Academic literature on the topic 'Glomerular filtration analysis'
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Journal articles on the topic "Glomerular filtration analysis"
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Riegel, JA. "Analysis of fluid dynamics in perfused glomeruli of the hagfish eptatretus stouti (Lockington)." Journal of Experimental Biology 201, no. 22 (November 1, 1998): 3097–104. http://dx.doi.org/10.1242/jeb.201.22.3097.
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The capillary tuft of glomeruli of the hagfish mesonephros contains both 'low'-pressure and 'high'-pressure glomerular vessels (LPGVs and HPGVs). The existence of the HPGV raised the possibility that pressure filtration could occur in the hagfish kidney when the blood pressure was sufficiently high. Therefore, measurements of glomerular capillary pressure were made in HPGVs and LPGVs whilst single glomeruli were perfused with hagfish Ringer's solution that contained the colloid Ficoll 70. Calculations of the effective colloid osmotic pressure in perfused capillaries were made; these showed that hydrostatic pressures within the HPGV were inadequate to effect pressure filtration except at high rates of perfusion. However, high rates of perfusion provoked perfusion pressures that exceeded the highest values measured in the renal blood supply of lightly anaesthetised hagfish. It was concluded that some process other than pressure filtration must account for formation of the primary urine by hagfish glomeruli. The proportion of the perfusate that became urine, the single glomerulus filtration fraction (SGFF), bore a strong positive relationship to the vascular resistance of perfused glomeruli. Both the SGFF and the vascular resistance were inversely related to the rate of perfusion except when that rate was very high. From these two observations it was concluded that at least two flow pathways exist in hagfish glomeruli: one that has a high vascular resistance and that contributes to the elaboration of the urine, and one that has a low vascular resistance and does not contribute to urine formation. The possible anatomical location of the various flow pathways through hagfish glomeruli and how they may function are discussed.
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Arendshorst, W. J., and C. W. Gottschalk. "Glomerular ultrafiltration dynamics: historical perspective." American Journal of Physiology-Renal Physiology 248, no. 2 (February 1, 1985): F163—F174. http://dx.doi.org/10.1152/ajprenal.1985.248.2.f163.
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Our knowledge of the structure and function of the renal glomerulus is reviewed in a historical context. The glomerular corpuscles were first described by Malpighi in 1666. Subsequent injection studies led to conflicting claims concerning a glomerular-tubular connection. This connection was accepted only after the convincing demonstration of the anatomical relationship essentially as we now know it by Bowman in 1842. Ludwig was the first to propose that the mechanism of separation of fluid in the glomeruli was by ultrafiltration. Estimates of the ultrafiltration forces in mammals led to conflicting speculation as to whether or not filtration-pressure equilibrium was reached in glomerular capillaries. Results of direct determinations in some Munich-Wistar rats indicate filtration pressure equilibrium, an ultrafiltration coefficient (Kf) of 0.08 nl X s-1 X mmHg-1, and a strong influence of plasma flow on filtration rate (GFR). In contrast, evidence has been presented that filtration dynamics in other Munich-Wistar rats and several other strains of rats are characterized by filtration disequilibrium, a Kf of 0.04 nl X s-1 X mmHg-1, and a weak dependence of GFR on plasma flow. In conscious and anesthetized rats, kidney GFR is usually relatively stable in the presence of renal vasodilation. Filtration disequilibrium is reported in the dog and equilibrium in the squirrel monkey. Although predictions for humans suggest filtration disequilibrium, final conclusions await an in-depth analysis of direct measurements.
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Dong, Jianghu J., Liangliang Wang, Jagbir Gill, and Jiguo Cao. "Functional principal component analysis of glomerular filtration rate curves after kidney transplant." Statistical Methods in Medical Research 27, no. 12 (June 20, 2017): 3785–96. http://dx.doi.org/10.1177/0962280217712088.
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This article is motivated by some longitudinal clinical data of kidney transplant recipients, where kidney function progression is recorded as the estimated glomerular filtration rates at multiple time points post kidney transplantation. We propose to use the functional principal component analysis method to explore the major source of variations of glomerular filtration rate curves. We find that the estimated functional principal component scores can be used to cluster glomerular filtration rate curves. Ordering functional principal component scores can detect abnormal glomerular filtration rate curves. Finally, functional principal component analysis can effectively estimate missing glomerular filtration rate values and predict future glomerular filtration rate values.
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Squarer, A., K. V. Lemley, S. Ambalavanan, B. Kristal, W. M. Deen, R. Sibley, L. Anderson, and B. D. Myers. "Mechanisms of progressive glomerular injury in membranous nephropathy." Journal of the American Society of Nephrology 9, no. 8 (August 1998): 1389–98. http://dx.doi.org/10.1681/asn.v981389.
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Glomerular function and structure were serially evaluated in 15 patients with membranous nephropathy who exhibited relapsing nephrosis and chronic depression of GFR. GFR declined from 56+/-8 (mean+/-SEM) at onset to 31+/-4 ml/min per 1.73 m2 after a 2- to 5-yr period of observation (P < 0.05). An analysis of filtration dynamics suggested persistent elevation of net ultrafiltration pressure. To examine a possible role for declining intrinsic glomerular filtration capacity as the basis for the observed hypofiltration, glomeruli in the baseline and a repeat biopsy (performed after a median of 28 mo) were subjected to morphometric analysis and mathematical modeling. Analysis of the baseline biopsy revealed a reduction in filtration slit frequency and thickening of the glomerular basement membrane, lowering computed hydraulic permeability by 66% compared with normal kidney donors. In contrast, filtration surface area was increased by 37% as a result of glomerular hypertrophy. The repeat biopsy revealed persistent depression of hydraulic permeability, primarily owing to foot process broadening. An additional finding was a decrease in filtration surface area from baseline in patent glomeruli, possibly due to encroachment on the capillary lumen of an increasingly widened basement membrane. Also, a striking increase in the prevalence of global glomerulosclerosis from 7+/-2% to 23+/-4% was found between the two biopsies, suggesting a significant loss of functioning nephrons. It is concluded that hypofiltration in membranous nephropathy is the consequence of a biphasic loss of glomerular ultrafiltration capacity, initially owing to impaired hydraulic permeability that is later exacerbated by a superimposed loss of functioning glomeruli and of filtration surface area.
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Drummond, I. A., A. Majumdar, H. Hentschel, M. Elger, L. Solnica-Krezel, A. F. Schier, S. C. Neuhauss, et al. "Early development of the zebrafish pronephros and analysis of mutations affecting pronephric function." Development 125, no. 23 (December 1, 1998): 4655–67. http://dx.doi.org/10.1242/dev.125.23.4655.
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The zebrafish pronephric kidney provides a simplified model of nephron development and epithelial cell differentiation which is amenable to genetic analysis. The pronephros consists of two nephrons with fused glomeruli and paired pronephric tubules and ducts. Nephron formation occurs after the differentiation of the pronephric duct with both the glomeruli and tubules being derived from a nephron primordium. Fluorescent dextran injection experiments demonstrate that vascularization of the zebrafish pronephros and the onset of glomerular filtration occurs between 40 and 48 hpf. We isolated fifteen recessive mutations that affect development of the pronephros. All have visible cysts in place of the pronephric tubule at 2–2.5 days of development. Mutants were grouped in three classes: (1) a group of twelve mutants with defects in body axis curvature and manifesting the most rapid and severe cyst formation involving the glomerulus, tubule and duct, (2) the fleer mutation with distended glomerular capillary loops and cystic tubules, and (3) the mutation pao pao tang with a normal glomerulus and cysts limited to the pronephric tubules. double bubble was analyzed as a representative of mutations that perturb the entire length of the pronephros and body axis curvature. Cyst formation begins in the glomerulus at 40 hpf at the time when glomerular filtration is established suggesting a defect associated with the onset of pronephric function. Basolateral membrane protein targeting in the pronephric duct epithelial cells is also severely affected, suggesting a failure in terminal epithelial cell differentiation and alterations in electrolyte transport. These studies reveal the similarity of normal pronephric development to kidney organogenesis in all vertebrates and allow for a genetic dissection of genes needed to establish the earliest renal function.
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Anderson, W. P., D. Alcorn, A. I. Gilchrist, J. M. Whiting, and G. B. Ryan. "Glomerular actions of ANG II during reduction of renal artery pressure: a morphometric analysis." American Journal of Physiology-Renal Physiology 256, no. 6 (June 1, 1989): F1021—F1026. http://dx.doi.org/10.1152/ajprenal.1989.256.6.f1021.
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The glomeruli of kidneys subjected to reduced perfusion pressure were examined morphometrically. The left renal artery was narrowed for 30 min in anesthetized dogs with (n = 6) or without (n = 7) converting-enzyme inhibition (captopril). The kidneys were then rapidly fixed by glutaraldehyde perfusion at high flow rate. In a comparison of glomeruli of kidneys subjected to pressure reduction in captopril-treated and untreated dogs, there was significantly greater mesangial contraction in the latter, but morphometric analysis revealed no significant differences in the glomerular surface area available for filtration as evidenced by glomerular capillary volume fractions, surface areas of the filtering basement membrane between epithelial and endothelial cells, or the length densities of the glomerular epithelial slits. In a comparison of the left (pressure reduction) and right (no pressure reduction) kidneys in the captopril-treated dogs, there was no significant effect of reduction of renal perfusion pressure per se on mesangial contraction or glomerular filtration surface area when angiotensin (ANG) II formation was blocked. Thus ANG II caused mesangial cell contraction after renal artery stenosis, but this did not significantly change glomerular ultrafiltration surface area.
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Scharschmidt, L. A., J. G. Douglas, and M. J. Dunn. "Angiotensin II and eicosanoids in the control of glomerular size in the rat and human." American Journal of Physiology-Renal Physiology 250, no. 2 (February 1, 1986): F348—F356. http://dx.doi.org/10.1152/ajprenal.1986.250.2.f348.
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We examined the possibility that glomerular prostaglandin E2 (PGE2) regulates the action of angiotensin II (ANG II) on mesangial contraction and filtration surface area. Using isolated rat glomeruli we indirectly assessed mesangial contraction and filtration surface area through measurements of glomerular planar surface area (GPSA) by image-analysis microscopy. ANG II reduced GPSA by approximately 20% in human and rat glomeruli, with threshold concentrations of 1 X 10(-13) M and maximum effect at 5 X 10(-11) M ANG II. Inhibition of glomerular PG synthesis with indomethacin or meclofenamate potentiated the threshold response of ANG II to reduce GPSA. Arachidonic acid (5 micrograms/ml) blunted both the threshold and the maximum responses of GPSA to ANG II. PGE2, 10(-8) and 10(-9) M, also decreased glomerular contraction to ANG II. Endoperoxide (EP) analogues decreased GPSA and EP 045, a thromboxane A2 (TXA2) receptor blocker, eliminated the contractile responses of glomeruli to the EP analogues. Authentic TXA2, synthesized from sheep platelet microsomes, also reduced GPSA. We conclude that glomerular products of arachidonate cyclooxygenation may either relax or contract the mesangium, thereby preserving or reducing filtration surface area. PGE2 exerts protective actions to reduce the mesangial contraction of ANG II, primarily through postreceptor effects. TXA2 may decrease glomerular filtration rate in certain diseases through direct actions on the mesangium.
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Uchio-Yamada, Kozue, Keiko Yasuda, Yoko Monobe, Ken-ichi Akagi, Osamu Suzuki, and Noboru Manabe. "Tensin2 is important for podocyte-glomerular basement membrane interaction and integrity of the glomerular filtration barrier." American Journal of Physiology-Renal Physiology 318, no. 6 (June 1, 2020): F1520—F1530. http://dx.doi.org/10.1152/ajprenal.00055.2020.
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Tensin2 (Tns2), an integrin-linked protein, is enriched in podocytes within the glomerulus. Previous studies have revealed that Tns2-deficient mice exhibit defects of the glomerular basement membrane (GBM) soon after birth in a strain-dependent manner. However, the mechanisms for the onset of defects caused by Tns2 deficiency remains unidentified. Here, we aimed to determine the role of Tns2 using newborn Tns2-deficient mice and murine primary podocytes. Ultrastructural analysis revealed that developing glomeruli during postnatal nephrogenesis exhibited abnormal GBM processing due to ectopic laminin-α2 accumulation followed by GBM thickening. In addition, analysis of primary podocytes revealed that Tns2 deficiency led to impaired podocyte-GBM interaction and massive expression of laminin-α2 in podocytes. Our study suggests that weakened podocyte-GBM interaction due to Tns2 deficiency causes increased mechanical stress on podocytes by continuous daily filtration after birth, resulting in stressed podocytes ectopically producing laminin-α2, which interrupts GBM processing. We conclude that Tns2 plays important roles in the podocyte-GBM interaction and maintenance of the glomerular filtration barrier.
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Myers, B. D., and L. Newton. "Cyclosporine-induced chronic nephropathy: an obliterative microvascular renal injury." Journal of the American Society of Nephrology 2, no. 2 (August 1991): S45. http://dx.doi.org/10.1681/asn.v22s45.
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Physiologic and morphologic techniques have been used to study kidneys of 200 cardiac transplant recipients treated with either low- or high-dose cyclosporine. After 12 months, both low- (4.6 +/- 0.4) and high-dose cyclosporine (6.3 +/- 0.3 mg/kg/24 h; P less than 0.01) were associated with depression of glomerular filtration rate below values in a third group of 100 recipients never exposed to cyclosporine by 40 to 47%. Determination of renovascular pressures and flows as well as analysis of transglomerular sieving of dextrans revealed renal vascular resistance in cyclosporine-treated recipients to be elevated greater than twofold, due largely to an increase in preglomerular resistance. Morphologic changes in renal tissue of both cyclosporine groups included an occlusive afferent arteriolopathy with downstream collapse or sclerosis of glomeruli. Ischemic nephrons were associated with patchy fibrosis of the surrounding interstitium. Follow-up for up to 9 yr reveals persistent but stable azotemia, on average. Longitudinal physiologic studies over a 48-month period (N = 15) during which cyclosporine was reduced in dosage (to 3.1 +/- 0.3 mg/kg) or withdrawn revealed a persistently reduced but constant level of glomerular filtration rate. Increasing ischemic glomerular collapse and sclerosis were observed at repeat renal biopsy. Remnant (spared) glomeruli exhibited hypertrophy; presumably elevated single nephron glomerular filtration rate maintained two-kidney glomerular filtration rate constant despite the declining fraction of functional glomeruli. By actuarial analysis, the cumulative incidence of end-stage renal failure in cardiac transplant recipients treated at this institution from 1980 onwards with continuous cyclosporine therapy has reached 10%.(ABSTRACT TRUNCATED AT 250 WORDS)
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Hladunewich, M. A., R. A. Lafayette, G. C. Derby, K. L. Blouch, J. W. Bialek, M. L. Druzin, W. M. Deen, and B. D. Myers. "The dynamics of glomerular filtration in the puerperium." American Journal of Physiology-Renal Physiology 286, no. 3 (March 2004): F496—F503. http://dx.doi.org/10.1152/ajprenal.00194.2003.
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We evaluated the glomerular filtration rate (GFR) during the second postpartum week in 22 healthy women who had completed an uncomplicated pregnancy. We used physiological techniques to measure GFR, renal plasma flow, and oncotic pressure and computed a value for the two-kidney ultrafiltration coefficient ( Kf). We compared these findings with those in pregnant women previously studied on the first postpartum day as well as nongravid women of reproductive age. Healthy female transplant donors of reproductive age permitted the morphometric analysis of glomeruli and computation of the single-nephron Kf. The aforementioned physiological and morphometric measurements were utilized to estimate transcapillary hydraulic pressure (ΔP) from a mathematical model of glomerular ultrafiltration. We conclude that postpartum day 1 is associated with marked glomerular hyperfiltration (+41%). A theoretical analysis of GFR determinants suggests that depression of glomerular capillary oncotic pressure, the force opposing the formation of filtrate, is the predominant determinant of early elevation of postpartum GFR. A reversal of the gestational hypervolemia and hemodilution, still evident on postpartum day 1, eventuates by postpartum week 2. An elevation of oncotic pressure in the plasma that flows axially along the glomerular capillaries to supernormal levels ensues; however, GFR remains modestly elevated (+20%) above nongravid levels. An analysis of filtration dynamics at this time suggests that a significant increase in ΔP by up to 16%, an ∼50% increase in Kf, or a combination of smaller increments in both must be invoked to account for the persistent hyperfiltration.
Dissertations / Theses on the topic "Glomerular filtration analysis"
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Walton, H. A. "The effect of structural modifications on the permeation properties of renal basement membrane." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382711.
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Roberts, Mark. "Assessment of glomerular dynamics in human pregnancy using theoretical analysis and dextran sieving coefficients." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336811.
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Akbari, Ayub. "Change in Referral Patterns to Nephrologists after Estimated Glomerular Filtration Rate (eGFR) Reporting: An interrupted time series analysis." Thesis, University of Ottawa (Canada), 2011. http://hdl.handle.net/10393/28785.
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Objectives: To update a Cochrane review of interventions to improve outpatient referral and to assess changes in referrals to nephrologists after initiating automatic estimated glomerular filtration rate (eGFR) reporting.
Methods: Systematic review using standardized Cochrane methods. Before and after study with interrupted time series analysis using data from retrospective chart review on referrals from family medicine to nephrology.
Results: Review added one new study and removed one for total of 17 studies. Referrals improved with education and structured referral sheets. Of 2766 eligible referrals for one-year pre-eGFR reporting to one-year post, 96.6% were reviewed. There was a 68.2% increase in referrals for chronic kidney disease (P < 0.01) and a 64.1% increase in total appropriate referrals (P =0.01) with no significant change in proportion of appropriate referrals (-2.5%, P=0.56).
Conclusion: Systematic review findings did not change from the previous review. eGFR reporting increased both appropriate and inappropriate referrals.
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Coelho, Fernanda Oliveira. "Efeitos renais da exposição crônica a nicotina em camundongos com deficiência de Klotho." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-09112015-124235/.
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A nicotina é o principal componente do tabaco e dos cigarros eletrônicos. A exposição crônica a nicotina, em quantidades semelhantes às atingidas pelo tabagismo humano, é responsável por piora da lesão renal aguda e da doença renal crônica. O gene klotho, predominantemente expresso no rim, foi descoberto após uma mutação insercional, com o surgimento de um fenótipo semelhante ao envelhecimento humano nos camundongos homozigotos para esse transgene. A proteína Klotho transmembrana tem ação de co-receptor do fator de crescimento fibroblástico 23 (FGF-23) e sua forma secretada atua em diversas vias intracelulares e em órgãos a distância. A deficiência de Klotho ocorre no envelhecimento, em situações que levam a lesão renal aguda e na doença renal crônica. A expressão reduzida de Klotho também agrava lesão renal aguda e participa da progressão da doença renal crônica, enquanto o seu aumento, ou a sua reposição, protegem dos processos inflamatórios e do estresse oxidativo. Neste estudo, objetivamos avaliar os efeitos renais, hemodinâmicos e sobre a expressão de Klotho da exposição crônica a nicotina e quais os efeitos dessa exposição nos animais haploinsuficientes para o transgene klotho (Kl+/-). Utilizamos para estas avaliações camundongos Kl+/- e seus controles wild type (Kl+/+), que foram expostos a nicotina (200 mcg/mL) ou veículo (sacarina 2%) diluídos em água por 28 dias. Ao final do estudo foram avaliados diurese, eletrólitos plasmáticos e urinários, ureia, aldosterona, ADH, FGF-23 e PTH intactos plasmáticos, expressão protéica renal de Klotho, alfa7-nAchR, NHE3, ENaC, NKCC2, AQP2, e-NOS, VEGF, MnSOD e renina, expressão genica renal de klotho, interleucinas, TBARS e GSH em tecido renal, taxa de filtração glomerular por FITC-inulina, pressão arterial e frequência cardíaca invasivas, sensibilidade baroreflexa e modulação autonômica cardíaca e periférica por análise espectral. Após a exposição a nicotina, os animais Kl+/+ apresentaram redução da expressão renal da proteína e do RNAm de Klotho e uma tendência a aumento dos níveis plasmáticos de FGF-23, associados a uma queda da diurese e da taxa de filtração glomerular, sem alteração dos níveis de ADH. Esses animais Kl+/+ também apresentaram aumento da sensibilidade barorreflexa em resposta ao nitroprussiato e um predomínio da modulação simpática cardíaca, com redução da expressão renal dos alfa7-nAchR. Os animais Kl+/- tiveram níveis renais ainda menores de Klotho após a exposição a nicotina, com aumento de TBARS, IL-6, uréia e aldosterona em relação aos Kl+/- não expostos. A diurese, a taxa de filtração glomerular e a expressão dos alfa7-nAchR não se reduziram e não houve aumento da sensibilidade barorreflexa após exposição a nicotina, com um predomínio da modulação parassimpática cardíaca, nesses animais Kl+/-. A ingesta hídrica, a pressão arterial e a frequência cardíaca foram semelhantes entre os 4 grupos. A proteinúria foi maior nos animais Kl+/- do que nos animais Kl+/+ após a exposição a nicotina. Podemos concluir que a exposição crônica à nicotina reduz a expressão renal de Klotho, estimula vias de inflamação, fibrose e estresse oxidativo renais e tem efeitos renais e sistêmicos diferentes de acordo com os níveis basais de KlothoNicotine is a major compound of tobacco and electronic cigarettes. Chronic exposure to nicotine concentrations that are similar to human smoke worsens acute kidney injury and chronic kidney disease. The klotho (Kl) gene is expressed predominantly by the kidney and was discovered after an unintentional insertional mutation that resulted, in transgenic homozygous mice, in a phenotype similar to human aging. Klotho transmembrane protein acts as a co-receptor to fibroblastic growth factor 23 (FGF-23) and the secreted form interacts in multiple intracellular pathways, with effects in distant organs. Klotho deficiency occurs in aging and in multiple acute kidney injury and chronic kidney disease etiologies, whereas klotho upregulation and replacement protect from inflammation and oxidative stress. Here, we investigated renal and hemodynamic effects of chronic nicotine exposure, its effects over renal expression of Kl, and compared wild type (Kl+/+) and Kl haploinsufficient mice (Kl+/-) in terms of the effects of that exposure. Kl+/- and Kl+/+ mice received nicotine (200 ?g/ml) or vehicle (saccharine 2%) in drinking water for 28 days. We evaluated diuresis, ions in serum and urine, urea, plasma and urinary levels of cotinine, aldosterone, plasma antidiuretic and parathyroid hormone, plasma FGF-23, protein expression of (immunoblotting for) Klotho and ?7 nicotinic acetylcholine receptor, NHE3, NKCC2, ENaC, aquaporin-2, e-NOS, VEGF and renin, klotho mRNA, kidney interleukines, TBARS and GSH, glomerular filtration rate by fluorescein isothiocyanate-inulin clearance, mean arterial pressure, heart rate, baroreflex sensitivity and autonomic cardiac and peripheral modulation by spectral analysis. After nicotine exposure, Kl+/+ mice showed decreased Klotho protein and mRNA and a tendency towards an elevation in plasma FGF-23, which were associated with both diuresis and glomerular filtration rate reductions, without modifications in ADH levels. Besides that, Kl+/+ animals increased baroreflex sensitivity after nitroprusside, a predominant sympathetic cardiac modulation and lower alfa7-nAchR kidney expression. Kl+/- mice reduced even more Klotho renal expression, with higher levels of TBARS, IL-6, urea and aldosterone. Diuresis, glomerular filtration rate, alfa7-nAchR expression and baroreflex sensitivity were the same of their controls. Cardiac parasympathetic modulation predominated in Kl+/- mice. Fluid intake, mean arterial pressure and heart rate were similar across the 4 groups. Renal protein excretion was higher in Kl+/- than in their controls after nicotine exposure. We can conclude that chronic nicotine exposure downregulates Klotho kidney expression induces inflammation and oxidative stress and stimulates fibrosis, with different renal and systemic responses according to basal Klotho levels
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Steinbruckner-Gaildraud, Ingrid. "Un nouveau marqueur d'évaluation de la filtration glomérulaire : la cystatine C sérique." Bordeaux 2, 2000. http://www.theses.fr/2000BOR2P040.
Full textBooks on the topic "Glomerular filtration analysis"
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Virginia. Department of Medical Assistance Services. Estimated glomerular filtration rate reporting among clinical laboratory providers: Report of the Virginia Department of Medical Assistance Services to the Governor and the General Assembly of Virginia. Richmond: Commonwealth of Virginia, 2007.
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Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.
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Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal phenotype in mitochondrial disease is proximal tubulopathy (Fanconi syndrome in the severest cases); however, as all regions of the nephron can be affected, from the glomerulus to the collecting duct, patients may also present with proteinuria, decreased glomerular filtration rate, nephrotic syndrome, water and electrolyte disorders, and renal tubular acidosis. Understanding of the relationship between underlying genotype and clinical phenotype remains incomplete in mitochondrial disease. Proximal tubulopathy typically occurs in children with severe multisystem disease due to mtDNA deletion or mutations in nDNA affecting mitochondrial function. In contrast, glomerular disease (focal segmental glomerulosclerosis) has been reported more commonly in adults, mainly in association with the m.3243A<G point mutation. Co-enzyme Q10 (CoQ10) deficiency has been particularly associated with podocyte dysfunction and nephrotic syndrome in children. Underlying mitochondrial disease should be considered as a potential cause of unexplained renal dysfunction; clinical clues include lack of response to conventional therapy, abnormal mitochondrial morphology on kidney biopsy, involvement of other organs (e.g. diabetes, cardiomyopathy, and deafness) and a maternal family history, although none of these features are specific. The diagnostic approach involves acquiring tissue (typically skeletal muscle) for histological analysis, mtDNA screening and oxidative phosphorylation (OXPHOS) complex function tests. A number of nDNA mutations causing mitochondrial disease have now been identified and can also be screened for if clinically indicated. Management of mitochondrial disease requires a multidisciplinary approach, and treatment is largely supportive as there are currently very few evidence-based interventions. Electrolyte deficiencies should be corrected in patients with urinary wasting due to tubulopathy, and CoQ10 supplementation may be of benefit in individuals with CoQ10 deficiency. Nephrotic syndrome in mitochondrial disease is not typically responsive to steroid therapy. Transplantation has been performed in patients with end-stage kidney disease; however, immunosuppressive agents such as steroids and tacrolimus should be used with care given the high incidence of diabetes in mitochondrial disease.
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Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi, and Brian B. Ratliff. Pathophysiology of acute kidney injury. Edited by Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.
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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.
Book chapters on the topic "Glomerular filtration analysis"
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Pedersen, Michael, Pietro Irrera, Walter Dastrù, Frank G. Zöllner, Kevin M. Bennett, Scott C. Beeman, G. Larry Bretthorst, Joel R. Garbow, and Dario Livio Longo. "Dynamic Contrast Enhancement (DCE) MRI–Derived Renal Perfusion and Filtration: Basic Concepts." In Methods in Molecular Biology, 205–27. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_12.
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AbstractDynamic contrast-enhanced (DCE) MRI monitors the transit of contrast agents, typically gadolinium chelates, through the intrarenal regions, the renal cortex, the medulla, and the collecting system. In this way, DCE-MRI reveals the renal uptake and excretion of the contrast agent. An optimal DCE-MRI acquisition protocol involves finding a good compromise between whole-kidney coverage (i.e., 3D imaging), spatial and temporal resolution, and contrast resolution. By analyzing the enhancement of the renal tissues as a function of time, one can determine indirect measures of clinically important single-kidney parameters as the renal blood flow, glomerular filtration rate, and intrarenal blood volumes. Gadolinium-containing contrast agents may be nephrotoxic in patients suffering from severe renal dysfunction, but otherwise DCE-MRI is clearly useful for diagnosis of renal functions and for assessing treatment response and posttransplant rejection.Here we introduce the concept of renal DCE-MRI, describe the existing methods, and provide an overview of preclinical DCE-MRI applications to illustrate the utility of this technique to measure renal perfusion and glomerular filtration rate in animal models.This publication is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction is complemented by two separate publications describing the experimental procedure and data analysis.
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Irrera, Pietro, Lorena Consolino, Walter Dastrù, Michael Pedersen, Frank G. Zöllner, and Dario Livio Longo. "Dynamic Contrast Enhanced (DCE) MRI-Derived Renal Perfusion and Filtration: Experimental Protocol." In Methods in Molecular Biology, 429–41. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_25.
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AbstractDynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) can provide a noninvasive way for assessing renal functional information following the administration of a small molecular weight gadolinium-based contrast agent. This method may be useful for investigating renal perfusion and glomerular filtration rates of rodents in vivo under various experimental (patho)physiological conditions. Here we describe a step-by-step protocol for DCE-MRI studies in small animals providing practical notes on acquisition parameters, sequences, T1 mapping approaches and procedures.This chapters is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This experimental protocol chapter is complemented by two separate chapters describing the basic concept and data analysis.
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Ku, Min-Chi, María A. Fernández-Seara, Frank Kober, and Thoralf Niendorf. "Noninvasive Renal Perfusion Measurement Using Arterial Spin Labeling (ASL) MRI: Basic Concept." In Methods in Molecular Biology, 229–39. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_13.
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AbstractThe kidney is a complex organ involved in the excretion of metabolic products as well as the regulation of body fluids, osmolarity, and homeostatic status. These functions are influenced in large part by alterations in the regional distribution of blood flow between the renal cortex and medulla. Renal perfusion is therefore a key determinant of glomerular filtration. Therefore the quantification of regional renal perfusion could provide important insights into renal function and renal (patho)physiology. Arterial spin labeling (ASL) based perfusion MRI techniques, can offer a noninvasive and reproducible way of measuring renal perfusion in animal models. This chapter addresses the basic concept of ASL-MRI.This chapter is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction chapter is complemented by two separate chapters describing the experimental procedure and data analysis.
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Longo, Dario Livio, Pietro Irrera, Lorena Consolino, Phillip Zhe Sun, and Michael T. McMahon. "Renal pH Imaging Using Chemical Exchange Saturation Transfer (CEST) MRI: Basic Concept." In Methods in Molecular Biology, 241–56. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_14.
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AbstractMagnetic Resonance Imaging (MRI) has been actively explored in the last several decades for assessing renal function by providing several physiological information, including glomerular filtration rate, renal plasma flow, tissue oxygenation and water diffusion. Within MRI, the developing field of chemical exchange saturation transfer (CEST) has potential to provide further functional information for diagnosing kidney diseases. Both endogenous produced molecules as well as exogenously administered CEST agents have been exploited for providing functional information related to kidney diseases in preclinical studies. In particular, CEST MRI has been exploited for assessing the acid-base homeostasis in the kidney and for monitoring pH changes in several disease models. This review summarizes several CEST MRI procedures for assessing kidney functionality and pH, for monitoring renal pH changes in different kidney injury models and for evaluating renal allograft rejection.This chapter is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction chapter is complemented by two separate chapters describing the experimental procedure and data analysis.
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Jerome, Neil Peter, Anna Caroli, and Alexandra Ljimani. "Renal Diffusion-Weighted Imaging (DWI) for Apparent Diffusion Coefficient (ADC), Intravoxel Incoherent Motion (IVIM), and Diffusion Tensor Imaging (DTI): Basic Concepts." In Methods in Molecular Biology, 187–204. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0978-1_11.
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AbstractThe specialized function of the kidney is reflected in its unique structure, characterized by juxtaposition of disorganized and ordered elements, including renal glomerula, capillaries, and tubules. The key role of the kidney in blood filtration, and changes in filtration rate and blood flow associated with pathological conditions, make it possible to investigate kidney function using the motion of water molecules in renal tissue. Diffusion-weighted imaging (DWI) is a versatile modality that sensitizes observable signal to water motion, and can inform on the complexity of the tissue microstructure. Several DWI acquisition strategies are available, as are different analysis strategies, and models that attempt to capture not only simple diffusion effects, but also perfusion, compartmentalization, and anisotropy. This chapter introduces the basic concepts of DWI alongside common acquisition schemes and models, and gives an overview of specific DWI applications for animal models of renal disease.This chapter is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction chapter is complemented by two separate chapters describing the experimental procedure and data analysis.
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Srivastava, Devesh Kumar, and Pradeep Kumar Tiwari. "Chronic Kidney Disease Prediction Using Data Mining Algorithms." In Handbook of Research on Disease Prediction Through Data Analytics and Machine Learning, 92–111. IGI Global, 2021. http://dx.doi.org/10.4018/978-1-7998-2742-9.ch006.
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In today's contemporary world, it is important to know about the odds of having a disease because of changing living standards of the population overall in the continent. The disease on which the authors are working is chronic kidney disease. Once the person gets chronic kidney disease (CKD), his working capability decreases along with other adverse effects. It is possible to get rid of diseases like CKD with new methodologies that will help us to predict the stage of kidney disease at an early stage. Under big data analytics, data may be structured, unstructured, quasi- or semi-structured. The CKD detected and predicted by applying classification models: support vector machine (SVM), K-nearest neighbor (KNN), and logistic regression algorithm. It helps in predicting the likelihood of occurrence of disease on various different features. The two algorithms KNN and SVM are compared to find the algorithm that gives better accuracy. Further regression technique has been used to detect the disease based on, which the stages are classified by using GFR (glomerular filtration rate) formula.
Conference papers on the topic "Glomerular filtration analysis"
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De Senneville, B. Denis, P. Desbarats, M. Ries, C. T. W. Moonen, and N. Grenier. "Automatic Region Tracking for MR Glomerular Filtration Rate Analysis." In 2006 International Conference on Image Processing. IEEE, 2006. http://dx.doi.org/10.1109/icip.2006.312999.
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Rafeeque, Ameena, and Mohammed Fasihul Alam. "The effect of Renin Angiotensin System Blockers versus Calcium Channel Blockers on Progression towards Hypertensive Chronic Kidney Disease: A comprehensive systematic review based on Randomized Controlled Trials." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0162.
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Background: Decline in estimated Glomerular filtration rate (eGFR) is associated with further progression of chronic kidney disease. Evidence suggests that Renin Angiotensin System blockers (RAS), which can be angiotensin-receptor blockers (ARBs) or Angiotensin converting enzymes Inhibitors (ACEIs), have reno- protective effect, but results are variable. Similarly, effects of Calcium channel blockers (CCBs) are shown to have a role in protecting renal function but differ across studies. Hence, the relative effect of ARBs or ACEIs as well as CCBs, and their administration as monotherapy, remain uncertain. Purpose: To summarize and determine the pooled effect of RAS versus CCBs on progression towards hypertensive CKD amongst diabetic as well as non-diabetic patients with CKD of any stage from I-IV. Data sources: All language studies in PubMed, the Cochrane Library Central, Clinical Registry of unpublishedTrials, WHO, Embase, Scopus, ProQuest, reference lists, and expert contacts up to September 2019. Study selection: This study included all the full text articles that studied diabetic and non-diabetic patients with eGFR ≥ 15 ml/min per 1.73m3 or Urinary albumin excretion levels (UAE) ≤ 300mg/d during RAS based treatment an intervention in direct comparison with CCBs treatment based approach as comparator at baseline and at the end of follow-up. However, pooling of all the included studies using meta-analysis was not feasible due to substantial study heterogeneity and the small number of included studies that are meta-analyzable. So, studies were selected for systematic review, and out of which, all the meta-analyzable studies were quantitatively analyzed on the basis of main outcomes such as (i) Relative risk for CKD progression and (ii) Mean differences in SBP and DBP for both the arms. Doi plot and funnel plot were used for detection of publication bias. Results: Review with seven included trials, and metaanalysis using IVhet model was done on three studies for primary CKD outcome and four studies for secondary BP outcomes. RAS blockers and CCBs did not show any statistically significant differences in terms of its effects on further progression CKD with RR of 0.90 [95% CI 0.69, 1.16]. Moreover, there was no statistically significant difference in BP from baseline to final end points between CCBs and RAS inhibitors with WMD of -2.09 mmHg [95% CI -5.96, 1.79] for mean SBP change and -0.71 mmHg [95% CI -2.16, 0.73] for mean DBP change. Conclusion: Evidence asserts no difference between RAS and CCB concerning the risk of progression for CKD and in terms of mean BP differences. However, the study have its own set of limitations due to which more well designed and well conducted RCTs with robust findings are required to confirm the inferences based on this review.