scholarly journals Mesoamerican nephropathy: A not so unknown chronic kidney disease

Author(s):  
Mariel Fabiola Valdivia Mazeyra ◽  
Patricia Muñoz Ramos ◽  
Rosario Serrano ◽  
Marina Alonso Riaño ◽  
Yohana Gil Giraldo ◽  
...  
2018 ◽  
Vol 94 (6) ◽  
pp. 1205-1216 ◽  
Author(s):  
Rebecca S.B. Fischer ◽  
Chandan Vangala ◽  
Sreedhar Mandayam ◽  
Denis Chavarria ◽  
Ramón García-Trabanino ◽  
...  

2015 ◽  
Vol 72 (10) ◽  
pp. 714-721 ◽  
Author(s):  
Catharina Wesseling ◽  
Berna van Wendel de Joode ◽  
Jennifer Crowe ◽  
Ralf Rittner ◽  
Negin A Sanati ◽  
...  

2014 ◽  
Vol 71 (Suppl 1) ◽  
pp. A27.1-A27 ◽  
Author(s):  
Catharina Wesseling ◽  
Berna van Wendel de Joode ◽  
Jennifer Crowe ◽  
Ralf Rittner ◽  
Kristina Jakobsson

PLoS ONE ◽  
2018 ◽  
Vol 13 (3) ◽  
pp. e0193056 ◽  
Author(s):  
Julia Wijkström ◽  
Channa Jayasumana ◽  
Rajeewa Dassanayake ◽  
Nalin Priyawardane ◽  
Nimali Godakanda ◽  
...  

2019 ◽  
Vol 317 (5) ◽  
pp. F1111-F1121 ◽  
Author(s):  
Yuka Sato ◽  
Carlos A. Roncal-Jimenez ◽  
Ana Andres-Hernando ◽  
Thomas Jensen ◽  
Dean R. Tolan ◽  
...  

An epidemic of chronic kidney disease of unknown etiology (Mesoamerican nephropathy) has emerged in hot regions of Central America. We have demonstrated that dehydration associated with recurrent heat exposure causes chronic kidney disease in animal models. However, the independent influence of core body temperature on kidney injury has not been explored. In the present study, we tested the hypothesis that kidney injury could be accelerated by increasing body temperature independent of external temperature. Wild-type mice were exposed to heat (39.5°C, 30 min, 2 times daily) with or without the mitochondrial uncoupling agent 2,4-dinitrophenol (DNP) for 10 days. Core temperature, renal function, proteinuria, and renal histological and biochemical analyses were performed. Isolated mitochondria markers of oxidative stress were evaluated from kidney tissue. DNP increased body core temperature in response to heat by 1°C (42 vs. 41°C), which was transient. The mild increase in temperature correlated with worsening albuminuria ( R = 0.715, P < 001), renal tubular injury, and interstitial infiltration of monocytes/macrophages. Tubular injury was marked in the outer medulla. This was associated with a reduction in kidney tissue ATP levels (nonheated control: 16.71 ± 1.33 nmol/mg and DNP + heat: 13.08 ± 1.12 nmol/mg, P < 0.01), reduced mitochondria, and evidence for mitochondrial oxidative stress. The results of the present study suggest that kidney injury in heat stress is markedly worsened by increasing core temperature. This is consistent with the hypothesis that clinical and subclinical heat stroke may play a role in Mesoamerican nephropathy.


2017 ◽  
Author(s):  
Gearoid M McMahon

Chronic interstitial nephritis is a progressive kidney disease with a wide variety of causes characterized by the presence of tubulointerstitial fibrosis, inflammation, and tubular atrophy. Most patients with advanced chronic kidney disease will have at least some degree of chronic interstitial nephritis present on a renal biopsy. However, there is a subset of renal diseases that specifically target the interstitium, leading to a progressive decline in kidney function. This review discusses the pathology and pathophysiology of chronic interstitial nephritis. In addition, common causes are reviewed, with a particular emphasis on recently described variants, including genetic causes of interstitial nephritis, Mesoamerican nephropathy, Balkan endemic nephropathy, and IgG4-related kidney disease. Key words: Chronic Kidney Disease, Inflammation, Fibrosis, 


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