Carlos Rotellar

Ten Years’ Experience With Continuous Ambulatory Peritoneal Dialysis

Up to January 1989, 171 patients were trained at our center on continuous ambulatory peritoneal dialysis (CAPD), and 17 on continuous cyclic peritoneal dialysis (CCPD). Over 10 years, we have gained 5,068 patient-months experience. Patient survival was 60% and 31% at 5 and 10 years, respectively. In contrast, diabetics had a survival of 32% at 5 years. Major complications included 499 new episodes of peritonitis, 304 exit-site infections, 22 hernias, five bowel perforations, one hydrothorax, and three episodes of sclerosing encapsulating peritonitis. Our technique survival has been 62% and 40% at 5 and 10 years, respectively. We believe that CAPD is a viable dialysis technique for long-term treatment of chronic renal failure and it should be offered as an option to intermittent hemodialysis.

Right atrium thrombosis in patients on hemodialysis

Vascular access has been the Achilles heel of hemodialysis for many years, and placement of temporary subclavian and internal jugular vein catheters has been a daily practice for the nephrologist. Now, concern about central vein stenosis, well described with the use of subclavian catheters in end-stage renal disease (ESRD), has prompted the use of internal jugular vein permanent catheters to avoid this complication, so as not to hinder future arteriovenous grafts. Permanent catheter access is not without its own special problems, and we describe here two patients that developed thrombosis of the right atrium while receiving hemodialysis through a permanent internal jugular catheter.

Bilateral nephrectomy and dialysis as an option for patients with bilateral renal cancer.

Six patients who underwent bilateral nephrectomy for renal carcinoma were placed on maintenance dialysis; of these, 1 patient had a renal transplant. A 5-year 44% survival of these patients was observed. We feel that radical nephrectomy followed by chronic dialysis is a reasonable alternative and offers a fair prognosis to patients with bilateral renal cancer in which partial nephrectomy is not possible.

Clinical Aspects of Bowel Perforation in Patients Undergoing Continuous Ambulatory Peritoneal Dialysis

Since the advent of the Tenckhoff catheter (1968) and the introduction of continuous ambulatory peritoneal dialysis (CAPD) by Popovich et al. in 1976, peritoneal dialysis (PD) has gaine:d popularity for the treatment of end-stage renal failure. By the end of 1990 there were 16,484 patients on chronic peritoneal dialysis in the United States (13.5% of all dialysis patients) (1). However, as lwith any mode of therapy, it is not free of complicati,ons. Major complications of PD include peritonitis, exit-site infection, bowel perforation, hydrothorax, and sclerosing encapsulating peritonitis (SEP) (2). In this paper, we review the clinical aspects of bowel perforation in patients on continuous peritoneal dialysis.

Exophthalmos: rare complication of A-V fistula used for hemodialysis.

Carlos Rotellar, MD, Department of Medicine, Division of Nephrology, The Medical Center, Georgetown University, Washington, DC 20007 (USA) Dear Sir Complications of all forms of vascular access for dialysis have been described including infection, thrombosis, steal syndrome, aneurysm, pseudoaneurysm (hematu-ria), venous hypertension, cardiac failure, lymphocele, skin necrosis, internal hypertrophy and dislodgement (bleeding) [1, 2]. We report here exophthalmos as an unusual vascular access complication. A 56-year-old white male with obstructive uropathy started hemodialysis through a fistula in the left elbow in June 1980. He developed severe swelling of the left arm 2 weeks after the fistula was created. Subsequently, swelling of the left side of the neck and face occurred in association with external jugular vein distention. Dialyzer natural venous pressure was markedly elevated. A fistulogram was performed showing a long stenosed segment of the left cephalic vein with numerous shoulder collaterals. The subclavian vein had an aneurysmal dilatation immediately prior to the left jugular vein. The left jugular vein filled in a retrograde fashion. There was a complete obstruction to flow at the junction of the innominate vein with the jugular vein; the superior vena cava was patent. One month later, a bypass was performed. The cephalic vein was brought into opposition with the brachial vein. The end of the cephalic vein was sewn to the brachial vein without difficulty. Subsequently, the patient noted decreased vision in the left eye and was found to have a 6-mm exophthalmos. CT scan of the orbit showed retro-orbital edema and dilated veins (fig. 1). The fistula in the left arm was surgically occluded and both the edema and exophthalmos decreased dramatically. To our knowledge, this is the first report of exophthalmos and retroorbital edema secondary to the use of A-V fistula for hemodialysis. Fig. 1. CT scan. References Brenner, B.M.; Rector, F.C., Jr.: The kidney, pp. 2490–2543 (Saunders, Philadelphia 1981). Mennes P.A.; Gilula L.A.; Anderson C.B.; Etheredge

Treatment of idiopathic membranous glomerulonephritis.

Carlos Rotellar, MD, Nephrology Division, Georgetown University Hospital, 3800 Reservoir Road, N.W. Washington, DC 20007 (USA) Dear Sir, We have read with interest the editorial by Garatini et al. [1] in the January 1987 issue of your journal. It is interesting to note that after many years of dealing with idiopathic membranous glomerulonephritis we do not know how to treat it, and what is more frustrating, we do not understand the disease. At the recent meeting of the American Society of Nephrology held in Washington, D.C., there was a debate on how to treat idiopathic membranous glomerulonephritis. No treatment and steroids, with or without cytotoxic drugs, were discussed, and again frustration was the result of the meeting because no answer was arrived at. The treatment of idiopathic membranous glomerulonephritis with these drugs is based on the good results obtained with them in the treatment of minimal change disease. However, the rationale of this is unclear due to the fact that these two diseases have probably very little in common. Membranous glomerulonephritis is thought to be caused by deposition of immune complexes (IC) in the basement membrane of the capillary wall of the glomeru-lus (in situ formation and/or deposition of circulating IC). Several studies have shown that removal of the antigen in the so called secondary membranous glomerulonephritis produces its resolution [2]. Idiopathic membranous glomerulonephritis is caused by the IC but the antigen is unknown. It may be that in some cases of idiopathic membranous glomerulonephritis the body is unable to clear the antigen. Though it is not clear why, it could be due to a deficiency in the antibody production (antigen in excess of antibody), production of low-affinity antibodies (‘bad antibodies’) and/or decreased activity of the reticuloendothelial system, in a word, a failure of the immune system to clear the antigen from the body. If this is so, then we should try to correct the deficiencies of the immune system to improve the rate of IC elimination instead of suppressing it even more. Obviously we would not like to increase the production of low-affinity antibodies (bad antibodies) because, if so, we would probably make the situation worse. However, if some cases of idiopathic membranous glomerulonephritis are due to a low production of antibodies and/or low activity of the reticuloendothelial system, the stimulation of either or both may cure the disease. Several substances can stimulate the immune system, e.g., Bacillus Calmette-Guérin (BCG), levamisole, or thymic hormones [2] and we do not know which one is safer. However, we feel that some efforts should be directed to investigate what role the immune stimulation can play in the treatment of idiopathic membranous glomerulonephritis.

Effect of urine osmolality on urinary red cell morphology.

Stephen N. Turitzin, MD, Georgetown University, Medical Center, Nephrology Division, 3800 Reservoir Road, Washington, DC 20007 (USA) Dear Sir, We have read with interest the article by De Caes-tecker et al. [1] on the localization of hematuria by red cell analyzers and phase contrast microscopy. We disagree with their conclusion that urine osmolality does not affect the urinary erythrocyte cell size distribution. Although this may be true for situations in which high urine osmolality is encountered, it is not the case for hypotonic urine. As part of a larger study of urinary red cell morphology following extracorporeal shock wave lithotripsy [2], we examined erythrocyte size distributions in mixtures of blood and urine of different tonicities. We found that low urine osmolality substantially altered red cell size determined by cell counter. Urine collected from a healthy male volunteer was diluted with varying proportions of distilled water to produce samples with a range of osmolalities from 68 to 758 mosm/kg. One hundred microliters of whole blood was mixed with 10 ml of each of these urine samples. After 30–60 min incubation, 50 μl of each mixture were added to 25 ml of isotonic buffer for determination of cell size distributions and median cell volume using a cell counter (Electrozone/Celloscope Model 112 CLT, Ill.). Cell counts were made before and after addition of a lysing agent (Zapoglobinll, Coulter Electronics, Fla.) to eliminate counts due to nonerythrocyte debris. We found that above 210 mosm/kg osmolality had little effect on red cell size, but that below this value median cell volume fell. Figure 1 shows red cell size distributions in urine samples with osmolalities of 89, 140, and 247 mosm/kg. The mean median cell volume in eight urine samples with osmolalities between 68 and 201 • · 89 mOsm/Kg * a 140 mOsm/Kg ■ ■ 247 mOsm/Kg Fig. 1. Cell size frequency distributions of erythrocytes incubated in urines of three different osmolalities. mosm/kg was 46.6 ± 14.2 fl (mean ± SD), while the mean median red cell volume in ten urine samples with osmolalities between 228 and 758 mosm/kg was 101.1 ± 9.5 fl. This difference was