A quantitative study of indium-111-oxine platelet kinetics in acute and chronic renal transplant rejection.

Thirteen patients were investigated on 22 occasions at times varying from 1 day to 10 years after living family donor or cadaver renal transplantation. Platelet survival in the circulation, and in vivo platelet distribution and sites of deposition and sequestration was quantitatively determined with Indium-111-oxine (In-111-oxine) labelled platelets and a scintillation camera interfaced with a computer assisted imaging system. In all patients platelet survival was shortened and the platelet survival curve exponential. In patients with no evidence of transplant rejection and those with chronic rejection, there was no measurable or visible accumulation of labelled platelets in the kidney. The sequestration pattern of In-111 labelled platelets at the end of platelet life span was within normal limits and located in the reticuloendothelial system. In those patients with acute transplant rejection, platelet survival was shortened. Labelled platelets accumulated in the kidney: this was clearly visualized on scintigraphy and reflected by a significant increase in the radioactivity count density of the kidney. Platelets not deposited in the transplant were sequestrated in the reticuloendothelial system. This study demonstrates the diagnostic value of In-111 labelled platelet kinetics in the investigation of acute renal failure after renal transplantation. This investigation appears of limited clinical value in chronic rejection.

Analgesic nephropathy. Local experience in Bloemfontein.

In a prospective study we found analgesic nephropathy (AN) to be responsible for approximately 13% of all cases of end-stage renal disease being treated at our renal unit in Bloemfontein. There seemed to be a lack of awareness of this preventable cause of chronic renal failure among the general public and the medical profession alike. The study also confirms previous reports regarding the potential reversibility of AN and its association with peptic ulcer disease and urothelial cancer. Certain cystoscopic and histological changes in the bladder urothelium were present in varying combinations in all our patients with AN and these may be regarded as specific and more objective aids in establishing this elusive diagnosis.

Bladder urothelium in analgesic-associated nephropathy--a valuable diagnostic aid.

A brownish discoloration of the bladder mucosa on cystoscopy and the histological findings in a bladder biopsy specimen of submucosal vascular basement membrane thickening, pigment or chronic inflammatory changes in the absence of infection were present in various combinations in all our patients with analgesic-associated nephropathy. None of these findings was present in a control group of patients with other established causes of renal function impairment. More objective diagnostic aids may lead to a greater awareness and earlier diagnosis of this preventable cause of chronic renal failure.

The effect of oral isoniazid on human lymphocyte subpopulations.

After oral administration of isoniazid (INH) to volunteers, a significant reduction in circulating T lymphocytes and a significant increase in B lymphocytes was found. These findings suggest that INH may be useful as an immunosuppressive agent.

Increased concentrations of serum free fatty acids falsely increase serum thyroxine as determined by competitive protein-binding.

Markedly increased concentrations of free fatty acids after a fatty meal and heparin injection already have been shown to falsely increase thyroxine values measured by competitive protein-binding techniques, where ethanol extraction in used. We report here the effect of lesser increases. In 10 patients receiving heparin during hemodialysis we found significant increases in serum thyroxine by competitive protein-binding (mean, 20 nmol/l) and in free fatty acid concentrations (164 micronmol/l). Thyroxine measured as iodine did not change significantly. In seven subjects who had fasted for 27 h, we also noted significant increases in thyroxine by competitive protein-binding (mean 63 nmol/l) and in free fatty acid concentrations (624 micronmol/l). In a single subjects, serial measurements showed a close association of the two variables and the overall correlation between the increases was good. This artefact limits the value of many currently used thyroxine methods because it imposes restrictions on transport of samples and selection of patients.