Correlation analysis between renal papillae Hounsfield density (PHD) and endoscopic papillary description in stone formers.

We aimed to evaluate the correlation between endoscopic papillary abnormalities (PA) and high renal papilla Hounsfield density (PHD) on CT scan in patients who underwent flexible ureteroscopic treatment (fURS) for renal stones. We retrospectively assessed patients from a prospectively collected database who were treated with fURS for renal stones between May 2016 and October 2020. PHD was measured on preoperative CT-scan by a radiologist blinded from the intraoperative aspect of the papillae. Correlation was examined between high PHD (≥ 43 HU) and PA described in fURS, stone composition, metabolic abnormalities, … Out of 159 consecutive cases, 131 were eligible for analysis with available preoperative CT-scan. Median age was 55 years (IQR 43-67) and median PHD was 40 (IQR 36-45). Eighty patients (61%) had PHD < 43, and 51 patients (39%) had PHD ≥ 43. In univariate and multivariate analysis, only young age (p-value = 0.017) and insufficient diuresis (p-value = 0.008) were correlated with high PHD. No significant correlation was found with PA described during endoscopy, including the intensity of Randall's plaques. In this study, high PHD appears to be only a sign of insufficient diuresis, with no significant correlation with potential PA.

Contralateral renal change in a unilateral ureteral obstruction rat model using intravoxel incoherent motion diffusion-weighted imaging.

OBJECTIVES: Most functional magnetic resonance research has primarily examined alterations in the affected kidney, often neglecting the contralateral kidney. Our study aims to investigate whether imaging parameters accurately depict changes in both the renal cortex and medulla in a unilateral ureteral obstruction rat model, thereby showcasing the utility of intravoxel incoherent motion (IVIM) in evaluating contralateral renal changes. METHODS: Six rats underwent MR scans and were subsequently sacrificed for baseline histological examination. Following the induction of left ureteral obstruction, 48 rats were scanned, and the histopathological examinations were conducted on days 3, 7, 10, 14, 21, 28, 35, and 42. The apparent diffusion coefficient (ADC), pure molecular diffusion (D), pseudodiffusion (D*), and perfusion fraction (f) values were measured using IVIM. RESULTS: On the 10th day of obstruction, both cortical and medullary ADC values differed significantly between the UUO10 group and the sham group (p < 0.01). The cortical D values showed statistically significant differences between UUO3 group and sham group (p < 0.01) but not among UUO groups at other time point. Additionally, the cortical and medullary f values were statistically significant between the UUO21 group and the sham group (p < 0.01). Especially, the cortical f values exhibited significant differences between the UUO21 group and the UUO groups with shorter obstruction time (at time point of 3, 7, 10, 14 day) (p < 0.01). CONCLUSIONS: Significant hemodynamic alterations were observed in the contralateral kidney following renal obstruction. IVIM accurately captures changes in the unobstructed kidney. Particularly, the cortical f value exhibits the highest potential for assessing contralateral renal modifications.

Renal papillary tip biopsy in stone formers: a review of clinical safety and insights.

Alexander Randall first published renal papillary tip findings from stone formers in 1937, paving the way for endoscopic assessment to study stone pathogenesis. We performed a literature search to evaluate the safety of papillary tip biopsy and clinical insights gained from modern renal papillary investigations. A search on the topic of renal papillary biopsy provided an overview of Randall's plaques (RP), classification systems for renal papillary grading, and a summary of procedure type, complications, and outcomes. Within 26 identified manuscripts, 660 individuals underwent papillary tip biopsy percutaneously (n = 562), endoscopically (n = 37), or unspecified (n = 23). Post-operative hemoglobin changes were similar to controls. One individual (0.2%) reported fever > 38°, and long-term mean serum creatinine post-biopsy (n = 32) was unchanged. Biopsies during ureteroscopy or PCNL added ~20-30 min of procedure time. Compared to controls, papillary plaque-containing tissue had upregulation in pro-inflammatory genes, immune cells, and cellular apoptosis. Urinary calcium and papillary plaque coverage were found to differ between RP and non-RP stone formers, suggesting differing underlying pathophysiology for these groups. Two renal papillary scoring systems have been externally validated and are used to classify stone formers. Overall, this review shows that renal papillary biopsies have a low complication profile with high potential for further research. Systematic adaption of a papillary grading scale, newer tissue analysis techniques, and the development of animal models of Randall's plaque may allow further exploration of plaque pathogenesis and identify targets for prevention therapies in patients with nephrolithiasis.

Confining calcium oxalate crystal growth in a carbonated apatite-coated microfluidic channel to better understand the role of Randall's plaque in kidney stone formation.

Effective prevention of recurrent kidney stone disease requires the understanding of the mechanisms of its formation. Numerous in vivo observations have demonstrated that a large number of pathological calcium oxalate kidney stones develop on an apatitic calcium phosphate deposit, known as Randall's plaque. In an attempt to understand the role of the inorganic hydroxyapatite phase in the formation and habits of calcium oxalates, we confined their growth under dynamic physicochemical and flow conditions in a reversible microfluidic channel coated with hydroxyapatite. Using multi-scale characterization techniques including scanning electron and Raman microscopy, we showed the successful formation of carbonated hydroxyapatite as found in Randall's plaque. This was possible due to a new two-step flow seed-mediated growth strategy which allowed us to coat the channel with carbonated hydroxyapatite. Precipitation of calcium oxalates under laminar flow from supersaturated solutions of oxalate and calcium ions showed that the formation of crystals is a substrate and time dependent complex process where diffusion of oxalate ions to the surface of carbonated hydroxyapatite and the solubility of the latter are among the most important steps for the formation of calcium oxalate crystals. Indeed when an oxalate solution was flushed for 24 h, dissolution of the apatite layer and formation of calcium carbonate calcite crystals occurred which seems to promote calcium oxalate crystal formation. Such a growth route has never been observed in vivo in the context of kidney stones. Under our experimental conditions, our results do not show any direct promoting role of carbonated hydroxyapatite in the formation of calcium oxalate crystals, consolidating therefore the important role that macromolecules can play in the process of nucleation and growth of calcium oxalate crystals on Randall's plaque.

Renal expression of AQP1 in the high-fat nutritional obesity of rat / Expresión renal de AQP1 en la obesidad nutricional alta en grasas en ratas

AQP1 plays an essential role in maintaining body water balance. In the kidney, AQP1 is localized to the apical and basolateral membrane of epithelial cells in the proximal tubule and descending thin limb of Ansa nephroni (Henle's loop) where it reabsorbs the vast majority of filtered water. The growing epidemic of obesity and metabolic diseases particularly obesity-related kidney disease is getting more and more attention in this century. However, a full understanding of mechanisms involved to the progressive renal disease is still unclear, in particular AQPs in the kidney of obesity. In this paper, we examined the localization of AQP1 in renal cortex and medulla of ND (normal diet) and HFD (high-fat diet) at rats. In the renal cortex and medulla, immunolight microscopy revealed weak expression of AQP1 in the apical and basolateral membrane of epithelial cells at the proximal straight/convoluted tubule of HFD compared with ND, respectively. The same result was confirmed in the thick descending limb and descending thin limb of Henle's loop. In the high-fat nutritional obesity of rats, decreased AQP1 levels may not directly cause serious obesity-related kidney disease, e.g. chronic kidney disease, even end-stage renal disease. But at least, AQPs (AQP1 in this study) was one of initially conditions to the incentive of obesity-related kidney disease.

Las acuoporinas tipo 1 (AQP1) constituyen una parte esencial en el mantenimiento del equilibrio del agua en el cuerpo. En el riñón, la AQP1 se localiza en la membrana apical y basolateral de las células epiteliales, en el túbulo proximal y en el segmento descendente del Ansa nephroni o asa nefrónica (asa de Henle), donde reabsorbe la gran mayoría de agua filtrada. La creciente epidemia de obesidad y enfermedades metabólicas en el siglo actual, hacen que la enfermedad renal relacionada con la obesidad esté recibiendo cada vez más atención. Sin embargo, aún no existe un conocimiento definitivo de los mecanismos implicados en la enfermedad renal progresiva, en particular los relacionados a las acuoporinas renales en la obesidad. En este trabajo, examinamos la localización de AQP1 en la corteza y la médula renales de la dieta normal (DN) y dieta alta en grasa (DAG) en ratas. En la corteza y médula renales, la microscopía de luz reveló una expresión débil de AQP1 en la membrana apical y basolateral de las células epiteliales en el túbulo contorneado proximal del grupo DAG en comparación con el grupo DN, respectivamente. El mismo resultado se confirmó en la porción descendente gruesa y en la porción descendente delgada del asa nefrónica. En ratas del grupo DAG, la disminución de los niveles de AQP1 pudo no ser la causa directa de una enfermedad renal grave relacionada con obesidad, como por ejemplo, enfermedad renal crónica, o una enfermedad renal terminal. No obstante, en este estudio, la expresión renal de AQP1 constituyó una de las condiciones iniciales para inducir la enfermedad renal relacionada con obesidad.

Expression of V2R and AQPs in the renal medulla of high-fat nutritional obesity of rat / Expresión de V2R y AQPs en la médula renal de ratas con obesidad nutricional alta en grasas

Recent evidence has indicated that adipose tissue produces bioactive substances that contribute to obesity-related kidney disease, altering the renal function and structure. Eight of the AQPs are expressed in the kidney, where several of them contribute to water absorption and maintenance of body water balance. In the study, we mainly examined the localization of AQP2, AQP3 and V2R in renal medulla of Normal Diet (ND) and High-fat Diet (HFD) of rats, respectively. In renal medulla of HFD, immunolight microscopy revealed weak expression of AQP2 at the apical plasma membrane and intracellular vesicles of principal cells of the IMCD and OMCD. AQP3 and V2R expression also observed a decrease in immunolabelling in the IMCD and OMCD. It was suggested that excess lipid accumulation may lead to lipotoxicity and may be the major driver of organ dysfunction such as water reabsorption dysfunction, which may be resulted from abnormal response of rphan G-protein-coupled receptors in kidney.

La evidencia reciente ha indicado que el tejido adiposo produce sustancias bioactivas que contribuyen a la enfermedad renal relacionada con la obesidad, alterando la función y la estructura renal. Ocho de los AQP se expresan en el riñón, donde varios de ellos contribuyen a la absorción de agua y al mantenimiento del equilibrio hídrico corporal. En el estudio, examinamos principalmente la localización de AQP2, AQP3 y V2R en la médula renal de ratas con dieta normal (ND) y ratas con dieta alta en grasas (HFD). En la médula renal del grupo HFD, la microscopía electrónica de barrido reveló una expresión débil de AQP2 en la membrana plasmática apical y las vesículas intracelulares de las células principales de IMCD y OMCD. La expresión de AQP3 y V2R también observó una disminución en el inmunomarcador en IMCD y OMCD. Se sugiere que el exceso de acumulación de lípidos puede conducir a lipotoxicidad y ser el principal impulsor de la disfunción orgánica, como la disfunción de reabsorción de agua, que puede ser el resultado de la respuesta anormal de los receptores acoplados a proteína rphan G en el riñón.