Paul Donohoe

The use of opioid analgesia in end-stage renal disease patients managed without dialysis: recommendations for practice.

The numbers of patients dying with end-stage renal disease (ESRD), particularly those managed conservatively (without dialysis) or withdrawing from dialysis is increasing rapidly in developed countries. There is growing awareness of the extensive symptom control needs of these patients. Pain is a common problem, and has been both under-recognized and under-treated. It is challenging to manage, largely because of the constraints very poor renal function places on use of medication. Although pharmacological reviews of opioid use in renal failure have been published, there is a need for clinical recommendations to aid palliative and renal specialists in providing effective pain control. This review describes the pharmacological evidence for and against the use of the different opioid medications, and translates this into clinical recommendations for ESRD patients managed conservatively, not for those on dialysis for whom there are different pharmacological considerations. Acetaminophen (paracetamol) is recommended at Step 1 of the World Health Organization ladder. Of the Step 2 analgesics, tramadol is the least problematic, although dose reduction and increased dosing interval are required, and caution should be exercised. Of the Step 3 analgesics, fentanyl, alfentanil and methadone are recommended. There is limited evidence for buprenorphine, although theoretical reasons why it may be a good choice for these patients. Hydromorphone and oxycodone cannot be recommended because of extremely limited evidence, although each is likely a better choice than morphine or diamorphine. Morphine and diamorphine themselves are not recommended because of known accumulation of potentially toxic metabolites.

Predictors of Renal Outcome in HIV-Associated Nephropathy

BACKGROUND Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is an important cause of end-stage renal disease among African American patients. This study was performed to study the epidemiology of HIVAN in a predominantly black African population and the impact of highly active antiretroviral therapy and other factors on the development of end-stage renal disease. METHODS We retrospectively identified all patients with HIVAN, defined by biopsy or strict clinical criteria, in 8 clinics in the United Kingdom. Baseline renal function, HIV parameters, renal pathological index of chronic damage, and responses to highly active antiretroviral therapy were analyzed, and factors associated with adverse renal outcome were identified. RESULTS From 1998 through 2004, we studied 16,834 patients, 61 of whom had HIVAN. HIVAN prevalence in black patients was 0.93%, and HIVAN incidence in those without renal disease at baseline was 0.61 per 1000 person-years. After a median of 4.2 years, 34 patients (56%) had developed end-stage renal disease. There were no significant differences in renal function and HIV parameters at baseline, time to initiation of highly active antiretroviral therapy, and rates of HIV RNA suppression between the 20 patients who developed end-stage renal disease >3 months after receiving the HIVAN diagnosis and the 23 patients who maintained stable renal function. However, the index of chronic damage score was significantly higher in those who developed end-stage renal disease (P < .001), and an index of chronic damage score >75 was associated with shorter renal survival (P < .001). CONCLUSIONS Whereas overall patient survival suggested an important benefit of highly active antiretroviral therapy, no additional renal benefit of early initiation of highly active antiretroviral therapy or viral suppression could be demonstrated in this large cohort of patients with established HIVAN. Severity of chronic kidney damage, as quantified by biopsy, was the strongest predictor of renal outcome.

Unusual presentation of aortic dissection with bilateral testicular pain and rapidly deteriorating renal function.

THE CASE 43-year-old male former smoker with a history of dilated cardiomyopathy secondary to hypertenAsion, intermittent claudication, obesity, and hypercholesterolemia, attended the Accident and Emergency Department with a 24-hour history of sharp central chest pain and some dyspnea. Although this was his first presentation with chest pain, he had attended the Accident and Emergency Departments at other hospitals twice during the preceding 6 months with loin pain and testicular pain. On these occasions, he was diagnosed with and treated for pyelonephritis and epididymitis, respectively, after receiving previous inpatient urology reviews with normal results on testicular ultrasonography. On this visit to our hospital, his vital signs and physical examination were normal. Cardiovascular examination revealed normal heart sounds, with no added murmurs, and equal pulses and blood pressures bilaterally. An electrocardiogram showed left axis deviation and a nondynamic 1-mm ST segment depression across the lateral chest leads. Arterial blood gases were normal on room air, with a pH of 7.39, partial pressure of oxygen of 11.7kPa, partial pressure of carbon dioxide of 5.32 kPa, and bicarbonate of 23.8 mmol. However, blood tests revealed impaired renal function (serum creatinine, 142 mmol/L), with elevated D-Dimer levels (>8000 ng/ml) and a hemoglobin level of 15g/dL (MCV 85fl). His chest x-ray image was normal, with no obvious mediastinal widening. On the basis of his symptoms, the accident and emergency team became concerned about a pulmonary embolus; however, an urgent computed tomography (CT) pulmonary angiogram did not show any evidence of pulmonary emboli. The following day, his chest pain had resolved, but sudden and sharp bilateral testicular pain developed, similar to that previously experienced. The general