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UROLOGY, NEPHROLOGY AND ANDROLOGY (159 journals)                     

Showing 1 - 159 of 159 Journals sorted alphabetically
Acta Urológica Portuguesa     Open Access   (Followers: 1)
Actas Urológicas Españolas     Full-text available via subscription   (Followers: 3)
Actas Urológicas Españolas (English Edition)     Full-text available via subscription   (Followers: 1)
Advances in Chronic Kidney Disease     Full-text available via subscription   (Followers: 11)
Advances in Urology     Open Access   (Followers: 13)
African Journal of Nephrology     Open Access  
African Journal of Urology     Open Access   (Followers: 7)
AJP Renal Physiology     Hybrid Journal   (Followers: 8)
Aktuelle Urologie     Hybrid Journal   (Followers: 4)
American Journal of Kidney Diseases     Hybrid Journal   (Followers: 42)
American Journal of Men's Health     Open Access   (Followers: 9)
American Journal of Nephrology     Full-text available via subscription   (Followers: 38)
Andrologia     Hybrid Journal   (Followers: 2)
Andrology     Hybrid Journal   (Followers: 4)
Andrology & Gynecology : Current Research     Hybrid Journal   (Followers: 4)
Andrology and Genital Surgery     Open Access   (Followers: 7)
Andrology-Open Access     Open Access  
Annales d'Urologie     Full-text available via subscription  
Arab Journal of Nephrology and Transplantation     Open Access   (Followers: 1)
Arab Journal of Urology     Open Access   (Followers: 7)
Archives of Clinical Nephrology     Open Access   (Followers: 2)
Archivio Italiano di Urologia e Andrologia     Open Access   (Followers: 1)
Archivos Españoles de Urología     Open Access  
Asian Journal of Andrology     Open Access   (Followers: 1)
Asian Journal of Urology     Open Access   (Followers: 3)
Bangladesh Journal of Urology     Open Access   (Followers: 5)
BANTAO Journal     Open Access  
Basic and Clinical Andrology     Open Access  
BJU International     Hybrid Journal   (Followers: 34)
BJUI Compass     Open Access   (Followers: 2)
BMC Nephrology     Open Access   (Followers: 11)
BMC Urology     Open Access   (Followers: 14)
Canadian Journal of Kidney Health and Disease     Open Access   (Followers: 8)
Canadian Urological Association Journal     Open Access   (Followers: 2)
Cancer Urology     Open Access   (Followers: 2)
Cardiorenal Medicine     Full-text available via subscription   (Followers: 1)
Case Reports in Nephrology     Open Access   (Followers: 5)
Case Reports in Nephrology and Dialysis     Open Access   (Followers: 9)
Case Reports in Urology     Open Access   (Followers: 12)
Clinical and Experimental Nephrology     Hybrid Journal   (Followers: 4)
Clinical Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 22)
Clinical Kidney Journal     Open Access   (Followers: 4)
Clinical Medicine Insights : Urology     Open Access   (Followers: 3)
Clinical Nephrology     Full-text available via subscription   (Followers: 8)
Clinical Nephrology and Urology Science     Open Access   (Followers: 6)
Clinical Queries: Nephrology     Hybrid Journal   (Followers: 1)
Cuadernos de Cirugía     Open Access   (Followers: 3)
Current Opinion in Nephrology & Hypertension     Hybrid Journal   (Followers: 10)
Current Opinion in Urology     Hybrid Journal   (Followers: 12)
Current Urology     Open Access   (Followers: 10)
Current Urology Reports     Hybrid Journal   (Followers: 5)
Der Nephrologe     Hybrid Journal  
Der Urologe     Hybrid Journal   (Followers: 1)
Diabetic Nephropathy     Open Access   (Followers: 1)
EMC - Urología     Full-text available via subscription  
Enfermería Nefrológica     Open Access   (Followers: 1)
European Urology     Full-text available via subscription   (Followers: 33)
European Urology Focus     Hybrid Journal   (Followers: 5)
European Urology Oncology     Hybrid Journal   (Followers: 1)
European Urology Open Science     Open Access   (Followers: 10)
Forum Nefrologiczne     Full-text available via subscription  
Geriatric Nephrology and Urology     Hybrid Journal   (Followers: 7)
Giornale di Clinica Nefrologica e Dialisi     Open Access  
Herald Urology     Open Access   (Followers: 2)
Hong Kong Journal of Nephrology     Open Access   (Followers: 3)
Human Andrology     Partially Free   (Followers: 2)
IJU Case Reports     Open Access  
Indian Journal of Nephrology     Open Access   (Followers: 2)
Indian Journal of Urology     Open Access   (Followers: 5)
International Brazilian Journal of Urology     Open Access   (Followers: 5)
International Journal of Nephrology     Open Access   (Followers: 2)
International Journal of Nephrology and Renovascular Disease     Open Access   (Followers: 2)
International Journal of Urology     Hybrid Journal   (Followers: 12)
International Urology and Nephrology     Hybrid Journal   (Followers: 7)
Jornal Brasileiro de Nefrologia     Open Access  
Journal für Urologie und Urogynäkologie/Österreich     Hybrid Journal  
Journal of Clinical Nephrology     Open Access   (Followers: 2)
Journal of Clinical Urology     Hybrid Journal   (Followers: 14)
Journal of Endoluminal Endourology     Open Access  
Journal of Endourology     Hybrid Journal   (Followers: 2)
Journal of Endourology Case Reports     Hybrid Journal  
Journal of Genital System & Disorders     Hybrid Journal   (Followers: 3)
Journal of Integrative Nephrology and Andrology     Open Access   (Followers: 2)
Journal of Kidney Cancer and VHL     Open Access  
Journal of Lower Genital Tract Disease     Hybrid Journal  
Journal of Nephrology     Hybrid Journal   (Followers: 4)
Journal of Nephrology Research     Open Access   (Followers: 3)
Journal of Pediatric Nephrology     Open Access   (Followers: 5)
Journal of Renal Care     Hybrid Journal   (Followers: 8)
Journal of Renal Nursing     Full-text available via subscription   (Followers: 12)
Journal of Renal Nutrition     Hybrid Journal   (Followers: 28)
Journal of Renal Nutrition and Metabolism     Open Access   (Followers: 1)
Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 31)
Journal of The Egyptian Society of Nephrology and Transplantation     Open Access  
Journal of Translational Neurosciences     Open Access  
Journal of Urology     Full-text available via subscription   (Followers: 46)
Journal of Urology & Nephrology     Open Access   (Followers: 2)
Kidney Disease and Transplantation     Open Access   (Followers: 4)
Kidney Diseases     Open Access   (Followers: 3)
Kidney International     Hybrid Journal   (Followers: 46)
Kidney International Reports     Open Access   (Followers: 3)
Kidney Medicine     Open Access  
Kidney Research Journal     Open Access   (Followers: 6)
Kidneys (Počki)     Open Access   (Followers: 1)
Nature Reviews Nephrology     Full-text available via subscription   (Followers: 22)
Nature Reviews Urology     Full-text available via subscription   (Followers: 13)
Nefrología (English Edition)     Open Access  
Nefrología (Madrid)     Open Access  
Nephro-Urology Monthly     Open Access   (Followers: 1)
Nephrology     Hybrid Journal   (Followers: 13)
Nephrology Dialysis Transplantation     Hybrid Journal   (Followers: 27)
Nephron     Hybrid Journal   (Followers: 4)
Nephron Clinical Practice     Full-text available via subscription   (Followers: 4)
Nephron Experimental Nephrology     Full-text available via subscription   (Followers: 4)
Nephron Extra     Open Access   (Followers: 1)
Nephron Physiology     Full-text available via subscription   (Followers: 4)
Neurourology and Urodynamics     Hybrid Journal   (Followers: 1)
OA Nephrology     Open Access   (Followers: 2)
Open Access Journal of Urology     Open Access   (Followers: 6)
Open Journal of Nephrology     Open Access   (Followers: 5)
Open Journal of Urology     Open Access   (Followers: 6)
Open Urology & Nephrology Journal     Open Access  
Pediatric Urology Case Reports     Open Access   (Followers: 7)
Portuguese Journal of Nephrology & Hypertension     Open Access   (Followers: 1)
Progrès en Urologie     Full-text available via subscription  
Progrès en Urologie - FMC     Full-text available via subscription  
Prostate Cancer and Prostatic Diseases     Hybrid Journal   (Followers: 6)
Renal Failure     Open Access   (Followers: 12)
Renal Replacement Therapy     Open Access   (Followers: 4)
Research and Reports in Urology     Open Access   (Followers: 4)
Revista de Nefrología, Diálisis y Trasplante     Open Access   (Followers: 1)
Revista Mexicana de Urología     Open Access   (Followers: 1)
Revista Urologia Colombiana     Open Access  
Saudi Journal of Kidney Diseases and Transplantation     Open Access   (Followers: 2)
Scandinavian Journal of Urology     Hybrid Journal   (Followers: 7)
Seminars in Nephrology     Hybrid Journal   (Followers: 11)
The Prostate     Hybrid Journal   (Followers: 8)
Therapeutic Advances in Urology     Open Access   (Followers: 4)
Trends in Urology & Men's Health     Partially Free   (Followers: 1)
Ukrainian Journal of Nephrology and Dialysis     Open Access   (Followers: 1)
Uro-News     Hybrid Journal   (Followers: 1)
Urolithiasis     Hybrid Journal   (Followers: 2)
Urologia Internationalis     Full-text available via subscription   (Followers: 2)
Urologia Journal     Hybrid Journal  
Urologic Clinics of North America     Full-text available via subscription   (Followers: 4)
Urologic Nursing     Full-text available via subscription   (Followers: 4)
Urologic Radiology     Hybrid Journal  
Urological Science     Open Access  
Urologicheskie Vedomosti     Open Access  
Urologie in der Praxis     Hybrid Journal  
Urologie Scan     Hybrid Journal  
Urology     Hybrid Journal   (Followers: 33)
Urology Annals     Open Access   (Followers: 4)
Urology Case Reports     Open Access   (Followers: 3)
Urology Practice     Full-text available via subscription   (Followers: 2)
Urology Times     Free   (Followers: 3)
Urology Video Journal     Open Access   (Followers: 1)
World Journal of Nephrology and Urology     Open Access   (Followers: 15)
World Journal of Urology     Hybrid Journal   (Followers: 11)


Similar Journals
Journal Cover
Nephron Physiology
Number of Followers: 4  
  Full-text available via subscription Subscription journal
ISSN (Print) 1660-2137 - ISSN (Online) 1660-2137
Published by Karger Homepage  [122 journals]
  • Renal Oxygenation Characteristics in Healthy Native Kidneys: Assessment
           with Blood Oxygen Level-Dependent Magnetic Resonance Imaging
    • Abstract: Objective: To explore the characteristics of blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI) in healthy native kidneys. Methods: Seventy-nine patients without chronic kidney disease underwent BOLD-MRI with T2* spoiled gradient recalled echo sequences. BOLD images were analyzed using R2*map software to produce an R2* pseudo-color map. Cortical and medullary R2* values were analyzed in both kidneys and in both sexes. Different regional R2* values in the cortex and medulla were also analyzed. Physiological indices including age, height, weight, body mass index, body surface area, and estimated glomerular filtration rate (eGFR) were recorded. Correlations between R2* value and physiological indices were determined. Results: Renal cortical R2* values were lower than values in the medulla (p < 0.001). Female and male cortical R2* values were also lower than the corresponding values in the medulla (p < 0.001). Renal medullary R2* values in the lower renal pole were lower than values in the middle and upper poles (p = 0.001). Age was positively correlated with R2* values in the medulla (r = 0.32, p = 0.004). eGFR was negatively correlated with both cortical R2* values (r = -0.26, p = 0.02) and medullary R2* values (r = -0.29, p = 0.009). Conclusions: BOLD-MRI can directly visualize renal oxygenation. There was variation in the oxygenation of different regions of the kidney. Renal cortical and medullary oxygenation in healthy kidneys decreased with patient age. eGFR also decreased with patient age.
      Nephron Physiol 2014;128:47-54
  • Mineralocorticoid and SGK1-Sensitive Inflammation and Tissue Fibrosis
    • Abstract: Effects of mineralocorticoids are not restricted to regulation of epithelial salt transport, extracellular volume and blood pressure; mineralocorticoids also influence a wide variety of seemingly unrelated functions such as inflammation and fibrosis. The present brief review addresses the role of mineralocorticoids in the orchestration of these latter processes. Mineralocorticoids foster inflammation as well as vascular, cardiac, renal and peritoneal fibrosis. Mechanisms involved in mineralocorticoid-sensitive inflammation and fibrosis include the serum- and glucocorticoid-inducible kinase 1 (SGK1), which is genomically upregulated by mineralocorticoids and transforming growth factor β (TGF-β), and stimulated by mineralocorticoid-sensitive phosphatidylinositide 3-kinase. SGK1 upregulates the inflammatory transcription factor nuclear factor-#954;B, which in turn stimulates the expression of diverse inflammatory mediators including connective tissue growth factor. Moreover, SGK1 inhibits the degradation of the TGF-β-dependent transcription factors Smad2/3. Mineralocorticoids foster the development of TH17 cells, which is compromised following SGK1 deletion. Excessive SGK1 expression is observed in a wide variety of fibrosing diseases including lung fibrosis, diabetic nephropathy, glomerulonephritis, obstructive kidney disease, experimental nephrotic syndrome, obstructive nephropathy, liver cirrhosis, fibrosing pancreatitis, peritoneal fibrosis, Crohn's disease and celiac disease. The untoward inflammatory and fibrosing effects of mineralocorticoids could be blunted or even reversed by mineralocorticoid receptor blockers, which may thus be considered in the treatment of inflammatory and/or fibrosing disease.
      Nephron Physiol 2014;128:35-39
  • Mineralocorticoid-Induced Sodium Appetite and Renal Salt Retention:
           Evidence for Common Signaling and Effector Mechanisms
    • Abstract: An increase in renal sodium chloride (salt) retention and an increase in sodium appetite are the body's responses to salt restriction or depletion in order to restore salt balance. Renal salt retention and increased sodium appetite can also be maladaptive and sustain the pathophysiology in conditions like salt-sensitive hypertension and chronic heart failure. Here we review the central role of the mineralocorticoid aldosterone in both the increase in renal salt reabsorption and sodium appetite. We discuss the working hypothesis that aldosterone activates similar signaling and effector mechanisms in the kidney and brain, including the mineralocorticoid receptor, the serum- and glucocorticoid-induced kinase SGK1, the ubiquitin ligase NEDD4-2, and the epithelial sodium channel ENaC. The latter also mediates the gustatory salt sensing in the tongue, which is required for the manifestation of increased salt intake. Effects of aldosterone on both the brain and kidney synergize with the effects of angiotensin II. Thus, mineralocorticoids appear to induce similar molecular pathways in the kidney, brain, and possibly tongue, which could provide opportunities for more effective therapeutic interventions. Inhibition of renal salt reabsorption is compensated by stimulation of salt appetite and vice versa; targeting both mechanisms should be more effective. Inhibiting the arousal to consume salty food may improve a patient's compliance to reducing salt intake. While a better understanding of the molecular mechanisms is needed and will provide new therapeutic options, current pharmacological interventions that target both salt retention and sodium appetite include mineralocorticoid receptor antagonists and potentially inhibitors of angiotensin II and ENaC.
      Nephron Physiol 2014;128:8-16
  • Genetic, Molecular and Clinical Determinants for the Involvement of
           Aldosterone and Its Receptors in Major Depression
    • Abstract: Major depression (MDE) has metabolic and neuroendocrine correlates, which point to a biological overlap between MDE and cardiovascular diseases. Whereas the hypothalamic-pituitary-adrenocortical axis has long been recognized for its involvement in depression, the focus was mostly on cortisol/corticosterone, whereas aldosterone appears to be the ‘forgotten' stress hormone. Part of the reason for this is that the receptors for aldosterone, the mineralocorticoid receptors (MR), were thought to be occupied by glucocorticoids in most parts of the brain. However, recently it turned out that aldosterone acts selectively in relevant mood-regulating brain areas, without competing with cortisol/corticosterone. These areas include the nucleus of the solitary tract (NTS), the amygdala and the paraventricular nucleus of the hypothalamus. These regions are intimately involved in the close relationship between emotional and vegetative symptoms. Genetic analysis supports the role of aldosterone and of MR-related pathways in the pathophysiology of depression. Functional markers for these pathways in animal models as well as in humans are available and allow an indirect assessment of NTS function. They include heart rate variability, baroreceptor reflex sensitivity, blood pressure, salt taste sensitivity and slow-wave sleep. MR activation in the periphery is related to electrolyte regulation. MR overactivity is a risk factor for diabetes mellitus and a trigger of inflammatory processes. These markers can be used not only to assist the development of new treatment compounds, but also for a personalized approach to treat patients with depression and related disorders by individual dose titration with an active medication, which targets this system.
      Nephron Physiol 2014;128:17-25
  • Effect of Mineralocorticoids on Acid-Base Balance
    • Abstract: Aldosterone is classically associated with the regulation of salt and potassium homeostasis but has also profound effects on acid-base balance. During acidosis, circulating aldosterone levels are increased and the hormone acts in concert with angiotensin II and other factors to stimulate renal acid excretion. Pharmacological blockade of aldosterone action as well as inherited or acquired syndromes of impaired aldosterone release or action impair the renal response to acid loading and cause hyperkalemic renal tubular acidosis. The mineralocorticoid receptor (MR) mediating the genomic effects of aldosterone is expressed in all cells of the distal nephron including all subtypes of intercalated cells. In acid-secretory type A intercalated cells, aldosterone stimulates proton secretion into urine, whereas in non-type A intercalated cells, aldosterone increases the activity of the luminal anion exchanger pendrin stimulating bicarbonate secretion and chloride reabsorption. Aldosterone has also stimulatory effects on proton secretion that may be mediated by a non-genomic pathway. In addition, aldosterone indirectly stimulates renal acid excretion by enhancing sodium reabsorption through the epithelial sodium channel ENaC. Increased sodium reabsorption enhances the lumen-negative transepithelial voltage that facilitates proton secretion by neighboring intercalated cells. This indirect coupling of sodium reabsorption and proton secretion is thought to underlie the fludrocortisone-furosemide test for maximal urinary acidification in patients with suspected distal renal tubular acidosis. In patients with CKD, acidosis-induced aldosterone may contribute to progression of kidney disease. In summary, aldosterone is a powerful regulator of renal acid excretion required for normal acid-base balance.
      Nephron Physiol 2014;128:26-34
  • Impact of Aldosterone on Osteoinductive Signaling and Vascular
    • Abstract: Vascular calcification is frequently found already in early stages of chronic kidney disease (CKD) patients and is associated with high cardiovascular risk. The process of vascular calcification is not considered a passive phenomenon but involves, at least in part, phenotypical transformation of vascular smooth muscle cells (VSMCs). Following exposure to excessive extracellular phosphate concentrations, VSMCs undergo a reprogramming into osteo-/chondroblast-like cells. Such ‘vascular osteoinduction' is characterized by expression of osteogenic transcription factors and triggered by increased phosphate concentrations. A key role in this process is assigned to cellular phosphate transporters, most notably the type III sodium-dependent phosphate transporter Pit1. Pit1 expression is stimulated by mineralocorticoid receptor activation. Therefore, aldosterone participates in the phenotypical transformation of VSMCs. In preclinical models, aldosterone antagonism reduces vascular osteoinduction. Patients with CKD suffer from hyperphosphatemia predisposing to vascular osteogenic transformation, potentially further fostered by concomitant hyperaldosteronism. Clearly, additional research is required to define the role of aldosterone in the regulation of osteogenic signaling and the consecutive vascular calcification in CKD, but more generally also other diseases associated with excessive vascular calcification and even in individuals without overt disease.
      Nephron Physiol 2014;128:40-45
  • On the Pleotropic Actions of Mineralocorticoids
    • Abstract: Classical effects of mineralocorticoids include stimulation of Na+ reabsorption and K+ secretion in the kidney and other epithelia including colon and several glands. Moreover, mineralocorticoids enhance the excretion of Mg2+ and renal tubular H+ secretion. The renal salt retention following mineralocorticoid excess leads to extracellular volume expansion and hypertension. The increase of blood pressure following mineralocorticoid excess is, however, not only the result of volume expansion but may result from stiff endothelial cell syndrome impairing the release of vasodilating nitric oxide. Beyond that, mineralocorticoids are involved in the regulation of a wide variety of further functions, including cardiac fibrosis, platelet activation, neuronal function and survival, inflammation as well as vascular and tissue fibrosis and calcification. Those functions are briefly discussed in this short introduction to the special issue. Beyond that, further contributions of this special issue amplify on mineralocorticoid-induced sodium appetite and renal salt retention, the role of mineralocorticoids in the regulation of acid-base balance, the involvement of aldosterone and its receptors in major depression, the mineralocorticoid stimulation of inflammation and tissue fibrosis and the effect of aldosterone on osteoinductive signaling and vascular calcification. Clearly, still much is to be learned about the various ramifications of mineralocorticoid-sensitive physiology and pathophysiology.
      Nephron Physiol 2014;128:1-7
  • Insulin Receptor and the Kidney: Nephrocalcinosis in Patients with
           Recessive INSR Mutations
    • Abstract: Background/Aims: Donohue and Rabson-Mendenhall syndrome are rare autosomal recessive disorders caused by mutations in the insulin receptor gene, INSR. Phenotypic features include extreme insulin resistance, linear growth retardation, paucity of fat and muscle, and soft tissue overgrowth. The insulin receptor is also expressed in the kidney, where animal data suggest it plays a role in glomerular function and blood pressure (BP) regulation, yet such a role in the human kidney is untested. Patients with biallelic INSR mutations provide a rare opportunity to ascertain its role in man. Methods: Retrospective review of patients with INSR mutations. Data for BP, renal imaging, plasma creatinine and electrolyte levels, as well as urine protein, albumin and calcium excretion were sought from the treating clinicians. Results: From 33 patients with INSR mutations, data were available for 17 patients. Plasma creatinine was low (mean ± SD: 25 ± 9 μmol/l) and mean plasma electrolyte concentrations were within the normal range (n = 13). Systolic BP ranged between the 18th and 91st percentile for age, sex, height and weight (n = 9; mean ± SD: 49 ± 24). Twenty-four-hour urinary calcium data were available from 10 patients and revealed hypercalciuria in all (mean ± SD: 0.32 ± 0.17 mmol/kg/day; normal
  • Contents Vol. 26, 2014
    • Abstract:
      Nephron Physiol 2014;126:I-IV
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
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