Acute hydrothorax complicating peritoneal dialysis: a case report.

INTRODUCTION: Acute hydrothorax is an uncommon but a well-recognized complication of peritoneal dialysis. No single test is definitive for diagnosis. Although it is not a life-threatening condition, hydrothorax often requires abandonment of peritoneal dialysis. Delay in diagnosis can lead to worsening of the clinical status. CASE PRESENTATION: A 33-year-old Caucasian woman with lupus, who was successfully treated with temporary peritoneal dialysis 17 years previously, presented with acute dyspnea and a right pleural effusion after recommencing peritoneal dialysis. Investigations eliminated infective, cardiac, and primary respiratory causes. Peritoneal dialysis-related hydrothorax was suggested by biochemistry, and a pleuroperitoneal leak was definitively confirmed by using a Tc-99 m DTPA (diethylene triamine penta-acetic acid) scintigraphy scan. Subsequently, she underwent video-assisted thoracoscopy-guided talc pleurodesis and was able to return successfully to peritoneal dialysis. CONCLUSION: Although our case is not the first report that describes the occurrence of acute hydrothorax in peritoneal dialysis, it is an important condition to recognize for the wider general medical community. Furthermore, this case demonstrates that peritoneal dialysis can be continued with a hydrothorax, provided the underlying cause can be corrected. We review the literature pertaining to the utility and reliability of different diagnostic approaches to hydrothorax.

Optimising intraperitoneal gentamicin dosing in peritoneal dialysis patients with peritonitis (GIPD) study.

BACKGROUND: Antibiotics are preferentially delivered via the peritoneal route to treat peritonitis, a major complication of peritoneal dialysis (PD), so that maximal concentrations are delivered at the site of infection. However, drugs administered intraperitoneally can be absorbed into the systemic circulation. Drugs excreted by the kidneys accumulate in PD patients, increasing the risk of toxicity. The aim of this study is to examine a model of gentamicin pharmacokinetics and to develop an intraperitoneal drug dosing regime that maximises bacterial killing and minimises toxicity. METHODS/DESIGN: This is an observational pharmacokinetic study of consecutive PD patients presenting to the Royal Brisbane and Women's Hospital with PD peritonitis and who meet the inclusion criteria. Participants will be allocated to either group 1, if anuric as defined by urine output less than 100 ml/day, or group 2: if non-anuric, as defined by urine output more than 100 ml/day. Recruitment will be limited to 15 participants in each group. Gentamicin dosing will be based on the present Royal Brisbane & Women's Hospital guidelines, which reflect the current International Society for Peritoneal Dialysis Peritonitis Treatment Recommendations. The primary endpoint is to describe the pharmacokinetics of gentamicin administered intraperitoneally in PD patients with peritonitis based on serial blood and dialysate drug levels. DISCUSSION: The study will develop improved dosing recommendations for intraperitoneally administered gentamicin in PD patients with peritonitis. This will guide clinicians and pharmacists in selecting the most appropriate dosing regime of intraperitoneal gentamicin to treat peritonitis. TRIAL REGISTRATION: ACTRN12609000446268.

Assessment of arterial stiffness, oxidative stress and inflammation in acute kidney injury.

BACKGROUND: It is well know that arterial stiffness, oxidative stress and inflammation are features of chronic kidney disease. The arterial changes have a multitude of potential interconnected causes including endothelial dysfunction, oxidative stress, inflammation, atherosclerosis and vascular calcification. There is evidence that arterial stiffness becomes progressively worse as CKD progresses. The contribution of the biochemical changes of uremic toxicity to arterial stiffness is less clear. The aim of this study is to elucidate the vascular changes in acute kidney injury. We hypothesise that arterial stiffness will be increased during acute kidney injury and this will return to normal after kidney function recovers. METHODS/DESIGN: One hundred and forty four patients with acute kidney injury defined as an acute increase in serum creatinine to > 133 micromol/l or urea > 14.3 mmol/l or urine output < 410 ml/day will be recruited. Baseline measures of aortic pulse wave velocity, augmentation index, and brachial and central blood pressure will be recorded along with blood measures for oxidative stress and inflammation. Repeat measures will be taken at six and 12 months after the onset of the acute kidney injury. DISCUSSION: The role and contribution of the biochemical changes to arterial stiffness in the acute phase of kidney disease is not known. This study will primarily assess the time course changes in pulse wave velocity from the onset of acute kidney injury and after recovery. In addition it will assess augmentation index, central blood pressure and oxidative stress and inflammation. This may shed light on the contribution of biochemical kidney toxins on arterial stiffness in both acute kidney injury and chronic kidney disease. TRIAL REGISTRATION: ACTRN 12609000285257.

Evaluation and initial management of acute kidney injury.

The evaluation and initial management of patients with acute kidney injury (AKI) should include: (1) an assessment of the contributing causes of the kidney injury, (2) an assessment of the clinical course including comorbidities, (3) a careful assessment of volume status, and (4) the institution of appropriate therapeutic measures designed to reverse or prevent worsening of functional or structural kidney abnormalities. The initial assessment of patients with AKI classically includes the differentiation between prerenal, renal, and postrenal causes. The differentiation between so-called "prerenal" and "renal" causes is more difficult, especially because renal hypoperfusion may coexist with any stage of AKI. Using a modified Delphi approach, the multidisciplinary international working group, generated a set of testable research questions. Key questions included the following: Is there a difference in prognosis between volume-responsive and volume-unresponsive AKI? Are there biomarkers whose patterns (dynamic changes) predict the severity and recovery of AKI (maximal stage of AKI, need for RRT, renal recovery, mortality) and guide therapy? What is the best biomarker to assess prospectively whether AKI is volume responsive? What is the best biomarker to assess the optimal volume status in AKI patients? In evaluating the current literature and ongoing studies, it was thought that the answers to the questions posed herein would improve the understanding of AKI, and ultimately patient outcomes.

Uremic toxins: a new focus on an old subject.

The uremic syndrome is characterized by an accumulation of uremic toxins due to inadequate kidney function. The European Uremic Toxin (EUTox) Work Group has listed 90 compounds considered to be uremic toxins. Sixty-eight have a molecular weight less than 500 Da, 12 exceed 12,000 Da, and 10 have a molecular weight between 500 and 12,000 Da. Twenty-five solutes (28%) are protein bound. The kinetics of urea removal is not representative of other molecules such as protein-bound solutes or the middle molecules, making Kt/V misleading. Clearances of urea, even in well-dialyzed patients, amount to only one-sixth of physiological clearance. In contrast to native kidney function, the removal of uremic toxins in dialysis is achieved by a one-step membrane-based process and is intermittent. The resulting sawtooth plasma concentrations of uremic toxins contrast with the continuous function of native kidneys, which provides constant solute clearances and mass removal rates. Our increasing knowledge of uremic toxins will help guide future treatment strategies to remove them.

Renal replacement therapy in acute renal failure.

Acute renal failure (ARF) is a common condition in hospitalized patients. The aetiology and physiological characteristics differ from those of chronic renal failure (CRF) and both conditions should be approached differently. At present, the approach to the management of ARF is very heterogeneous. Attempts have therefore been made to improve consensus and to standardize treatment in the Acute Dialysis Quality Initiative (ADQI). Technology for the treatment of ARF is expanding. Traditional intermittent haemodialysis (IHD) is still a major treatment modality but continuous renal replacement therapies (CRRT) and slow, low-efficiency daily dialysis (SLEDD) are commonly used alternatives. Each modality has advantages and disadvantages, but to date no evidence exists for the superiority of one over the other. On the other hand, the availability of multiple options allows us to provide tailor-made treatment: the best modality is chosen depending on local expertise and the individual clinical scenario. Practice guidelines based on the best available evidence and the author's opinion are suggested.

Do circulating cytokines really matter in sepsis?

Sepsis remains the major cause of mortality worldwide, claiming millions of lives each year. The past decade has seen major advances in the understanding of the biological mechanisms involved in this complex process. Unfortunately, no definitive therapy yet exists that can successfully treat sepsis and its complications. In this review, we will address the significance of circulating cytokines in the pathophysiology of sepsis and its relevance to new approaches in extracorporeal therapies.