Jean-Michel Pochet

Post-renal transplant syndrome of transient lower limb joint pain: description under a tacrolimus-based immunosuppression.

The occurrence of a post-renal transplant syndrome of lower limbs joint pain has been reported extensively over the last decade. Clinical examination of the symptomatic joints is often unremarkable and magnetic resonance imaging reveals abnormalities of the bone marrow suggestive of edema and/or hemorrhage. The main striking features of this syndrome are the spontaneous resolution of the symptoms within a few weeks as well as of the marrow abnormalities. This syndrome has been attributed to cyclosporine, given in the immunosuppression regimen or to epiphyseal impactions. We here document the occurrence of this syndrome in 5 kidney graft recipients given a tacrolimus-based immunosuppression.

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.

HYPEROXALURIA : AN UNDERESTIMATED CAUSE OF RAPIDLY PROGRESSIVE RENAL FAILURE

Abstract Hyperoxaluria is rarely considered as a cause of rapidly progressive renal failure. A case is reported of a patient in whom rapidly renal failure developed after subtotal small bowel resection. A diagnosis of calcium oxalate deposits nephropathy was confirmed by renal biopsy. This cause of renal failure may be underestimated and should be systematically searched for in all patients with malabsorption.

Metabolic alkalosis in the intensive care unit

Address for correspondence : Olivier Devuyst, MD, PhD Division of Nephrology, UCL Medical School 10 Avenue Hippocrate B-1200 Brussels, Belgium Tel : 32-2-764 1855; Fax : 32-2-764 5453; devuyst@nefr.ucl.ac.be Metabolic alkalosis is considered as the most common acid-base disorder encountered in patients treated in intensive care unit (ICU) (1). This entity is associated with a poor prognosis, as attested by mortality rates going up to 45 % if blood pH is ≥ 7.55, and even to 80% if blood pH is ≥ 7.65. The prognosis is worst when metabolic alkalosis is associated with respiratory alkalosis (2). This poor prognosis not necessarily reflects a causal relationship but is rather due to the severity of the underlying disease(s). However, severe metabolic alkalosis by itself may have detrimental consequences in acutely ill patients (3). It alters tissue oxygenation, by shifting the oxygenhemoglobin dissociation curve to the left, thereby impairing tissue oxygen delivery. Although this effect is short-lived (6-8 hours), it may be superimposed on the hypoxemia due to compensatory hypoventilation, secondary to the rise in blood pH (4). These deleterious effects may be especially important in patients with chronic respiratory diseases, in whom metabolic alkalosis could prompt the need for artificial ventilation or compromize the weaning of such therapy. Metabolic alkalosis is also associated with ventilation-perfusion mismatches which further enhance hypoxemia (5). The tissue oxygenation of these patients is also impaired by the vasoconstriction associated with alkalosis (6). In addition to a decrease in brain perfusion, metabolic alkalosis lowers the threshold for seizures and may be responsible for confusion and coma (6). Finally, metaMETABOLIC ALKALOSIS IN THE INTENSIVE CARE UNIT

Belgian consensus statement on the diagnosis and management of patients with atypical hemolytic uremic syndrome

In the last decade, significant progress has been made in the understanding and the treatment of patients with atypical Hemolytic Uremic Syndrome (aHUS). aHUS has emerged as a disease largely cause...

The patient with metabolic alkalosis

ABSTRACT Metabolic alkalosis defined by the increase of both plasma HCO3- level (>26 mmol/L) and blood arterial pH (>7.43) is quite frequent and usually accompanied by hypokalemia. Its pathogenesis requires both the generation of alkalosis and its maintenance. Generation may be due to excessive hydrogen ion loss by the gastrointestinal tract (e.g. vomiting) or by the kidney (e.g. use of loop diuretics) or may be due to exogenous base gain. Maintenance reflects the inability of the kidney to excrete the excess of bicarbonate because of hypovolemia, chloride depletion, hypokalemia, hyperaldosteronism, renal failure or a combination of these factors. The evaluation of volemic status and measurement of urinary Cl- and plasma levels of renin and aldosterone are crucial to identify the cause(s) of metabolic alkalosis. The cornerstone of treatment is the correction of existing depletions and the prevention of further losses. In vomiting-induced chloride depletion alkalosis, infusion of potassium chloride restores the excretion of bicarbonate by the kidney.

Any use for alternative lock solutions in the prevention of catheter-related blood stream infections?

The prevention of catheter-related blood stream infections (CRBSI) in hemodialysis (HD) patients remains a challenge because of high morbidity and mortality associated to CRBSI. Alternative locking solutions (ALS) containing an antithrombotic substance with additional antimicrobial or antibiofilm properties (citrate, ethylenediaminetetraacetic acid [EDTA], 70% ethanol, thrombolytics) with or without the addition of molecules with specific antimicrobial activity (antibiotics, taurolidine, paraben-methylene-blue) has been proposed with the aim to prevent or eradicate intraluminal biofilm colonization and subsequent CRBSI. In this review, we examine the available evidence concerning their efficacy and potential side effects, in order to determine whether ALS should be implemented widely or only in selected cases.

Group C streptococcal psoas abscess associated with a homolateral hip joint prosthesis infection: a case report.

Abstract An abscess in the psoas muscle is rare and frequently misdiagnosed. A delay in the diagnosis can increase its mortality rate. Some clinical signs can help the clinician but they all are not always present, and not at the same time. We describe in this paper a case report of an association between a psoas abscess and a homolateral hip joint prosthesis infection. It was suspected because of no improvement in clinical state despite treatment of the abscess by antibiotics and drainage, and it required finally other complementary therapeutic solutions. The pathogenic microorganism was a group C streptococcus. We discuss all these points and thereafter we suggest some recommendations for the clinician.

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