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Veterinary Radiology & Ultrasound : the... 2013Ultrasound findings of the canine kidney include a hyperechoic cortex and a hypo to anechoic medulla. In this study, the sonographic appearance of the outer renal...
Ultrasound findings of the canine kidney include a hyperechoic cortex and a hypo to anechoic medulla. In this study, the sonographic appearance of the outer renal medulla in dogs without evidence of renal disease is described. Dogs that underwent abdominal ultrasound over a 6-month period were subjected to review and then divided into six groups based on body weight (kg): < 4.9, 5.0-9.9, 10-19.9, 20-29.9, 30-39.9, and ≥ 40. Chi-square analysis was used to determine if the frequency of a hyperechoic outer medulla was significantly different between weight groups, sex, and age (P-value < 0.05). Of the 145 dogs that met the inclusion criteria, 45 had a hyperechoic outer medulla relative to the cortex and inner medulla. In the remaining dogs, the outer medulla was isoechoic to the cortex. Dogs less than 5 kg had the highest frequency of a hyperechoic outer medulla (P < 0.0001) and dogs greater than 40 kg did not have a hyperechoic outer medulla (P < 0.0001). Sex had no influence on the presence or absence of the hyperechoic outer medulla; however, younger dogs were overrepresented (6.4 ± 0.6 years compared with 7.8 ± 0.4 years; P = 0.04). Ultrasound descriptions of the canine kidney have not taken into account the contributions of the renal cortex and outer medulla. Based on this study of dogs with no clinically significant renal disease, the outer medulla can be isoechoic or hyperechoic to the cortex and a hyperechoic outer medulla is more commonly seen in small breed dogs.
Topics: Animals; Body Weight; Dogs; Female; Kidney Medulla; Male; Prospective Studies; Ultrasonography
PubMed: 23738847
DOI: 10.1111/vru.12069 -
Journal of Comparative Physiology. B,... Nov 2018Mammalian kidneys play an essential role in balancing internal water and salt concentrations. When water needs to be conserved, the renal medulla produces concentrated... (Review)
Review
Mammalian kidneys play an essential role in balancing internal water and salt concentrations. When water needs to be conserved, the renal medulla produces concentrated urine. Central to this process of urine concentration is an osmotic gradient that increases from the corticomedullary boundary to the inner medullary tip. How this gradient is generated and maintained has been the subject of study since the 1940s. While it is generally accepted that the outer medulla contributes to the gradient by means of an active process involving countercurrent multiplication, the source of the gradient in the inner medulla is unclear. The last two decades have witnessed advances in our understanding of the urine-concentrating mechanism. Details of medullary architecture and permeability properties of the tubules and vessels suggest that the functional and anatomic relationships of these structures may contribute to the osmotic gradient necessary to concentrate urine. Additionally, we are learning more about the membrane transporters involved and their regulatory mechanisms. The role of medullary architecture and membrane transporters in the mammalian urine-concentrating mechanism are the focus of this review.
Topics: Animals; Humans; Kidney Medulla; Membrane Transport Proteins; Urine
PubMed: 29797052
DOI: 10.1007/s00360-018-1164-3 -
Histology and Histopathology Jun 2017Recently, gold nanoparticles (GNPs) have shown promising applications in targeted drug delivery and contrast imaging. Although in vitro cytotoxicity of GNPs has been...
Recently, gold nanoparticles (GNPs) have shown promising applications in targeted drug delivery and contrast imaging. Although in vitro cytotoxicity of GNPs has been thoroughly studied, there are limited data on in vivo toxicity of GNPs. In this study, we evaluated the effects of intraperitoneally injected 10 nm and 50 nm GNPs (5 μg/animal) on the expression of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) on day 1 and day 5, post-exposure. The results of immunohistochemistry showed that both 10 nm and 50 nm GNPs induced an acute phase expression of proinflammatory cytokines in renal cortex and medulla. This proinflammatory response was comparatively more intense in renal medulla than cortex. All the three cytokines were undetectable in control cortex and medulla. In conclusion, both 10 nm and 50 nm GNPs caused an acute phase induction of proinflammatory cytokines in cortex and medulla of rat kidneys. An intense immunostaining of proinflammatory cytokines in renal medulla warrants further studies to evaluate the nephrotoxicity of GNPs to validate the safe application of GNPs for contrast imaging in renal insufficiency.
Topics: Animals; Cytokines; Disease Models, Animal; Gold; Immunohistochemistry; Inflammation; Kidney Cortex; Kidney Medulla; Male; Metal Nanoparticles; Rats; Rats, Wistar
PubMed: 27678417
DOI: 10.14670/HH-11-825 -
Advances in Internal Medicine 1974
Review
Topics: Aldosterone; Angiotensin II; Animals; Cardiac Output; Desoxycorticosterone; Extracellular Space; Humans; Hypertension; Hypertension, Malignant; Hypertension, Renal; Kidney; Kidney Medulla; Kidney Transplantation; Lipids; Plasma Volume; Pressoreceptors; Prostaglandins; Renin; Sodium; Transplantation, Homologous
PubMed: 4360963
DOI: No ID Found -
American Journal of Physiology.... Jun 2003The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced... (Review)
Review
The unique role of nitric oxide (NO) in the regulation of renal medullary function is supported by the evidence summarized in this review. The impact of reduced production of NO within the renal medulla on the delivery of blood to the medulla and on the long-term regulation of sodium excretion and blood pressure is described. It is evident that medullary NO production serves as an important counterregulatory factor to buffer vasoconstrictor hormone-induced reduction of medullary blood flow and tissue oxygen levels. When NO synthase (NOS) activity is reduced within the renal medulla, either pharmacologically or genetically [Dahl salt-sensitive (S) rats], a super sensitivity to vasoconstrictors develops with ensuing hypertension. Reduced NO production may also result from reduced cellular uptake of l-arginine in the medullary tissue, resulting in hypertension. It is concluded that NO production in the renal medulla plays a very important role in sodium and water homeostasis and the long-term control of arterial pressure.
Topics: Animals; Blood Pressure; Humans; Kidney Medulla; Nitric Oxide; Renal Circulation; Vasoconstriction
PubMed: 12736168
DOI: 10.1152/ajpregu.00701.2002 -
Current Problems in Diagnostic Radiology 2008The kidneys can harbor a wide variety of lesions, many of which can be visualized by computed tomography and magnetic resonance imaging. In this article, the pertinent... (Comparative Study)
Comparative Study Review
The kidneys can harbor a wide variety of lesions, many of which can be visualized by computed tomography and magnetic resonance imaging. In this article, the pertinent renal anatomic relationships as well as the histologic composition and function of the renal medulla and sinus are reviewed. Additionally, computed tomography and magnetic resonance imaging features of renal sinus and medullary lesions in adult patients are presented. This article reviews the salient imaging features of various malignant, benign neoplastic, and nonneoplastic lesions of the sinus and medulla.
Topics: Adult; Contrast Media; Female; Humans; Kidney Calices; Kidney Diseases; Kidney Medulla; Magnetic Resonance Imaging; Male; Middle Aged; Radiographic Image Enhancement; Sensitivity and Specificity; Tomography, X-Ray Computed
PubMed: 18823867
DOI: 10.1067/j.cpradiol.2007.09.002 -
Kidney & Blood Pressure Research 2016Recent studies have indicated that local inflammatory mediators are importantly involved in the regulation of renal function. However, it remains unknown how such local...
BACKGROUND/AIMS
Recent studies have indicated that local inflammatory mediators are importantly involved in the regulation of renal function. However, it remains unknown how such local inflammation is triggered intracellularly in the kidney. The present study was designed to characterize the inflammasome centered by Nlrp3 in the kidney and also test the effect of its activation in the renal medulla.
METHODS AND RESULTS
By immunohistochemistry analysis, we found that inflammasome components, Nlrp3, Asc and caspase-1, were ubiquitously distributed in different kidney areas. The caspase-1 activity and IL-1β production were particularly high in the renal outer medulla compared to other kidney regions. Further confocal microscopy and RT-PCR analysis showed that Nlrp3, Asc and caspase-1 were particularly enriched in the thick ascending limb of Henle's loop. In anesthetized mice, medullary infusion of Nlrp3 inflammasome activator, monosodium urate (MSU), induced significant decreases in sodium excretion and medullary blood flow without changes in mean arterial blood pressure and renal cortical blood flow. Caspase-1 inhibitor, Ac-YVAD-CMK and deletion of Nlrp3 or Asc gene abolished MSU-induced decreases in renal sodium excretion and MBF.
CONCLUSION
Our results indicate that renal medullary Nlrp3 inflammasomes represent a new regulatory mechanism of renal MBF and sodium excretion which may not depend on classical inflammatory response.
Topics: Animals; Blood Flow Velocity; Gene Deletion; Inflammasomes; Kidney Medulla; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; NLR Family, Pyrin Domain-Containing 3 Protein
PubMed: 27010539
DOI: 10.1159/000443424 -
Current Opinion in Nephrology and... Jan 2002Accumulating evidence favors the notion that perfusion of the medulla of the kidney is regulated through the effects of nitric oxide. Reduction of nitric oxide... (Review)
Review
Accumulating evidence favors the notion that perfusion of the medulla of the kidney is regulated through the effects of nitric oxide. Reduction of nitric oxide production in the medulla by local tissue infusion of nitric oxide synthase blockers leads to reduction of medullary blood flow, salt retention and hypertension. Conversely, infusion of L-arginine to increase nitric oxide abrogates hypertension and enhances medullary blood flow in animal models. Nitric oxide levels can also be controlled through its consumption by reactive oxygen species. Thus, medullary oxidative stress might influence blood pressure and sodium balance through changes in nitric oxide. Nitric oxide inhibits sodium chloride reabsorption by the thick ascending limb and collecting duct. The likelihood that some forms of hypertension result directly from pathological alteration of transporters, channels, regulatory elements or enzymes that affect medullary nitric oxide seems high.
Topics: Animals; Humans; Hypertension; Kidney Medulla; Nitric Oxide; Reactive Oxygen Species; Reference Values; Renal Circulation; Sodium
PubMed: 11753093
DOI: 10.1097/00041552-200201000-00014 -
Pflugers Archiv : European Journal of... Nov 1998Cells of the renal medulla, which are exposed under normal physiological conditions to widely fluctuating extracellular solute concentrations, respond to hypertonic... (Review)
Review
Cells of the renal medulla, which are exposed under normal physiological conditions to widely fluctuating extracellular solute concentrations, respond to hypertonic stress by accumulating the organic osmolytes glycerophosphorylcholine (GPC), betaine, myo-inositol, sorbitol and free amino acids. Increased intracellular contents of these osmolytes are achieved by a combination of increased uptake (myo-inositol and betaine) and synthesis (sorbitol, possibly GPC), decreased degradation (GPC) and reduced osmolyte release. In the medulla of the concentrating kidney, accumulation of organic osmolytes, which do not perturb cell function even at high concentrations, allows the maintenance of "normal" intracellular concentrations of inorganic electrolytes. Adaptation to decreasing extracellular solute concentrations, e.g. diuresis, is achieved primarily by activation of pathways allowing the efflux of organic osmolytes, and secondarily by inactivation of production (sorbitol) and uptake (betaine, myo-inositol) and stimulation of degradation (GPC). Apart from modulation of the osmolyte content, osmolality-dependent reorganization of the cytoskeleton and expression of specific stress proteins (heat shock proteins) may be further, as yet poorly characterized, components of the regulatory systems involved in the adaptation of medullary cells to osmotic stress.
Topics: Adaptation, Physiological; Animals; Diuresis; Extracellular Space; Heat-Shock Proteins; Humans; Hypertonic Solutions; Kidney Medulla; Kinetics
PubMed: 9799394
DOI: 10.1007/s004240050710 -
Acta Physiologica (Oxford, England) Jul 2011This is an informal personal review of the development over time of my ideas about the concentrating mechanism of the mammalian renal papilla. It had been observed that... (Review)
Review
This is an informal personal review of the development over time of my ideas about the concentrating mechanism of the mammalian renal papilla. It had been observed that animals with a need to produce a concentrated urine have a long renal papilla. I saw the function of the long papilla in desert rodents as an elongation of the counter-current concentrating mechanism of the inner medulla. This model led me to overlook contrary evidence. For example, in many experiments, the final urine has a higher osmolality than that of the tissue at the tip of the papilla. In addition, we had observations of the peristalsis of the renal pelvis surrounding the papilla. The urine concentration falls if the peristalsis is stopped. I was wrong; together, these lines of evidence show that the renal papilla is not just an elongation of the inner medulla. We are left without a full explanation of the concentrating mechanism of the mammalian renal papilla. It is hoped that other researchers will tackle this interesting problem.
Topics: Animals; Kidney Concentrating Ability; Kidney Medulla; Kidney Pelvis; Osmolar Concentration; Peristalsis; Urea; Urine
PubMed: 21281458
DOI: 10.1111/j.1748-1716.2011.02261.x