Chronic Kidney Disease

Meet the patient

A 58-year-old man with 12 years of type 2 diabetes comes for a routine review. He feels entirely well. His eGFR has drifted from 78 to 52 over two years, his urine albumin-to-creatinine ratio is 140 mg per g, and his blood pressure is 148 over 92. He takes metformin, glimepiride and atorvastatin.[1][3]

Two exam questions are now live and you must answer both: how fast is this kidney failing, and what do you add today? He is the face of CKD — silent, progressive, and entirely treatable if you stage it correctly and do not reach for one drug at a time. Everything below answers those two questions at consultant depth.[1]

The KDIGO definition — the line you must be able to recite

CKD is decreased kidney function — GFR below 60 mL per min per 1.73 m squared — or markers of kidney damage, or both, of at least 3 months duration, regardless of the underlying cause. The KDIGO conference that fixed the operational thresholds defined it as GFR below 60 mL per min per 1.73 m squared or a urine albumin-to-creatinine ratio above 30 mg per g. Say "chronic renal failure" in a viva and you have already lost the mark — the definition and its classification have evolved away from that binary term.[10][11]

The two criteria run on either logic. Kidney damage shows itself as albuminuria — a urine albumin-to-creatinine ratio above 30 mg per g in the KDIGO definition. Or a GFR below 60 mL per min per 1.73 m squared, sustained for at least 3 months — the duration that separates CKD from acute kidney injury, and the reason you always hunt for a baseline creatinine before labelling anything chronic.[10][11]

Classification — read the risk off the CGA heat-map

Stage the patient on three axes because each one changes what you do. The Cause axis drives disease-specific therapy (immunosuppression for lupus, tolvaptan for ADPKD, relief of obstruction). The G and A axes drive referral, monitoring frequency and how aggressively you deploy cardiorenal protection.[1]

The G axis — GFR categories:[1]

The A axis — albuminuria categories, screened on a spot urine albumin-to-creatinine ratio:[13]

[12] [13]

Plot the G and A axes together and you read the KDIGO heat-map — green, yellow, orange, red. The meta-analysis behind the heat-map shows the two axes raise risk independently of each other: end-stage kidney disease hazard ratios of 4, 29 and 454 at eGFRs of 60, 45 and 15 versus 95, and of 5, 13 and 28 at ACRs of 30, 300 and 1000 mg per g versus 5 mg per g. G3b or worse with A3 is the red cell — refer those patients. The counter-intuitive pearl that examiners love: albuminuria predicts progression and death in its own right, even when the GFR is preserved — a patient in G2 A3 (near-normal GFR, heavy proteinuria) fares worse than one in G3a A1 (reduced GFR, clean urine).[10][12]

Who gets CKD — and why it kills them

CKD is one of the commonest non-communicable diseases on earth, and most of your CKD patients will die of cardiovascular disease, not of kidney failure. Hold both facts at once — the first sets your screening duty, the second sets your treatment priority.[1]

[1]

The global prevalence is 10 to 13 percent of adults, climbing above 25 percent in the over-65s — though in the elderly a slice of that burden is the benign age-related GFR decline rather than progressive disease. CKD was the tenth leading cause of years of life lost globally, and its mortality is still rising while cardiovascular and cancer deaths fall.[1]

Risk factors cluster into three groups. Susceptibility — older age, family history, low birth weight, lower socio-economic status, and ethnic minorities (Black, Hispanic, South Asian, Indigenous Australian, Native American; APOL1 risk variants explain much of the excess FSGS and hypertension-attributed nephropathy in Black patients). Initiation — the direct causes: diabetes, hypertension, glomerulonephritis, polycystic kidney disease, obstruction, recurrent infection, autoimmune disease, HIV, nephrotoxins. Progression — the accelerators: heavy proteinuria, poor blood pressure control, poor glycaemic control, smoking, obesity, African ancestry, and ongoing nephrotoxin exposure.[1]

Why the kidney keeps dying — the final common pathway

Whatever the original insult, CKD progresses through one final common pathway — and every modern therapy is designed to interrupt it. That is the sentence that earns the pathophysiology marks.[1]

The cascade runs: nephron loss, then hyperfiltration of the survivors, then glomerulosclerosis, tubulointerstitial fibrosis, and further nephron loss — a self-perpetuating cycle. Surviving nephrons raise their single-nephron GFR to hold total GFR (the Brenner hypothesis); the cost is intraglomerular hypertension, podocyte injury, basement-membrane leak and proteinuria. Filtered protein then activates proximal tubular cells into a pro-fibrotic state. Proteinuria is therefore both a marker and a mediator of progression — which is why lowering it changes outcomes.[1]

Angiotensin II is the central effector — it constricts the efferent arteriole and drives intraglomerular pressure. Block it (ACE inhibitor or ARB, finerenone) and you drop that pressure. SGLT2 inhibition works from the other end: by restoring tubuloglomerular feedback it contracts the afferent arteriole and normalises intraglomerular pressure — a haemodynamic effect independent of glucose lowering, which is exactly why dapagliflozin and empagliflozin protect non-diabetic kidneys.[4][5]

As GFR falls, the systemic complications emerge in a predictable order — anaemia (EPO deficiency), CKD-mineral and bone disorder (phosphate retention, FGF-23 rise, secondary hyperparathyroidism), metabolic acidosis, sodium and water retention, hyperkalaemia, dyslipidaemia. They are not random; they are the direct consequence of losing nephron function, and the mnemonic KUSMAUL (below) holds them in one breath.[1]

What you will find — CKD is silent until it is not

CKD is notoriously silent until G3b to G4. Most early disease is found not by symptoms but by a routine eGFR and urine ACR in a diabetic, a hypertensive, or an older patient. By the time uraemic symptoms appear, the GFR is usually below 20 to 25.[1]

Earliest markers — all picked up on testing, not on history. Nocturia (the concentrating mechanism has gone), frothy urine (proteinuria), mild hypertension, mild fatigue, and an asymptomatic anaemia on a routine count. A new blood pressure reading in a young person, or proteinuria on a medical examination, must trigger an eGFR and a urine ACR.[1]

Established uraemic syndrome — anorexia, nausea, metallic taste, weight loss, fatigue, pruritus, restless legs, sexual dysfunction, easy bruising, impaired concentration; in advanced disease asterixis, myoclonus, seizures and uraemic encephalopathy. Uraemic pericarditis (pleuritic pain, friction rub) and uraemic frost are rare now but are classic stems — and both are absolute indications for urgent dialysis.[1]

Go looking for the cause. Diabetic retinopathy supports diabetic kidney disease; ballotable cystic kidneys point to ADPKD; haematuria with red-cell casts and a rapidly rising creatinine means glomerulonephritis; prostatism with hydronephrosis means obstruction; a malar rash with arthralgia means lupus; palpable purpura with sinusitis means ANCA vasculitis. A focused system enquiry and a skin, fundus, abdominal and neurological exam narrows the differential fast.[1]

The first fork — is this CKD or AKI?

Before anything else, separate CKD from acute kidney injury — the management is radically different and the single most useful discriminator is an old blood test. AKI evolves over hours to days, is often reversible, and the kidneys are normal or enlarged on ultrasound. CKD evolves over months to years, is irreversible, and the kidneys are small and echogenic.[1]

Three more mimics to exclude. Age-related GFR decline — no albuminuria, no damage markers, so not CKD by KDIGO. Prerenal azotaemia — volume depletion, BUN-to-creatinine above 20, responds to fluids. Rapidly progressive glomerulonephritis — eGFR falls over 50 percent in under three months with haematuria and red-cell casts; biopsy and immunosuppress urgently.[1]

The bedside round — three questions in parallel

At the bedside answer three questions at once: what is the cause, how fast is it progressing, and what complications are present? That frame keeps the assessment focused rather than a rambling systems review.[1]

History — establish tempo and cause. Pull every previous creatinine and eGFR to compute the annual decline and separate CKD from AKI. Then chase the cause: diabetes duration and control, hypertension, recurrent childhood UTIs (reflux), obstruction, nephrotoxins (NSAIDs, lithium, tenofovir, calcineurin inhibitors, herbal remedies), autoimmune symptoms, recent infections, and family history of kidney disease or hearing loss (Alport). Screen for uraemic, volume and cardiovascular symptoms.[1]

Examination — volume status first. JVP, blood pressure in both arms and posturally, peripheral and sacral oedema, basal crackles, S3 gallop. Then ballotable kidneys (ADPKD, hydronephrosis), a palpable bladder (obstruction), renal bruits (renovascular), hepatosplenomegaly (polycystic liver, amyloid). Skin for pallor, excoriations, uraemic frost, half-and-half nails, palpable purpura. Cardiovascular for a pericardial friction rub (dialysis indication) and signs of heart failure.[1]

Investigations — confirm, define the cause, detect the complications

Pursue all three goals in parallel: confirm the diagnosis and stage, define the cause, and find the complications. None of them waits for the other.[1]

Bloods. Creatinine and eGFR by the CKD-EPI 2021 race-free equation (more accurate than MDRD, especially at higher GFR); trend over three months to confirm chronicity. Urea and electrolytes — sodium, potassium, bicarbonate (acidosis when bicarbonate below 22). Full blood count for the normocytic normochromic anaemia that appears at G3b. Iron studies, bone profile (calcium low or normal, phosphate high, PTH high), 25-hydroxyvitamin D, HbA1c, lipids, and an autoimmune and virology screen when the cause is unclear.[1]

Urine is irreplaceable. The urine albumin-to-creatinine ratio quantifies albuminuria and is the single most important prognostic marker — at least 30 mg per g defines CKD if chronic. Urine microscopy discriminates the cause: dysmorphic red cells and red-cell casts mean glomerular bleeding; white-cell casts mean pyelonephritis or interstitial nephritis; granular muddy-brown casts mean acute tubular necrosis.[1]

Imaging — renal ultrasound on every new diagnosis. Size, cortical thickness, echogenicity, cysts, stones, hydronephrosis, asymmetry. Renal biopsy when the cause is unclear, the disease may be treatable, or the result changes management — heavy or rising proteinuria, active sediment, rapidly progressive glomerulonephritis, suspected lupus or vasculitis. Do not biopsy a small scarred kidney.[1]

Cardiovascular risk assessment is non-negotiable. ECG, lipid profile, blood pressure, glucose, smoking status — and stress testing or angiography for symptoms. Cardiovascular disease is the leading cause of death in CKD, and reducing it is as important as slowing the GFR decline.[1]

The emergencies — calcium first, dialyse for AEIOU

CKD rarely presents as an acute resuscitation; the emergencies are its complications. The two that kill within minutes are severe hyperkalaemia and the uraemic emergencies. Recognise them and act within minutes — this section carries no jokes.[1]

Uraemic emergencies needing urgent dialysis — the AEIOU mnemonic. A severe metabolic Acidosis (pH below 7.1 or bicarbonate below 10, unresponsive to bicarbonate); Electrolyte derangement — refractory hyperkalaemia; Intoxications with dialysable poisons (lithium, salicylate, methanol, ethylene glycol, metformin); O fluid Overload refractory to diuretics with pulmonary oedema; Uraemia with pericarditis, encephalopathy, intractable vomiting, or bleeding from platelet dysfunction. Any one needs urgent dialysis via a temporary central venous catheter while a definitive access is planned.[1]

The supporting emergencies. Severe metabolic acidosis is treated with sodium bicarbonate (oral for chronic mild acidosis, intravenous in emergencies, watching volume and sodium). Refractory fluid overload with pulmonary oedema gets high-dose loop diuretic (furosemide 80 to 250 mg IV), oxygen, morphine, nitrate infusion and CPAP or NIV — and urgent dialysis or haemofiltration if it fails. Symptomatic severe anaemia with heart failure gets intravenous iron first; transfuse only for haemodynamic instability, and carefully, because of fluid overload and sensitisation before transplant.[1]

The four pillars — deployed together, not in sequence

The single most important conceptual shift of the past decade: the four disease-modifying therapies are started together, not one after another. In any patient with CKD and albuminuria (A2 or A3) or an eGFR below 60, you deploy RAAS blockade, SGLT2 inhibition, finerenone in diabetics, and multifactorial cardiovascular risk reduction as a combination. Each pill interrupts a different mechanism of progression, and the trials were additive on top of maximised background therapy.[1]

Pillar 1 — RAAS blockade

First-line in any CKD with albuminuria (UACR at least 30 mg per g) or hypertension. ACE inhibitors and ARBs dilate the efferent arteriole, lower intraglomerular pressure, cut proteinuria by 30 to 50 percent, and slow progression. Titrate to the maximum tolerated dose.[1]

Named doses — ramipril 2.5 to 10 mg once daily, losartan 50 to 100 mg once daily, irbesartan 150 to 300 mg once daily. Expect a small reversible creatinine rise (up to 30 percent) on starting; stop and investigate if it exceeds 30 percent or hyperkalaemia is refractory. Never combine an ACE inhibitor with an ARB — no extra benefit, more harm.[1]

Pillar 2 — SGLT2 inhibition

Start an SGLT2 inhibitor in any CKD with eGFR above 20, regardless of diabetes status (KDIGO 2024). The mechanism is tubuloglomerular feedback restoration, not glucose lowering — which is exactly why it protects non-diabetic kidneys too. Dapagliflozin 10 mg once daily or empagliflozin 10 mg once daily reduce progression to end-stage kidney disease, cardiovascular death and hospitalisation for heart failure by roughly 30 percent; canagliflozin 100 mg once daily is the CREDENCE alternative.[3][4][5]

[3] [4] [5]

Pillar 3 — finerenone

In type 2 diabetics with CKD and albuminuria already on maximum RAAS blockade, add finerenone 10 to 20 mg once daily. This is the non-steroidal mineralocorticoid receptor antagonist — a third, additive pillar. Monitor potassium: hold if it rises above 5.5. The hyperkalaemia risk is lower than with spironolactone or eplerenone, which are not recommended for CKD progression per se.[6]

[6]

Pillar 4 — multifactorial cardiovascular risk reduction

Because cardiovascular disease is the leading cause of death, this pillar is as important as slowing the GFR decline — and it is the single biggest determinant of survival. Target blood pressure below 130 over 80 mm Hg in CKD with albuminuria (loosen to under 140 over 90 in the frail elderly). Add a thiazide if eGFR above 30, switch to a loop diuretic if below 30, and layer in a calcium-channel blocker or beta-blocker as needed.[1]

Give a statin to every CKD patient over 50 — atorvastatin 20 to 80 mg or rosuvastatin 20 mg daily — and reduce intensity on dialysis. Target HbA1c around 7 to 8 percent, encourage smoking cessation, salt restriction and weight management, and use an antiplatelet for established vascular disease.[2]

[2]

The complications — KUSMAUL, treated in parallel

The complications of CKD spell KUSMAUL: potassium, uraemia, salt, mineral, anaemia, uraemic toxins, lipids. Treat them in parallel with the pillars, not after.[1]

Anaemia — iron first, then a restrained ESA

Investigate before you attribute anaemia to CKD — B12, folate, ferritin and transferrin saturation, occult blood, haemolysis, paraprotein. Then give iron before and alongside any erythropoiesis-stimulating agent. In patients undergoing maintenance haemodialysis, the PIVOTAL trial showed that proactive high-dose intravenous iron sucrose (400 mg monthly, withheld only when ferritin exceeded 700 micrograms per L or transferrin saturation reached 40 percent or more) beat a reactive low-dose strategy (iron only when ferritin fell below 200 micrograms per L or transferrin saturation below 20 percent) on a composite of myocardial infarction, stroke, heart-failure hospitalisation or death — with no excess infections and lower ESA dose requirements.[14]

If you use an erythropoiesis-stimulating agent, never aim for a normal haemoglobin. TREAT targeted a haemoglobin of approximately 13 g per dL with darbepoetin in diabetics with CKD and doubled stroke (hazard ratio 1.92) without reducing death or cardiovascular events; the partial-correction arm of the Drueke trial sat at 10.5 to 11.5 g per dL — a risk-benefit balance that, as the TREAT authors concluded, will make the stroke risk outweigh the benefits for many patients.[7][8]

[7] [8]

CKD-mineral and bone disorder

Treat the triad — high phosphate, disturbed calcium and raised PTH — and act on trends, not a single abnormal value. The KDIGO 2017 CKD-MBD update (for G3a to G5 and dialysis patients) frames management as decreasing phosphate levels, maintaining calcium levels and addressing elevated parathyroid hormone, and warns to avoid hypercalcaemia while treating secondary hyperparathyroidism — the reason to be cautious with calcium-based phosphate binders and active vitamin D analogues when the calcium is already high. Restrict dietary phosphate first, then bind it with meals.[15]

Acidosis, hyperkalaemia, fluid

Metabolic acidosis — correct it, because correction changes outcomes. In a randomised trial of 134 CKD patients with creatinine clearance 15 to 30 mL per min per 1.73 m squared and serum bicarbonate 16 to 20 mmol per L, oral sodium bicarbonate slowed the decline in kidney function (1.88 versus 5.93 mL per min per 1.73 m squared), cut rapid progression (9 versus 45 percent) and reduced progression to end-stage renal disease (6.5 versus 33 percent), with improved nutritional markers.[16] Chronic hyperkalaemia — dietary restriction plus a potassium binder, so RAAS blockade stays on board. Patiromer (initial dose 4.2 g or 8.4 g twice daily in the pivotal trial) lowered serum potassium by a mean of 1.01 mmol per L at 4 weeks in hyperkalaemic CKD patients on RAAS inhibitors, and withdrawal to placebo let hyperkalaemia recur (60 versus 15 percent).[17] Sodium zirconium cyclosilicate 10 g three times daily for 48 hours, then 5 g once daily, maintained normokalaemia over 28 days in the HARMONIZE trial.[18] Fluid overload — salt restriction, daily weights and loop diuretics titrated to dry weight; escalate to dialysis when it becomes diuretic-refractory.

Nephrotoxins — the single commonest reversible cause of decline

NSAIDs are the commonest reversible cause of CKD decline — avoid them. Ibuprofen, naproxen, diclofenac, the COX-2 inhibitors all constrict the afferent arteriole and undo your RAAS blockade. Add high-dose or long-term PPIs (interstitial nephritis), tenofovir disoproxil (switch to tenofovir alafenamide), unmonitored lithium and calcineurin inhibitors, aminoglycosides, iodinated contrast, and herbal remedies (Aristolochia, St John's wort, Chinese preparations).[1]

Plan renal replacement therapy early, dialyse late

Refer to nephrology at eGFR below 30 (G4) — early enough for education, modality choice, vascular access and transplant evaluation. Create an arteriovenous fistula six months before the expected dialysis start (it needs 6 to 12 weeks to mature and frequently needs revision). Refer for transplant evaluation at eGFR below 20; a pre-emptive living-donor transplant gives the longest graft and patient survival.[1]

There is no absolute eGFR threshold to start dialysis. The IDEAL trial showed early initiation (eGFR 10 to 14) was not superior to late initiation (eGFR 5 to 7) in asymptomatic patients. Dialyse for the AEIOU emergencies or for symptomatic uraemia, fluid overload or electrolyte derangement that medicine can no longer control. For older patients with multiple comorbidities, comprehensive conservative care is a legitimate pathway.[1]

Specific subtypes and scenarios

Diabetic kidney disease is the single largest cause of CKD worldwide — screen with annual UACR and eGFR from diagnosis in type 2 and from five years after diagnosis in type 1. Treat with the full four-pillar regimen, tight glycaemic control (HbA1c around 7 to 8 percent), and mandatory SGLT2 inhibition. Biopsy only if atypical — short duration, no retinopathy in type 1, rapid decline, haematuria, or active sediment.[3][6]

Hypertensive nephrosclerosis is second commonest — long-standing hypertension, bland urine, small symmetric kidneys. Treat to blood pressure below 130 over 80 with RAAS blockade first-line. Suspect renovascular disease if there is flash pulmonary oedema, asymmetry greater than 1.5 cm, an abdominal bruit, or a steep creatinine rise on starting an ACE inhibitor or ARB.[1]

Autosomal dominant polycystic kidney disease (ADPKD) — family history, bilateral palpable kidneys, hypertension, haematuria, intracranial aneurysms. Tolvaptan 60 to 120 mg per day in two divided doses slows the rise in kidney volume and the GFR decline in rapidly progressive disease (Mayo class 1C to 1D). Monitor liver enzymes monthly for 18 months then three-monthly (idiosyncratic hepatotoxicity), and ensure free access to water. Avoid in advanced CKD, hepatobiliary disease and pregnancy.[9]

[9]

The glomerulonephritides. IgA nephropathy (the commonest primary GN) gets RAAS blockade, SGLT2 inhibition, and targeted-release budesonide or systemic steroids in selected high-risk patients. Membranous nephropathy gets RAAS blockade plus rituximab in high-risk disease. FSGS gets RAAS blockade plus steroids, calcineurin inhibitors or mycophenolate. Lupus nephritis and ANCA vasculitis need combined nephrology and rheumatology — biopsy, induction with cyclophosphamide or rituximab plus glucocorticoids, then maintenance with mycophenolate or azathioprine.[1]

How CKD patients come to harm — the classic pitfalls

These are the preventable errors examiners press on. None of them is rare; all of them are avoidable.[1]

• Calling AKI-on-CKD "stable CKD" because nobody looked for a baseline creatinine — the commonest diagnostic error.[1]
• Missing bilateral renal artery stenosis before starting an ACE inhibitor or ARB — a creatinine rise over 30 percent or new hyperkalaemia is the clue.[1]
• Overusing calcium-based phosphate binders — drives the vascular calcification that then kills the patient.[1]
• Escalating an ESA without correcting iron first, then aiming for a normal Hb — TREAT and Drueke 2006 showed the ceiling.[7][8]
• Continuing NSAIDs or high-dose PPIs in advanced CKD.[1]
• Forgetting to renally dose-adjust — metformin, NOACs, gabapentin, opioids, antibiotics.[1]
• Creating an AV fistula too late, or failing to refer for transplant early — the patient arrives needing emergency dialysis through a femoral line.[1]
• Failing to vaccinate against hepatitis B before dialysis.[1]

Prognosis and disposition

CKD prognosis is dominated by cardiovascular mortality, which exceeds the risk of reaching dialysis in most early-CKD cohorts. The KDIGO CGA stage is the best single predictor. G1 to G3a with normal albuminuria has minimal impact on life expectancy with treatment. G3b to G4 carry 5 to 10 percent annual mortality, mostly cardiovascular. G5 carries 10 to 20 percent annual mortality on dialysis, with 50 percent five-year survival — comparable to several cancers. A living-donor transplant roughly doubles survival, with 90 percent five-year graft survival.[1]

Primary care manages G1 to G3a CKD with stable albuminuria and controlled cardiovascular risk, monitoring eGFR and UACR annually. Refer to nephrology at eGFR below 30, persistent A2 or A3 albuminuria despite RAAS blockade, a GFR decline over 5 mL per min per year, refractory hypertension, heavy or rising proteinuria, active sediment, anaemia with Hb below 100, refractory hyperkalaemia or acidosis, or suspected glomerulonephritis or inherited disease.[1]

Special populations

Pregnancy in CKD — high maternal and fetal risk: pre-eclampsia (often superimposed), fetal growth restriction, prematurity, and accelerated maternal GFR decline, especially with baseline eGFR below 40, heavy proteinuria or hypertension. Preconception, switch the ACE inhibitor or ARB to labetalol, methyldopa or nifedipine, and avoid mycophenolate, cyclophosphamide, warfarin, statin, spironolactone and SGLT2 inhibitors. Aspirin 75 to 150 mg daily from 12 weeks reduces pre-eclampsia.[1]

The elderly — the age-related GFR decline may be overestimated by creatinine-based equations; cystatin C is more accurate and flags "shrunken pore syndrome". Be more permissive with blood pressure (under 140 over 90 in the frail elderly), avoid polypharmacy, renally dose-adjust every drug, and consider comprehensive conservative care in the very elderly with multiple comorbidities.[1]

Paediatric CKD — causes differ: congenital anomalies of the kidney and urinary tract (CAKUT, the largest single cause), hereditary nephritis (Alport), reflux nephropathy, cystinosis. Growth failure, metabolic bone disease and anaemia dominate; the goal is a pre-emptive transplant.[1]

Evidence, guidelines and regional differences

The evidence base has been rebuilt in a decade by four classes of trial. The SGLT2 inhibitor outcome trials (CREDENCE, DAPA-CKD, EMPA-KIDNEY) proved disease modification independent of diabetes. The non-steroidal MRA trials (FIDELIO-DKD, FIGARO-DKD) added finerenone. SHARP established statin-based lipid lowering in CKD. The ESA target trials (TREAT, Drueke 2006, CHOIR, CREATE) set the Hb ceiling. The result is a four-pillar combination that simply did not exist before 2010.[1][2][3][4][5][6][7][8][9]

Controversies to handle calmly. The optimal blood pressure target in the elderly (SPRINT supports lower but excluded diabetes); whether SGLT2 inhibitors work below eGFR 20 (trials excluded this group); whether bisphosphonates are safe in advanced CKD; whether to continue RAAS blockade in stage 4 to 5 CKD; and the best dialysis start time (IDEAL supports later, symptomatic initiation).[1]

The mantra, and the mnemonics

The high-yield traps, correctly stated. The KDIGO definition is more than 3 months — not "chronic renal failure". Albuminuria A2 is 30 to 300 mg per g, A3 over 300 — the cut-off is 30, not 150. The GFR cut-off is below 60, not below 30 (which is G4). ACE inhibitor or ARB, never both combined. SGLT2 inhibitors work in non-diabetic CKD. ESA target Hb 100 to 120; over 130 kills. Metformin is safe to eGFR 30, not 60. A kidney under 9 cm is irreversibly scarred — do not biopsy.[1][7][8]

Ward-round test — three stems, thirty seconds each

Stem 1 — the diabetic from the top of the topic (answer)

A 58-year-old with type 2 diabetes, eGFR 52, urine ACR 140 mg per g, blood pressure 148 over 92, on metformin and atorvastatin. What do you add today? Model: This is diabetic kidney disease, stage G3a A2, and the kidney is failing faster than the GFR alone suggests because albuminuria is the dominant prognostic marker. Add the four pillars together: an ACE inhibitor or ARB (ramipril, titrated; the blood pressure target is below 130 over 80), an SGLT2 inhibitor — dapagliflozin 10 mg or empagliflozin 10 mg (mandatory in diabetic CKD with albuminuria, eGFR above 20), finerenone 10 to 20 mg on top of the RAAS blockade (monitor potassium), and multifactorial cardiovascular risk reduction (he is already on a statin; tighten glycaemia and add smoking and salt advice). Do not sequence them — start the combination.[1][3][4][5][6]

Stem 2 — peaked T waves at 3am (answer)

A 64-year-old on ramipril and spironolactone for CKD G4 arrives with potassium 7.1 and wide QRS complexes. Walk me through the first 15 minutes. Model: This is imminent cardiac arrest — humour off, act in order. Calcium gluconate 10 percent 10 mL slow IV over 2 to 5 minutes to stabilise the myocardium first. Then shift potassium: 10 units soluble insulin IV plus 25 to 50 g of 50 percent dextrose, and 10 to 20 mg nebulised salbutamol; add sodium bicarbonate 50 to 100 mmol IV if acidotic. Then remove it: furosemide 40 to 80 mg IV and an oral binder, haemodialysis if refractory. Stop the ramipril and the spironolactone immediately. Recheck potassium and ECG within 1 to 2 hours.[1]

Stem 3 — the small asymmetric kidney (answer)

An eGFR of 38 is found in a 70-year-old started on ramipril three weeks ago; creatinine has risen 35 percent. Renal ultrasound shows kidneys of 8.2 cm and 9.8 cm. What is going on and what do you do? Model: Two traps firing at once. The asymmetry greater than 1.5 cm suggests renovascular disease, and the 35 percent creatinine rise on starting the ACE inhibitor is the classic clue to bilateral renal artery stenosis — stop the ramipril and investigate with Doppler ultrasound or MR angiography (avoid iodinated contrast). Separately, a kidney under 9 cm is irreversibly scarred — do not biopsy it; there is nothing treatable to find and a real bleeding risk. The plan is renovascular workup, blood pressure control with a calcium-channel blocker, and nephrology referral.[1]

References

1. [1]Levin A, Ahmed SB, Carrero JJ, et al. Executive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknowns Kidney Int, 2024.PMID 38519239
2. [2]Baigent C, Landray MJ, Reith C, et al. The effects of lowering LDL cholesterol with simvastatin plus ezetimibe in patients with chronic kidney disease (Study of Heart and Renal Protection): a randomised placebo-controlled trial Lancet, 2011.PMID 21663949
3. [3]Perkovic V, Jardine MJ, Neal B, et al. Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy N Engl J Med, 2019.PMID 30990260
4. [4]Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease N Engl J Med, 2020.PMID 32970396
5. [5]Herrington WG, Staplin N, Wanner C, et al. Empagliflozin in Patients with Chronic Kidney Disease N Engl J Med, 2023.PMID 36331190
6. [6]Bakris GL, Agarwal R, Anker SD, et al. Effect of Finerenone on Chronic Kidney Disease Outcomes in Type 2 Diabetes N Engl J Med, 2020.PMID 33264825
7. [7]Pfeffer MA, Burdmann EA, Chen CY, et al. A trial of darbepoetin alfa in type 2 diabetes and chronic kidney disease N Engl J Med, 2009.PMID 19880844
8. [8]Drüeke TB, Locatelli F, Clyne N, et al. Normalization of hemoglobin level in patients with chronic kidney disease and anemia N Engl J Med, 2006.PMID 17108342
9. [9]Torres VE, Chapman AB, Devuyst O, et al. Tolvaptan in patients with autosomal dominant polycystic kidney disease N Engl J Med, 2012.PMID 23121377
10. [10]Webster AC, Nagler EV, Morton RL, et al. Chronic Kidney Disease Lancet, 2017.PMID 27887750
11. [11]Levey AS, de Jong PE, Coresh J, et al. The definition, classification, and prognosis of chronic kidney disease: a KDIGO Controversies Conference report Kidney Int, 2011.PMID 21150873
12. [12]Gansevoort RT, Matsushita K, van der Velde M, et al. Lower estimated GFR and higher albuminuria are associated with adverse kidney outcomes. A collaborative meta-analysis of general and high-risk population cohorts Kidney Int, 2011.PMID 21289597
13. [13]Bakris GL. Microalbuminuria: what is it? Why is it important? What should be done about it? J Clin Hypertens (Greenwich), 2001.PMID 11416691
14. [14]Macdougall IC, White C, Anker SD, et al. Intravenous Iron in Patients Undergoing Maintenance Hemodialysis N Engl J Med, 2019.PMID 30365356
15. [15]Ketteler M, Block GA, Evenepoel P, et al. Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder: Synopsis of the Kidney Disease: Improving Global Outcomes 2017 Clinical Practice Guideline Update Ann Intern Med, 2018.PMID 29459980
16. [16]de Brito-Ashurst I, Varagunam M, Raftery MJ, Yaqoob MM. Bicarbonate supplementation slows progression of CKD and improves nutritional status J Am Soc Nephrol, 2009.PMID 19608703
17. [17]Weir MR, Bakris GL, Bushinsky DA, et al. Patiromer in patients with kidney disease and hyperkalemia receiving RAAS inhibitors N Engl J Med, 2015.PMID 25415805
18. [18]Kosiborod M, Rasmussen HS, Lavin P, et al. Effect of sodium zirconium cyclosilicate on potassium lowering for 28 days among outpatients with hyperkalemia: the HARMONIZE randomized clinical trial JAMA, 2014.PMID 25402495