ABSTRACT
There have been few published reports regarding rehabilitation for nephrotic syndrome. We compared the clinical outcomes of three cases of nephrotic syndrome with different treatment courses during 5 weeks of early rehabilitation.We report on three cases of nephrotic syndrome. Case 1 was a 67-year-old male who showed good progress after steroid treatment. Quadriceps torque and exercise capacity were increased after intervention. Case 2, a 78-year-old male, demonstrated resistance to steroid treatment. Quadriceps torque was decreased and exercise capacity was increased after intervention. Case 3 was an 83-year-old male who received nutrition therapy and diuretics without steroid treatment. Quadriceps torque and exercise capacity were decreased post-intervention.Early rehabilitation should be considered even if the steroid treatment course is different; furthermore, it is necessary to carefully consider the optimal exercise load in patients with nephrotic syndrome for whom regardless of whether or not steroid treatment is used.
Subject(s)
Nephrotic Syndrome/drug therapy , Nephrotic Syndrome/rehabilitation , Quadriceps Muscle/physiology , Aged , Aged, 80 and over , Case-Control Studies , Humans , Male , Muscle Strength Dynamometer/statistics & numerical data , Nephrotic Syndrome/diagnosis , Steroids/therapeutic use , Torque , Treatment Outcome , Walk Test/methods , Walk Test/statistics & numerical dataABSTRACT
Glucose-stimulated insulin secretion (GSIS) by pancreatic ß cells is biphasic. However, the physiological significance of biphasic GSIS and its relationship to diabetes are not yet fully understood. This study demonstrated that impaired first-phase GSIS follows fasting, leading to increased blood glucose levels and brain glucose distribution in humans. Animal experiments to determine a possible network between the brain and ß cells revealed that fasting-dependent hyperactivation of AMP-activated protein kinase in the hypothalamus inhibited first-phase GSIS by stimulating the ß-adrenergic pancreatic nerve. Furthermore, abnormal excitability of this brain-ß cell neural axis was involved in diabetes-related impairment of first-phase GSIS in diabetic animals. Finally, pancreatic denervation improved first-phase GSIS and glucose tolerance and ameliorated severe diabetes by preventing ß cell loss in diabetic animals. These results indicate that impaired first-phase GSIS is critical for brain distribution of dietary glucose after fasting. Furthermore, ß cells in individuals with diabetes mistakenly sense that they are under conditions that mimic prolonged fasting. The present study provides additional insight into both ß cell physiology and the pathogenesis of ß cell dysfunction in type 2 diabetes.
