摘要:

In a previous study we examined the role of antigenic electrical charge as a factor influencing glomerular immune complex (IC) localization in the rabbit. From that study patterned after chronic serum sickness nephritis it was demonstrated that the administration of charge-modified cationic bovine serum albumin (BSA) of isoelectric point (pI) ≧ 9.5 invariably resulted in heavy subepithelial deposits, whereas native BSA (anionic, pI 4.5) produced principally mesangial deposits. In order to investigate the mechanism by which the immune deposits formed, passive serum sickness was induced in New Zealand white rabbits by unilaterally perfusing kidneys of nonimmunized rabbits with five alternating cycles of saline, antigen and antibody, or immunized rabbits with saline and antigen alone. Localization of BSA and IgG along the glomerular basement membrane (GBM) occurred only after exposure to cationic BSA and antibody; non-immunized animals perfused with cationic BSA and antibody to cationic BSA uniformly developed generalized, diffuse nearly linear deposits of IgG and BSA along the GBM. Similar deposits, which became progressively more granular after exposure to circulating antibody, were seen after the perfusion of cationic BSA alone into animals actively immunized with cationic or native BSA. Ultrastructural examination showed effacement of foot processes and isolated, irregular subepithelial and subendothelial deposits. Control perfusion employing alternating cycles of native BSA and anti-native BSA antibody, cationic BSA and normal sheep IgG, or native BSA alone in animals actively immunized with native or cationic BSA failed to develop glomerular IgG deposits. All control kidneys were normal on ultrastructural examination. We conclude that epimembranous deposits induced by cationic BSA are formed locally in the GBM and that in the perfused rabbit kidney a cationic antigen is a requirement for in situ IC formation in the subepithelial spac

ISSN:1660-8151    

DOI:10.1159/000183165

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

The effects of intrarenal administration of isoproterenol on excretion of urinary enzymes were examined in dogs. Urinary N-acetyl-β-D-glucosaminidase (NAG) and glutamyl transpeptidase (γ-GTP) originated from lysosomes and the brush border membrane of the kidney, respectively. NAG excretion was elevated for 10 min by isoproterenol (0.2 µg/kg/min) without a drastic change in glomerular filtration rate and renal blood flow. This elevation was inhibited by pretreatment with d, l-propranolol (0.6 mg/kg bolus injection 0.3 mg/kg/30 min) but less so by d-propranolol. Urinary γ-GTP excretion was little affected by isoproterenol. In light of these findings, the possibility that β-receptors may be involved in the excretion of NAG has to be consid

ISSN:1660-8151    

DOI:10.1159/000183166

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

Clinically important hyperkalemia occurred in 2 patients receiving a single small dose of potassium chloride by mouth. In spite of normal or near normal renal function, both subjects manifested abnormalities predisposing to impaired potassium homeostasis including hypoaldosteronism, autonomic dysfunction, or diabetes mellitus. It is suggested that in this type of patient the oral dose of potassium be as small as possible, taken with meals or given as a slow-release preparation.

ISSN:1660-8151    

DOI:10.1159/000183167

出版商:S. Karger AG    

年代:1984

数据来源: Karger

摘要:

A 6-year and 8-month-old boy on chronic intermittent peritoneal dialysis for end stage kidney disease presented with severe diarrhea, abdominal distension, cramps, tenesmus and vomiting. Barium enema showed rigidity and irregularity of the mucosa of the sigmoid and distal descending colon, with ‘thumb print like’ appearance, findings compatible with ischemic colitis. The institution of hemodialysis and discontinuation of the peritoneal dialysis resulted in a marked clinical and radiological improvement. Kidney transplantation performed a month later was associated with a complete cure of his intestinal dise

ISSN:1660-8151    

DOI:10.1159/000183168

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000183169

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000183170

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000183171

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000183172

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000183173

出版商:S. Karger AG    

年代:1984

数据来源: Karger

ISSN:1660-8151    

DOI:10.1159/000183174

出版商:S. Karger AG    

年代:1984

数据来源: Karger