Carotid endarterectomy in patients with renal insufficiency: Should selection criteria be different in patients with renal insufficiency?

The objective of this study was to elucidate the relationship between outcomes from carotid endarterectomy (CEA) in patients with and without renal insufficiency. Carotid endarterectomy is one of the most commonly performed vascular procedures. The role of cardiac comorbidity in carotid endarterectomy has been extensively studied. The relationship between renal failure and surgical outcomes has also been studied for both coronary artery bypass grafting and lower extremity occlusive disease. However, the role of renal insufficiency in relationship to decision making regarding surgical intervention for carotid stenosis is not well defined. The authors hypothesized that the outcomes from CEA were negatively influenced by renal dysfunction. A retrospective review was made of consecutive CEAs performed at their institution from 1990 to 1995. Patients were grouped into 2 categories according to their renal function. Group A, 448 patients (90%) with creatinine level 1.8 mg/dL or less, and group B, 49 patients (10%) with creatinine levels more than 1.8 mg/dL. Data from patients on dialysis are presented but were excluded for the purpose of analysis. Included in the study were 497 patients with a mean age of 70 +/-8.9 and 74 +/-8.9 for groups A and B, respectively. Preoperative creatinine was 1.1 (+/-0.25) mg/dL for group A and 2.5 (+/-0.81) mg/dL for group B. Outcomes were as follows: perioperative cardiac events 5.4% vs 28.6%, stroke rates 2.7% vs 2.0%, and mortality rates 0.9% vs 8.2%, for groups A and B, respectively. At 60-month follow-up the stroke rates were 7.6% vs 6.1 %, and the mortality rates 22.8% vs 59.2%, for groups A and B, respectively. While patients with chronic renal insufficiency have no increased risk of perioperative or long-term neurologic events, perioperative and long-term mortality rates are significantly increased. This significant reduction in survival should prompt a more cautious application of CEA in patients with increased creatinine.     

Nephroprotection: how to slow the progression of chronic renal insufficiency?

Most nephropathies are characterized by a progression that may result in end-stage renal failure (ESRF). Apart from the specific treatment implemented when possible, ESRF may be delayed by nephroprotective therapy. Following the definition of the risk factors likely to induce progressive renal disease, the various therapeutic strategies that may play a nephroprotective role are reviewed. The potential results are described with regard to published data, in particular randomised trials, as recommended by the evidence-based medicine principles. Blockade of the renin-angiotensin system plays a major role in terms of nephroprotection. However, this strategy should not replace lifestyle measures and pharmacological treatment of the metabolic disorders associated to nephropathies.     

Can renal fibrosis be reversed?

New therapeutic approaches are needed to address the current epidemic of chronic kidney disease. Beyond delaying the inevitable onset of end-stage kidney disease the ultimate dream of clinical therapy is disease regression. Degradation of the interstitial matrix proteins is potentially feasible, especially before the interstitial scar becomes highly organized. Currently the specific matrix-degrading proteases that perform this function in vivo have not been clearly identified although several candidates have been suggested. Reversing renal fibrosis will also mandate removal of interstitial myofibroblasts that are the major source of the fibrosis-associated interstitial matrix proteins. However, the greater therapeutic challenge pertains to the current inability to regenerate intact functional nephrons in a site where they have been destroyed. In chronic tubulointerstitial damage that typifies all progressive kidney diseases, it is not interstitial matrix accumulation per se that leads to renal functional decline but rather its destructive effects on neighboring cells. In particular, loss of peritubular capillaries and tubules are the morphological features that underlie declining renal function. Recent advances in several basic scientific fields of investigation such as matrix biology, developmental biology, angiogenesis, and stem cell biology have identified new candidate therapeutic targets. A powerful new molecular tool-box is at our disposal that can be used to begin to translate recent discoveries into the clinical research arena with the goal of reversing renal fibrosis in a functionally meaningful way.     

Can acute renal failure be prevented?

Correction of salt and volume depletion is paramount in the prevention of renal damage. Measures which stimulate intense filtration of glomeruli in acute renal failure, such as the use of atrial natriuretic peptide analogues, theophylline, dopamine, or growth factors should be regarded with caution, since they all increase metabolic workload in the outer medulla and hence aggravate medullary hypoxia. Neither frusemide, dopamine nor dopexamine have been shown to be better than aggressive saline loading in preventing acute renal failure in at risk patients. Until new clinical studies emerge, avoidance of nephrotoxic insults where possible, monitoring of circulating concentrations of potentially nephrotoxic drug levels and volume loading coupled with supportive measures is recommended. When volume depletion persists, usual blood pressure cannot be restored and patients remain oliguric, early referral to the intensive care unit is paramount. The mortality rate in patients with acute renal failure is high; therefore, measures which reduce the incidence and progression of renal dysfunction will be of benefit.     

Can peritoneal dialysis be used as a long term therapy for end stage renal disease?

Over the last 25 years, since the introduction of CAPD, the use of PD has increased greatly and over this period many advances in technique have been made. As is well known, that home and self-dialysis, such as PD, cost less than in-center HD and can provide excellent survival and a high level of patient rehabilitation. To date however, the demonstration that PD can provide long term dialysis has been limited to a small number of patients. The next few decades will see a marked increase in the worldwide dialysis population, particularly as older and sicker patients are accepted into dialysis. It is likely that worldwide pressures related to cost containment will favour the use of cost effective therapies, such as PD. However, the increased use of PD will continue, only if we continue to improve its efficacy and do not waste the economic benefits gained over HD. We are challenged to improve and develop PD in a way that optimises patient medical and psychosocial outcomes while minimizing costs. This may be achieved by using more biocompatible solutions, hopefully inexpensive, that will maintain the peritoneal membrane intact for long periods, will better preserve the membrane's transport characteristics over time, and thus reduce the main causes of drop out from dialysis.     

The diabetic patient: renal insufficiency like other kidney failures?

The number of patients requiring renal replacement therapy because of diabetic nephropathy has been relentlessly increasing, and diabetes mellitus is now the leading cause of end stage renal disease in most Western Countries. Diabetic nephropathy has specificities. First, it tends to progress rapidly toward end stage renal disease. Second, patients with diabetic nephropathy are at increased risk of cardiovascular disease, when compared to patients with non diabetic nephropathy; similarly to what has been shown for diabetic patients on dialysis. Third, patients with diabetic nephropathy tend to be more severely anemic than patients with non-diabetic chronic kidney disease. Finally, small studies suggest that patients with diabetic nephropathy could have lower serum concentrations of parathyroid hormone than patients with non-diabetic nephropathy and similar glomerular filtration rate.     

Can traumacel be used in the treatment of chronic wounds?

Traumacel (calcium salt of oxidised cellulose) has previously only been used in the treatment of acute wounds. To assess its safety and effectiveness in the management of chronic wounds a 12-week pilot study was undertaken which involved 11 patients with 15 non-healing leg ulcers and assessed ulcer size, ulcer pain and degree of exudate. Five ulcers healed within the study period. Significant pain relief was experienced by three patients. Use of the dressing did not appear to be related to a reduction in exudate. No patients experienced sensitisation to the product or had to be withdrawn because of adverse effects. Traumacel was found to be safe in the management of chronic ulceration, and appeared to promote healing in some recalcitrant ulcers.