Abstract
This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:
Our objective is to systematically assess the benefits and harms of diuretics for people at all stages of CKD.
Background
Description of the condition
Chronic kidney disease (CKD) is a worldwide public health problem and has major social and economic implications (Zhang 2008). In the USA and the UK, the prevalence is about 11% to 16% (Ackland 2013) and the prevalence in other countries ranges from approximately 1% to 30% (Mani 2005; Obrador 2014). The problem is further aggravated because of lack of healthcare providers and facilities mainly in developing country. CKD is defined as abnormalities of kidney structure or function, present for more than three months, with implications for health (KDIGO 2013). The criteria for CKD are markers of kidney damage (one or more of albuminuria, urine sediment abnormalities, electrolyte and other abnormalities due to tubular disorders, abnormalities detected by histology structural abnormalities detected by imaging and history of kidney transplantation) or decreased glomerular filtration rate (GFR) (< 60 mL/min/1.73 m²) (KDIGO 2013). CKD may complicate comorbid conditions such as cardiac diseases, anaemia and bone disease. Disease progression may be altered by appropriate therapies and lifestyle changes (CDC 2010).
Description of the intervention
The principal use of diuretics in CKD is to reduce blood pressure and treat swelling (oedema) (Sica 2011a). Diuretics facilitate the action of angiotensin‐converting enzyme inhibitors (ACEis) and other antihypertensive drugs to reduce the risk of coronary vascular disease among people with CKD (Carter 2004; NKF K/DOQI 2002). Diuretics can also help to control potassium levels in people with elevated potassium levels (hyperkalaemia). Long‐acting diuretics administered with antihypertensive drugs have been shown to increase patients' compliance with drug therapy (Sica 2011a). There are three main types of diuretics: thiazides, loop diuretics and potassium‐sparing diuretics. Thiazide diuretics act on distal tubules; loop diuretics on the thick ascending limb of loop of Henle; and potassium‐sparing diuretics on collecting tubules.
Commonly used thiazide diuretics include chlorthalidone, hydrochlorothiazide, indapamide and metolazone. The long‐acting nature of chlorthalidone results in better control (1.5 to 2 times more potent) of blood pressure than hydrochlorothiazide (Ernst 2006; Sica 2011a); however chlorthalidone results in a higher risk of hypokalaemia. Absorption of metolazone is very poor and hence requires appropriate titration.
Bumetanide, furosemide and torsemide are frequently used loop diuretics. The bioavailability of loop diuretics is not affected by the presence of CKD. Loop diuretics should be reserved for conditions of clinically significant fluid overload (e.g. heart failure and significant fluid retention with vasodilator drugs, such as minoxidil) or with advanced kidney failure and can be combined with thiazide‐type diuretics (Sica 2011b).
Frequently‐administered potassium‐sparing diuretics are triamterene, amiloride, spironolactone and eplerenone. These drugs are further classified as those that inhibit epithelial sodium channels and mineralocorticoid receptor inhibitors. Drug choice is dependent on disease severity; as severity increases, people on thiazides are switched to loop diuretics or combined drug therapy (James 2014; KDIGO 2013; Sica 2011a; Sica 2011b).
Adverse events related to diuretic administration are dose‐dependent (Sica 2011a), but commonly include hypotension, decreased GFR, electrolyte abnormalities and hyperkalaemia. The Eighth Joint International Commission guidelines recommends some blood pressure control (less than 140/90 mm Hg for general hypertensive population less than 60 years, diabetics or non‐diabetic CKD patients) (James 2014) while the KDIGO 2013 guidelines recommend blood pressure less than 130/80 mm Hg for patients with albumin excretion ≥ 30 mg/24 h (KDIGO 2013; Palevsky 2013). The Eighth Joint International Commission guidelines also recommends that initial or add on hypertensive therapy with ACEi or angiotensin receptor blocker (ARB) will improve kidney outcomes in people with CKD (James 2014).
How the intervention might work
Diuretics trigger a range of mechanisms, including braking phenomenon. Braking phenomenon leads to post‐diuretic sodium retention. Presence or absence of sodium retention leads to two different phenomena (NKF K/DOQI 2002). There can be no tendency to retain sodium; in that case the normal S‐shaped dose response relationship is observed. The S‐shaped response curve indicates that the optimal dose led to maximum diuretic response and additional doses will not increase the effect. Where there is a tendency to retain sodium, the S‐shaped curve shifts right and down, indicating that the optimal dose did not result in an appropriate dose response. This effect is termed diuretic resistance, and hence, a higher dose may be required (NKF K/DOQI 2002). The site of action for all diuretics (with the exception of spironolactone) is in the luminal space. Glomerular filtration has a minor role in diuretic entry into the urinary compartment, largely because all diuretics are bound to protein (Sica 2011a).
Thiazides increase sodium, potassium and magnesium excretion and decrease calcium excretion. Thiazide‐induced hypokalaemia is associated with increased blood glucose, and treatment of thiazide‐induced hypokalaemia may reverse glucose intolerance and may prevent diabetes (Sica 2011b). Thiazide‐induced hyperuricaemia occurs as a result of volume contraction and competition with uric acid for renal tubular secretion (Sica 2011b). Adverse interactions include the blunting of thiazide effects by nonsteroidal anti‐inflammatory drugs and the potential to increase fatigue, lethargy, and increase in glucose when combined with beta‐blockers (Sica 2011b).
Loop diuretics increase sodium, potassium, hydrogen ion, calcium and magnesium excretion.
Potassium‐sparing diuretics increase sodium excretion and decrease potassium, hydrogen ion, calcium and magnesium excretion.
Diuretics will lower blood pressure and potentiate the effects of ACEis, ARBs and other antihypertensive agents, including calcium‐channel blockers by reducing extracellular fluid volume (Sica 2011a). Dosing is empiric and frequently determined by the elimination of oedema for CKD stage 4 to 5. Spironolactone leads to natriuretic response in patients with cirrhosis and ascites or heart failure, particularly used with a loop or a thiazide‐type diuretic or both (Sica 2011a).
Why it is important to do this review
CKD is an important, common condition that can complicate other comorbidities and itself lead to increased morbidity and mortality. This review intends to systematically assess the benefits and harms of diuretics for people at all stages of CKD. Diuretics are important class of drugs but there is little evidence to guide clinicians regarding which diuretics are most effective, safest in these patients, or when switching should occur from one type of diuretic to another in this population.
There is limited evidence about the appropriate time to convert from one class of diuretic to another. There is need to assess existing differences for controlling blood pressure for loop diuretics without any effect on volume loss. Furthermore, there is limited information available for titrating dose appropriately for blood pressure control.
The safety and efficacy of diuretics alone or in combination need to be addressed. The safety issue of combining loop diuretics with thiazide diuretics compared with higher doses of loop diuretics has not been addressed, nor is the safety and efficacy of use of loop diuretics in patients on haemolysis known.
The body of evidence concerning the blood pressure‐lowering response of loop diuretics compared with ACEis is insufficient. There is limited evidence relating to adverse events associated with diuretics among people at all stages of CKD (NKF K/DOQI 2002; Sica 2011a). Hence, a systematic review is required to investigate these issues to better inform clinical decision making.
Objectives
Our objective is to systematically assess the benefits and harms of diuretics for people at all stages of CKD.
Methods
Criteria for considering studies for this review
Types of studies
All randomised controlled trials (RCTs) and quasi‐RCTs (RCTs in which allocation to treatment was obtained by alternation, use of alternate medical records, date of birth or other predictable methods) looking at diuretics for people with all stages of CKD regardless of dose, diuretic type or duration of administration.
Types of participants
Inclusion criteria
Participants in the included studies will be adults at all stages of CKD, irrespective of dialysis requirements, kidney transplant recipients and those with comorbidities such as cardiovascular disease (CVD), anaemia, and bone disease. But they will be considered separately in analyses.
Exclusion criteria
No exclusions will be applied.
Types of interventions
We will investigate diuretic versus another diuretic; diuretic versus placebo; or diuretic versus no treatment. We will also consider treatment frequency, duration, and mode of administration as modifiers of treatment effects. We plan to include thiazides (chlorthalidone, hydrochlorothiazide, indapamide, metolazone), loop diuretics (bumetanide, furosemide, torsemide) and potassium sparing diuretics (triamterene, amiloride, spironolactone, eplerenone) in our assessment or various combinations.
Types of outcome measures
Primary outcomes
All‐cause mortality
End‐stage kidney disease
Acute kidney injury
Efficacy in controlling blood pressure
Doubling of serum creatinine
Anaemia, mineral metabolism, low blood pressure feeling lightheaded, trouble breathing, belly or muscle cramps, nausea or vomiting, peritonitis, hernia and dialysis disequilibrium syndrome especially in participants with CKD under dialysis
Graft loss, graft survival, rejection, and infections for kidney transplant participants.
Secondary outcomes
Blood pressure at end of treatment
Electrolyte abnormalities (hyperkalaemia, hypokalaemia, hyponatraemia, hypomagnesaemia, hypercalcaemia)
Rate of estimated GFR decline over time
Changes in proteinuria
Incidence of ESKD
Cardiovascular mortality and morbidity.
Search methods for identification of studies
Electronic searches
We will search the Cochrane Renal Group's Specialised Register through contact with the Trials' Search Co‐ordinator using search terms relevant to this review (Appendix 1). The Cochrane Renal Group’s Specialised Register contains studies identified from the following sources.
Monthly searches of the Cochrane Central Register of Controlled Trials (CENTRAL)
Weekly searches of MEDLINE OVID SP
Handsearching of renal‐related journals and the proceedings of major renal conferences
Searching of the current year of EMBASE OVID SP
Weekly current awareness alerts for selected renal journals
Searches of the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov.
Studies contained in the Specialised Register are identified through search strategies for CENTRAL, MEDLINE, and EMBASE based on the scope of the Cochrane Renal Group. Details of these strategies, as well as a list of handsearched journals, conference proceedings and current awareness alerts, are available in the Specialised Register section of information about the Cochrane Renal Group.
Searching other resources
Reference lists of review articles, relevant studies and clinical practice guidelines.
Letters seeking information about unpublished or incomplete studies to investigators known to be involved in previous studies.
Data collection and analysis
Selection of studies
The search strategy described will be used to obtain titles and abstracts of studies that may be relevant to the review. The titles and abstracts will be screened independently by two authors, who will discard studies that are not applicable; however studies and reviews that might include relevant data or information on studies will be retained initially. Two authors will independently assess retrieved abstracts and, if necessary the full text, of these studies to determine which studies satisfy the inclusion criteria.
Data extraction and management
Data extraction will be carried out independently by two authors using standard data extraction forms. Studies reported in non‐English language journals will be translated before assessment. Where more than one publication of one study exists, reports will be grouped together and the publication with the most complete data will be used in the analyses. Where relevant outcomes are only published in earlier versions these data will be used. Any discrepancy between published versions will be highlighted.
Assessment of risk of bias in included studies
The following items will be independently assessed by two authors using the risk of bias assessment tool (Higgins 2011) (Appendix 2).
Was there adequate sequence generation (selection bias)?
Was allocation adequately concealed (selection bias)?
-
Was knowledge of the allocated interventions adequately prevented during the study (detection bias)?
Participants and personnel
Outcome assessors
Were incomplete outcome data adequately addressed (attrition bias)?
Are reports of the study free of suggestion of selective outcome reporting (reporting bias)?
Was the study apparently free of other problems that could put it at a risk of bias?
Measures of treatment effect
For dichotomous outcomes such as mortality due to CKD or associated comorbidity at six months to five years, results will be expressed as risk ratio (RR) with 95% confidence intervals (CI). Where continuous scales of measurement are used to assess the effects of treatment for example creatinine clearance, serum creatinine, proteinuria, and GFR the mean difference (MD) will be used, or the standardised mean difference (SMD) if different scales have been used.
We will convert extracted data to the above measures for treatment effects if given in other forms. We will extract or calculate 95% CI for all data.
Unit of analysis issues
The unit of analysis issue will depend on types of studies i.e. parallel RCTs/clustered RCTs/cross‐over RCTs/studies with multiple interventional groups. For cross‐over RCTs and clustered randomised RCTs, effect estimates and their errors will be meta‐analysed by using generic inverse‐variance method in RevMan. For studies with multiple interventional groups, we will use multiple treatment meta‐analysis (Higgins 2011).
Dealing with missing data
Any further information required from the original author will be requested by written correspondence (e.g. emailing or writing to corresponding author) and any relevant information obtained in this manner will be included in the review. Evaluation of important numerical data such as screened, randomised patients as well as intention‐to‐treat, as‐treated and per‐protocol population will be carefully performed. Attrition rates, for example drop‐outs, losses to follow‐up and withdrawals will be investigated. Issues of missing data and imputation methods (for example, last‐observation‐carried‐forward) will be critically appraised (Higgins 2011).
Assessment of heterogeneity
Heterogeneity will be analysed using a Chi² test on N‐1 degrees of freedom, with an alpha of 0.05 used for statistical significance and with the I² test (Higgins 2003). I² values of 25%, 50% and 75% correspond to low, medium and high levels of heterogeneity. Since heterogeneity may be seen in treatment effects across stages of CKD, the effect estimate will be reported for separate groups rather than overall effects. Therapeutic intent will also be an important source of heterogeneity to be explored (indication for treatment – as fluid retention and hypertension may represent different treatment goals and may have different effects). Also, duration of diuretic use and co‐administration of diuretic with other class commonly co‐administered like ACEis and ARBs will also be considered as important factor affecting heterogeneity.
Assessment of reporting biases
If possible, funnel plots will be used to assess for the potential existence of small study bias (Higgins 2011).
Data synthesis
Data will be pooled using the random‐effects model but the fixed‐effect model will also be used to ensure robustness of the model chosen and susceptibility to outliers.
Subgroup analysis and investigation of heterogeneity
Subgroup analysis will be used to explore possible sources of heterogeneity (e.g. patient age; outpatient versus hospitalised patients; presence or absence of comorbidities such as diabetes, coronary heart disease, anaemia and bone disease; intravenous versus oral administration; and CKD stage). Heterogeneity among participants could be related to age and renal pathology for example, CKD stage, cause of renal pathology‐diabetic nephropathy. Heterogeneity in treatments could be related to prior agent(s) used and the agent, dose and duration of therapy (e.g. differences between thiazide diuretics, loop diuretics and potassium‐sparing diuretics, dose, duration of therapy, short‐acting vs. long‐acting diuretics). Adverse effects will be tabulated and assessed using descriptive techniques because they are likely to be different for various agents. Where possible, the risk difference with 95% CI will be calculated for each adverse effect, either compared with no treatment or another agent.
Sensitivity analysis
We will perform sensitivity analyses to explore the influence of the following factors on effect size:
Repeating the analysis excluding unpublished studies
Repeating the analysis taking account of risk of bias, as specified
Repeating the analysis excluding any very long or large studies to establish how much they dominate the results
Repeating the analysis excluding studies using the following filters: diagnostic criteria, language of publication, source of funding (industry versus other), country.
Repeating analysis excluding studies in which the diuretic is used in combination with another diuretic class (e.g. thiazide‐type plus potassium‐sparing).
Acknowledgements
We would like to thank:
The Cochrane Renal Group for their valuable guidance.
The referees for their feedback and advice during the preparation of this protocol.
The Indian Council of Medical Research and South Asian Cochrane Network and Centre, Prof. BV Moses & ICMR Centre for Advanced Research & Training in Evidence‐Based Healthcare, CMC Vellore for supporting the training program as well as making the Cochrane Library free for India.
Professor Prathap Tharyan, Director, South Asian Cochrane Network and Centre; CMC Vellore for his guidance during the training workshop.
Management, Vice‐Chancellor, Deans, Heads of Departments and Faculty members of our departments of Sri. Ramachandra University for continuing inspiration and support.
Family members for their continuing inspiration and support.
Appendices
Appendix 1. Electronic search strategies
| Database | Search terms |
| CENTRAL |
|
| MEDLINE |
|
| EMBASE |
|
Appendix 2. Risk of bias assessment tool
| Potential source of bias | Assessment criteria |
|
Random sequence generation Selection bias (biased allocation to interventions) due to inadequate generation of a randomised sequence |
Low risk of bias: Random number table; computer random number generator; coin tossing; shuffling cards or envelopes; throwing dice; drawing of lots; minimization (minimization may be implemented without a random element, and this is considered to be equivalent to being random). |
| High risk of bias: Sequence generated by odd or even date of birth; date (or day) of admission; sequence generated by hospital or clinic record number; allocation by judgement of the clinician; by preference of the participant; based on the results of a laboratory test or a series of tests; by availability of the intervention. | |
| Unclear: Insufficient information about the sequence generation process to permit judgement. | |
|
Allocation concealment Selection bias (biased allocation to interventions) due to inadequate concealment of allocations prior to assignment |
Low risk of bias: Randomisation method described that would not allow investigator/participant to know or influence intervention group before eligible participant entered in the study (e.g. central allocation, including telephone, web‐based, and pharmacy‐controlled, randomisation; sequentially numbered drug containers of identical appearance; sequentially numbered, opaque, sealed envelopes). |
| High risk of bias: Using an open random allocation schedule (e.g. a list of random numbers); assignment envelopes were used without appropriate safeguards (e.g. if envelopes were unsealed or non‐opaque or not sequentially numbered); alternation or rotation; date of birth; case record number; any other explicitly unconcealed procedure. | |
| Unclear: Randomisation stated but no information on method used is available. | |
|
Blinding of participants and personnel Performance bias due to knowledge of the allocated interventions by participants and personnel during the study |
Low risk of bias: No blinding or incomplete blinding, but the review authors judge that the outcome is not likely to be influenced by lack of blinding; blinding of participants and key study personnel ensured, and unlikely that the blinding could have been broken. |
| High risk of bias: No blinding or incomplete blinding, and the outcome is likely to be influenced by lack of blinding; blinding of key study participants and personnel attempted, but likely that the blinding could have been broken, and the outcome is likely to be influenced by lack of blinding. | |
| Unclear: Insufficient information to permit judgement | |
|
Blinding of outcome assessment Detection bias due to knowledge of the allocated interventions by outcome assessors. |
Low risk of bias: No blinding of outcome assessment, but the review authors judge that the outcome measurement is not likely to be influenced by lack of blinding; blinding of outcome assessment ensured, and unlikely that the blinding could have been broken. |
| High risk of bias: No blinding of outcome assessment, and the outcome measurement is likely to be influenced by lack of blinding; blinding of outcome assessment, but likely that the blinding could have been broken, and the outcome measurement is likely to be influenced by lack of blinding. | |
| Unclear: Insufficient information to permit judgement | |
|
Incomplete outcome data Attrition bias due to amount, nature or handling of incomplete outcome data. |
Low risk of bias: No missing outcome data; reasons for missing outcome data unlikely to be related to true outcome (for survival data, censoring unlikely to be introducing bias); missing outcome data balanced in numbers across intervention groups, with similar reasons for missing data across groups; for dichotomous outcome data, the proportion of missing outcomes compared with observed event risk not enough to have a clinically relevant impact on the intervention effect estimate; for continuous outcome data, plausible effect size (difference in means or standardized difference in means) among missing outcomes not enough to have a clinically relevant impact on observed effect size; missing data have been imputed using appropriate methods. |
| High risk of bias: Reason for missing outcome data likely to be related to true outcome, with either imbalance in numbers or reasons for missing data across intervention groups; for dichotomous outcome data, the proportion of missing outcomes compared with observed event risk enough to induce clinically relevant bias in intervention effect estimate; for continuous outcome data, plausible effect size (difference in means or standardized difference in means) among missing outcomes enough to induce clinically relevant bias in observed effect size; ‘as‐treated’ analysis done with substantial departure of the intervention received from that assigned at randomisation; potentially inappropriate application of simple imputation. | |
| Unclear: Insufficient information to permit judgement | |
|
Selective reporting Reporting bias due to selective outcome reporting |
Low risk of bias: The study protocol is available and all of the study’s pre‐specified (primary and secondary) outcomes that are of interest in the review have been reported in the pre‐specified way; the study protocol is not available but it is clear that the published reports include all expected outcomes, including those that were pre‐specified (convincing text of this nature may be uncommon). |
| High risk of bias: Not all of the study’s pre‐specified primary outcomes have been reported; one or more primary outcomes is reported using measurements, analysis methods or subsets of the data (e.g. subscales) that were not pre‐specified; one or more reported primary outcomes were not pre‐specified (unless clear justification for their reporting is provided, such as an unexpected adverse effect); one or more outcomes of interest in the review are reported incompletely so that they cannot be entered in a meta‐analysis; the study report fails to include results for a key outcome that would be expected to have been reported for such a study. | |
| Unclear: Insufficient information to permit judgement | |
|
Other bias Bias due to problems not covered elsewhere in the table |
Low risk of bias: The study appears to be free of other sources of bias. |
| High risk of bias: Had a potential source of bias related to the specific study design used; stopped early due to some data‐dependent process (including a formal‐stopping rule); had extreme baseline imbalance; has been claimed to have been fraudulent; had some other problem. | |
| Unclear: Insufficient information to assess whether an important risk of bias exists; insufficient rationale or evidence that an identified problem will introduce bias. |
What's new
| Date | Event | Description |
|---|---|---|
| 26 October 2017 | Amended | Protocol withdrawn as the authors could not comply with editorial timelines. |
Contributions of authors
Draft the protocol: PBS, PS, BWCS, SCH
Study selection: PBS, PS
Extract data from studies: PBS, SCH
Enter data into RevMan: PBS, SCH
Carry out the analysis: PBS, BWCS,
Interpret the analysis: PBS, PS, BWCS, SCH
Draft the final review: PBS, PS, BWCS, SCH
Disagreement resolution: PBS, PS, BWCS
Update the review: PBS, PS, BWCS, SCH
Sources of support
Internal sources
None known, Other.
External sources
None known, Other.
Declarations of interest
Pankaj B Shah: None known
Periasamy Soundararajan: None known
Bernard WC Sathiyasekaran: None known
Sanjeev C Hegde: None known
Notes
Protocol withdrawn as the authors could not comply with editorial timelines.
Withdrawn from publication for reasons stated in the review
References
Additional references
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