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)

Acute movement disorder associated with reversible bilateral basal ganglia lesions is an increasingly recognized syndrome in patients with end-stage renal disease, especially in the setting of concurrent diabetes mellitus. We report an elderly man with end-stage diabetic nephropathy treated by daily automated peritoneal dialysis who developed subacute symptoms of gait disturbance, dysarthria, dysphagia and lethargy. Computed tomography and magnetic resonance imaging of the head revealed bilateral symmetrical basal ganglia lesions. Repeat imaging 3 weeks later showed that these lesions had regressed spontaneously. However, his neurological symptoms improved slowly. These findings were similar to 23 other cases in the literature. Review of these cases shows that clinical features were predominantly bradykinesia, gait disturbance and concurrent metabolic acidosis (observed in 90% of cases). The pathogenesis of this condition has not been clearly defined, but uraemia may be an aggravating factor in predisposed patients, particularly in the presence of diabetic microvascular disease. There is no specific treatment for this condition; supportive measures are the mainstay of management. In the majority of patients, neurological improvement lags behind regression of basal ganglia lesions seen with neuroimaging, and the long-term outcome is variable.
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PMID:Bilateral basal ganglia lesions in patients with end-stage diabetic nephropathy. 1819 7

A 38-year-old man gradually developed gait instability, dysarthria, and dysphagia over two months associated with an elevated blood pressure after starting hemodialysis therapy for diabetic nephropathy. Brain MRI studies indicated vasogenic edema in the brainstem, extending from the lower midbrain to the upper medulla oblongata. The patient's high blood pressure was refractory to treatment, and his neurological disabilities and MRI abnormalities progressed. FDG-PET, MR spectroscopy, and cerebrospinal fluid studies did not suggest neoplastic pathologies. The patient was diagnosed with a brainstem variant of reversible posterior leukoencephalopathy syndrome, and received three courses of steroid pulse therapy. After the pulse therapy, the clinical manifestations and MR findings improved. By maintaining strict management of blood pressure and body water balance during hemodialysis, he did not experience any further clinical exacerbation, and the lesion on MR images continued to regress. Ten months after the pulse therapy, T1-weighted images showed slightly hyperintense signal. This case suggests that reversible posterior leukoencephalopathy syndrome (RPLS) may take a chronic clinical course without acute onset.
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PMID:[Brainstem variant of reversible posterior leukoencephalopathy syndrome with a prolonged clinical course: a case report]. 1908 30