Arthur Gordon

Vascular Calcification and Peripheral Necrosis in a Renal Transplant Recipient Reversal of Lesions Following Subtotal Parathyroidectomy

In the patient described progressive vascular calcification and digital necrosis developed after successful renal transplantation. The development of these lesions was associated with hypercalcemia and evidence of secondary hyperparathyroidism, and occurred in the face of a low calcium-phosphorus product. After the removal of three and a half hyperplastic parathyroid glands, the cutaneous lesions healed, and there was a marked reduction in the degree of vascular calcification. It is suggested that these lesions developed as a result of secondary hyperparathyroidism, and they may represent a form of calciphylaxis in man.

Reversal of an Inborn Sphingolipidosis (Fabry's Disease) by Kidney Transplantation

Abstract A 38-year-old man with Fabrys disease (α-galactosidosis) received a cadaver kidney transplant in September 1969. After surgery, plasma and urine trihexosyl ceramide was successfully maint...

Disordered calcium and phosphorus metabolism during maintenance hemodialysis: Correlation of clinical, roentgenographic and biochemical changes

Abstract The incidence and progression of renal osteodystrophy and soft tissue calcification in sixteen patients undergoing maintenance hemodialysis (MHD) for eight to thirty-eight months at Mount Sinai Hospital, Los Angeles, were determined by clinical and roentgenographic observation. The most common symptom was pruritus, which occurred in every patient. Ocular, periarticular or arterial calcification, usually asymptomatic, appeared or worsened during MHD in at least thirteen patients. Roentgenographic signs of hyperparathyroidism were present in nine of ten patients who underwent dialysis for more than one year, and appeared or progressed during dialysis in at least five. Stress fractures and reduction in bone density occurred in three patients. The mean serum levels immediately before and after dialysis were calcium 9.16 and 10.28 mg/100 ml, inorganic phosphate 7.94 and 3.85 mg/100 ml, blood urea nitrogen 87.5 and 25.7 mg/100 ml, and creatinine 12.97 and 5.08 mg/100 ml. The increment in serum calcium during dialysis was partly due to the high calcium level of the dialysate (6.87 ± 0.58 mg/100 ml), but there was considerable variation between patients which was only partly explained by individual differences in the correction of hyperphosphatemia and uremia. Although some patients showed a fall in predialysis serum phosphate levels in the first few months, high levels eventually developed in all; this constituted the most striking difference between the present series and that reported from Fulham Hospital, London, in which the incidence of osteodystrophy and soft tissue calcification was much lower. This difference resulted partly from insufficient ingestion of phosphate-binding antacids and inadequate control of dietary phosphate intake, but it may also have reflected a more severe disorder of parathyroid cell proliferation (mitotic autonomy) in uremic patients in Los Angeles than in London.

Extended hemodialysis in children with chronic renal failure

Five adolescents from 12 to 15 years of age with end-stage renal disease weredialyzed intermittently for periods of 1 to 6 months, using a low-resistance, pumpless, no-prime dialyzer (single layer of a standard two-layer Kiil). Minimal difficulties were observed with the silastic-teflon arteriovenous cannula. A relatively unrestricted diet was permitted with limitation of fluids to 1 L. and no added salt. Hypertension responded to removal of fluid by ultrafiltration. In adolescents weighing 28 to 52 kilograms, extended hemodialysis 2 to 3 times weekly for periods of 16 to 21 hours was found to be simple, without serious complications, and adequate to control the symptoms of uremia. This method of intermittent hemodialysis is recommended for children in preparation for live or cadaveric renal homotransplantation.

Sorbent Regeneration of Peritoneal Dialysate: an Approach to Ambulatory Dialysis

Sorbent regeneration of peritoneal dialysate has been shown to be feasible in experimental and preliminary clinical studies and provides a realistic basis for the optimization of dialysis therapy and the potential development of an ambulatory dialysis system. Peritoneal dialysis efficiency can be significantly enhanced by continuous dialysate flow techniques and the mass transfer of uremic solutes can be theoretically augmented by the increased dialysis time made possible by a wearable design. Further optimization of end stage renal failure therapy may be achieved by the combined use of various methods for blood purification.

Current Status of Dialysate Regeneration for the Treatment of Chronic Uremia

The removal of uremic solutes from dialysate by chemical compounds with adsorptive capacity provides a methodology for achieving a major reduction in the volume of dialysate necessary for conducting effective dialysis. Sorbent regeneration of dialysate permits a system with a small volume of recirculating dialysate to maintain maximal blood to dialysate concentration gradients and to potentially achieve mass transfer efficiency equal to that of a large volume recirculating or single pass dialysate flow system. Activated carbon, by virtue of its ability to adsorb organic nitrogenous compounds has served as the basic component of virtually all sorbent systems applied to the treatment of uremia. Yatzidis(1) demonstrated that activated carbon could adsorb creatinine, uric acid, phenols, indolic compounds, guanidines and organic acids. The adsorption of endogenous uremic metabolites of middle molecular weight configuration has also been demonstrated and there is presumptive clinical evidence derived from patients treated with sorbent systems that activated carbon probably adsorbs all organic uremic metabolites, known or as yet unidentified, which are of toxic significance(2–4). Unfortunately, there is one exception to this remarkable affinity of carbon for nitrogenous uremic metabolites.