Methoxamine inhibits noradrenaline release through activation of ?1- and ?2-adrenoceptors in rat isolated kidney: involvement of purines and prostaglandins

1993 ◽  
Vol 347 (3) ◽  
pp. 273-279 ◽  
Author(s):  
C. Bohmann ◽  
P. Schollmeyer ◽  
L. C. Rump
Keyword(s):  
Noradrenaline Release ◽  
Isolated Kidney ◽  
Kidney Involvement

Sarcoid relapse with isolated kidney involvement

2006 ◽  
Vol 1 (2) ◽  
pp. 170-172 ◽  
Author(s):  
Giuseppe Famularo ◽  
Giulio Cesare Nicotra ◽  
Giovanni Minisola ◽  
Claudio De Simone
Keyword(s):  
Isolated Kidney ◽  
Kidney Involvement

Correlation Between Noradrenaline Fluxes, Metabolism and Compartmentalisation in Human Platelets

1982 ◽  
Vol 48 (01) ◽  
pp. 062-066 ◽  
Author(s):  
Chantal Legrand ◽  
Véronique Dubernard ◽  
Philippe Meyer
Keyword(s):  
Noradrenaline Release ◽  
Human Platelets ◽  
Release Of Noradrenaline ◽  
Storage Pool ◽  
Platelet Storage ◽  
Efflux Of Noradrenaline ◽  
Preferential Localization

Summary(3H) noradrenaline was taken up by human platelets and partially converted into sulfoconjugated noradrenaline. This uptake was inhibited by drugs which have been previously shown to impair the uptake of 5-HT (ouabain, chlorimipramine) or the storage of 5-HT (tyramine, reserpine) by platelets. In addition, tyramine and reserpine stimulated the formation of sulfoconjugated noradrenaline. The efflux of noradrenaline from platelets was measured in parallel and was found to be directly related to the proportion of non metabolized to metabolized noradrenaline in the cells. Unlike tyramine, which induced a similar release of noradrenaline and 5-HT, reserpine was less effective at inducing noradrenaline release than 5-HT release. This study indicates a preferential localization of noradrenaline in the granular pool of human platelets with the existence of an extragranular sulfoconjugated pool which is increased when the granular storage of noradrenaline is impaired. Studies of noradrenaline fluxes and metabolism may be useful in the understanding of both acquired and inherited platelet storage pool defects.

DETERMINING OF MONOCLONAL GAMMOPATHY IN NEPHROLOGICAL PATIENTS

2019 ◽  
Vol 23 (2) ◽  
pp. 82-90
Author(s):  
L. B. Lysenko ◽  
N. V. Chebotareva ◽  
N. N. Mrykhin ◽  
V. V. Rameev ◽  
T. V. Androsova ◽  
...  
Keyword(s):  
Renal Diseases ◽  
Chronic Glomerulonephritis ◽  
Al Amyloidosis ◽  
Hematological Neoplasms ◽  
Cast Nephropathy ◽  
Number Of Patients ◽  
Light Chain Disease ◽  
Kidney Involvement ◽  
Cryoglobulinemic Glomerulonephritis ◽  
Electrophoresis Of Proteins

BACKGROUND. Мonoclonal gammopathy (MG) is not only the state preceding of hematological neoplasms, but also associated with non- hematological diseases, in particular damage of kidneys. Earlier diagnosis of MG represents an important area in treating patients with renal diseases associated with MG. THE AIM: To determine the frequency of MG among therapeutic and nephrological patients for optimization of methods of their diagnosis and treatment. PATIENTS AND METHODS: In common, 11392 patients were analyzed within 4 years (2013-2016). The standard clinical examination was conducted. Method of an electrophoresis of proteins of serum of blood and the 24-hour urine, method of immunofixation of proteins of serum and urine, and method of free light chains definition in serum (Freelite) were used for MG identification. RESULTS: MG is diagnosed in 174 of 11392 patients: 49 % of men and 51 % of women aged from 18 up to 85 years. MG was found 2.1 times more often in nephrological patient than in patients of therapeutic departments. Among patients of this group, AL-amyloidosis with kidney involvement was diagnosed in 41 %, cryoglobulinemic glomerulonephritis – in 18 %, chronic glomerulonephritis – in 35 %, also there was small number of patients with light chain disease and cast-nephropathy. 86 % of nephrological patients had less than 5 g/l of monoclonal protein that corresponds oligo secretory MG, and at 46 % from them – less than 1 g/l, other 10 % had MG of 5-10 g/l, and only in 4.42 % of patients MG more 10g/l was defined. CONCLUSION: We conclude that MG, especially oligo secretory form, play a significant role in pathogenesis of renal damage. It is important to apply sensitive methods – immunofixation of proteins and method «Freelite» for nephrological patients.

Features of the oxidative status in patients with lupus nephritis

2020 ◽  
Vol 24 (1) ◽  
pp. 39-44
Author(s):  
E. V. Smirnova ◽  
E. V. Proskurnina ◽  
T. N. Krasnova
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Lupus Nephritis ◽  
Blood Plasma ◽  
Respiratory Burst ◽  
Oxidative Status ◽  
Free Radical Production ◽  
Radical Production ◽  
Neutrophil Activity ◽  
Kidney Involvement

BACKGROUND. Oxidative status impairment plays a significant role in the pathogenesis of SLE and lupus nephritis (LN). The data about oxidative status in this disease are incomplete, that’s why it’s necessary to use a new approach to study it. THE AIM: To study oxidative status in SLE patients with kidney involvement. PATIENTS AND METHODS:53 patients with SLE were included in this prospective study, among them 40 patients with different severity of kidney involvement, control group were 87 healthy donors. Oxidative stress parameters were measured: antioxidant activity (AOA) of blood plasma and parameters, characterizing the state of the main source of reactive oxygen species (ROS) – neutrophils, more specifically: specific spontaneous neutrophil activity, specific stimulated activity (peak and integral), coefficient of respiratory burst attenuation, representing the rate of free radical production decrease after stimulation, the higher the value of this parameter, the slower is free radical production decrease. RESULTS. It was shown elevation of neutrophil free radical-producing activity parameters and elevation of blood plasma AOA in patients with LN, comparing to healthy controls. Immunosuppressive therapy with glucocorticosteroids (GCS) and cytostatics (CS) increased blood plasma AOA comparing to monotherapy with GCS. A correlation between oxidative status impairment and intensity of inflammatory reactions was found: correlation of respiratory burst attenuation coefficient with blood sedimentation rate was shown. Reduction of spontaneous free radical-producing neutrophil activity was found in LN patients with NS, which might be the result of neutrophil functional activity attenuation in high disease activity. CONCLUSION. The increased free radical-producing neutrophil activity was shown, which might be the cause of oxidative stress in SLE with LN. It seems warranted investigation of these parameters in samples of larger volume to search targets aimed at neutrophils. The necessity of antioxidant therapy in patients with SLE seems doubtful, as they show significant increase of blood plasma AOA, which might result from compensatory reaction of human organism to oxidative stress and therapy with GCS and CS.

Platelet-activating factor and the kidney

1986 ◽  
Vol 251 (1) ◽  
pp. F1-F11 ◽  
Author(s):  
D. Schlondorff ◽  
R. Neuwirth
Keyword(s):  
De Novo ◽  
Mesangial Cells ◽  
Biological Activities ◽  
Platelet Activating Factor ◽  
Calcium Ionophore ◽  
Initial Step ◽  
Renal Physiology ◽  
Dependent Manner ◽  
Glomerular Mesangial Cells ◽  
Isolated Kidney

Platelet-activating factor (PAF) represents a group of phospholipids with the basic structure of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine. A number of different cells are capable of producing PAF in response to various stimuli. The initial step of PAF formation is activation of phospholipase A2 in a calcium-dependent manner, yielding lyso-PAF. During this step arachidonic acid is also released and can be converted to its respective cyclooxygenase and lipoxygenase products. The lyso-PAF generated is then acetylated in position 2 of the glycerol backbone by a coenzyme A (CoA)-dependent acetyltransferase. An additional pathway may exist whereby PAF is generated de novo from 1-alkyl-2-acetyl-sn-glycerol by phosphocholine transferase. PAF inactivation in cells and blood is by specific acetylhydrolases. PAF exhibits a variety of biological activities including platelet and leukocyte aggregation and activation, increased vascular permeability, respiratory distress, decreased cardiac output, and hypotension. In the kidney PAF can produce decreases in blood flow, glomerular filtration, and fluid and electrolyte excretion. Intrarenal artery injection of PAF may also result in glomerular accumulation of platelets and leukocytes and mild proteinuria. PAF increases prostaglandin formation in the isolated kidney and in cultured glomerular mesangial cells. PAF also causes contraction of mesangial cells. Upon stimulation with calcium ionophore the isolated kidney, isolated glomeruli and medullary cells, and cultured mesangial cells are capable of producing PAF. The potential role for PAF in renal physiology and pathophysiology requires further investigation that may be complicated by 1) the multiple interactions of PAF, prostaglandins, and leukotrienes and 2) the autocoid nature of PAF, which may restrict its action to its site of generation.

scholarly journals Pathomechanisms in the Kidneys in Selected Protozoan Parasitic Infections

2021 ◽  
Vol 22 (8) ◽  
pp. 4209
Author(s):  
Karolina Kot ◽  
Natalia Łanocha-Arendarczyk ◽  
Michał Ptak ◽  
Aleksandra Łanocha ◽  
Elżbieta Kalisińska ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Molecular Mechanisms ◽  
Kidney Injury ◽  
Therapeutic Interventions ◽  
Parasitic Infections ◽  
Injury Mechanisms ◽  
Kidney Involvement ◽  
Leishmania Spp ◽  
Apoptosis Process ◽  
Insight Into

Leishmaniasis, malaria, toxoplasmosis, and acanthamoebiasis are protozoan parasitic infections. They remain important contributors to the development of kidney disease, which is associated with increased patients’ morbidity and mortality. Kidney injury mechanisms are not fully understood in protozoan parasitic diseases, bringing major difficulties to specific therapeutic interventions. The aim of this review is to present the biochemical and molecular mechanisms in kidneys infected with Leishmania spp., Plasmodium spp., Toxoplasma gondii, and Acanthamoeba spp. We present available mechanisms of an immune response, oxidative stress, apoptosis process, hypoxia, biomarkers of renal injury in the serum or urine, and the histopathological changes of kidneys infected with the selected parasites. Pathomechanisms of Leishmania spp. and Plasmodium spp. infections have been deeply investigated, while Toxoplasma gondii and Acanthamoeba spp. infections in the kidneys are not well known yet. Deeper knowledge of kidney involvement in leishmaniasis and malaria by presenting their mechanisms provides insight into how to create novel and effective treatments. Additionally, the presented work shows gaps in the pathophysiology of renal toxoplasmosis and acanthamoebiasis, which need further research.

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