while many aspects of the illness are still unknown. Current data show that many hospitalized COVID-19 patients suffer from kidney damage, in the form of proteinuria, hematuria or acute kidney injury (AKI). AKI is especially prevalent among severe and critically ill COVID-19 patients and is a predictor of mortality. The pathophysiology of AKI in COVID-19 is unclear. Early reports of histopathologic examination from autopsied kidney tissue show SARS-CoV-2 viral particles in renal tubular cells and podocytes, suggesting direct viral infection, as well as findings of acute tubular necrosis, while rhabdomyolysis-associated AKI and glomerulopathies may also occur. As of today, only remdesivir has been authorized to treat COVID-19. Ongoing research investigates potential of anti-viral and anti-inflammatory agents along with safety and efficacy of commonly prescribed drugs such as renin-angiotensin-aldosterone system blockers. This review discusses the prevalence of AKI and its association with outcome, while highlighting possible mechanisms of AKI and suggesting organ protective measures to prevent the development of kidney damage.

Protein energy wasting (PEW), mostly characterized by decreased body stores of protein and energy sources, particularly in the skeletal muscle compartment, is highly prevalent in patients with moderate to advanced chronic kidney disease (CKD). Fibroblast growth factor 23 (FGF23) is an endocrine hormone secreted from bone and has systemic actions on skeletal muscle. In CKD, FGF23 is elevated and its coreceptor α-klotho is suppressed. Multiple lines of evidence suggest that FGF23 is interconnected with various mechanisms of skeletal muscle wasting in CKD, including systemic and local inflammation, exaggerated oxidative stress, insulin resistance (IR), and abnormalities in adipocytokine metabolism. Investigation of metabolic actions of FGF23 on muscle tissue could provide new insights into metabolic and nutritional abnormalities observed in patients with CKD.

Renal osteodystrophy is a common problem in renal failure patients. Bone pain is a common manifestation of renal osteodystrophy. The aim of the study was to assess the intensity of chronic bone pain via visual analog scale (VAS) and its relationship with parathyroid hormone, health-related quality of life (HRQoL), and depression in hemodialysis patients. Ninety-five patients recruited were asked to rate chronic bone pain via VAS. Depressive symptoms and HRQoL were assessed by Beck Depression Inventory (BDI) and Short-Form 36, respectively. VAS was positively correlated with intact parathyroid hormone (r = +0.322, p = 0.001), phosphorus (r = +0.300, p = 0.003), alkaline phosphatase (r = +0.275, p = 0.009), and negatively correlated with physical component (r = –0.320, p = 0.002) and mental component summary scores (r = –0.247, p = 0.016). In multivariate linear regression analysis, logVAS was independently associated with serum phosphorus (β = 0.072, 95% confidence interval: 0.020–0.123, p = 0.007), log intact parathyroid hormone (β = 0.176, 95% confidence interval: 0.041–0.310, p = 0.011), and physical component summary score (β = –0.018, 95% confidence interval: –0.031–(–0.005), p = 0.008). VAS is correlated with bone metabolism markers, namely, intact parathyroid hormone, and may be used to assess the intensity of chronic bone pain. The intensity of chronic bone pain is related with HRQoL in hemodialysis patients.

We aimed to evaluate impact of spironolactone (S) on cardiovascular toxicity of concomitant use of radiotherapy (RT) and trastuzumab (T). S, an aldosterone receptor antagonist, is known to ameliorate the cardiac damage. S ameliorates anthracycline -induced cardiotoxicity, there is no data regarding to effect of S on both T and radiation-induced cardiotoxicity. Eighty rats were divided into eight groups: group (G) 1 was defined as control group. G2, G3 and G4 were RT, S and T groups respectively. G5, G6, G7 and G8 were RT + T, T + S, RT + S and RT + T + S groups respectively. Rats were sacrificed at 6th hour; 21st and 100th days after RT. Heart and thoracic aorta samples were taken for microscopical examination. Cardiac inflammation and fibrosis scores and; TGF-β expression were not significantly different within study groups at 6th hour and 21st days of RT. By 100th days of RT fibrosis scores and TGF-β expression in cardiac samples were significantly different between study groups (p values were 0.004 and 0.002 respectively). Pair-wise comparisons revealed that both cardiac fibrosis scores and TGF-β expression levels were higher in G5 when compared to G8 (p values were 0.046 and 0.028 respectively). Moreover the TGF-β expression was higher in G5 when compared to G2 (p = 0.046). We could not demonstrate any significant differences with respect to inflammation, fibrosis and TGF-β expression in thoracic aorta samples between study groups. Although S had a protective effect on cardiac tissue it had no protective effect on thoracic aorta when administered with RT + T.