ஜர்னல் ஆஃப் நெப்ராலஜி & தெரபியூட்டிக்ஸ்

The overall incidence of malignancy after renal transplantation is three to five times higher than in general population. As a result malignancy is the third most common cause of death in renal recipients. Three cases are given below of de novo renal allograft tumor occurring after transplantation. Case 1 is about a 57-year old female patient who underwent kidney transplant (LRKT) with zero haplotype match from her cousin and the case 2 discuss about a 45-year old female who developed ESRD secondary to chronic glomerulonephritis v/s hypertensive sclerosis. Last case report discusses about 46-year old Caucasian male with a history of Ig A and Granulomatosis with polyangiitis received LRKT from his brother.

A 25 year-old man presented with reversible posterior leukoencephalopathy syndrome manifesting as seizure, loss of consciousness and severe hypertension. He had contracted end stage kidney disease due to Alport syndrome and was treated with continuous ambulatory peritoneal dialysis for one year. Because his residual renal function was declining, he had refractory hypertension for several months before admission. On the admission, brain T-2 intensified magnetic resonance imaging revealed hyperintensive changes that were restricted to the cortex and the subcortical white matter of the parietal lobe, temporal lobe and posterior lobe. His clinical symptoms were improved by appropriate control of blood pressure using antihypertensive drugs and fluid depletion by continuous hemodiafiltration. Previous hyperintensive lesions disappeared in brain magnetic resonance imaging. He was transferred to maintenance hemodialysis three times weekly and discharged. One month later, he had a seizure attack again because of refractory hypertension which may be derived from low compliance with sodium and water restriction. We report here a reversible posterior leukoencephalopathy syndrome patient on peritoneal dialysis with severe hypertension and volume overload.

In essential hypertension, peripheral sympathetic nerve activity is generally thought to be increased regardless of salt sensitivity or insensitivity. Recent reports suggest that the cause may be abnormal central nervous system enhancement. However, other several reports have shown that a central sympathetic inhibitory system, the neuronal nitric oxide synthase system, may be strongly enhanced in salt-sensitive hypertensive Dahl rats, an animal model of salt-sensitive hypertension. These two facts lead to questions what happens finally in peripheral sympathetic activity and what is the relationship between sympathetic nerves and hypertension. In this review, we will show evidences for enhancement of central sympathetic inhibitory system, putative cause for up-regulation of central neuronal nitric oxide synthase system, and a role of its function, then lastly we consider the relationship between hypertension and sympathetic nerves in a rat model, with a focus on salt-sensitive hypertension.