Furosemide Increases the Risk of Hyperparathyroidism in Chronic Kidney Disease

2016 ◽  
Vol 43 (6) ◽  
pp. 421-430 ◽  
Author(s):  
Raquel F.V. Vasco ◽  
Rosa M.A. Moyses ◽  
Roberto Zatz ◽  
Rosilene M. Elias
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Biochemical Parameters ◽  
Estimated Glomerular Filtration Rate ◽  
Excretion Rate ◽  
Strong Predictor ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Advanced Stages

Background: Diuretics are widely used in patients with chronic kidney disease (CKD). While thiazide-like diuretics limit urinary calcium excretion, loop diuretics (LD) promote calcium wasting, which might facilitate the development of secondary hyperparathyroidism (HPT2). We sought to investigate, in CKD patients not on dialysis, the influence of either hydrochlorothiazide (Hydro) or furosemide (Furo) on circulating parathyroid hormone (PTH) and whether such actions are determined by the effects of these compounds on calcium excretion. Methods: Electronic charts of all nephrology outpatients (CKD stages 2-5) who were given Hydro or Furo were included. We assessed estimated glomerular filtration rate (eGFR), biochemical parameters and 24-hour calcium excretion. Hyperparathyroidism was defined as PTH >65 pg/ml. Results: Out of 275 patients, 108 (29%) were taking Hydro and 167 (61%) Furo. Patients on Hydro were younger, mostly female and had higher eGFR. The median 24-hour urinary calcium excretion in the overall cohort was 41 (22, 76), being lower in Furo than in Hydro patients (37 (16, 68) vs. 47 (26, 88) mg/24 h, respectively, p = 0.016). Logistic regression showed that, after adjustment for eGFR, calcium excretion rate was found not to increase the risk ratio for HPT2, whereas Furo was a strong predictor of HPT2. Conclusion: Furo increased the risk of HPT2 among CKD patients compared to Hydro. This effect was independent of eGFR or calcium excretion. The use of LD in CKD, currently preferred in advanced stages, should be reappraised.

Determinants and outcomes associated with urinary calcium excretion in chronic kidney disease

2021 ◽  
Author(s):  
Jing Liu ◽  
Maria Clarissa Tio ◽  
Ashish Verma ◽  
Insa M Schmidt ◽  
Titilayo O Ilori ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion ◽  
Atherosclerotic Cardiovascular Disease ◽  
Clinical Events ◽  
Males And Females ◽  
End Stage ◽  
Egfr Decline

Abstract Context Abnormalities in calcium metabolism are common in chronic kidney disease (CKD). Diminished urinary calcium excretion may promote vascular calcification, and increased urinary calcium excretion may lead to nephrolithiasis and nephrocalcinosis, conditions associated with CKD. Objective To study predictors of urinary calcium excretion and its association with adverse clinical outcomes in CKD. Design, Setting and Patients This study assessed 3,768 non-dialysis participants in the Chronic Renal Insufficiency Cohort study from April 2003 to September 2008. Participants were followed up to October 2018. Exposure Clinically plausible predictors of urinary calcium excretion and 24-hour urinary calcium excretion at baseline. Main Outcome Measures Urinary calcium excretion; incident end stage kidney disease (ESKD), CKD progression (50% estimated glomerular filtration rate (eGFR) decline or incident ESKD), all-cause mortality, and atherosclerotic cardiovascular disease events. Results eGFR was positive correlated with 24-hour urinary calcium excretion. The variables most strongly associated with 24-hour urinary calcium excretion were 24-hour urinary sodium (β=0.19 and 0.28 in males and females), serum parathyroid hormone (β=-0.22 and -0.20), loop diuretics (β=0.36 and 0.26), thiazide diuretics (β=-0.49 and -0.53), and self-identified black race (β=-0.23 and -0.27). Lower urinary calcium excretion was associated with greater risks of outcomes, but these associations were greatly attenuated or nullified after adjustment for baseline eGFR. Conclusion Urinary calcium excretion is markedly lower in individuals with CKD compared to general population. Determinants of urinary calcium excretion differed between sexes and levels of CKD. Significant associations between urinary calcium excretion and adverse clinical events were substantially confounded by eGFR.

scholarly journals Urinary Calcium Excretion and Risk of Chronic Kidney Disease in the General Population

2017 ◽  
Vol 2 (3) ◽  
pp. 366-379 ◽  
Author(s):  
Jacob M. Taylor ◽  
Lyanne M. Kieneker ◽  
Martin H. de Borst ◽  
Sipke T. Visser ◽  
Ido P. Kema ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
General Population ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Calcium Excretion

scholarly journals Effects of calcium-modulating hormones on thiazide receptor density.

1996 ◽  
Vol 7 (7) ◽  
pp. 1052-1057 ◽  
Author(s):  
P Blakely ◽  
D A Vaughn ◽  
D D Fanestil
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Ion ◽  
Excretion Rate ◽  
Urinary Calcium ◽  
Plasma Calcium ◽  
Urinary Calcium Excretion ◽  
Ion Concentration ◽  
Calcium Excretion ◽  
Calcitropic Hormones ◽  
Calcium Ion Concentration

Thiazide diuretic drugs act in the distal convoluted tubule (DCT) to inhibit a Na+Cl- cotransporter and enhance reabsorption of luminal calcium. The density of receptors for thiazides in the rat DCT is known to be increased by adrenocortical steroids, furosemide, and bendroflumethiazide, but decreased by ischemia. Because the DCT is a physiologic site of action by calcitonin and parathyroid hormone, this study examined the effects of these calcitropic hormones in thyroparathyroidectomized Sprague-Dawley rats on (1) the density of the rat thiazide receptor (TZR), as quantitated by binding of (3H)metolazone to renal membranes, and (2) urinary electrolyte excretion rate. Salmon calcitonin (sCT) (20 to 100 ng/h) (1) increased the density of the renal TZR twofold, an effect that is maximal by 6 h after sCT administration, and (2) decreased urinary calcium excretion rate. Adequate dietary calcium must be provided for the effects of sCT to be observed. Regression analysis demonstrated that renal TZR density correlated negatively with total urinary calcium excretion rate but not with plasma calcium ion concentration. In addition, neither rat calcitonin (rCT), at doses that cause hypocalcemia, nor parathyroid hormone, at doses that cause hypercalcemia, produce direct effects on TZR density in the DCT of the thyroparathyroidectomized rat. Our findings indicate that upregulation of TZR by sCT, which occurs independently of plasma calcium-ion concentration, is likely via a calcitonin-like receptor other than that for rat calcitonin itself.

Phosphate binders in patients with chronic kidney disease: Between the new and the old.

2019 ◽  
pp. 2-3
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Estimated Glomerular Filtration Rate ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Phosphate Binders ◽  
Advanced Chronic Kidney Disease ◽  
Phosphate Retention ◽  
Stage 4 ◽  
Dietary Phosphate

Impaired phosphate excretion by the kidney leads to Hyperphosphatemia. It is an independent predictor of cardiovascular disease and mortality in patients with advanced chronic kidney disease (stage 4 and 5) particularly in case of dialysis. Phosphate retention develops early in chronic kidney disease (CKD) due to the reduction in the filtered phosphate load. Overt hyperphosphatemia develops when the estimated glomerular filtration rate (eGFR) falls below 25 to 40 mL/min/1.73 m2. Hyperphosphatemia is typically managed with oral phosphate binders in conjunction with dietary phosphate restriction. These drugs aim to decrease serum phosphate by binding ingested phosphorus in the gastrointestinal tract and its transformation to non-absorbable complexes [1].

Potential effect of pharmaceutical care to improve outcomes in patients with chronic kidney disease-mineral bone disorder in Sulaimani dialysis centers

2020 ◽  
pp. 82-94
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Pharmaceutical Care ◽  
Biochemical Parameters ◽  
Positive Impact ◽  
Potential Effect ◽  
Care Group ◽  
Mineral Bone Disorder ◽  
Bone Disorder

Objective: the present study was aimed to evaluate the role of pharmaceutical services in improving the outcome of mineral bone disorder in patients with advanced chronic kidney disease. Methodology: One hundred and twenty patients with chronic kidney disease-mineral bone disorder (CKD-MBD) screened for eligibility, seventy-six patients enrolled in the study and randomly allocated into two groups: pharmaceutical care and usual care, both groups interviewed by the pharmacist using specific questionnaire for assessing the quality of life (QoL). All the drug related problems (DRPs) including drug-drug interactions (DDIs) were recorded by the pharmacist. Blood samples were collected and utilized for analyzing the levels of vitamin D, phosphorous, calcium, albumin and parathyroid hormone at baseline and three months after. The pharmaceutical care group received all the educations about their medications and how to minimize DRPs; improve the QoL. Additionally, the pharmaceutical intervention included correcting the biochemical parameters. Results: Pharmaceutical care significantly improved patients QoL and minimized DRPs and DDIs. It was also effective in improving the biochemical parameters. Conclusion: Pharmaceutical care has a positive impact on improving the outcome of patients with CKD-MBD through attenuating DRPs, improving the biochemical parameters and the QoL.

scholarly journals FGF-23 and Phosphate in Children with Chronic Kidney Disease: A Cross-Sectional Study in Kazakhstan

Medicina ◽  
2020 ◽  
Vol 57 (1) ◽  
pp. 15
Author(s):  
Altynay Balmukhanova ◽  
Kairat Kabulbayev ◽  
Harika Alpay ◽  
Assiya Kanatbayeva ◽  
Aigul Balmukhanova
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Ckd Stage ◽  
Advanced Stages ◽  
Fgf 23 ◽  
Stage 1

Background and objectives: Chronic kidney disease (CKD) in children is a complex medical and social issue around the world. One of the serious complications is mineral-bone disorder (CKD-MBD) which might determine the prognosis of patients and their quality of life. Fibroblast growth factor 23 (FGF-23) is a phosphaturic hormone which is involved in the pathogenesis of CKD-MBD. The purpose of the study was to determine what comes first in children with CKD: FGF-23 or phosphate. Materials and Methods: This cross-sectional study included 73 children aged 2–18 years with CKD stages 1–5. We measured FGF-23 and other bone markers in blood samples and studied their associations. Results: Early elevations of FGF-23 were identified in children with CKD stage 2 compared with stage 1 (1.6 (1.5–1.8) pmol/L versus 0.65 (0.22–1.08), p = 0.029). There were significant differences between the advanced stages of the disease. FGF-23 correlated with PTH (r = 0.807, p = 0.000) and phosphate (r = 0.473, p = 0.000). Our study revealed that the elevated level of FGF-23 went ahead hyperphosphatemia and elevated PTH. Thus, more than 50% of children with CKD stage 2 had the elevating level of serum FGF-23, and that index became increasing with the disease progression and it achieved 100% at the dialysis stage. The serum phosphate increased more slowly and only 70.6% of children with CKD stage 5 had the increased values. The PTH increase was more dynamic. Conclusions: FGF-23 is an essential biomarker, elevates long before other markers of bone metabolism (phosphate), and might represent a clinical course of disease.

scholarly journals Associations among Heavy Metals and Proteinuria and Chronic Kidney Disease

Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 282
Author(s):  
Hui-Ju Tsai ◽  
Chih-Hsing Hung ◽  
Chih-Wen Wang ◽  
Hung-Pin Tu ◽  
Chiu-Hui Li ◽  
...  
Keyword(s):  
Heavy Metals ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
General Population ◽  
Estimated Glomerular Filtration Rate ◽  
Synergistic Effects ◽  
Blood Lead ◽  
Southern Taiwan ◽  
The Mean ◽  
Traditional Risk Factors

Background: The prevalence of chronic kidney disease (CKD) is increasing annually in Taiwan. In addition to traditional risk factors, heavy metals contribute to the development of CKD. The aim of this study was to investigate associations among heavy metals and proteinuria and CKD in the general population in Southern Taiwan. We also explored the interaction and synergetic effects among heavy metals on proteinuria. Methods: We conducted a health survey in the general population living in Southern Taiwan between June 2016 and September 2018. Seven heavy metals were measured: blood lead (Pb) and urine nickel (Ni), chromium (Cr), manganese (Mn), arsenic (As), copper (Cu), and cadmium (Cd). Proteinuria was measured using reagent strips. CKD was defined as an estimated glomerular filtration rate (eGFR) of <60 mL/min/1.73 m2. Results: The mean age of the 2447 participants was 55.1 ± 13.2 years and included 977 males and 1470 females. Participants with high blood Pb and high urine Ni, Mn, Cu, and Cd were significantly associated with proteinuria. Interactions between blood Pb and urine Cr, and between urine Cd and Cu, had significant effects on proteinuria. The participants with high blood Pb and high urine Cu were significantly associated with an eGFR of <60 mL/min/1.73 m2. Conclusion: High blood Pb and high urine Cu may be associated with proteinuria and an eGFR of <60 mL/min/1.73 m2. High urine Ni, Mn, and Cd were significantly associated with proteinuria. Co-exposure to Cd and Cu, and Pb and Cr, may have synergistic effects on proteinuria.

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