Michel Tintillier

Acute renal failure secondary to oxalosis in a recipient of a simultaneous kidney-pancreas transplant: was mycophenolate the cause?

Mycophenolate mofetil (MMF) is now the preferred antimetabolite for post-transplant immunosuppression [1]. Although leucopenia and diarrhoea are the main side effects, there are case reports of a malabsorption syndrome caused by MMF [2]. Oxalosis, either primary or secondary, is a wellrecognised cause for renal failure. Secondary hyperoxaluria is caused by increased intestinal oxalate absorption and can be aggravated by excessive dietary oxalate intake. Particular gastro-intestinal disorders such as short bowel syndrome, chronic inflammatory bowel disease and fat malabsorption syndromes, e.g. chronic pancreatitis, are known to increase the risk of secondary hyperoxaluria [3]. Oxalosis causing renal allograft failure has also been reported [4,5]. To our knowledge, MMF has not previously been implicated in the development of secondary hyperoxaluria and acute renal failure in kidney or kidney–pancreas transplant patients. We report a patient with prolonged MMF-associated diarrhoea who presented with acute renal failure caused by oxalosis.

Late-onset primary hyperoxaluria triggered by hypothyroidism and presenting as rapidly progressive renal failure--description of a new mutation.

Primary hyperoxaluria type 1 (PH1) is a rare autosomal metabolic recessive disease, caused by the deficiency of the liver peroxysomal alanine:glyoxylate aminotransferase (AGT), characterized by accumulation of calcium oxalate crystals in kidneys and others organs. We present the case of an elderly woman with PH1, presenting as acute renal failure. Precipitation of calcium oxalate crystals was probably due to amiodarone-induced severe hypothyroidism. Residual AGT activity is associated with the G170R (G630A) mutation. A new mutation of AGT, called R36C, was also discovered; the role of this new mutation is actually not known.

Peritoneal dialysis and an inguinal hernia.

THE LANCET • Vol 362 • December 6, 2003 • www.thelancet.com 1893 RNA and resistance to aminoglycoside antibiotics in clones of Streptomyces lividans carrying DNA from Streptomyces tenjimariensis. Mol Gen Genet 1985; 200: 415–21. 16 Kelemen GH, Cundliffe E, Financsek I. Cloning and characterization of gentamicin-resistance genes from Micromonospora purpurea and Micromonospora rosea. Gene 1991; 98: 53–60. 17 Thompson J, Skeggs PA, Cundliffe E. Methylation of 16S ribosomal RNA and resistance to the aminoglycoside antibiotics gentamicin and kanamycin determined by DNA from the gentamicinproducer, Micromonospora purpurea. Mol Gen Genet 1985; 201: 168–73. 18 Nelson KE, Clayton RA, Gill SR, et al. Evidence for lateral gene transfer between Archaea and bacteria from genome sequence of Thermotoga maritima. Nature 1999; 399: 323–29. 19 Ochman H, Lawrence JG, Groisman EA. Lateral gene transfer and the nature of bacterial innovation. Nature 2000; 405: 299–304. 20 Lipsitch M, Samore MH. Antimicrobial use and antimicrobial resistance: a population perspective. Emerg Infect Dis 2002; 8: 347–54. 21 Kurokawa H, Yagi T, Shibata N, Shibayama K, Arakawa Y. Worldwide proliferation of carbapenem-resistant gram-negative bacteria. Lancet 1999; 354: 955. 22 Gonzalez-Zorn B, Courvalin P. VanA-mediated high level glycopeptide resistance in MRSA. Lancet Infect Dis 2003; 3: 67–68. 23 Martinez-Martinez L, Pascual A, Jacoby GA. Quinolone resistance from a transferable plasmid. Lancet 1998; 351: 797–99. 24 Bootsma, HJ, van Dijk H, Vauterin P, Verhoef J, Mooi FR. Genesis of BRO -lactamase-producing Moraxella catarrhalis: evidence for transformation-mediated horizontal transfer. Mol Microbiol 2000; 36: 93–104. 25 Gomis-Ruth FX, Moncalian G, Perez-Luque R, et al. The bacterial conjugation protein TrwB resembles ring helicases and F1-ATPase. Nature 2001; 409: 637–41.

Aeroportia and Pneumatosis Intestinalis in a Hemodialysis Patient

Hepatic portal venous gas (HPVG), the existence of gas in the hepatic portal venous system, is associated with a high mortality rate. It is rarely described in patients on chronic hemodialysis. We report a case of HPVG in an 84-year-old man who was on hemodialysis. He experienced abdominal pain, nausea, and vomiting during the dialysis session. Abdominal tomodensitometry revealed the presence of HPVG and numerous air-fluid levels with pneumatosis intestinalis in the context of severe mesenteric atherosclerosis. The patients condition gradually worsened, and he died soon afterwards. Early detection of HPVG and pneumatosis intestinalis signs is crucial for prompt diagnosis and management of acute mesenteric infarction.

An Unusual Abdominal X-ray

78 Hong Kong J Nephrol • October 2008 • Vol 10 • No 2 Department of Nephrology, Clinique et Maternité Sainte Elisabeth, Namur, Belgium. Correspondence to: Dr. M. Tintillier, 15 Place Louise Godin, B-5000 Namur, Belgium. Fax: (+32) 81-711903; E-mail: m.tintillier@skynet.be A 71-year-old Caucasian male was referred by his general physician for dyspnea, mild hypertension and sustained elevation of serum creatinine. Relevant past history included chronic kidney disease and mitral insufficiency. His glomerular filtration rate was calculated to be 12.23 mL/min according to the Modification of Diet in Renal Disease equation. Because of his advanced renal failure, due most probably to nephroangiosclerosis, hemodialysis was started. After 10 days, a peritoneal catheter (Tenckhoff Swan-neck double-cuff pigtail-right) was implanted via a paramedial approach without incident. After contrast injection, fluoroscopic control was made to confirm the position of the catheter in the Douglas space. Two weeks later, an attempt to infuse dialysis fluid via the peritoneal dialysis catheter was made unsuccessfully, and a catheter flow obstruction was observed. Plain abdominal radiography showed migration of the tip of the catheter in the left flank; a central opacity was also noted (Panel A). Further questioning of the patient revealed that the round opacity within the image was a silicone abdominal reservoir of a urinary sphincter prosthesis (AMS 800; American Medical Systems Inc., Minnetonka, MN, USA). The AMS 800 artificial urinary sphincter is the most commonly used device and is the criterion standard for the treatment of incontinence caused by intrinsic sphincter dysfunction. It is composed of a pressureregulating balloon, an inflatable cuff, and a control pump. The balloon has a dual function: it is a pressure regulator and a fluid reservoir. Balloon reservoirs are typically placed in the lower abdomen. The inflatable cuff has a variable length that compresses the urethra or the bladder neck circumferentially. The cuff is placed around the bulbar urethra in adult males. For women and children, the bladder neck is the only site that should be used. The control pump contains unidirectional valves, a delayed-fill resistor, a locking mechanism, and An Unusual Abdominal X-ray