scholarly journals The relation of anthropometric measurements and insulin resistance in patients with polycystic kidney disease

2016 ◽  
Vol 4 (3) ◽  
pp. 127-134
Author(s):  
Bennur Esen ◽  
Emel Sağlam Gokmen ◽  
Mahmut Kaya ◽  
Burak Ozkan ◽  
Ahmet Engin Atay

AbstractObjectiveTo examine the frequency of insulin resistance (IR) and its relation with anthropometric measurements in patients with autosomal dominant polycystic kidney disease (ADPKD).Material and MethodsNonobese 82 patients with ADPKD and 58 age matched healthy controls were enrolled into the study. None of participants were diabetic or receiving renal replacement therapies (RRT). IR was determined by homeostasis model assessment of insulin resistance (HOMA-IR) formula. Tanita body composition analyzer was used for anthropometric measurements. Creatinine clearance of participant were assessed by the modification of diet in renal diseases (MDRD).ResultsPatients with ADPKD had significantly higher level of urea and creatinine, microalbuminuria, and lower level of MDRD. Body fat distribution and HOMA-IR in both the groups were similar. Systolic and diastolic blood pressure of patients were higher than those of controls.ConclusionWe failed to determine a higher frequency of IR among patients with ADPKD.

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 38
Author(s):  
Zhiwei Qiu ◽  
Jinzhao He ◽  
Guangying Shao ◽  
Jiaqi Hu ◽  
Xiaowei Li ◽  
...  

Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disease characterized by progressive enlargement of fluid-filled cysts derived from renal tubular epithelial cells, which has become the fourth leading cause of end-stage renal diseases. Currently, treatment options for ADPKD remain limited. The purpose of this study was to discover an effective therapeutic drug for ADPKD. With virtual screening, Madin-Darby canine kidney (MDCK) cyst model, embryonic kidney cyst model and kidney-specific Pkd1 knockout mouse (PKD) model, we identified obacunone as a candidate compound for ADPKD drug discovery from a natural antioxidant compound library. In vitro experiments showed that obacunone significantly inhibited cyst formation and expansion of MDCK cysts and embryonic kidney cysts in a dose-dependent manner. In vivo, obacunone treatment significantly reduced the renal cyst development in PKD mice. Western blot and morphological analysis revealed that obacunone served as a NRF2 activator in ADPKD, which suppressed lipid peroxidation by up-regulating GPX4 and finally restrained excessive cell proliferation by down-regulating mTOR and MAPK signaling pathways. Experimental data demonstrated obacunone as an effective renal cyst inhibitor for ADPKD, indicating that obacunone might be developed into a therapeutic drug for ADPKD treatment.


2011 ◽  
Vol 20 (03) ◽  
pp. 241-247
Author(s):  
Rumeyza Kazancioglu ◽  
Vecihi Memili ◽  
Savas Ozturk ◽  
Meltem Gursu ◽  
Çigdem Kutlu ◽  
...  

1994 ◽  
Vol 5 (5) ◽  
pp. 1266-1270
Author(s):  
A Meyrier ◽  
P Simon

Over the last 26 yr, 33 cases and/or families of patients with autosomal dominant polycystic kidney disease (ADPKD) and a particular appearance of the eyes have been observed. ADPKD was unremarkable and in most cases had led to the usual slow development of end-stage renal failure. The facial feature concerned the upper eyelid, which drooped obliquely over the eyeball with a fold hiding the upper segment of the iris (blepharochalasis). The aspect was so typical that the diagnosis of ADPKD was suggested on first contact with new renal patients. All affected patients were white, of various origins, including French, Polish, Scandinavian, Italian, and Spanish. In retrospect, drooping eyelids had been present in the parents and/or grandparents who had died of renal failure, with or without an established diagnosis of ADPKD. In order to disclose the cosegregation of blepharochalasis with ADPKD, the screening of its prevalence in a well-circumscribed region with a catchment population of 410,000 was undertaken. The facial feature was found in 24 (32%) of 75 ADPKD families. Family transmission was confirmed in those kindreds, because at least two members suffered from ADPKD. Cosegregation was sought by analyzing family group photographs taken over several generations, the oldest member of which was born in 1973. All members with blepharochalasis had died of renal failure or are presently being followed up for ADPKD. A bibliographic search showed that the association of ocular and/or eyelid deformities and various inborn renal diseases is far from rare, suggesting a simultaneous event in the embryonic timetable.(ABSTRACT TRUNCATED AT 250 WORDS)


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Bei Liu ◽  
Song-Chang Chen ◽  
Yan-Mei Yang ◽  
Kai Yan ◽  
Ye-Qing Qian ◽  
...  

Abstract Autosomal dominant polycystic kidney disease (ADPKD) is one of the most frequently inherited renal diseases caused by mutations in PKD1 and PKD2. We performed mutational analyses of PKD genes in 49 unrelated patients using direct PCR-sequencing and multiplex ligation-dependent probe amplification (MLPA) for PKD1 and PKD2. RT-PCR analysis was also performed in a family with a novel PKD2 splicing mutation. Disease-causing mutations were identified in 44 (89.8%) of the patients: 42 (95.5%) of the patients showed mutations in PKD1 and 2 (4.5%) showed mutations in PKD2. Ten nonsense, 17 frameshift, 4 splicing and one in-frame mutation were found in 32 of the patients. Large rearrangements were found in 3 patients and missense mutations were found in 9 patients. Approximately 61.4% (27/44) of the mutations are first reported with a known mutation rate of 38.6%. RNA analysis of a novel PKD2 mutation (c.595_595 + 14delGGTAAGAGCGCGCGA) suggested monoallelic expression of the wild-type allele. Furthermore, patients with PKD1-truncating mutations reached end-stage renal disease (ESRD) earlier than patients with non-truncating mutations (47 ± 3.522 years vs. 59 ± 11.687 years, P = 0.016). The mutation screening of PKD genes in Chinese ADPKD patients will enrich our mutation database and significantly contribute to improve genetic counselling for ADPKD patients.


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