Eric Taylor

Vascular theory of the formation of Randall plaques.

The relationship between calcium-based calculi and Randall plaques is well documented, but the role these plaques play in the early process of urinary stone formation remains unknown. The vascular hypothesis of Randall plaque formation has been proposed, and recent works support this concept. The renal papilla’s vascular environment is subject to relative hypoxia, hyperosmolar surroundings, and turbulent blood flow. These factors together create an environment prone to vascular injury and may potentiate Randall plaque precipitation. Recent data support the similarity between the vascular calcification process itself and urinary stone formation. Furthermore, epidemiological studies have suggested an association between urinary stones, adverse cardiovascular events, and vascular calcification risk factors. The concept that an initial vascular insult precipitates a Randall plaque and subsequent urolithiasis is compelling and represents an area in need of continued research. This may lead to future novel treatment approaches to urolithiasis.

Complications associated with percutaneous nephrolithotomy.

The increasing global prevalence of nephrolithiasis continues to burden the healthcare delivery systems of industrialized nations and exact a disproportionate humanitarian toll on populations of the developing world (1). In the United States alone, the prevalence of nephrolithiasis is nearly twice the rate reported in the 1960s (2-5). The subsequent rise in surgical interventions for nephrolithiasis has resulted in the development of new minimally invasive technologies and techniques, but it has also led to the resurgence of established methods such as percutaneous nephrolithotomy (PNL).

Determinants of nephrostomy tube dislodgment after percutaneous nephrolithotomy.

BACKGROUND AND PURPOSE Percutaneous nephrolithotomy (PCNL) traditionally necessitates the placement of a nephrostomy tube at the conclusion of the surgical procedure. Although tubeless PCNL has become more popular, patients with complex problems still need traditional nephrostomy tube drainage. The goal of this study was to investigate whether patient body mass index (BMI) impacted inadvertent nephrostomy tube dislodgement. Furthermore, we hoped to determine whether nephrostomy tube type impacted tube dislodgement rates. METHODS A retrospective review between 2005 and 2012 of 475 consecutive PCNL cases was undertaken. Patients were categorized based on the type of nephrostomy tube placed. BMI was examined as a continuous variable. The primary outcome of nephrostomy tube dislodgment was determined based on imaging obtained at the time of PCNL and postoperative hospitalization. Logistic regression analysis was then used to adjust for nephrostomy tube type and BMI. RESULTS Overall, 24 (5.5%) total patients experienced nephrostomy tube dislodgment postoperatively. The mean BMI for patients experiencing nephrostomy tube dislodgment was 39.7 vs 30.9 for those without tube dislodgment (P<0.0001; 95% confidence interval [CI] 4.6 to 12.9). Using logistic regression and adjusting for the use tube type, BMI was an independent predictor of tube dislodgement (P<0.001). For each unit of increase in BMI, the likelihood of tube dislodgment increased by 6% (1.06). After adjusting for BMI, however, nephrostomy tube type was not found to be an independent predictor of nephrostomy tube dislodgment. CONCLUSIONS Nephrostomy tube type did not influence nephrostomy tube dislodgment rates. As a patients BMI increased, the likelihood of tube dislodgment increased in a directly proportionate fashion. This is possibly because of the nephrostomy tube being fixed directly to the mobile skin associated with their fat pannus. Although the nephrostomy tube type itself did not affect tube dislodgment rates, a redesigned nephrostomy tube or fixation device should take into account the above findings related to obese patients to reduce the likelihood of nephrostomy tube dislodgment.

Significant differences in struvite and cystine stone frequency seen among Chinese nephrolithiasis patients living in North America compared to those living in China

Background Interracial disparities in nephrolithiasis prevalence have been reported, but the interplay between genetics and the environment for urinary stone disease risk factors is poorly understood. To examine how environment may alter genetic predisposition for stone formation, we established the International Chinese Consortium on Nephrolithiasis (ICCON) as a multi-institutional collaboration to examine patterns of nephrolithiasis presentation between Chinese patients living in different countries. Methods Chinese patients undergoing percutaneous nephrolithotomy (PCNL) at six participating institutions in China and North America over 4 years were reviewed retrospectively. Patient demographics and clinical data were compared between Chinese patients living in China and North America. Results A total of 806 patients were included, encompassing 721 Chinese patients living in China and 85 living in North America. Nephrolithiasis patients living in China were more likely to be male (67% vs. 56%, P=0.02), present at a younger age (48.6±15.0 vs. 55.0±13.0 years, P<0.01), and have a lower BMI (24.6±4.0 vs. 25.9±5.7, P=0.04) but were less likely to form struvite stones (5.5% vs. 14.1%, P<0.01). No cystine stone patients were seen in North American Chinese patients, whereas 1.8% of nephrolithiasis patients living in China presented with cystine stones. Similar rates of calcium-based and uric acid calculi as well as urinary pH were seen among both groups. Conclusions Significant differences exist between Chinese nephrolithiasis patients living in China compared to those living in North America, highlighting the importance of environmental factors in addition to genetics in modulating risk for urinary stone disease.

Moderation may be the best fad diet for urinary stone disease.

With recent increases in obesity throughout the United States and other industrialized nations, fad diets continue to gain in popularity. Although little formal research has been undertaken regarding the health impact of these fads, each has its own questionable health benefits as well as potential health risks, including lithogenic effects (1).

Making sense of dietary calcium and urinary stone disease

The regulation of dietary and supplemental calcium intake in relation to urinary stone disease is not well understood (1). For instance, why do most patients with primary hyperparathyroidism with markedly increased serum and urinary calcium not have a history of urinary stone disease?

Reactive oxygen species may unite many mechanisms by which calcium oxalate stones form

The pathogenesis of calcium oxalate nephrolithiasis remains a mystery, but the suggestion that it is simply due to perturbations in urinary super saturations remains an inadequate explanation (1). It is likely due to much more complex and nuanced mechanisms that incorporate inorganic and organic components. How these components propagate into Randall plaques or calculi or even where these stone-forming events occur (vasa recta, collecting ducts, or the basement membrane of the loops of Henle) is debatable. Metabolic derangements leading to uncontrolled reactive oxygen species (ROS) generation or a reduced antioxidant capacity to alleviate oxidative stresses may play a role in Randall plaque formation through tissue damage and/or ROS-induced altered gene expression.

The link between metabolic syndrome and nephrolithiasis: a white whale for understanding urinary stone disease

The incidence of nephrolithiasis has risen steadily over recent decades, as has the rates of the metabolic syndrome. Several factors have contributed to this, including the increased incidence of obesity; more than 30% of Americans have a body mass index (BMI) >30. The etiologies for both are complex and multifactorial, but a consistently demonstrable relationship does exist between the two. Patients with either affliction are prone to the other, with the highest incidence of stones found in those with several factors leading to the metabolic syndrome (1). Furthermore, several of the disease process (hypertension, atherosclerosis, diabetes mellitus, or dyslipidemia) related to the metabolic syndrome each are associated with an increased risk of nephrolithiasis. The reason for this is unclear, and likely goes beyond just poor dietary factors leading to serum and urine chemistries ideal for renal calculus formation. No underlying mechanism has yet been identified correlating these processes to one another. Continued basic and translational research is needed to understand how these diseases are linked. While a growing body of epidemiologic data supports these associations, they only serve to highlight the importance of further research to truly understand the underlying mechanisms driving these links. As translational research continues to expand in the field of nephrolithiasis, newly generated knowledge will fill the gaps brought to light by these epidemiologic data.

Alexander Randall may have had it right after all.

Several theories exist regarding the pathogenesis of urinary calculi, and the early incipient events leading to calculus formation remain the most controversial. The authors detail a theory by which microscopic Randall plaques (RP) lead to calcium oxalate calculi in idiopathic calcium oxalate stone formers (1). Outlined is a process by which RP form in the basement membrane of the loops of Henle and spread through the interstitium through mineral deposition in an organic matrix, eventually eroding through the urothelium. Once exposed to the urinary milieu, precipitation of minerals and organic substances occurs based on urinary constituents. The process leading to RP formation is not yet fully defined, but one must consider an alternative theory based on a more vascular process. In short, formation may be RP due to a process similar to how atherosclerotic lesions form in arteries as the vasa recta that surround the tubules have turbulent flow, relative hypoxia, and hyperosmolarity which is an ideal environment for vascular injury and a calcifying process. The early events leading to RP and calcium oxalate stone formation has yet to be determined, but is likely multifactorial and represents an area of research fit for collaboration beyond our fellow urologic colleagues.

Balancing the utility of new technology against cost in urinary stone disease

Several advances in endourologic technology have allowed for a greater scope of care to be provided to urologic patients via a minimally invasive approach. The greatest of these is likely the current generation of flexible ureteroscopes which allow for a level of maneuverability, with or without active secondary deflection, that rarely prevent lower pole renal access via a retrograde approach.