Excess Calcium, Magnesium and Phosphorus Deposition in the Epigastric Artery of Dialysis Patients Undergoing Renal Transplantation

ABSTRACT Objective: Vascular calcification contributes to cardiovascular disease on dialysis patients. Arterial mineral content is modified but not well defined. We aim to define what is the concentration of calcium, magnesium and phosphorus in the epigastric artery of adult dialysis patients undergoing renal transplantation. Methods: All renal allograft recipients who underwent surgery at our centre between May 2003 and December 2005 and consented to be taken small samples of epigastric artery were included in our cross-sectional study. Histological, radiological and spectrometric methods were used to measure vascular calcification, deposits and concentrations of calcium, phosphorus and magnesium in epigastric artery, which were correlated with clinical and biochemical characteristics. Mineral vascular content was compared with corresponding samples from cadaveric renal donors free from renal disease (control group). Results: Calcium and magnesium concentrations in epigastric artery were much higher in recipients (n = 100) than in donors (n = 30). Histologically confirmed calcifications were more frequent in recipients. Calcium and magnesium content in epigastric artery were correlated directly with recipient age, pre-transplant serum P and Ca × P product. A high content of calcium and magnesium in this artery was observed in recipients with media and intimal calcification. Multivariate logistic regression showed that dialysis vintage > 3.5 years and calcium concentration in epigastric artery ≥ 4500 mg/kg wet weight were independent predictors of histological calcification. Conclusion: Excess mineral deposition is observed in the epigastric artery of dialysis patients, where the recipient's age, serum P, Ca × P product and time on dialysis play a decisive role.

Sodium storage in human tissues is mediated by glycosaminoglycan expression.

The current paradigm regarding sodium handling in animals and humans postulates that total body sodium is regulated predominately via regulation of extracellular volume. Active sodium storage independent of volume retention is thought to be negligible. However, studies in animals, hypertensive patients, and healthy humans suggest water-free storage of sodium in skin. We hypothesized that tissue sodium concentrations ([Na]T) found in humans vary and reflect regulation due to variable glycosaminoglycan content due to variable expression of XYLT-1. Twenty seven patients on dialysis and 21 living kidney transplant donors free of clinically detectable edema were studied. During surgery, abdominal skin, muscle, and arteries were biopsied. [Na]T was determined by inductively coupled plasma-optical emission spectrometry, semiquantitative glycosaminoglycan content with Alcian stain, and XYLT-1 expression by real-time PCR. [Na]T of arteries were ranging between 0.86 and 9.83 g/kg wet wt and were significantly higher in arteries (4.52 ± 1.82 g/kg) than in muscle (2.03 ± 1.41 g/kg; P < 0.001) or skin (3.24 ± 2.26 g/kg wet wt; P = 0.038). For individual patients [Na]T correlated for skin and arterial tissue (r = 0.440, P = 0.012). [Na]T also correlated significantly with blinded semiquantitative analysis of glycosaminoglycans staining (r = 0.588, P = 0.004). In arteries XYLT-1 expression was also correlated with [Na]T (r = 0.392, P = 0.003). Our data confirm highly variable [Na]T in human skin and muscle and extend this observation to [Na]T in human arteries. These data support the hypothesis of water-independent sodium storage via regulated glycosaminoglycan synthesis in human tissues, including arteries.

Recurrent abscess at site of laparoscopic cholecystectomy port due to spilled gallstones.

Spillage of gallstones is common during laparoscopic cholecystectomy and may lead to intra-abdominal abscesses and sinus formation. We describe two patients with recurrent abscess at the site of epigastric port due to presence of large spilled stone in the parietes following laparoscopic cholecystectomy. Removal of the stone led to resolution of symptoms.