Riad Darwish

Acquired Renal Cystic Disease in Renal Transplant Recipients

End-stage kidneys are known to undergo cystic transformation in patients treated with long-term hemodialysis. Little has been published, however, on the occurrence of acquired renal cystic disease (ACD) in renal transplant recipients. The available clinical and histopathological data were gathered on 22 renal transplant recipients who had undergone either necropsy or nephrectomy. None of our patients exhibited cystic changes in their donor kidneys. However, 11 patients (50%) had ACD of the native kidneys while the remaining patients lacked ACD. The duration of dialysis prior to transplantation was significantly longer and the life of the functional transplant kidney was significantly shorter in the ACD group as compared to the noncystic group. The combined duration of ESRD (dialysis + transplantation), however, was comparable in the two groups. It thus appears that the presence of a functioning renal allograft somehow retards the evolution of cystic changes in the diseased native kidneys. 1 of the patients in the ACD group exhibited superimposed multifocal clear cell carcinoma of the affected kidney, while none of the patients in the noncystic group exhibited renal neoplasm.

Urinary excretion and deficiency of prothrombin in nephrotic syndrome

Plasma and urinary prothrombin concentration and plasma prothrombin activity were measured in a group of 17 patients with the nephrotic syndrome. An immunologic assay using a monospecific antibody against human prothrombin was employed in the measurement of prothrombin concentration in the plasma and urine. Prothrombin-deficient plasma was used as the substrate in the measurement of plasma prothrombin activity. A control group consisting of five normal volunteers was included for comparison. Both the activity and concentration of prothrombin were significantly lower in the nephrotic group as compared with the control group. Significant quantities of immunoreactive prothrombin were detected in the urine of the majority of nephrotic patients. This study has provided unequivocal evidence of urinary excretion and acquired deficiency of prothrombin in the nephrotic syndrome.

Dialysis hypoxemia: Role of dialyzer membrane and dialysate delivery system

Arterial blood gas values, carbon monoxide diffusion capacity, oxygen consumption, carbon dioxide production, respiratory quotient, minute ventilation, and pulmonary capillary blood flow were determined before and during hemodialysis. In addition, the effect of single passage through the dialyzer on blood carbon dioxide tension, pH, and bicarbonate concentration was evaluated. Acetate-based dialysate was used in all experiments. Cellulosic dialyzer with single-pass dialysate delivery system was used in one group, and polyacrylonitrile dialyzers with recirculating delivery system in another. Although hypoxemia occurred in both groups, it was more severe in the former group. Dialyzer carbon dioxide loss was significantly greater with single-pass dialysate delivery system and cellulosic dialyzers than with recirculating delivery system and polyacrylonitrile dialyzer. To differentiate the role of dialysate delivery system from that of the membrane, the experiments were repeated using recirculating delivery system and cellulosic dialyzer. This resulted in marked attenuation of hypoxemia and dialyzer carbon dioxide tension losses. Since other experimental conditions were the same, the observed differences were thought to be due to the difference in the mode of dialysate delivery. It thus appears that the mode of dialysate delivery per se can modify the changes in arterial oxygen tension during hemodialysis and should be added to the list of factors implicated in the genesis of dialysis hypoxemia.

Focal renal cortical necrosis associated with zomepirac

Anaphylactoid shock, disseminated intravascular coagulation, and anuric renal failure requiring dialysis occurred in a patient receiving zomepirac sodium for toothache. Although renal function showed gradual improvement after seven days of anuria, the recovery was slow and incomplete. Renal biopsy three weeks after the onset of renal failure revealed evidence of focal renal cortical necrosis. Association of zomepirac administration with renal cortical necrosis is not known to have been previously demonstrated. This observation adds another dimension to the previously reported renal complications of nonsteroidal anti-inflammatory agents, especially zomepirac. The proportions of lymphocyte subsets, as defined with monoclonal antibodies, and the proliferative response to mitogens were normal. The patients lymphocytes showed no proliferative response to zomepirac. Serum complement components and immunoglobulin levels were within normal limits, and radioallergosorbent testing gave negative results. The mechanism of anaphylactoid reaction to zomepirac in this case, therefore, remains unclear.