Ischemic nephropathy: where are we now?

Identification and reversing the loss of kidney function beyond occlusive disease of the renal arteries poses a major clinical challenge. Recent studies indicate that atherosclerotic renal artery stenosis develops as a function of age and is commonly associated with other microvascular disease, including nephrosclerosis and diabetic nephropathy. The risks of renal artery stenosis are related both to declining kidney function and to accelerated cardiovascular disease, with increased morbidity and mortality. Newer drugs, including agents that block the renin-angiotensin system, have improved the level of BP control for renovascular hypertension. Progressive renovascular disease during medical therapy can produce refractory hypertension, congestive heart failure, and renal failure with tubulointerstitial fibrosis. Recent studies indicate a complex interplay of oxidative stress, endothelial dysfunction, and activation of fibrogenic cytokines as a result of experimental atherosclerosis and renal hypoperfusion. Advances in imaging and interventional devices offer major new opportunities to prevent progressive loss of kidney function. Recent series indicate that although 25 to 30% of patients with impaired renal function can recover glomerular filtration after revascularization, many have no apparent change in kidney function and 19 to 25% experience a significant loss of kidney function, in some cases as a result of atheroemboli. To select patients who are most likely to benefit from vascular intervention, clinicians should understand the pathophysiology of developing ischemic nephropathy and the potential hazards of revascularization in the setting of diffuse atherosclerotic disease. Further research should be directed toward identification of critical disease, regulation of fibrogenesis, and the interaction with other atherosclerotic processes.     

Diagnostic criteria for renovascular disease: where are we now?

Renovascular disease, especially atherosclerotic renal artery stenosis (ARAS) in older subjects, is commonly encountered in clinical practice. This is at least in part due to the major advances in non-invasive imaging techniques that allow greater diagnostic sensitivity and accuracy than ever before. Despite increased awareness of ARAS, renal revascularization is less commonly performed, likely as a result of several prospective, randomized, clinical trials which fail to demonstrate major benefits of renal revascularization beyond medical therapy alone. Primary care physicians are less likely to investigate renovascular disease and nephrologists likely see more patients after a period of unsuccessful medical therapy with more advanced ARAS. The goal of this review is to revisit current diagnostic and therapeutic paradigms in order to characterize more clearly which patients will likely benefit from further evaluation and intensive treatment of renal artery stenosis.     

Immunosuppression for kidney transplantation: Where are we now and where are we going?

Advances in immunosuppression have propelled kidney transplantation from a scientific curiosity to the optimal treatment for patients with end stage kidney disease. Declining rates of acute rejection have led to improvements in short term kidney transplant survival, culminating in incrementally better long term patient and allograft outcomes. Contextualized around established immune-suppressing drug targets, this review summarizes the history of the clinical science and highlights the pivotal trials that have led to present-day treatment standards at the level of both individual agents and multidrug regimens for kidney recipients. Finally, recently approved and emerging therapies are discussed, with an emphasis on challenges faced by clinicians managing this increasingly complex patient population.     

Transanal endoscopic microsurgery: where are we now?

AIMS: This review of literature aimed to assess the role and establish the current status of transanal endoscopic microsurgery (TEM) in the management of benign and malignant rectal lesions. METHODS: A review of the literature was undertaken through the Medline database and by cross-referencing previous publications, thus identifying 54 relevant publications on TEM in the management of rectal lesions. Aggregated results of various parameters were calculated but statistical comparisons deemed unsuitable due to heterogeneity of data. RESULTS: The TEM procedure is associated with good functional results, morbidity of 4% and zero procedure-related mortality. The local recurrence rates after TEM excision is 4.5% (range 0-14) for benign rectal lesions, 6% (0-13) for T(1) cancers, 14% (range 0-50) for T(2) cancers and 20% (range 14-67%) for T(3) cancers. Local recurrences after TEM can be surgically salvaged with good disease free survival rates. CONCLUSIONS: The TEM procedure clearly offers the benefits of good exposure of the operative field allowing extremely precise dissection and access to high rectal lesions unresectable by other methods. For pTis and low risk pT(1) lesions, the oncological results are comparable to the more traditional formal resection. The routine use of TEM for high-risk pT(1) and higher stage lesions is not an oncologically sound choice at the present moment.     

Persistent postoperative pain: where are we now?

There has been considerable interest and controversy around persistent postoperative pain for several years. Most of the available data arise from studies with methodological problems (especially its definition in terms of duration, severity, and effect on quality of life and function); however, more recent investigations have begun to address these issues. Although the quoted incidence varies considerably, analysis of the most conservative data shows that there is no doubt that persistent postoperative pain is a significant clinical problem and a burden to those who suffer from it. There is a wealth of literature describing factors associated with increased likelihood of persistent postoperative pain. Although it is difficult to be precise, it is clear that psychosocial factors probably play a role in some situations and that significant preoperative pain, severe immediate postoperative pain, and nerve damage are often good predictors. There are some data indicating that the incidence and severity of persistent postoperative pain can be reduced by special perioperative interventions; however, as yet, the evidence is not compelling and consistent. A reliable prevention strategy is not yet emerging from the published literature and considerably more work is required to deliver this.     

Anal fistula plug: Where were we,where are we now?

The controversy associated with the treatment of complex fistula disease is rooted within the balance of the therapeutic index—highly efficacious techniques, such as fistulotomy, have unfavorably high rates in incontinence. Unfortunately, safer techniques, such as fibrin glue and anal fistula plugs sacrifice better cure rates for lower rates of post-operative incontinence. This article will discuss the use of the anal fistula plug (AFP) from its inception, evolution of technique, and its predictors of success, while summarizing the literature on the bioprosthetic anal fistula plugs in the management of anal fistulas.     

Arterial stiffness in dialysis patients: where are we now?

Patients with end-stage renal disease treated by chronic dialysis have an impressive mortality, which more than half of this mortality is attributable to cardiovascular disease. Despite stratification for sex, race, and the presence of diabetes, cardiovascular disease mortality is 10–30 times higher in dialysis patients compared to general population. In dialysis patients, both atherosclerosis (mainly affecting the intima of the arteries) and arteriosclerosis (affecting predominantly the media of large- and middle-sized arteries diffusely) are highly prominent. Arteriosclerosis characterized by reduced arterial compliance (i.e., reduced elasticity of the arteries) is due to increased fibrosis, loss of elastic fibers, and extensive vessel wall calcification. Arteriosclerosis is closely related to arterial stiffness. A generally accepted mechanistic view is that an increase in arterial stiffness causes a premature return of reflected waves in late systole, increasing central pulse pressure, thus systolic. An increased arterial stiffness can increase the risk of stroke through several mechanisms, including an increase in central pulse pressure, influencing arterial remodeling both at the site of the extracranial and intracranial arteries, increasing carotid wall thickness, and the development of stenosis and plaques, and the likelihood of plaque rupture. Very importantly, it was also suggested that arterial stiffness itself independently plays a role in exacerbating chronic kidney disease progression. This review deals briefly with the definition of arterial stiffness, methods of measuring arterial stiffness and pathophysiology of arterial stiffness, and factors related with arterial stiffness.