Nicola Di Paolo

Peritoneal Sclerosis: One or Two Nosological Entities?

The frequency, pathology, animal models, pathogenesis, clinical manifestations, diagnostic criteria, therapy and prevention of peritoneal sclerosis are reviewed. Many of these aspects have a bimodal configuration which suggests that peritoneal sclerosis, usually considered a single pathology in peritoneal dialysis, is actually two distinct nosological entities: simple sclerosis and sclerosing peritonitis. The former is very frequent, with minor anatomical alterations and low clinical impact; it is reproducible in animals by means of peritoneal dialysis, and is clearly due to the poor biocompatibility of peritoneal dialysis solutions. The latter is rare, with radical anatomical alterations and high mortality requiring valid methods of diagnosis, therapy and prevention; it can only be reproduced in animal models by means other than peritoneal dialysis and seems to be due to factors both related and unrelated to peritoneal dialysis.

Morphological and Morphometric Changes in Mesothelial Cells during Peritoneal Dialysis in the Rabbit

The morphometric and morphological changes in the mesothelial cell population were studied in rabbits in peritoneal dialysis with lactate and bicarbonate buffer solution. During dialysis the mesothelial population underwent radical changes in morphology and morphometric analysis showed a significant increase in cell size. Light microscope examination showed two types of changes: hyperplasia of the mesothelial cell with diameters of up to 80 microns, nucleus proportional to the cytoplasm, a large nucleole giving an owls eye appearance and cytoplasm rich in granular material. The second change was multiple nuclei and arrest of cell division. Nuclear division occurred, but no separation of the cytoplasm. The cells became larger than 200 microns, packed with nuclei and relatively little cytoplasm. Electron microscopy confirmed that the hyperplastic cells had perfect structure whereas the polynucleate cells contained vacuoles and little cytoplasmic reticulum. Immunohistochemistry using monoclonal antibodies SK2-27 and SK 60-61 specific to cytokeratins 14, 16, 17 and 8, 18, respectively, identified the cells as mesothelial. The changes were related to the glucose content of the peritoneal dialysis solution. Glucose is therefore the bioincompatible agent that modifies the mesothelium during peritoneal dialysis, causing it to become hyperplastic or blocking replication.

Videothoracoscopic obliteration of pleuroperitoneal fistula in continuous peritoneal dialysis

Hydrothorax during peritoneal dialysis is a very tedious complication. Many authors have described techniques of performing diagnosis and therapeutic procedures to take care of these complications. We describe a method to perform diagnosis and therapy by videothoracoscopy. Videothoracoscopy permits identification and closure of the tiny flaws in the diaphragm.

Fibrosis and Sclerosis: Different Disorders or Different Stages?

Peritoneal sclerosis is very common in peritoneal dialysis (PD) patients. It can vary from the mild, clinically silent sclerosis always present after years of PD, to rare but dramatic and often fatal cases. In our opinion, peritoneal sclerosis is a single disorder, so its variable manifestations are different stages of one nosological entity: this opinion relies mainly on strong connections in pathophysiology. In our view, the frequency, pathology, animal models, etiology and pathogenesis often show a bimodal configuration with suggests that peritoneal sclerosis is actually two distinct nosological entities: simple sclerosis and sclerosing peritonitis. The former is very frequent, with minor anatomical alterations and low clinical impact; it is reproducible in animals by means of PD, and is clearly due to the poor biocompatibility of PD. The latter is rare, with radical anatomical alterations and high mortality; it can only be reproduced in animal models by means other than PD and seems to be due to factors both related and unrelated to PD.

Cerivastatin Induces Rhabdomyolysis and Acute Renal Failure

Accessible online at: www.karger.com/journals/nef Dear Sir, Information on the safety of statins in the mass media has recently caused alarm among consumers. However, statins adequately meet therapeutic needs when LDL cholesterol exceeds levels set by guidelines of major countries. Cases of rhabdomyolysis associated with cerivastatin used in combination with other drugs, such as gemfibrozil and cyclosporins [1–3], have been reported, and in some cases rhabdomyolysis has led to acute renal failure (ARF) [4]. Here we report the case of a patient treated with cerivastatin only, who developed rhabdomyolysis and ARF. The patient had a family history of hypercholesterolemia and had been taking 200 mg/day cerivastatin for about a year. Six months before admission to hospital, prostate cancer was diagnosed and treated with 100 mg/day cyproterone acetate. Five months before admission, he took 500 mg aspirin for sudden diffuse muscular pain. The pain increased. He did not take further aspirin, and the symptoms subsided over a few days. He did not seek medical advice. Four days before admission, he again had diffuse muscular pain. This time he took 600 mg nimesulide in 48 h, while still on cerivastatin. The pain increased, the urine became dark, he experienced severe weakness with general malaise and was rushed to hospital. On admission, blood chemistry showed rhabdomyolysis and ARF (CPK 34,090 IU/l, myoglobinemia 21,931 ng/ml, LDH 5,890 IU/l, SGOT 885 IU/l, SGPT 875 IU/l, creatinine 2.3 mg/dl, BUN 112 mg/dl, creatine clearance 9.6 ml/min). Urinalysis showed microhematuria, tubule proteinuria and high tubule enzymes (NAG 18.32 Ìg/l and AAP 77.0 Ìg/l). Diuresis was 250 ml/day. Electromyography showed severe diffuse myopathy in all regions tested. Histochemistry and immunohistochemistry of a biopsy from the left vastus lateralis showed diffuse myopathic alterations with myocellular necrosis. Prompt alkaline and diuretic therapy restored diuresis (13,000 ml/day). After 2 days, the rhabdomyolytic crisis began to subside, and after 2 weeks blood chemistry was again normal with creatinine clearance 96 ml/min. EMG 18 days after admission was normal. Follow-up of the neoplastic disease was negative. All other organs and systems were found to be normal. A review of the scanty literature and the data of our patient suggests the following observations: (1) Combined with other drugs or alone, cerivastatin may cause rhabdomyolysis [5]. (2) Cyproterone acetate has been used for several decades and has never been associated with reports of muscle damage or interference with antilipemic drugs. (3) The patient appears to have had a slight rhabdomyolytic event a few months before admission, exacerbated by 500 mg aspirin. (4) The last episode of rhabdomyolysis was preceded by a large dose of nimesulide taken for muscle pain. The clinical data suggest damage to muscle, renal tubules (with ARF) and liver. Cerivastatin presumably triggered rhabdomyolysis which was prodromal for several months. Worsening of muscle pain after aspirin and onset of severe rhabdomyolysis with ARF after nimesulide suggest that FANS may promote muscle damage induced by cerivastatin.

THE SELF-LOCATING PERITONEAL CATHETER: FIFTEEN YEARS OF EXPERIENCE

504 During the past 30 years, many attempts have been made to modify the Tenckhoff peritoneal catheter in order to improve its function and efficiency (1–3). The catheter is a serious issue in peritoneal dialysis because it creates a communication between the abdominal cavity and the outside world, thus exposing patients to potentially severe complications, some of which can be reduced using new connection systems (4–6). Nevertheless, these complications tend to limit the use of peritoneal dialysis, although it is more physiological than hemodialysis. It is therefore logical to try and improve the function and biocompatibility of peritoneal catheters (6). Peritoneal catheters often become dislocated, leading to malfunction and need for replacement since it is usually not possible to restore them to their correct position. In 1995, with the aim of preventing this complication, the Nephrology Department of the University Hospital of Siena designed a new catheter, similar to the Tenckhoff catheter in form but with a 12-g high specific weight tungsten cylinder incorporated in the abdominal extremity. We call this new catheter the “self-locating peritoneal catheter” (SLPC) (7,8). Our catheter maintains the original form and internal diameter of the Tenckhoff catheter for most of its length, but the external diameter increases in the last 2 cm, where we do not find the usual perforations. This new catheter has some important physical characteristics: