Sodium Intake and Renal Outcomes: A Systematic Review

Smyth, Andrew; O’Donnell, Martin J.; Yusuf, Salim; Clase, Catherine M.; Teo, Koon; Canavan, Michelle; Reddan, Donal; Mann, Johannes F.E.

doi:10.1093/ajh/hpt294

Cited by 68 publications

(49 citation statements)

References 29 publications

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“…Results did not differ in sensitivity analyses excluding high-risk groups such as those with hypertension, heart failure, diabetes mellitus, or CKD. Smyth et al 14 then performed a systematic review evaluating the relationship between sodium intake and kidney outcomes in individuals with and without CKD (n = 8,129). Their results showed that in individuals with CKD, there was an association between high sodium intake and decline in GFR, as well as an increase in proteinuria, whereas the association of low and usual sodium intake with outcomes did not differ.…”

Section: How Does This Study Compare With Prior Studies?mentioning

confidence: 99%

Don’t Pass the Salt: Evidence to Support Avoidance of High Salt Intake in CKD

Leonberg‐Yoo

Sarnak

2017

American Journal of Kidney Diseases

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Section: How Does This Study Compare With Prior Studies?mentioning

confidence: 99%

Don’t Pass the Salt: Evidence to Support Avoidance of High Salt Intake in CKD

Leonberg‐Yoo

Sarnak

2017

American Journal of Kidney Diseases

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“…The efficacy of severe fluid restriction (<1 l/day) with or without sodium restriction was evaluated in two RCTs, but neither study showed any benefit [71,72]. Another systematic review evaluating the effect of sodium restriction on renal outcomes in diverse populations also showed that there is reasonable evidence to support an association between high sodium intake (>4.6 g/day) and adverse renal outcomes, but not between low sodium intake and better renal outcomes [73]. It should be noted that sodium restriction appears to have competing effects on both the heart and the kidney, lowering blood pressure and activating the RAAS.…”

Section: Established Treatment Strategiesmentioning

confidence: 99%

Current and Potential Therapeutic Strategies for Hemodynamic Cardiorenal Syndrome

et al. 2015

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Background: Cardiorenal syndrome (CRS) encompasses conditions in which cardiac and renal disorders co-exist and are pathophysiologically related. The newest classification of CRS into seven etiologically and clinically distinct types for direct patient management purposes includes hemodynamic, uremic, vascular, neurohumoral, anemia- and/or iron metabolism-related, mineral metabolism-related and protein-energy wasting-related CRS. This classification also emphasizes the pathophysiologic pathways. The leading CRS category remains hemodynamic CRS, which is the most commonly encountered type in patient care settings and in which acute or chronic heart failure leads to renal impairment. Summary: This review focuses on selected therapeutic strategies for the clinical management of hemodynamic CRS. This is often characterized by an exceptionally high ratio of serum urea to creatinine concentrations. Loop diuretics, positive inotropic agents including dopamine and dobutamine, vasopressin antagonists including vasopressin receptor antagonists such as tolvaptan, nesiritide and angiotensin-neprilysin inhibitors are among the pharmacologic agents used. Additional therapies include ultrafiltration (UF) via hemofiltration or dialysis. The beneficial versus unfavorable effects of these therapies on cardiac decongestion versus renal blood flow may act in opposite directions. Some of the most interesting options for the outpatient setting that deserve revisiting include portable continuous dobutamine infusion, peritoneal dialysis and outpatient UF via hemodialysis or hemofiltration. Key Messages: The new clinically oriented CRS classification system is helpful in identifying therapeutic targets and offers a systematic approach to an optimal management algorithm with better understanding of etiologies. Most interventions including UF have not shown a favorable impact on outcomes. Outpatient portable dobutamine infusion is underutilized and not well studied. Revisiting traditional and novel strategies for outpatient management of CRS warrants clinical trials.

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“…Ako je ovaj mehanizam oštećen, viši krvni pritisak je potreban da održi ekskreciju natrijuma za dato op-terećenje natrijumom što rezultuje hroničnim povećanjem krvnog pritiska [33]. Hipertenzija predstavlja ravnotežu između unosa natrijuma i izlučivanja natrijuma preko bubrega što vodi poremećaju srednjeg arterijskog pritiska [34].…”

Section: Bubregom Uslovljena Hipertenzijaunclassified

Kidney and hypertension

Jovanović¹

2014

Biomedicinska istraž.

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Kratak sadržajHipertenzija može biti uzrok i posledica bolesti bubrega. U današnjem društvu su i hipertenzija i bolest bubrega postale epidemijske i udružene sa povećanim rizikom od kardiovaskularnih bolesti. Poslednjih dekada brojne kliničke, eksperimentalne i genetske studije pokazuju da bubreg igra važnu ulogu u esencijalnoj hipertenziji. Međutim, malo se zna o direktnom mehanizmu na koji bubreg indukuje hipertenziju ili zašto krvni pritisak raste kod bolesnika sa bolestima bubrega. U ovom radu je opisana patofiziologija esencijalne hipertenzije i njena veza sa hroničnim bolestima bubrega i kardiovaskularnim bolestima. Posebno je opisan uticaj natrijuma, renin angiotenzin aldosteron sistema, simpatikusa kao i medijatora vazokonstrikcije i vazodilatacije na razvitak hipertenzije uzrokovane bubrezima. Sem toga, opisani su i medijatori koji započinju i održavaju progresiju hroničnih bolesti bubrega kao i njihov uticaj na hipertenziju. UvodHipertenzija je uz dijabetes jedna od najčešćih bolesti današnjice i moglo bi se reći da se javlja gotovo epidemijski. Preko 65 miliona ljudi u Sjedinjenim Američkim Državama (SAD) ima hipertenziju, a svake godine se dijagnostikuje oko 2 miliona novih bolesnika [1,2]. Najčešća je esencijalna hipertenzija koja nastaje kao posledica kompleksnih interakcija multiplih sistema bez jasne etiologije i predstavlja jedan od kardiovaskularnih (KV) faktora rizika. The Seventh Report of the Joint National Committee (JNC 7) definiše dva stadijuma hipertenzije: stadijum 1 hipertenzije -sistolni krvni pritisak 140-159 mmHg i dijastolni krvni pritisak 90-99 mmHg, i stadijum 2 hipertenzije -sistolni krvni pritisak ≥ 160 mmHg i dijastolni krvni pritisak ≥ 100 mmHg [2]. Adekvatna kontrola krvnog pritiska je potrebna u cilju prevencije KV komplikacija (infarkta miokarda, srčane insuficijencije), ali i moždanog udara i bolesti bubrega. Hroničnu insuficijenciju bubrega (HIB) ima 25 miliona stanovnika u SAD, a u terminalnoj fazi insuficijencije bubrega je preko 500 000. Hipertenzija je, pored dijabetesa, vodeći uzrok HIB koja se definiše kao smanjenje izračunate jačine glomerulske filtracije (JGF) ispod 60 ml/ min/1,73 m 2 . Ovo smanjenje JGF je udruženo sa KV komplikacijama, povećanim brojem hospitalizacija, ali i povećanim mortalitetom [3]. The National Kidney Faundation KDOQI vodiči preporučuju skrining svih bolesnika sa HIB na hipertenziju. Visina krvnog pritiska kod ovih bolesnika mora biti bolje kontrolisana i njihove vrednosti moraju biti niže nego u opštoj populaciji: ispod 130/80 mmHg kod bolesnika bez proteinurije i ispod 125/75 mmHg kod bolesnika sa proteinurijom [4].Najnovijim ispitivanjima utvrđeno je da su hronične bolesti bubrega i hipertenzija dve bolesti predodređene još u detinjstvu. Podaci iz "The National Health and Nutrition Examination Survey" potvrđuju da krvni pritisak kod dece i adolescenata u SAD raste i to sa prevalencijom hipertenzije oko 4% i pre-hipertenzije oko 10% [5]. Približno 50% dece sa HIB ima hipertenziju koja uzrokuje bržu progresiju bolesti [6]. Rani znak ošte...

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Sodium Intake and Renal Outcomes: A Systematic Review

Cited by 68 publications

References 29 publications

Don’t Pass the Salt: Evidence to Support Avoidance of High Salt Intake in CKD

Don’t Pass the Salt: Evidence to Support Avoidance of High Salt Intake in CKD

Current and Potential Therapeutic Strategies for Hemodynamic Cardiorenal Syndrome

Kidney and hypertension

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