{"id":5115,"date":"2020-11-19T22:45:13","date_gmt":"2020-11-19T22:45:13","guid":{"rendered":"http:\/\/edren.org\/ren\/?page_id=5115"},"modified":"2025-10-08T10:57:28","modified_gmt":"2025-10-08T10:57:28","slug":"ckd-summary-overview","status":"publish","type":"page","link":"https:\/\/edren.org\/ren\/handbook\/unithdbk\/ckd\/ckd-summary-overview\/","title":{"rendered":"CKD summary overview"},"content":{"rendered":"<h3>Overview<\/h3>\n<p>Most chronic kidney disease (CKD) is diagnosed and managed in primary care.\u00a0 The advice on this page is based largely on consensus CKD guidelines from <a href=\"https:\/\/kdigo.org\/wp-content\/uploads\/2017\/02\/KDIGO_2012_CKD_GL.pdf\">KDIGO<\/a> and <a href=\"https:\/\/www.nice.org.uk\/guidance\/cg182\">NICE<\/a> and <a href=\"https:\/\/kdigo.org\/guidelines\/diabetes-ckd\/\">diabetes guidelines<\/a> from KDIGO.\u00a0 A general approach is summarised here.\u00a0 Further details on each of the sections of this diagram are given below:<\/p>\n<p><a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-full wp-image-5236\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren.jpg\" alt=\"\" width=\"1200\" height=\"900\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren.jpg 1200w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren-300x225.jpg 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren-1024x768.jpg 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren-768x576.jpg 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/11\/CKD-figures-for-Edren-150x113.jpg 150w\" sizes=\"auto, (max-width: 1200px) 100vw, 1200px\" \/><\/a><\/p>\n<p>&nbsp;<\/p>\n<h3>1) Diagnose CKD and determine likely cause<\/h3>\n<h5><strong>Definition of CKD<\/strong><\/h5>\n<p>CKD is defined by KDIGO as &#8220;abnormalities of kidney structure or function, present for at least 3 months, with implications for health&#8221;.\u00a0 Therefore the new finding of an elevated serum creatinine may be CKD or an acute kidney injury.<\/p>\n<p>CKD is staged according to eGFR and albuminuria.\u00a0 Some patients with structural abnormalities (e.g. cysts) may have CKD despite normal eGFR and no albuminuria.<\/p>\n<p>&nbsp;<\/p>\n<h5><strong>Proteinuria<\/strong><\/h5>\n<p>Checking for proteinuria is important in:<\/p>\n<ul style=\"list-style-type: disc;\">\n<li>diagnosing CKD (some patients can have proteinuria as the only sign of CKD &#8211; i.e. with normal GFR and kidney imaging; for example this is the case in many patients with nephrotic syndrome; it is generally unhelpful to screen for proteinuria in an unselected, asymptomatic population)<\/li>\n<li>risk-stratification to guide management (e.g. patients with proteinuria may benefit from ACE\/ARB to delay CKD progression)<\/li>\n<li>risk-stratification to guide prognostication (e.g. patients with proteinuria are at greater risk of cardiovascular disease and CKD progression)<\/li>\n<li>monitoring CKD progression \/ response to treatment<\/li>\n<\/ul>\n<p>For further information on how to check for proteinuria and h<span style=\"font-family: 'Source Sans Pro';\">ow to interpret results, see <a href=\"https:\/\/edren.org\/ren\/handbook\/unithdbk\/ckd\/proteinuria\/\">here<\/a>.\u00a0\u00a0<\/span><\/p>\n<p>&nbsp;<\/p>\n<h5><strong>Determining the cause of CKD<\/strong><\/h5>\n<p>The commonest causes of CKD in Scotland are vascular disease and diabetes.\u00a0 There are of course many other causes however, so it is worth considering the likely aetiology and in particular ensuring that reversible causes are not missed.\u00a0 Look for features of multi-system disease and review all medications, including over-the-counter medications such as NSAIDs and herbal remedies.<\/p>\n<p>Important diagnoses not to miss include:<\/p>\n<ul style=\"list-style-type: disc;\">\n<li>urinary tract obstruction<\/li>\n<li>drug causes of interstitial nephritis \/ scarring (NSAIDs, 5-asa drugs, rarely PPIs, lithium)<\/li>\n<li>paraprotein-related kidney disease<\/li>\n<li>multisystem inflammatory disease (vasculitis, lupus)<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<p>Consider a renal USS if (NICE guidelines):<\/p>\n<div class=\"itemizedlist indented\">\n<ul class=\"itemizedlist\" style=\"list-style-type: disc;\">\n<li class=\"listitem\">accelerated progression of CKD<\/li>\n<li class=\"listitem\">visible or persistent invisible haematuria<\/li>\n<li class=\"listitem\">symptoms of urinary tract obstruction<\/li>\n<li class=\"listitem\">family history of polycystic kidney disease and are aged over 20 years<\/li>\n<li class=\"listitem\">GFR &lt; 30 ml\/min\/1.73 m<sup>2<\/sup>\u00a0(GFR category G4 or G5)<\/li>\n<li>&#8230;and consider the likely utility of scanning in context of age \/ frailty \/ co-morbidities etc. (not everybody with CKD needs an USS!)<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<\/div>\n<h3>2) Risk-stratify<\/h3>\n<p>Management is dictated by risk of CKD progression.\u00a0 This can be assessed using the KDIGO &#8220;traffic light&#8221; grading of GFR and albuminuria:<\/p>\n<p><a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-5118 size-large\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights-1024x768.png\" alt=\"\" width=\"980\" height=\"735\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights-1024x768.png 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights-300x225.png 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights-768x576.png 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights-150x113.png 150w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Traffic-lights.png 1440w\" sizes=\"auto, (max-width: 980px) 100vw, 980px\" \/><\/a><\/p>\n<p>Patients in the orange and red categories are at high risk of progression.<\/p>\n<p>Other methods of risk stratification include:<\/p>\n<ul style=\"list-style-type: disc;\">\n<li>looking at historic trends in serum Cr \/ eGFR (ideally on a graph if possible)<\/li>\n<li>using the kidney failure 4-variable risk <a href=\"https:\/\/kidneyfailurerisk.com\/\">equation<\/a><\/li>\n<li>factoring in what is known about the natural history of the underlying kidney disease (e.g. diabetic kidney disease is often progressive)<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<h3>3) Delay CKD progression<\/h3>\n<p>In some CKD subgroups, renin-angiotensin system inhibitors (RASi &#8211; i.e. ACE inhibitors or angiotensin receptor blockers) and SGLT2i have been shown to slow progression of CKD.\u00a0 The patients in whom there is an evidence base to support these drugs is shown here:<\/p>\n<p><a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-5121 size-large\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1-1024x768.png\" alt=\"\" width=\"980\" height=\"735\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1-1024x768.png 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1-300x225.png 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1-768x576.png 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1-150x113.png 150w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-with-DKD-1.png 1440w\" sizes=\"auto, (max-width: 980px) 100vw, 980px\" \/><\/a> <a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-5122 size-large\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD-1024x768.png\" alt=\"\" width=\"980\" height=\"735\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD-1024x768.png 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD-300x225.png 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD-768x576.png 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD-150x113.png 150w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/RASi-without-DKD.png 1440w\" sizes=\"auto, (max-width: 980px) 100vw, 980px\" \/><\/a> <a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-5123 size-large\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD-1024x768.png\" alt=\"\" width=\"980\" height=\"735\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD-1024x768.png 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD-300x225.png 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD-768x576.png 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD-150x113.png 150w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-with-DKD.png 1440w\" sizes=\"auto, (max-width: 980px) 100vw, 980px\" \/><\/a> <a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone wp-image-5124 size-large\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD-1024x768.png\" alt=\"\" width=\"980\" height=\"735\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD-1024x768.png 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD-300x225.png 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD-768x576.png 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD-150x113.png 150w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/SGLT2i-without-DKD.png 1440w\" sizes=\"auto, (max-width: 980px) 100vw, 980px\" \/><\/a><\/p>\n<p>RASi have been shown to reduce the risk of end-stage renal failure by ~30% (i.e. relative risk reduction 0.3).\u00a0 In patients already established on RASi, SGLT2i have been shown to reduce the risk of renal progression and death by ~40% (i.e. relative risk reduction 0.4) &#8211; a benefit that is realised even in patients <em>without<\/em> diabetes.\u00a0 The absolute risk reduction (ARR) depends on the starting risk.\u00a0 Therefore patients with low risk of progression to ESKD (e.g. green on the KDIGO risk table) will have a low ARR and a NNT that is measured in the high-100s to 1000s.\u00a0 Patients with a moderate-to-high baseline risk of progression (KDIGO orange \/ red) stand to benefit enormously from these drugs and would have NNTs in the 10s to low-100s.<\/p>\n<p>We recommend considering these drugs in patients at risk of progression, taking into account other factors such as:<\/p>\n<ul style=\"list-style-type: disc;\">\n<li>patient preference<\/li>\n<li>other co-morbidities (e.g. in heart failure, RASi and SGLT2i might confer an ever greater mortality benefit)<\/li>\n<li>effect on cardiovascular risk (i.e. not just effect on CKD progression)<\/li>\n<li>glycaemic control in diabetes<\/li>\n<li>polypharmacy<\/li>\n<li>competing risk of death from other causes (e.g. elderly patients with CKD are more likely to die from non-renal causes before reaching end-stage renal failure; of course they may still benefit from the cardiovascular effects of RASi)<\/li>\n<\/ul>\n<p>In draft guidance:<\/p>\n<ul style=\"list-style-type: disc;\">\n<li><a href=\"https:\/\/www.nice.org.uk\/news\/article\/nice-recommend-dapagliflozin-for-people-with-chronic-kidney-disease\">NICE<\/a> recommend dapagliflozin 10 mg od for CKD as an add-on to ACEi\/ARB (or if ACEi\/ARB not tolerated) and if eGFR 25 &#8211; 75 ml\/min and uACR &gt; 22.6 mg\/mmol (in NHSL we have taken 25 mg\/mmol as a convenient, user-friendly threshold)<\/li>\n<li>the <a href=\"https:\/\/ukkidney.org\/node\/1129\">UKKA<\/a> recommend SGLT2i in patients with CKD and uACR &gt; 25 mg\/mmol, excluding individuals with ADPKD or on immunosuppressive medication.<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<h5><strong><span style=\"font-family: 'Source Sans Pro';\">RASi and SGLT2i algorithms<\/span><\/strong><\/h5>\n<p><strong><span style=\"font-family: 'Source Sans Pro';\">For patients without diabetes:<\/span><\/strong><\/p>\n<ul style=\"list-style-type: disc;\">\n<li>consider RASi if uACR &gt; 30 mg\/mmol (uPCR &gt; 50) and hypertension<\/li>\n<li>consider RASi if uACR &gt; 70 mg\/mmol (uPCR &gt; 100) regardless of blood pressure<\/li>\n<li>consider SGLT2i if uACR &gt; 25 mg\/mmol (uPCR &gt; 50) in patients who are already established on maximum-dose RASi (or if RASi contraindicated)<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<p><strong>For patients with T2DM not on insulin:<\/strong><\/p>\n<ul style=\"list-style-type: disc;\">\n<li>consider RASi if uACR &gt; 3 mg\/mmol regardless of blood pressure<\/li>\n<li>consider SGLT2i in all patients with CKD (i.e. if eGFR &lt; 60 or uACR &gt; 3)<\/li>\n<li>consider metformin in all patients with CKD and eGFR &gt; 30 ml\/min (as per BNF)<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<p><strong>For patients with T1DM or T2DM on insulin:<\/strong><\/p>\n<ul style=\"list-style-type: disc;\">\n<li>consider RASi if uACR &gt; 3 mg\/mmol regardless of blood pressure<\/li>\n<li>discuss use of SGLT2i with diabetes team (risk of euglycaemic ketoacidosis)<\/li>\n<\/ul>\n<p>&nbsp;<\/p>\n<h5><strong>Prescribing RASi<\/strong><\/h5>\n<p>It is unusual to start RASi if serum potassium &gt; 5 mmol\/l or eGFR &lt; 15.\u00a0 However, for patients who stand to gain a lot (e.g. diabetic kidney disease with albuminuria) it is often appropriate to tolerate a higher serum potassium (e.g. up to 6 mmol\/l) and to consider strategies to lower potassium (dietary restriction, diuretics, novel binders).\u00a0 Discuss with renal if unsure.\u00a0 We have more advice on our <a href=\"http:\/\/edren.org\/ren\/gp-info\/ace-inhibitors-how-to-start\/\">ACE inhibitor<\/a> page.<\/p>\n<p>&nbsp;<\/p>\n<h5><strong>Prescribing SGLT2i<\/strong><\/h5>\n<p>See our page on <a href=\"https:\/\/edren.org\/ren\/handbook\/unithdbk\/prescribing\/sglt2i-how-to-start\/\">initiating SGLT2i<\/a> in patients with and without diabetes.\u00a0 SGLT2i for CKD are now approved by the SMC and on the NHS Lothian formulary.<\/p>\n<p>&nbsp;<\/p>\n<h3>4) Address cardiovascular risk<\/h3>\n<p>Patients with CKD have elevated cardiovascular risk.\u00a0 In addition to standard measures that apply to the general population, consider offering atorvastatin (starting dose 20 mg) if:<\/p>\n<ul style=\"list-style-type: disc;\">\n<li>GFR &lt; 60 and age &gt; 40<\/li>\n<li>GFR &lt; 60 and age &gt; 18 with diabetes<\/li>\n<li>CKD 1 \u2013 2 with albuminuria<\/li>\n<\/ul>\n<p>Increase to 40 mg daily if not achieving appropriate lipid targets (e.g. NICE recommend if reduction in non-HDL cholesterol &lt; 40%) and eGFR &gt; 30.<\/p>\n<p>Guidelines differ in their recommended target blood pressures.\u00a0 In most patients (with or without CKD) it is usually appropriate to target an office blood pressure of 130\/80 or 150\/90 in the frail elderly.\u00a0 See our <a href=\"http:\/\/edren.org\/ren\/gp-info\/blood-pressure-targets-in-renal-disease\/\">blood pressure pages<\/a> for a more nuanced approach.<\/p>\n<p>&nbsp;<\/p>\n<h3>5) Monitor<\/h3>\n<p>Patients with CKD should have blood pressure, U&amp;Es and proteinuria (e.g. uACR) monitored.\u00a0 This figure suggests monitoring frequency (with the numbers representing the number of tests per year):<\/p>\n<p><a href=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignnone size-large wp-image-5128\" src=\"http:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7-1024x768.png\" alt=\"\" width=\"980\" height=\"735\" srcset=\"https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7-1024x768.png 1024w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7-300x225.png 300w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7-768x576.png 768w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7-150x113.png 150w, https:\/\/edren.org\/ren\/wp-content\/uploads\/2020\/09\/Slide7.png 1440w\" sizes=\"auto, (max-width: 980px) 100vw, 980px\" \/><\/a><\/p>\n<p>It is sensible to adjust this according to patient preferences \/ characteristics.\u00a0 For example, patients opting for predominantly conservative management may not need any monitoring at all.\u00a0 Newly diagnosed patients may need more frequent monitoring, until stability has been established.<\/p>\n<p>&nbsp;<\/p>\n<h3>6) Referral to renal<\/h3>\n<p>See our <a href=\"http:\/\/edren.org\/ren\/gp-info\/when-to-refer-to-the-renal-unit\/\">referral guidelines<\/a>.\u00a0 Some common indications for referral in CKD are given in the summary figure at the top of this page.\u00a0 If you have questions regarding the diagnosis or management of CKD that may not warrant formal referral to the renal clinic, please make use of our e-mail advice line (<a href=\"mailto:rie.renaladvice@luht.scot.nhs.uk\">rie.renaladvice@luht.scot.nhs.uk<\/a>).\u00a0 Please note that this advice line is for health professionals seeking advice about patients in Lothian &amp; Borders.<\/p>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Overview Most chronic kidney disease (CKD) is diagnosed and managed in primary care.\u00a0 The advice on this page is based largely on consensus CKD guidelines from KDIGO and NICE and diabetes guidelines from KDIGO.\u00a0 A general approach is summarised here.\u00a0 Further details on each of the sections of this diagram\u2026<\/p>\n<p> <a class=\"continue-reading-link\" href=\"https:\/\/edren.org\/ren\/handbook\/unithdbk\/ckd\/ckd-summary-overview\/\"><span>Continue reading<\/span><i class=\"crycon-right-dir\"><\/i><\/a> <\/p>\n","protected":false},"author":6,"featured_media":0,"parent":5365,"menu_order":9,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_lmt_disableupdate":"no","_lmt_disable":"","footnotes":""},"class_list":["post-5115","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/pages\/5115","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/users\/6"}],"replies":[{"embeddable":true,"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/comments?post=5115"}],"version-history":[{"count":28,"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/pages\/5115\/revisions"}],"predecessor-version":[{"id":6712,"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/pages\/5115\/revisions\/6712"}],"up":[{"embeddable":true,"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/pages\/5365"}],"wp:attachment":[{"href":"https:\/\/edren.org\/ren\/wp-json\/wp\/v2\/media?parent=5115"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}