Differential Determinants of Tubular Phosphate Reabsorption: Insights on Renal Excretion of Phosphates in Kidney Disease

2018 ◽  
Vol 47 (5) ◽  
pp. 300-303 ◽  
Author(s):  
Nahid Tabibzadeh ◽  
Romuald Mentaverri ◽  
Maïté Daroux ◽  
Rafik Mesbah ◽  
Alexia Delpierre ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Iron Supplementation ◽  
Renal Excretion ◽  
Multivariable Analysis ◽  
Tubular Reabsorption ◽  
Phosphate Metabolism ◽  
Estimated Gfr ◽  
Phosphate Reabsorption ◽  
Renal Threshold ◽  
Tubular Phosphate Reabsorption

We assessed the tubular reabsorption of phosphate (TRP) and maximal renal threshold for phosphate reabsorption to glomerular filtration rate (TmPi/GFR) and their determinants in 64 stages 2–4 chronic kidney disease (CKD) patients in order to define the early changes in phosphate metabolism in CKD. In multivariable analysis, TmPi/GFR correlates were estimated GFR (eGFR), intact parathyroid hormone (iPTH), and hemoglobin (R2 = 0.417), while TRP correlates were eGFR, iPTH, 24-h phosphaturia, and calcitriol (R2 = 0.72). This suggests that TmPi/GFR and TRP, respectively, assess hemoglobin-phosphate and bowel-kidney phosphate regulation axis. Iron supplementation based on TmPi/GFR or earlier phosphate restriction based on TRP should be investigated in view of modifying clinical outcomes in CKD.

scholarly journals Early post-transplantation hypophosphatemia is associated with elevated FGF-23 levels

2011 ◽  
Vol 164 (5) ◽  
pp. 839-847 ◽  
Author(s):  
Andrea Trombetti ◽  
Laura Richert ◽  
Karine Hadaya ◽  
Jean-Daniel Graf ◽  
François R Herrmann ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Tubular Reabsorption ◽  
Phosphate Metabolism ◽  
Multivariate Models ◽  
Intact Pth ◽  
Post Transplantation ◽  
Estimated Gfr ◽  
Renal Tubular Reabsorption ◽  
Renal Tubular ◽  
Fgf 23

BackgroundWe examined the hypothesis that high FGF-23 levels early after transplantation contribute to the onset of hypophosphatemia, independently of parathyroid hormone (PTH) and other factors regulating phosphate metabolism.MethodsWe measured serum phosphate levels (sPi), renal tubular reabsorption of Pi (TmPi/GFR), estimated GFR (eGFR), intact PTH (iPTH), calcitriol, intact (int) and C-terminal (Cter) FGF-23, dietary Pi intake and cumulative doses of glucocorticoids in 69 patients 12 days (95% confidence interval, 10–13) after renal transplantation.ResultsHypophosphatemia was observed in 43 (62%) of the patients 12 days after transplantation. Compared with non-hypophosphatemic subjects, their post-transplantation levels of intact and CterFGF-23 were higher (195 (108–288) vs 48 (40–64) ng/l, P<0.002 for intFGF-23; 205 (116–384) vs 81 (55–124) U/ml, P<0.002, for CterFGF-23). In all subjects, Cter and intFGF-23 correlated inversely with sPi (r=−0.35, P<0.003; −0.35, P<0.003, respectively), and TmPi/GFR (r=−0.50, P<0.001; −0.54, P<0.001, respectively). In multivariate models, sPi and TmPi/GFR were independently associated with FGF-23, iPTH and eGFR. Pre-transplant iPTH levels were significantly higher in patients developing hypophosphatemia after renal transplantation. Pre-transplant levels of FGF-23 were not associated with sPi at the time of transplantation.ConclusionIn addition to PTH, elevated FGF-23 may contribute to hypophosphatemia during the early post-renal transplant period.

Synthetic atrial natriuretic factor decreases renal tubular phosphate reabsorption in rats

1985 ◽  
Vol 249 (2) ◽  
pp. F315-F318
Author(s):  
T. G. Hammond ◽  
A. Haramati ◽  
F. G. Knox
Keyword(s):  
Parathyroid Hormone ◽  
Atrial Natriuretic Factor ◽  
Tubular Reabsorption ◽  
Phosphate Reabsorption ◽  
Natriuretic Factor ◽  
Tubular Phosphate Reabsorption ◽  
Renal Tubular ◽  
Filtered Load ◽  
Atrial Natriuretic

Atrial natriuretic factor (ANF), a family of peptides isolated from cardiac atria, has marked effects on sodium excretion. A synthetic 26 amino acid sequence of ANF peptide has also been shown to be phosphaturic. However, it is difficult to assess whether the phosphaturia is due to changes in tubular reabsorption of phosphate without control of filtered load of phosphate. In the present study, the hypothesis that ANF peptide decreases tubular phosphate reabsorption was tested by using graded phosphate infusions of 0, 1, 2, and 3 mumol/min in thyroparathyroidectomized rats. Further, reabsorbed phosphate was similarly assessed in rats infused with parathyroid hormone (PTH) to allow comparison with a known phosphaturic hormone. ANF peptide decreased reabsorbed phosphate compared with saline controls (2.72 +/- 0.28 mumol/ml GFR compared with 3.35 +/- 0.35, P less than 0.05) but not as much as a maximally phosphaturic dose of PTH (2.04 +/- 0.13 mumol/ml GFR). We conclude that synthetic ANF peptide decreases tubular phosphate reabsorption in vivo.

Renal effects of nitric oxide synthesis inhibition in cirrhotic rats

1994 ◽  
Vol 267 (6) ◽  
pp. R1454-R1460 ◽  
Author(s):  
N. M. Atucha ◽  
J. Garcia-Estan ◽  
A. Ramirez ◽  
M. C. Perez ◽  
T. Quesada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Excretion ◽  
Renal Plasma Flow ◽  
Tubular Reabsorption ◽  
Nitric Oxide Synthesis ◽  
Important Mediator ◽  
Experimental Liver Cirrhosis ◽  
Endogenous Nitric Oxide ◽  
And Control ◽  
Experimental Liver

In the present study, we have characterized the renal response to inhibition of endogenous nitric oxide (NO) synthesis [intravenous NG-nitro-L-arginine methyl ester (L-NAME) for 3 h] in anesthetized cirrhotic rats, with (ASC) and without (CIR) ascites, at doses that do not change blood pressure (BP). Administration of L-NAME induced opposite effects on water (UV) and sodium (UNaV) excretion in cirrhotic and control animals. Infusion of 1 microgram.kg-1.min-1 of L-NAME in CIR (n = 5) decreased renal plasma flow (RPF) at the end of the 3-h period, whereas UV, UNaV, and glomerular filtration rate (GFR) were unaltered. In contrast, infusion of L-NAME at 10 micrograms.kg-1.min-1 in six more CIR increased UV and UNaV significantly by the 1st h, without changes in BP or GFR, and these parameters remained elevated throughout the experiment. Infusion of 1 microgram.kg-1.min-1 in ASC (n = 6) did not change BP or GFR but significantly enhanced UV and UNaV after the 1st h. These effects were prevented by pretreatment with L-arginine (0.1 mg.kg-1.min-1) in another group of ASC infused with 1 microgram.kg-1.min-1 of L-NAME. These results indicate that, in ASC and CIR cirrhotic rats, inhibition of NO synthesis at nonpressor does improves renal excretion of sodium and water via a decrease in tubular reabsorption. NO is an important mediator of the renal excretory and hemodynamic alterations of experimental liver cirrhosis.

Zinc levels after iron supplementation in patients with chronic kidney disease

2004 ◽  
Vol 14 (3) ◽  
pp. 164-169 ◽  
Author(s):  
Denise Mafra ◽  
Lilian Cuppari ◽  
Déborah I.T Fávaro ◽  
Sı́lvia M.F Cozzolino
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Iron Supplementation ◽  
Zinc Levels

Renal excretion of cephapirin and cephaloridine: Evidence for saturable tubular reabsorption

1979 ◽  
Vol 25 (6) ◽  
pp. 870-876 ◽  
Author(s):  
Annie Arvidsson ◽  
Olof Borgå ◽  
Gunnár Alvan
Keyword(s):  
Renal Excretion ◽  
Tubular Reabsorption

MO547ASSOCIATION BETWEEN SERUM INDICES OF IRON METABOLISM AND CARDIOVASCULAR MORBIDITY IN PATIENTS WITH PREDIALYSIS CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Takeshi Hasegawa ◽  
Takahiro Imaizumi ◽  
Kenta Murotani ◽  
Takayuki Hamano ◽  
Masafumi Fukagawa
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Iron Metabolism ◽  
Iron Supplementation ◽  
Transferrin Saturation ◽  
Cox Proportional Hazards ◽  
Function Evaluation ◽  
Iron Deficient ◽  
Increased Risk ◽  
Reduced Risk

Abstract Background and Aims Patients with predialysis chronic kidney disease (CKD) have a greater risk of developing cardiovascular disease (CVD) events than the general population. Anaemia is the most frequent comorbidity in pre-dialysis CKD patients and is associated with an increase in CVD events. Iron deficiency is the most frequent cause of erythropoiesis-stimulating agents (ESAs) resistant anaemia in CKD patients and is modifiable by therapeutic intervention. However, the optimal ranges of iron markers are uncertain in predialysis CKD patients. Therefore, we aimed to investigate the association between serum indices of iron metabolism and the incidence of CVD events in patients with predialysis CKD using the CKD-Japan Cohort (CKD-JAC) data. Method We prospectively followed 1550 CKD patients aged 20-75 years with an estimated glomerular filtration rate (eGFR) &lt;60 mL/min/1.73 m2 for a mean of 4.21 years. We set serum transferrin saturation (TSAT) and ferritin levels as the main exposures to be tested. Our main outcome measures were any of the CVD events including fatal or non-fatal myocardial infarction, congestive heart failure (CHF), angina pectoris, arrhythmia, aorta dissection, cerebrovascular disorder, and peripheral artery diseases identified at each facility and adjudicated by the independent cardiac function evaluation committee. Multivariable Cox proportional hazards regression models were employed to examine the association between serum TSAT or ferritin levels with time to events. Death was considered as a competing risk with the Fine and Gray model. All models were stratified by facilities and adjusted for potential confounders as follows: age, sex, systolic blood pressure, diabetes mellitus, history of CHF, haemoglobin, serum calcium, serum phosphorus, intact parathyroid hormone, eGFR, proteinuria, ESAs, iron supplementation, renin-angiotensin system inhibitors, and beta-blockers. We also applied the multivariable fractional polynomial interaction (MFPI) approach to investigate whether TSAT levels are the effect modifier of the association between iron supplementation and the outcomes. Results In the overall cohort, 208 (13.4 %) patients developed CVD events (including 97 CHF) during the follow-up period (26.6 events/1000 person-year). The incidence rate of CVD events was the highest in the TSAT &lt; 20% category (33.0 events/1000 person-year). Compared to patients in the TSAT &gt; 40% category, those in the TSAT &lt; 20% category demonstrated an increased risk of CVD events (adjusted hazard ratio (AHR): 1.86, 95% confidence interval (CI): 1.06-3.26) and CHF events (AHR: 2.82, 95% CI: 1.15-6.89), respectively. Meanwhile, there was no association between serum ferritin levels and the risk of developing CVD or CHF events. MFPI analyses showed a reduced risk of CVD in patients receiving iron supplementation only in patients with TSAT &lt;20% (P for interaction=0.02). Conclusion Maintaining TSAT &gt;20% could be effective to reduce the risk of developing CVD events (especially CHF) in patients with predialysis CKD. Our analyses also suggest that iron-deficient patients with predialysis CKD may benefit from iron supplementation for reduced risk of CVD events.

scholarly journals Hypoxia-Inducible Factor Stabilizers in End Stage Kidney Disease: “Can the Promise Be Kept?”

2021 ◽  
Vol 22 (22) ◽  
pp. 12590
Author(s):  
Giuseppina Crugliano ◽  
Raffaele Serra ◽  
Nicola Ielapi ◽  
Yuri Battaglia ◽  
Giuseppe Coppolino ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Cardiovascular Events ◽  
Iron Supplementation ◽  
Hypoxia Inducible Factor ◽  
Current Treatment ◽  
Prolyl Hydroxylase ◽  
Individual Risk ◽  
Increased Risk ◽  
Gastrointestinal Side Effects ◽  
Iv Iron

Anemia is a common complication of chronic kidney disease (CKD). The prevalence of anemia in CKD strongly increases as the estimated Glomerular Filtration Rate (eGFR) decreases. The pathophysiology of anemia in CKD is complex. The main causes are erythropoietin (EPO) deficiency and functional iron deficiency (FID). The administration of injectable preparations of recombinant erythropoiesis-stimulating agents (ESAs), especially epoetin and darbepoetin, coupled with oral or intravenous(iv) iron supplementation, is the current treatment for anemia in CKD for both dialysis and non-dialysis patients. This approach reduces patients’ dependence on transfusion, ensuring the achievement of optimal hemoglobin target levels. However, there is still no evidence that treating anemia with ESAs can significantly reduce the risk of cardiovascular events. Meanwhile, iv iron supplementation causes an increased risk of allergic reactions, gastrointestinal side effects, infection, and cardiovascular events. Currently, there are no studies defining the best strategy for using ESAs to minimize possible risks. One class of agents under evaluation, known as prolyl hydroxylase inhibitors (PHIs), acts to stabilize hypoxia-inducible factor (HIF) by inhibiting prolyl hydroxylase (PH) enzymes. Several randomized controlled trials showed that HIF-PHIs are almost comparable to ESAs. In the era of personalized medicine, it is possible to envisage and investigate specific contexts of the application of HIF stabilizers based on the individual risk profile and mechanism of action.

scholarly journals Safety and efficacy of ferric citrate in phosphate reduction and iron supplementation in patients with chronic kidney disease

Oncotarget ◽  
2017 ◽  
Vol 8 (63) ◽  
pp. 107283-107294 ◽  
Author(s):  
Mei-Yi Wu ◽  
Ying-Chun Chen ◽  
Chun-Hung Lin ◽  
Yun-Chun Wu ◽  
Yu-Kang Tu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Iron Supplementation ◽  
Ferric Citrate ◽  
Safety And Efficacy

Abstract 15645: Carotid Artery Stenting and Endarterectomy in Patients With Stage 5 Chronic Kidney Disease: Insights of the Healthcare Cost and Utilization Project’s National Inpatient Sample

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Fabio V Lima ◽  
Tzyy Y Yen ◽  
Luis Gruberg
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery ◽  
Healthcare Cost ◽  
Carotid Artery Stenting ◽  
Hospital Admissions ◽  
Multivariable Analysis ◽  
Hospital Death ◽  
National Inpatient Sample ◽  
Artery Disease

Background: Carotid artery stenting (CAS) has evolved into a viable alternative for the treatment of symptomatic and asymptomatic high-grade carotid artery stenosis, particularly in patients considered to be at a high surgical risk for carotid endarterectomy (CEA). Hypothesis: There is limited data on the outcomes of patients with stage 5 chronic kidney disease (CKD) (GFR<15 mL/min/1.73 m 2 or dialysis) undergoing CEA or CAS. Methods: The Healthcare Cost and Utilization Project’s National Inpatient Sample was screened for hospital admissions of patients undergoing CAS and CEA from 2003-2012. Baseline clinical characteristics and outcomes were identified in patients with stage 5 CKD. The primary outcome was major adverse cardiac and cerebrovascular events (MACCE), defined as the composite of in-hospital death, acute myocardial infarction and acute cerebrovascular accident (CVA). Results: Our study population consisted of 1,723 patients that underwent CEA and 544 patients that underwent CAS. Patients undergoing CAS were younger and had significantly lower rates of coronary artery disease, hypertension and hyperlipidemia. CAS patients experienced significantly higher rates of MACCE compared with patients that underwent CEA, mainly driven by a higher rate of in-hospital strokes (Fig. 1). In a multivariable analysis, CAS (OR 1.53, 95% CI 1.19-1.98) was an independent predictor of MACCE. Conclusions: In patients with stage 5 CKD (GFR<15 mL/min/1.73 m 2 or dialysis ) undergoing internal carotid artery revascularization, CAS was associated with higher rates of in-hospital MACCE, driven by higher mortality and stroke rates when compared with CEA.

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