Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The glomerular filtration barrier separates the blood from the urinary space and consists of two major cell types: podocytes and fenestrated endothelial cells. Mesangial cells sit between the capillary loops and provide structural support. Proliferation and loss of mesangial cells both are central findings in a number of renal diseases, including diabetic nephropathy and mesangiolysis, respectively. Using cell-specific gene targeting, it was shown previously that vascular endothelial growth factor A (VEGF-A) production by podocytes is required for glomerular endothelial cell migration, differentiation, and survival. For further investigation of the effect of gene dose and VEGF-A knockdown within the glomerulus, mice that carry one hypomorphic VEGF-A allele and one podocyte-specific null VEGF-A allele (VEGFhypo/loxP,Neph-Cre+/-) were generated; in these mice, the "allelic dose" of VEGF-A is intermediate between glomerular-specific heterozygous and null states. VEGFhypo/loxP,Neph-Cre+/- mice die at 3 wk of age from renal failure. Although endothelial cell defects are observed, striking loss of mesangial cells occurs postnatally. In addition, differentiated mesangial cells cannot be found in glomeruli of podocyte-specific null VEGF-A mice (VEGFloxP/loxP,Cre+/-). Together, these results demonstrate a key role for VEGF-A production in the podocyte for mesangial cell survival and differentiation.
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PMID:Vascular endothelial growth factor a signaling in the podocyte-endothelial compartment is required for mesangial cell migration and survival. 1646 42

A 75-year-old man with diabetic nephropathy treated with hemodialysis visited to a medical office because of slight fever, and received intravenous glucose infusion without any vitamins. Thereafter, he noticed gait disturbance and began to tell inconsistent stories. He was admitted to our hospital due to aggravation of these symptoms. On admission, he was disoriented and not able to sit by himself because of severe truncal ataxia without weakness. He had also gaze direction nystagmus. Based on clinical features, we considered him as having Wernicke's encephalopathy (WE) and treated him with 100 mg thiamine per day. The thiamine supply diminished these symptoms soon. Plasma thiamine level prior to the administration was 7 ng/ml, which confirmed the diagnosis. MRI did not disclose any abnormalities frequently seen in WE. WE is a life-threatening disease, and 'early detection, early cure' is important for recovering without sequelae. The thiamine deficiency is often seen in dialysis patients because of dietary restrictions as well as its loss during dialysis. This case gives us the caution; when hemodialysis patients present acute/subacute gait disturbance and/ or abnormal mental state, we should consider WE. Furthermore, high-risk patients, such as elderly patients under hemodialysis may need some supplement including thiamine even at preclinical stage.
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PMID:[Wernicke encephalopathy in a non-alcoholic patient with diabetic nephropathy under hemodialysis]. 2059 67