Novel therapeutic approaches for COVID-19 in chronic kidney disease and transplant

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Antoney J. Ferrey ◽  
Ramy Hanna ◽  
Uttam G. Reddy ◽  
Ekamol Tantisattamo ◽  
Kamyar Kalantar-Zadeh ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Therapeutic Approaches ◽  
Novel Therapeutic

scholarly journals Novel therapeutic approaches for chronic kidney disease due to glomerular disorders

2016 ◽  
Vol 311 (1) ◽  
pp. F63-F65 ◽  
Author(s):  
Maria Del Nogal-Avila ◽  
Hector Donoro-Blazquez ◽  
Manish K. Saha ◽  
Caroline B. Marshall ◽  
Lionel C. Clement ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Clinical Trials ◽  
Kidney Disease ◽  
Therapeutic Strategies ◽  
Therapeutic Approaches ◽  
The Past ◽  
Disease Mechanisms ◽  
Toxic Drugs ◽  
Novel Therapeutic

Improved understanding of glomerular disease mechanisms over the past decade has led to the emergence of new and targeted therapeutic strategies for chronic kidney disease (CKD). Most promising among these are the administration of recombinant mutated human angiopoietin-like 4, sialic acid-related sugars that induce sialylation in vivo, compounds related to Bis-T-23, and immune depletion of the soluble urokinase receptor from the circulation. Taking these therapeutic strategies into clinical trials will be the first step away from repurposed and relatively toxic drugs currently used for treating kidney disease.

scholarly journals Recent Progress on Lipid Intake and Chronic Kidney Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Ke Pei ◽  
Ting Gui ◽  
Chao Li ◽  
Qian Zhang ◽  
Huichao Feng ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Lipid Metabolism ◽  
Kidney Disease ◽  
Recent Progress ◽  
Lipid Uptake ◽  
Vicious Cycle ◽  
Therapeutic Approaches ◽  
Lipid Abnormalities ◽  
Novel Therapeutic

The incidence of chronic kidney disease (CKD) is associated with major abnormalities in circulating lipoproteins and renal lipid metabolism. This article elaborates on the mechanisms of CKD and lipid uptake abnormalities. The viewpoint we supported is that lipid abnormalities directly cause CKD, resulting in forming a vicious cycle. On the theoretical and experiment fronts, this inference has been verified by elaborately elucidating the role of lipid intake and accumulation as well as their influences on CKD. Taken together, these findings suggest that further understanding of lipid metabolism in CKD may lead to novel therapeutic approaches.

Mechanisms of progression of chronic kidney disease

2015 ◽  
Author(s):  
Neil Turner
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Lower Risk ◽  
Progressive Disease ◽  
Serum Proteins ◽  
Direct Effects ◽  
Therapeutic Approaches ◽  
Podocyte Loss ◽  
Repair Mechanisms

Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.

AGE, RAGE and Diabetic Nephropathy

2010 ◽  
Vol 8 (2) ◽  
pp. 84
Author(s):  
MaÏté Daroux ◽  
Nicolas Grossin ◽  
Eric Boulanger ◽  
◽  
◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Advanced Glycation End Products ◽  
Specific Treatment ◽  
Therapeutic Approaches ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Immunohistochemical Studies

Diabetes is a disease that is present worldwide and which is associated with a large number of potential complications including chronic kidney disease (CKD). Several factors have been implicated in the development of the latter, including advanced glycation end-products (AGEs), which are formed from the interaction between sugar and proteins. AGE toxicity may be triggered via different mechanisms, especially by receptor binding. Immunohistochemical studies have demonstrated the presence of AGEs in all renal structures (vessels, glomeruli, tubules and the interstitium). They appear to be involved in the exacerbation of renal injury observed during diabetic nephropathy. At present, no specific treatment is yet available, although several therapeutic approaches are under development.

scholarly journals Developing better mouse models to study cisplatin-induced kidney injury

2017 ◽  
Vol 313 (4) ◽  
pp. F835-F841 ◽  
Author(s):  
Cierra N. Sharp ◽  
Leah J. Siskind
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Therapeutic Interventions ◽  
Low Doses ◽  
Dosing Regimen ◽  
Risk Of Mortality ◽  
Increased Risk ◽  
Novel Therapeutic

Cisplatin is a potent chemotherapeutic used for the treatment of many types of cancer. However, its dose-limiting side effect is nephrotoxicity leading to acute kidney injury (AKI). Patients who develop AKI have an increased risk of mortality and are more likely to develop chronic kidney disease (CKD). Unfortunately, there are no therapeutic interventions for the treatment of AKI. It has been suggested that the lack of therapies is due in part to the fact that the established mouse model used to study cisplatin-induced AKI does not recapitulate the cisplatin dosing regimen patients receive. In recent years, work has been done to develop more clinically relevant models of cisplatin-induced kidney injury, with much work focusing on incorporation of multiple low doses of cisplatin administered over a period of weeks. These models can be used to recapitulate the development of CKD after AKI and, by doing so, increase the likelihood of identifying novel therapeutic targets for the treatment of cisplatin-induced kidney injury.

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