Typology of intravesical prostatic protrusions, or so-called median lobes, in middle-aged and older men.

PURPOSE: Changes related to prostatic ageing include an increase of prostate volume and morphologic distortions of the prostatic edges in middle-aged and older men. These changes of the prostate exhibit a certain level of heterogeneity, which is clinically obvious for surgeons, radiologists, and anatomists, and which can be explained by the complex nature of the embryologic/anatomic development of the prostate. While the etiology of the median lobe has typically been attributed to a growth and protrusion of the prostatic area at the top of the utricle, we argue that this is not necessarily the case as intravesical protrusions of the prostate have also been observed laterally and anteriorly to the bladder neck, suggesting the involvement of other prostatic zones, thereby highlighting the need to refine the concept of the median lobe. MATERIAL: The current study examined a large series of 478 prostate magnetic resonance imaging scans (MRIs). Intravesical prostatic protrusions were classified, based on their topography: anterior (A), posterolateral (P), and dual (D). Data were analyzed using MedCalc®11.6.1.1.0 software. Pearson's correlations with coefficients (r) and P values were calculated for the patient's age, prostate volume, and IVPP size. RESULTS: An intravesical prostatic protrusion was observed in 27% of cases, with type A occurring in 18% (3% isolated), type P in 96% (81% isolated), and type D in 15%. CONCLUSION: The new insights regarding the variability in prostate anatomy will contribute to the improved management of prostate hypertrophy by radiologists and surgeons.

[Acute obstructive nephropathy: A pathophysiological view]. / Insuffisance rénale aiguë obstructive : une lecture physiopathologique.

Obstructive acute renal failure is a heterogeneous entity as the pathophysiology of intratubular obstruction is quite different from upper tract obstruction. In the former case, tubules are dilated due to a high hydrostatic pressure whereas pressures are normal in urinary upper tract. In the latter case, a high pressure above the ureteral obstacle is responsible for dilated renal cavities leading to extrinsic compression with no or only few dilated tubules though high hydrostatic pressure are recorded within tubules. Obstruction within tubules may be related to crystal formation, exfoliated cells, cellular debris and/or protein gels altogether with cell proliferation, proliferating cells, and recruitment of inflammatory cells. Though fibrosis may develop, the occurrence of atubular glomeruli in several nephrons due to an initial loss of tubular patency highlights the critical importance of maintaining a fluid flow within tubules in order to avoid uncontrolled tubular cell proliferation. The onset of tubular obstruction in few tubules, especially in crystal nephropathy is underestimated especially in chronic kidney disease patients, thus suggesting that some macromolecular solubilizing factors may be potential relevant therapy to prevent (and/or reverse) chronic kidney disease progression or decrease acute renal failure sequelae.

Plasma heme-induced renal toxicity is related to a capillary rarefaction.

Severe hypertension can lead to malignant hypertension (MH) with renal thrombotic microangiopathy and hemolysis. The role of plasma heme release in this setting is unknown. We aimed at evaluating the effect of a mild plasma heme increase by hemin administration in angiotensin II (AngII)-mediated hypertensive rats. Prevalence of MH and blood pressure values were similar in AngII and AngII + hemin groups. MH rats displayed a decreased renal blood flow (RBF), increased renal vascular resistances (RVR), and increased aorta and interlobar arteries remodeling with a severe renal microcirculation assessed by peritubular capillaries (PTC) rarefaction. Hemin-treated rats with or without AngII displayed also a decreased RBF and increased RVR explained only by PCT rarefaction. In AngII rats, RBF was similar to controls (with increased RVR). PTC density appeared strongly correlated to tubular damage score (rho = -0.65, p < 0.0001) and also renal Heme Oygenase-1 (HO-1) mRNA (rho = -0.67, p < 0.0001). HO-1 was expressed in PTC and renal tubules in MH rats, but only in PTC in other groups. In conclusion, though increased plasma heme does not play a role in triggering or aggravating MH, heme release appears as a relevant toxic mediator leading to renal impairment, primarily through PTC endothelial dysfunction rather than direct tubular toxicity.