Complications of CAPD

Allen R. Nissenson, Edward A. Ross

From the Department of Medicine, Division of Nephrology, UCLA School of Medicine, Los Angeles, California, and the Nephrology Section, UCI-Long Beach V A Program, Long Beach, California.


In the over seven years since CAPD began in earnest in the United States, much experience has been gained with the benefits and drawbacks of this form of therapy (1). As more patients remain on CAPD for long periods of time, a better appreciation for the incidence and importance of many complications has developed. This presentation will review the major complications of CAPD with emphasis on frequency of occurrence, diagnosis, treatment and prevention. It will not be all-inclusive, but will stress those complications that are most common and troublesome. Infection related complications, including peritonitis will not be reviewed here, as they are covered extensively elsewhere in this symposium.

Catheter related complications (2)

There are three major catheter-related complications seen in CAPD patients: pain, poor flow characteristics, and cuff erosion. The pattern of pain is the best clue to its etiology. Pain occurring during inflow is either sharp or burning. In the latter, it is likely related to the acidic pH (5.5) of the dialysate, and may be ameliorated by slightly raising dialysate pH with sodium bicarbonate injected into the dialysate just before instillation. In the former, the pain is caused by the position of the catheter tip atop or immediately adjacent to the bladder or bowel. Such pain occurs from dialysate streaming during infusion and is seen most commonly when catheters with a straight intraperitoneal segment are used. Occasionally repositioning the catheter will relieve the problem, but more often catheter replacement is necessary. When this is done, a curled catheter or other catheter design should preferentially be used. Finally, pain that occurs only at the end of inflow is generally related to overdistension of the abdomen .

This can be minimized by using the least hypertonic dialysate possible, lowest dialysate volume that permits adequate dialysis, and, if necessary , use of CCPD to minimize intra-abdominal pressure during exchanges.

Pain during outflow of dialysate generally occurs toward the end of drainage and may be caused by omental trapping in the catheter as drainage proceeds. Gentle irrigation of the catheter usually is sufficient to relieve this problem, though in extreme cases, catheter reposition or omentectomy may be necessary.

Constant pain during CAPD, in the absence of peritonitis or other intra-abdominal disease, almost always signifies catheter impingement on an intraabdominal organ. Such pain may be quite severe in the rectum, back or testes and usually requires catheter reposition or replacement.

Poor flow characteristics are a frequent problem in CAPD patients. Inflow obstruction is related to either a catheter kink, often in the subcutaneous tunnel, or occlusion of the catheter with fibrin debris. The former can be repaired surgically, while the latter may be corrected by catheter irrigation with saline or streptokinase (3).

Outflow obstruction is a much more frequent problem in CAPD patients. Stool-filled bowel enwrapping the catheter and preventing drainage is the most common cause of this complication and can be corrected by use of appropriate cathartics. Other causes of poor outflow include catheter malposition and obstruction by omentum or fibrin. Though catheter reposition for the former and use of irrigation with saline or streptokinase for the latter have met with some success, catheter replacement is usually necessary to correct this problem. Erosion of the distal cuff of a two-cuff Tenckhoff catheter through the exit site is commonly seen. In some patients this leads to persistent exit-site infection with eventual tunnel infection or peritonitis. In others the extruded cuff is an annoyance, but otherwise of little consequence. Careful shaving of the extruded cuff has been recommended by some, but the residual glue is difficult to remove and as irritating to the skin as the cuff itself. We, therefore, do not advocate this approach. Cuff extrusion can be avoided by meticulous attention to location of the exit-site during catheter placement with at least 3 cm between the exit site and the distal cuff . Catheters with only a single cuff or other subcutaneous anchoring system avoid this problem altogether .

Intra-peritoneal pressure related complications A linear rise in intra-abdominal pressure occurs with increasing intraperitoneal volume (IPV) whether the patient is lying, sitting or standing (4). For a given IPV, pressure is greatest with the patient seated and least with the patient supine. Though such pressures rarely exceed 12-14 cm H2O in most patients, this may be sufficient in some to cause hernia formation, dialysate leaks, abnormal pulmonary function and back pain.

Hernias have been reported in 10-20% of CAPD patients (5). The most common site is the midline incision from catheter placement, though this has been greatly minimized by use of a paramedian catheter insertion. Hernias also occur at pericatheter, umbilical, epigastric, ventral, diaphragmatic, and pelvic sites. Though not confirmed in all series, our impression is that such hernias are more common in the elderly, diabetics, multiparous women, and patients on corticosteroids. Such hernias may be of little consequence except cosmetically. On the other hand, incarceration, strangulation and acute intestinal obstruction may also result (6).

All patients should be carefully examined for hernias prior to starting CAPD. If they are present, they should be repaired. Hernias may be minimized by waiting at least 2 weeks before initiating CAPD after catheter placement, or by the use of CCPD. After hernia repair, peritoneal dialysis should be held for 10 days to 2 weeks to allow adequate tissue healing (7).

Dialysate leaks may occur early or late after catheter placement. Such leaks most commonly occur through the exit site, around the catheter, and into the layers of the abdominal wall. Leaks into the scrotom, penis, and vulva have also been described (8, 9). In addition, fluid leaks into the thoracic cavity may lead to massive hydrothorax and pulmonary compromise (10,11). We have found the same risk factors to apply to dialysate leaks as to hernia formation, as outlined above. The early leaks are related to inadequate catheter placement technique, usually coupled with premature use of high intraperitoneal volumes after catheter placement and are less common after a 10-14 day interval between placement and use. The use of a paramedian catheter insertion also minimizes incisionalleaks.

Dialysate leak should be suspected whenever a patient reports prolonged drainage time or progressive weight gain. To document a leak, in the absence of clinical signs, computerized tomography with contrast infused in the dialysate may be useful (12, 13). Such leaks may be managed conservatively with decreased dialysate volume and use of CCPD to minimize intraperitoneal pressure. If this approach is unsuccessful, temporary discontinuation of CAPD for 2-4 weeks with gradual reinstitution may be successful. Some patients require surgical exploration and repair of areas of fluid leak.

Massive hydrothorax, almost always right-sided, occurs occasionally in CAPD patients (10, II). Actual tears in the diaphragm have been found (14), but in most cases these cannot be identified. Much smaller congenital communications between pleural and peritoneal spaces have been proposed as causal in most patients. The diagnosis may be made by analysis of pleural fluid, in particular looking for a high glucose concentration. Such an analysis should be done within 30 minutes of instilling a fresh bag of dialysate into the peritoneum. Otherwise, rapid equilibrium of pleural fluid and blood glucose will confound the results ( 15) .The use of macroaggregated albumin labelled with 99m Technecium and injected intraperitoneally with subsequent scanning over the lungs may also be helpful (16).

Massive hydrothorax requires cessation of peri toneal dialysis, a switch to CCPD or IPD or initiation of hemodialysis (17). We do this for 4 weeks and then gradually reintroduce peritoneal fluid into the abdomen. If the effusion recurs, pleurodesis should be considered with talc, tetracycline, or a fibrin adhesive (Tissucol) (18, 19). If this is unsuccessful, peritoneal dialysis should be discontinued.

Infusion of 2 liters of dialysate into the abdomen of a CAPD patient produces a significant fall in functional pulmonary residual capacity, particularly marked with the patient supine (20) .These changes are seen in the first two weeks after initiation of CAPD, though seem to normalize with time on this modality. During episodes of peritonitis, however, substantial falls in arterial oxygen tension and vital capacity may occur, probably because of hypoventilation to minimize abdominal pain (21) . In the patient with underlying chronic pulmonary or cardiovascular disease, therefore, this may cause significant complications and should be minimized by judicious use of pain medications and supplementaloxygen.

Back pain is one of the commonest complications of CAPD .It may be caused by underlying musculoskeletal disease or deconditioning, aggravated by the postural changes induced by the intraperitoneal fluId load (22). Prevention is probably more important than treatment. Patients with underlying severe structural spine disease should be excluded from CAPD. Those patients with a history of mild chronic back pain should undergo thorough evaluation and be placed on a vigorous exercise program to strengthen the back and abdominal muscles and improve posture prior to starting CAPD. When back pain occurs in a patient already on CAPD, appropriate strengthening exercises should be prescribed. In addition, minimizing intraperitoneal volume or using CCPD might also be of benefit.

Metabolic complications

Substantial calories may derive from the absorption of glucose through the peritoneal cavity. This may represent 12-34% of total energy intake depending on the particular combination of solutions used on a given day (23). This added glucose load, when coupled with oral calorie intake, leads to a weight gain of 5-10% in most CAPD patients and gross obesity in a few. Minimizing the need for hypertonic dialysate by limiting fluid intake, decreasing oral calorie intake, and exercise all may be used to minimize this complication. Alternative dialysate osmotic agents might be ideal in this subset of patients, but are still under investigation.

Of even more concern, however, is hypertriglyceridemia seen in CAPD patients which is likely caused by the continuous large glucose load the patients are receiving. A rise in serum triglycerides of 10-15% occurs during the first 3 months of CAPD and is generally sustained (24). This abnormality is most marked in patients who are hypertriglyceridemic prior to starting on CAPD (25).

Cholesterol levels may rise slightly, but generally return to pre-CAPD levels within 6 months. The treatment of this abnormality is problematic (26). Limitation of carbohydrate intake (oral and dialysate) may be somewhat ameliorative. The use of lipid-Iowering agents, particularly clofibrate may be hazardous, causing severe myopathy and potentially lethal hyperkalemia. The intraperitoneal administration of insulin in non-diabetics has been tried, but with little success (27). Exercise training may be a useful adjunct to dietary manipulation (28).

Loss of amino acids and protein into the effluent dialysate is a potentially serious complication of CAPD. Two to three grams of amino acids are lost per day in direct proportion to their respective plasma concentrations (29). Plasma amino acid profiles are markedly deranged, similar to the pattern seen in chronic hemodialysis patients. The amino acid losses during CAPD per se, therefore, do not seem to account for this abnormality. Serum protein levels, on the other hand, fall into the low normal range in patients on CAPD and probably reflect their continuous loss across the peritoneal membrane. Losses of 9-12 grams per day can be expected, with 40 grams or more lost per day in patients with active peritonitis (30, 31). The minimal fall in serum albumin that is observed in most patients, despite significant dialysate losses, is attributable to decreased albumin catabolism and increased albumin synthesis (32). In addition, the low concentrations of serum urea nitrogen seen in CAPD patients for their level of protein intake results from a decrease in the fraction of protein metabolized to urea which in turn is caused by the substantial loss of nitrogen into dialysate in the form of protein and amino acids (33).

Anorexia, early satiety and nausea are common complaints of CAPD patients and may lead to inadequate nutrient intake. This coupled with the dialysate nitrogen losses described above may result in malnutrition. In some patients, in addition, oral calorie intake may decrease concomitant with absorption of intraperitoneal glucose. If the former is excessive, calorie malnutrition might ensue (34). Malnutrition is a particular problem in the stable CAPD patient during periods of peritonitis or other intercurrent illness that increases catabolism, and at all times in the diabetic and elderly CAPD patient. Careful, frequent assessment of nutritional status by a trained dietitian and judicious use of oral and if necessary parenteral nutritional supplements helps to minimize this potentially serious complication.

Other metabolic complications such as spontaneous hypoglycemia (35) and "contraction" alkalosis (36) have occurred in small numbers of patients undergoing CAPD and probably are a manifestation of severe underlying medical problems rather than the peritoneal dialysis per se.

Miscellaneous complications

Pseudomembranous colitis may occur as a complication of the antibiotic treatment of peritonitis. Only in rare occasions should that antibiotic be continued for the treatment of the peritoneal infection. Although the patient should avoid future use of the agent, recurrence is in general uncommon and may occur with a different antibiotic as well (37).

Cases of fatal pancreatitis have been reported in CAPD patients, but whether these truly represent a complication of this dialytic modality remains to be established (38). The clinical course is remarkable for the acute onset of hiccups, severe hyperglycemia, hemorrhagic peritoneal effluent, and shock. It must be distinguished from peritonitis, and may be related to recent episodes of peritonitis or use of antibiotics .

Chyloperitoneum is a rare complication of peritoneal dialysis (39). Trauma to the lymphatic system by the catheter causes leakage of chyle into the peritoneal cavity and abdominal pain characteristically aggravated by meals. Triglycerides and/or chylomicrons give the effluent a milky appearance. Surgical ligation of the leaking vessel may be necessary , although a trial of conservative management with low fat meals or hyperalimentation may be successful.

Hypertension is usually more easily controlled on CAPD than on hemodialysis, and some patients become hypotensive. Most likely due to excessive ultrafiltration, the patient may be managed with dialysate solutions oflow tonicity or given additional oral salt and water. Peripheral vascular disease can be symptomatically exacerbated by CAPD possibly related to this hypotensive effect. There is, however, no evidence that CAPD causes or enhances the progression of the occlusive disease. The significance of a reported approximately 20% incidence of worsened small and large vessel calcification in CAPD patients despite apparent control of hyperparathyroidism (40) has yet to be determined.

Apparently, synptomatic ischemia occurs in patients with pre-existing vascular insufficiency after a reduction in blood pressure (41 ) .Patients with known occlusive disease should avoid excess volume removal and overzealous treatment of hypertension. If vascular deterioration nevertheless continues, a change to hemodialysis may be beneficial.

Loss of peritoneal ultrafiltration capacity occurs when increased peritoneal membrane permeability leads to rapid dissipation of the dialysate-to-serum osmotic pressure gradient (42). This can necessitate the use of shorter exchange cycles or of dialysate solutions with higher dextrose concentrations. Acute and reversible impairments in ultrafiltration occur with the peritoneal inflammation of peritonitis. Progressive and permanent ultrafiltration failure has also been reported and can necessitate discontinuation of PD. Proposed mechanisms include peritoneal injury from recurrent episodes of peritonitis, dialysate solutions containing acetate buffer (43), hypertonic dialysate solutions, dialysate acidity, intraperitoneal antibiotics, plasticizers, particulate matter introduced from the plastic containers and tubing, and antiseptics used to spray tubing connections (44). Although the exact cause is unknown, the incidence of UP failure may increase with the duration of PD and is higher with CAPD compared to IPD (45).

Clinically, the syndrome of UP failure is often more of a problem than loss of solute clearance. In addition to peritoneal membrane sclerosis, inadequate flow through the catheter because of fibrin deposits or compartmentalization of the abdomen by adhesions can impair peritoneal clearances. Peritoneoscopy can be used to demonstrate and possibly lyse adhesions. Peritoneal air-contrast studies are done by first introducing the watersoluble contrast media and then instilling nitrous oxide (46). This technique may visualize fibrous bands, adhesions, and abscesses.

There are growing numbers of reported cases of sclerosing obstructive or encapsulating peritonitis. Patients typically have been on CAPD for at least one year and present with severe thickening and sclerosis of the peritoneum causing ultrafiltration failure, asthenia, weight loss, abdominal mass, abdominal pain and other symptoms of small bowel obstruction. Cases of severe sclerosis, especially those requiring surgical relief of bowel obstruction have high mortality rates. Although there is strong evidence that acetate-buffered dialysate solutions lead to this complication, patients using lactate solutions may also develop this problem. The etiology seems multifactorial, perhaps altered by abnormal individual host responses, and may include many of the causes listed above for the more common and less severe syndrome ofUF failure. In addition, proposed factors include beta-blocker medications, intraperitoneal antibiotics, disinfectants, and a response to the indwelling siliconized rubber tubing of the peritoneal catheter (47 , 48) .

Blood and peritoneal fluid eosinophilia may occur in CAPD patients. The syndrome of peritoneal eosinophilia usually occurs shortly after the initiation of PD, is typically asymptomatic, may be associated with mild blood eosinophilia and resolves spontaneously. Proposed mechanisms have included allergy or reaction to the plastics and other components of the connection system (49), and a reaction to the air introduced into the peritoneum at the time of catheter placement. Similar to pleural fluid eosinophilia after a pneumothorax, the !'eritoneal injection of air has been shown to cause transient peritoneal fluid eosinophilia (50). Blood eosinophilia may perhaps be caused by an allergic reaction to the antibiotics administered for peritonitis (51). Blood and peritoneal fluid eosinophilia has also been reported during fungal peritonitis (52).

Peritoneal bleeding can be caused by the pressure from the tip of the catheter. Usually the hemorrhage is relatively mild and self-limited and is due to erosion of small blood vessels. However, massive bleeding has been associated with the catheter perforating intra-abdominal organs (including the spleen) or perhaps adhesions (53), or traumatizing the peritoneum already injured from radiation therapy (54). A bloody dialysate effluent may also be caused by ovulation or retrograde menstruation.

The progression of renal osteodystrophy observed in many patients on CAPD is of great concern since some aspects ofCAPD could theoretically help improve the bone disease (55, 56). Depending on the serum calcium concentration, there can be positive mass transfer of calcium from 1.5% dextrose dialysate containing 7 mg/dl calcium. These solutions are recommended, especially since studies which reported improved osteitis fibrosa used that concentration (57). Dialysate with higher osmolality, however, can be associated with calcium loss and solutions with higher calcium levels have yet to become commercially available. CAPD does remove significant quantities of phosphorus and can help prevent hyperphosphatemia, but it does not eliminate the need for dietary phosphorus restriction and phosphate binders. In addition, even though approximately 13.6% of the circulating PTH is removed daily by CAPD (58), there is probably no effect on plasma levels.

Bone disease in CAPD patients can be worsened because of altered vitamin D metabolism. Not only do these patients have impaired 1 ,25(OH)2D3 synthesis, but D-binding protein, 1,25(OH)2D3 and 25(OH)D3 are lost into the dialysate (57, 59). 1,25(OH)2D3 should be administered to many of these patients, and the serum ionized (rather than total) calcium monitored.

As in hemodialysis, there has been a growing awareness of aluminum related bone disease in CAPD patients. The diagnostic criteria are the same and as controversial as those for hemodialysis patients (i.e. , bone biopsy or elevated serum aluminum levels after desferroximine infusion). Intravenous desferroximine is currently recommended for chelation therapy, but studies are underway examining the efficacy of subcutaneous, intramuscular, or intraperitoneal administration. Chelation has reportedly also been successful in treating aluminum-induced encephalopathy (60). When possible, aluminum containing phosphate binders should be replaced with calcium carbonate. Commercially available dialysate is not a significant source of aluminum (61).

A high incidence (5.4%) of calcium oxalate kidney stones has been reported in CAPD patients (62), and was associated with high urine oxalate concentrations. 1,25(OH)2D3 therapy may contribute to this problem by increasing the urine calcium level and thus the calcium-oxalate activity product.


  1. Nissenson AR, Gentile DE, Soderblom R, et al. Long-term morbidity and mortality of CAPD patients. (In press, 1986) Am. I. Kid. Dis.
  2. Gloor HI, Nichols WK, Sorkin MI, et al. Peritoneal access and related complications in CAPD. Am. I. Med. 1983; 74: 593-598.
  3. Wiegmann TB, Stuewe B, Duncan KA, et al. Effective use of streptokinase for peritoneal catheter failure. 1985; Amer. I. Kid Dis. 6: 119-123.
  4. TwardowskiZJ, ProwantBF, NolphKD, etal. High volume, low frequency CAPD. Kidney Int. 1983; 23: 64 70.
  5. Rocco MV, Stone WJ. Abdominal hernias in chronic peritoneal dialysis patients: A review. Perit. Dial. Bull. 1985; 5: 171-174.
  6. Madden MA, Beirne GJ, Zimmerman SW, et al. Acute bowel obstruction: An unusual complication of chronic peritoneal dialysis. Am. J. Kid. Dis. 1982; I: 219-221.
  7. Schleifer CR, Morfesis FA, Cupit M, et al. Management of hernias and Tenckhoff catheter complications in CAPD. Perit. Dial. Bull. 1984; 4: 146-150.
  8. Bennett RR, Bloom DA, Moore J. Penoscrotal edema complicating CAPD. Perit. Dial. Bull. 1983; 3: 165-166.
  9. Diaz-Buxo JA, Burgess P, Walker PJ: Peritoneovaginal fistula -unusual complication of peritoneal dialysis. Pent. Dial. Bull. 1983; 3: 142-143.
  10. Scheldewaert R, Bogaerts Y, Panwels R, et al. Management of a massive hydrothorax in a CAPD patient: A case report and a review of the literature. Perit. Dial. Bull. 1982; 2: 69 72.
  11. Singh S, Vaidya P, Dale A, et al. Massive hydrothorax complicating CAPD. 1983; Nephron, 1983; 34: 168-172.
  12. Twardowski ZJ , Tully RJ, Nichols WK, et al. CT in the diagnosis of subcutaneous leak sites during CAPD. Perit. Dial. Bull. 1984; 4: 163-166.
  13. Schultz Sa, Harmon TM, Nachtnebil KL. CT scanning with intraperitoneal contrast enhancement in a CAPD patient with localized edema. Perit. Dial. Bull. 1984; 4: 253-254.
  14. Pattison CW, Rodger RSC, Adu D, et al. Surgical treatment of hydrothorax complicating CAPD. Clin. Nephrol. 1984; 21: 191-193.
  15. Grefberg N, Danielson BG, Benson L, et al. Rightsided hydrothorax complicating peritoneal dialysis. Nephron 1983; 34: 130-134.
  16. Kennedy JM. Procedures used to demonstrate a pleuropentoneal communication: A review. Perit. Dial. Bull. 1985;5: 168-170.
  17. Townsend R, Fragola JA. Hydrothorax in a patient receiving CAPD. Successful treatment with IPD. Arch. Intern. Med. Bull. 1982; 142: 1571-1572.
  18. Benz RL, Schleifer CR. Hydrothorax in CAPD: Successful treatment with intrapleural tetracycline and a review of the literature. Am. J. Kid. Dis. 1985; 5: 136-140.
  19. Vlachojannis J, Boettcher I, Brandt L, et al. A new treatment for unilateral recurrent hydrothorax during CAPD. Pent. Dial. Bull. 1985; 5: 180-181.
  20. Gotloib L, Garmizo L, Vacak I, et al. Reduction of vital capacity due to increased intra-abdominal pressure during peritoneal dialysis. Perit. Dial. Bull. 1982; 2: 63-64.
  21. Taveira de Silva AM, Davis WB, Winchester JF, et al. Peritonitis, dialysate infusion and lung function in CAPD. Clin. Nephrol. 1985; 24: 79-83.
  22. Goodman CE, Husserl FE. Etiology, prevention and treatment of back pain in patients undergoing CAPD. Perit. Dial. Bull. 1983; 3: 119-122.
  23. Grodstein GP, Blumenkrantz MS, Kopple ID, et al. Glucose absorption during CAPD. Kidney Int 1981; 19: 564-567.
  24. Khanna R, Brechenridge C, Roncari C, et al. Lipid abnormalities in patients undergoing CAPD. Perit. Dial. Bull. 1982; 2: 513-515.
  25. Khanna R, Oreopoulos Do. "Complications of Peritoneal Dialysis Other Than Peritonitis". In Nolph KD, ed. Peritoneal Dialysis. Boston: Martinus NijhoffPublishers, 1985; 493-498.
  26. Golper T A: Treatment of Hyperlipidemia in Dialysis Patients. In Nissenson AR, Fine RN, eds. Dialysis Therapy. Philadelphia: Hanley & Belfus Publishers, In press, 1986.
  27. Beardsworth SF, Goldsmith HJ, Stanbudge BR. Intraperitoneal insulin cannot correct the hyperlipidemia of CAPD. Pent. Dial. Bull. 1983; 3: 126-127.
  28. Harter H. Endurance Exercise Training in Dialysis Patients. In Nissenson AR, Fine RN eds. Dialysis Therapy. Philadelphia: Hanley & Belfus Publisher, In press, 1986.
  29. Dombros N, Oren A, Marliss EB, et al. Plasma amino acid profiles and amino acid losses in patients undergoing CAPD. Perit. Dial. Bull. 1982; 2: 27-32.
  30. Blumenkrantz MJ, Gahl oM, Kopple ID, et al. Protein losses during peritoneal dialysis. Kidney Int. 1981; 19: 593-602.
  31. RubinJ, NolphKD, ArfaniaD, etal. Protein losses in CAPD. Nephron 1981; 28: 218-221.
  32. Kaysen GA, Schoenfeld PY. Albumin homeostasis in patients undergoing CAPD. Kidney Int. 1984; 25: 107-114.
  33. Blumenkrantz MJ, Kopple ID, Moran JK, et al. Nitrogen and urea metabolism during CAPD. Kidney Int. 1981; 20: 78-82.
  34. Von Baeyer H, Gahl oM, Riedinger H, et al. Adaptation of CAPD patients to the continuous peritoneal energy intake. Kidney Int. 1983; 23: 29-34.
  35. Smithand D, Khanna R, Ryan D, et at. Spontaneous hypoglycemia during CAPD. Perit. Dial. Bull. 1983; 3: 191-193.
  36. Tzamaloukas AH. "Contraction" alkalosis during treatment of hypoglycemia in CAPD patients. Perit. Dial. Bull. 1983; 3: 196-199.
  37. Barlett IG: Antibiotic-associated colitis. Disease-a month 1984; 30: 43.
  38. Pitrone F, Pellegrino E, Mileto G, Consolo F. May pancreatitis represent a CAPD complication? Report of two cases with a rapidly evolution to death. Int. I. Artif. Organs 1985; 8: 235.
  39. Pomeranz A, Reichenberg Y, Schurr D, Drukker A. Chyloperitoneum: A rare complication of peritoneal dialysis. Perit. Dial. Bull. 1984; 4: 35-37.
  40. Cassidy MID, Owen IP, Ellis HA, Dewar I, Robinson CI, Wilkinson R, Ward MK, Kerr DNS. Renal osteodystrophy and metastatic calcification in longterm continuous ambulatory peritoneal dialysis. Q. I. Med. 1985; 54: 29-48.
  41. Brown PM, Iohnston KW, Fenton SSA, Cattran DC. Symptomatic exacerbation of peripheral vascular disease with chronic ambulatory peritoneal dialysis. Clin. Neph. 1981; 16: 258-261.
  42. Wideroe TE, Smeby LC, Mjaland S, Dahl K, Berg KI, Aas TW. Long-term changes in transperitoneal water transport during continuous ambulatory peritoneal dialysis. Nephron 1984; 38: 238-247.
  43. Nolph KD, Ryan L, Moore H, Legrain M, Mion C, Oreopoulos DG. Factors affecting ultrafiltration in continuous ambulatory peritoneal dialysis. Perit. Dial. Bull. 1984; 4: 14-191.
  44. Iunor BIR, Briggs ID, Forwell MA, Dobbie IW, Henderson I. Sclerosing peritonitis -the contribution of chlorhexidine in alcohol. Pent. Dial. Bull. 1985; 5: 101-104.
  45. Slingeneyer A, Canaud B, Mion C. Permanent loss of ultrafiltration capacity of the peritoneum in long-term peritoneal dialysis: An epidemiological study. Nephron 1983; 33: 133-138.
  46. Tucker CT, Cunningham IT, Nichols AM, et at. Cannulography with peritoneal air contrast study. Contemporary Dialysis 1982; September, 3: 9-13.
  47. Hauglustaine D, van Meerbeek I, Monballyu I, Goddeens P, Lauwerijns I, Michielsen P. Sclerosing peritonitis with mural bowel fibrosis in a patient on long-termCAPD. Clin. Neph. 1984; 22: 158-162.
  48. Gandhi VC, Humayun HM, Ing TS, Daugirdas IT, Iablokow VR, Iwatsuki S, Geis WP, Hano IE. Sclerotic thickening of the peritoneal membrane in maintenance peritoneal dialysis patients. Arch. Intern. Med. 1980; 140: 1201-1203.
  49. Humayun HM, Ing TS, Daugirdas, IT, Gandhi VC, Popli S, Robinson IA, Hano IE, Zayas I. Peritoneal fluid eosinophilia in patients undergoing maintenance peritoneal dialysis. Arch. Intern. Med. 1981; 141: 1172-1173.
  50. Daugirdas IT, Leehey Dl, Popli S, Gandhi VC, Zayas I, Hoffman, W, Ing TS. Induction of peritoneal-fluid eosinophilia by intraperitoneal air in patients on continuous ambulatory peritoneal dialysis. New Engl. I. Med. 1985; 313: 1481.
  51. Chandran PKG, Humayun HM, Daugirdas IT, Nawab ZM, Gandhi VC, Ing TS. Blood eosinophilia in patients undergoing maintenance peritoneal dialysis. Arch. Intern. Med. 1985; 145: 114-116.
  52. Horisberger ID , Bille I, Wauters IP. Fungal eosinophilic peritonitis due to Alternaria in a patient on continuous ambulatory peritoneal dialysis. Perit. Dial. Bull. 1984; 4: 255-256.
  53. Shohat I, Shapira Z, Yussim A, Boner G. An unusual cause of massive intraperitoneal bleeding in CAPD. Perit. Dial. Bull. 1984; 4: 257-258.
  54. Hassell LH, Moore I, Conklin II. Hemoperitoneum during continuous ambulatory peritoneal dialysis: a possible complication of radiation induced peritoneal injury. Clin. Neph. 1984; 21: 241-243.
  55. Campese V, Easterling RE, Finkelstein F, Mat tern W, Ogden DA, Steiner RW, Oreopoulos DG . Renal osteodystrophy and the status of aluminum and other trace metals in CAPD patients: A panel review. Perit. Dial. Bull. 1984; 4: 129-135.
  56. Gokal R. Renal osteodystrophy in continuous ambulatory peritoneal dialysis. Perit. Dial. Bull. 1982; 2: 111-115.
  57. Zucchelli P, Catizone L, Casanova S, Fusaroli M, Fabbri L, Ferrari G. Renal osteodystrophy in CAPD patients. Mineral Electrolyte Metab. 1984; 10: 326-332.
  58. Delmez I, Slatopolsky E, Martin K, Gearing B, Harter H. The effects of continuous ambulatory peritoneal dialysis (CAPD) on parathyroid hormone (PTH) and mineral metabolism. Kidney Int. 1981; 19: 145.
  59. Shany S, Rapoport I, Goligorsky M, Yankowitz N, Suili I, Chaimovitz C. Losses of I, 25 and 24, 25-dihydroxycholecalciferol in the peritoneal fluid of patients treated with continuous ambulatory peritoneal dialysis. Nephron 1984; 36: 111-113.
  60. Bertholf RL, Roman JM, Brown S, Savory J, Wills MR. Aluminum hydroxide-induced osteomalacia, encephalopathy and hyperaluminemia in CAPD. Treatment with desferrioxamine. Perit. Dial. Bull. 1984; 4: 30-32.
  61. Mion C. Aluminium in continuous ambulatory peritoneal dialysis and post dilutional hemofiltration. Clin. Neph. 1985; 24: S88-S93.
  62. Oren A, Husdan H, Cheng PT, Khanna R, Pierratos A, Digenis G, Oreopoulos DG. Calcium oxalate kidney stones in patients on continuous ambulatory peritoneal dialysis. Kidney Int. 1984; 25: 534-538.