Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0235108 (tense)
2,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four of five patients with chronic renal failure developed tense bullae on the backs of their hands and fingers. In one of these patients the bullae were more widespread. In the fifth patient the lesions were limited to the fingers. The clinical picture resembled that of porphyria cutanea tarda, but porphyrin studies were consistently within normal limits. Histological studies showed subepidermal pressure bullae in each patient. In one of the patients immunohistology showed greenish fluorescence at the bases of the dermal papillae.
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PMID:Bullous dermatosis of chronic renal failure. 79 39

In chronic renal insufficiency resulting from destruction of the vast majority of nephrons, the surviving nephrons adapt their functions to the conditions of vigorous haemodynamic and osmolar overloads. They acquire an appropriate behaviour to preserve the principal renal functions and to achieve the balance of inner space. In the long period of time, similarly as in healthy people. Glomerulotubular balance as well as tubuloglomerular balance distinguish the remaining nephron function, while autoregulation of perfusion pressure along the glomerulus rapidly vanishes. All three regulation mechanisms are characteristic of the nephron function under physiologic conditions. Intense work of the remaining nephrons in chronic renal failure is under the high level controls of the group of hormones, among them are rennin-angiotensin system, arginine-vasopressin and atrial natriuretic peptide playing very important and particular roles. Comparison of different published studies emerge the idea that chronically increased arginine-vasopressin levels in chronic renal failure could block the autoregulation of blood flow and hydraulic pressure in glomeruli, which together with other mediator actions give high and fluctuating tense within remaining glomeruli, during every single cardiac cycle. It is probably the main event in the further course of kidney disease progression resulting in definite damage of the overloaded nephrons. Angiotensin II is one of reliably recognised mediators of unfavourable outcome in the process of nephron adaptation in chronic renal failure. Knowing the pathophysiologic processes in the remaining functionally adapted nephrons in chronic renal insufficiency determines a more adequate therapeutic approach in these patients.
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PMID:[Chronic renal insufficiency: 1) adaptation of nephron function in chronic renal insufficiency and 2) progression of chronic renal insufficiency]. 986 93

A 75-year-old Japanese man presented with pruritic blisters and macules on his trunk and extremities. He had been on hemodialysis for 4 years because of chronic renal failure, and in recent months, a polymethylmethacrylate membrane had been used for dialysis. After a change in dialysis membrane to a cellulose triacetate membrane, pruritic tense blisters developed on the extremities in combination with marked blood eosinophilia. Physical examination showed erythematous macules and tense blisters on the trunk and extremities. A biopsy specimen of an erythematous macule showed subepidermal vesicles and eosinophils that attached to the dermal-epidermal junction. Serum level of eosinophilic cationic protein was elevated. From clinical, histological, and immunological findings, a diagnosis of bullous pemphigoid was made. New blisters continued to erupt during the period in which the patient used the cellulose triacetate membrane dialyzer, and even after the use of clobetasol propionate. It resolved only after the patient came back to the use of a synthetic membrane dialyzer. We discontinued the use of clobetasol propionate, and neither bullous eruptions nor blood eosinophilia recurred. These observations suggest that cellulose membrane may be involved in the development of bullous pemphigoid through activation of eosinophils in the blood and the skin lesion, as in the present case.
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PMID:Development of bullous pemphigoid after change of dialysis membrane. 2416 26