ISSN:1660-8151    

DOI:10.1159/000182046

出版商:S. Karger AG    

年代:1981

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000182047

出版商:S. Karger AG    

年代:1981

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000182048

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The stimuli for compensatory renal growth following a decrease in functioning renal mass have interested a number of investigators. The existence of a humoral incitor and/or regulator of renal growth, renotropin, has been postulated; and three types of experiments have been performed to determine its existence. These include parabiotic, in vivo, and in vitro assays. In general, the three different methodologies support the existence of a renotropic factor (or factors) but further investigations are needed to clarify its precise roles in compensatory renal growth.

ISSN:1660-8151    

DOI:10.1159/000182049

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Approaches to treatment of lupus nephritis have been complicated by controversies in the definitions of the types of renal histology, the relevance of immunological and renal monitoring techniques as therapeutic guidelines, and lack of definitive clinical trials. It is suggested that demonstration of the efficacy of various therapeutic agents in clinical trials may be identified earlier by renal histological changes and/or assessment of drug toxicity compared to the time required for differences based on renal functional changes to emerge as ultimate measures of outcome.

ISSN:1660-8151    

DOI:10.1159/000182050

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Six interrelated abnormalities of Bartter’s syndrome are analyzed – juxtaglomerular hyperplasia, angiotensin resistance, altered kallikrein-kinin system, hyperprostaglandinuria, hypokalemia, and chloride-losing nephropathy. Arguments are advanced that any one of these could be the proximate cause and result in all the others. By the same token, each abnormality could be a consequence of any of the others and, furthermore, modulate the others by negative or positive feedback. Despite many recent insights, available data do not permit a definitive conclusion as to the locus of the primary abnormality. Rather, the syndrome presents as a remarkable biological counterpart to an electronic integrated circuit. The altered physiology of Bartter’s syndrome is reviewed and the pathogenesis of the syndrome analyzed in the light of recent liter

ISSN:1660-8151    

DOI:10.1159/000182051

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The renal cortex, outer medulla and inner medulla exhibit different profiles of drug metabolism. Mixed-function oxidase activity was present in cortex but not inner medulla. Cooxidation by prostaglandin endoperoxide synthetase was detected in inner medulla but not cortex. Both mixed-function oxidase and cooxidation were demonstrable in outer medulla. Urinary bladder carcinogens such as FANFT and benzidine and the renal carcinogen diethylstilbestrol were cooxidized by prostaglandin endoperoxide synthetase. Cooxidation could be a mechanism of activation of urinary bladder carcinogens and of nephrotoxic agents.

ISSN:1660-8151    

DOI:10.1159/000182052

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

3 patients with chronic renal failure due to lupus nephritis received kidney allografts from cadaver donors. Serological activity was present in 2 patients at the time of transplantation, and continued unabated despite intensive immunosuppressive therapy. Their allograft failed at 5 and 7 months after transplantation. Anti-DNA antibody in the allograft was found in 1 patient. The 3rd patient, with no serological activity at the time of transplantation, remained serologically negative, and her allograft functioned for 18 months. The persistence of serological activity in 1 patient, and the recovery of anti-DNA antibody from her allograft provide proof for the recurrence of lupus nephritis in the allograft.

ISSN:1660-8151    

DOI:10.1159/000182053

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Serious carbamazepine poisoning was treated by charcoal hemoperfusion with a 25% reduction in serum drug levels coincident with dramatic clinical improvement.

ISSN:1660-8151    

DOI:10.1159/000182054

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Results from many laboratories, including our own, support the following view of the status of renal blood flow (RBF) in acute renal failure (ARF). During the initiation phase of virtually all forms of experimental ARF, RBF appears to be substantially decreased. The mechanisms for the decrease in RBF vary depending on the model employed. However, we have shown that changes in cardiac output are involved in both HgCh and glycerol models of ARF. The degree to which the decreased RBF contributes to the impaired glomerular filtration rate (GFR) characterizing the initial phase of ARF also depends on the particular model that is studied. In terms of the maintenance phase of ARF, our studies show that total RBF is essentially normal in both glycerol and HgCU models of ARF. A general consensus exists that RBF is not related to the decreased GFR in the maintenance phase of ARF, regardless of the model of ARF employed. Results from this laboratory suggest, however, that a hemodynamic mechanism may still contribute to the decreased filtration in ARF despite the dissociation between total RBF and GFR. This mechanism may involve an increase in preglomerular resistance, either alone or in association with a decrease in postglomerular resistance. An extensive amount of research has been performed on the renal circulation in ARF over the past two decades. It appears that this research has basically confirmed Ole Munck’s impression of the role of renal blood flow in the pathophysiology of AR

ISSN:1660-8151    

DOI:10.1159/000182055

出版商:S. Karger AG    

年代:1981

数据来源: Karger