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Nephrology›Condition·Updated Jul 11, 2026·v1

Chronic Kidney Disease

Chronic kidney disease is a global health burden affecting ~850 million people, characterized by progressive loss of kidney function and high cardiovascular mortality. Modern management has evolved from RAASi monotherapy to a quadruple approach including SGLT2 inhibitors, nonsteroidal MRAs, and GLP-1 receptor agonists, which together can slow or halt progression. Early detection through eGFR and UACR screening is essential, as the condition is asymptomatic until advanced stages. Risk stratification using the KDIGO CGA system and the Kidney Failure Risk Equation guides therapy intensity and referral timing. Management also focuses on aggressive blood pressure control, correction of metabolic acidosis and anemia, hyperkalemia management to preserve RAASi, and timely preparation for renal replacement therapy. Key controversies include the role of cystatin C, the optimal BP target in the elderly, and the use of potassium binders for primary prevention.

High Evidence735 references·2,187 words·9 min read·v1
chronic kidney diseasenephrologykidney failureSGLT2 inhibitorsRAAS inhibitorsfinerenonehyperkalemiaalbuminuriaCKD-MBDanemia of CKDrenal replacement therapy

Quick Reference

RxDrug of choiceQuadruple therapy: RAAS inhibitor (ACEi/ARB) + SGLT2 inhibitor (dapagliflozin 10 mg or empagliflozin 10 mg) + nonsteroidal MRA (finerenone 10-20 mg) + GLP-1 receptor agonist (semaglutide 1.0 mg weekly) in appropriate populations
AltAlternativesARB if ACEi-intolerant; canagliflozin 100 mg as alternative SGLT2i; patiromer for hyperkalemia; roxadustat for anemia if injectables declined
⊘AvoidNSAIDs (all stages of CKD); non-dihydropyridine CCBs (diltiazem, verapamil) in CKD with heart failure; metformin if eGFR <30; nitrofurantoin if eGFR <30; high-dose rosuvastatin (>10 mg) if eGFR <30
DxTest of choiceSerum creatinine for eGFR (CKD-EPI 2021, race-free) + spot urine albumin-to-creatinine ratio; confirmatory cystatin C if eGFRcr 45-59 with A1
ScKey scoreKidney Failure Risk Equation (KFRE) - 5-year risk of ESKD; also KDIGO CGA heat map for baseline risk stratification
→When to refereGFR <30 mL/min/1.73 m², UACR >300 mg/g, rapidly progressive disease (≥50% eGFR decline over months), diagnostic uncertainty, severe complications (hyperkalemia, anemia, CKD-MBD, resistant hypertension)
CKD is common and deadly but highly treatable with contemporary quadruple therapy; early detection via eGFR+UACR screening and prompt initiation of guideline-directed medical therapy can slow progression, reduce cardiovascular mortality, and delay RRT by years.
Chronic kidney disease (CKD) is a progressive condition defined by persistent kidney damage or reduced function (eGFR <60 mL/min/1.73 m²) for >3 months [3][52]. It affects 10-14% of adults globally and is a leading cause of death, primarily from cardiovascular disease [30][54]. This concise guide integrates KDIGO 2024-2025 guidelines, focusing on staging (cause, GFR, albuminuria), evidence-based nephroprotection (RASi, SGLT2i, nsMRA, GLP-1 RA), acute management of life-threatening complications, and transition to renal replacement therapy.

Overview and Recommendations

Background

  • •CKD is defined by KDIGO as abnormalities of kidney structure or function present for >3 months, staged by cause, GFR (G1-G5), and albuminuria (A1-A3). It affects ~10-14% of the global adult population and was the cause of 1.2 million deaths in 2017, with projections to become the fifth leading cause of death by 2050. The condition was historically termed chronic renal failure; end-stage renal disease is now often replaced by the term kidney failure.
  • •The final common pathway is kidney fibrosis, driven by TGF-β signaling through Smad2/3, metabolic reprogramming (PFKFB3-driven histone lactylation), and hemodynamic stress from single-nephron hyperfiltration. RAAS and sympathetic activation amplify injury, while maladaptive autophagy, cellular senescence, and necroinflammation create self-propagating cycles of tubular damage and interstitial fibrosis.
  • •Diabetes and hypertension account for the majority of cases globally. Other etiologies include glomerular disease (e.g., IgA nephropathy, FSGS), tubulointerstitial disease, vascular disease (hypertensive nephrosclerosis), and cystic/congenital disorders (ADPKD). APOL1 risk variants in African-ancestry populations confer a substantially elevated lifetime risk. Acute kidney injury is a powerful independent risk factor, with a pooled adjusted HR of 8.8 for subsequent CKD.
  • •Landmark trials have reshaped therapy: PARADIGM-HF and DAPA-HF established SGLT2i benefits; DAPA-CKD and EMPA-KIDNEY proved nephroprotection in non-diabetic CKD; FIDELIO-DKD and FIGARO-DKD confirmed finerenone's cardiorenal effects; FLOW demonstrated GLP-1 RA benefit. The paradigm has shifted from RAASi monotherapy to quadruple therapy, achieving additive albuminuria reductions of 30-50%.
  • •Untreated or suboptimally managed CKD carries high mortality, 5-year mortality for a 65-year-old with stage 4 CKD approaches 45%, mostly from cardiovascular causes. Albuminuria (UACR ≥30 mg/g) and eGFR <60 mL/min/1.73 m² are multiplicative risk factors, with no threshold for albuminuria. Early detection and combination therapy can now delay kidney failure by >6 years and make remission (eGFR slope <1 mL/min/1.73 m²/yr) an increasingly attainable goal.

Evaluation

  • •Suspect CKD in any patient with exertional dyspnea, unexplained fatigue, nocturia, foamy urine, or dependent edema, though most early-stage patients are asymptomatic and detected incidentally on lab testing.
  • •Ask about long-standing diabetes, hypertension, family history of kidney disease, prior episodes of AKI, use of nephrotoxins (NSAIDs, herbal remedies, aristolochic acid), hematuria, flank pain, and systemic symptoms suggesting glomerulonephritis (sore throat, rash, arthritis, sinusitis).
  • •Examine blood pressure (volume-dependent hypertension is common), jugular venous pressure, presence of peripheral edema or pulmonary crackles, pallor (anemia when eGFR <30), fundoscopic changes (hypertensive/diabetic retinopathy), abdominal bruits, and signs of uremia (pericardial rub, asterixis, peripheral neuropathy, cognitive impairment).
  • •Order serum creatinine for eGFR using the CKD-EPI 2021 equation (without race) and spot urine albumin-to-creatinine ratio (UACR). Persistent eGFR <60 mL/min/1.73 m² for >3 months or UACR ≥30 mg/g establishes the diagnosis of CKD.
  • •If eGFRcr is 45-59 mL/min/1.73 m² without albuminuria (A1), obtain serum cystatin C. An eGFRcys <60 mL/min/1.73 m² confirms CKD; if eGFRcys ≥60, measured GFR (iohexol or inulin clearance) may be needed, up to 17% of this group do not have true CKD.
  • •Additional laboratories include serum electrolytes (K+, Na+, Cl-), bicarbonate, BUN, calcium, phosphate, intact PTH, CBC with differential, and serologies if active sediment or systemic disease is suspected (ANA, ANCA, anti-GBM, complements, hepatitis B/C, HIV, serum protein electrophoresis).
  • •Perform renal ultrasound as first-line imaging: assess kidney size (<9 cm suggests chronic scarring), cortical thickness, echogenicity, and exclude obstruction or cystic disease. Asymmetric kidneys suggest renovascular disease; larger kidneys with cysts suggest ADPKD.
  • •Consider native kidney biopsy when the cause remains uncertain after noninvasive workup and there is active urinary sediment (dysmorphic RBCs, RBC casts), nephrotic-range proteinuria (>3.5 g/day or UACR >3000 mg/g), rapidly progressive glomerulonephritis, or suspected systemic disease with renal involvement. Major complication rate is low (bleeding needing transfusion in 1.6%).
  • •Stage and risk stratify using the KDIGO CGA heat map: combine GFR category (G1-G5) and albuminuria category (A1-A3) to assign low, moderate, high, or very high risk for progression and cardiovascular mortality.
  • •Calculate the 5-year Kidney Failure Risk Equation (KFRE) using age, sex, eGFR, and UACR to estimate risk of ESKD and guide timing of nephrology referral and RRT planning (referral recommended when risk >3-5%).
  • •Assess for complications at every visit: anemia (Hb <10 g/dL), metabolic acidosis (serum bicarbonate <22 mmol/L), hyperkalemia (K+ >5.0 mmol/L, especially with RAASi), mineral bone disease (hyperphosphatemia, hypocalcemia, elevated PTH), and malnutrition (low albumin, muscle wasting, unintentional weight loss).
  • •Consider genetic testing in young-onset CKD (<40 years), strong family history, extrarenal features (e.g., hearing loss, cysts, hypomagnesemia), or when cause is unknown despite thorough evaluation. Monogenic causes are identified in 11-37% of such cases.

Management

  • •Initiate an ACE inhibitor or ARB at maximally tolerated dose for all patients with CKD and UACR ≥30 mg/g or hypertension. Lisinopril start 5-10 mg daily, target 40 mg daily; losartan start 25-50 mg daily, target 100 mg daily. A network meta-analysis showed ACEi reduces kidney failure by 39% (OR 0.61). Do not discontinue RAASi in advanced CKD, the STOP ACEi trial showed no benefit and a trend toward more ESKD events with discontinuation.
  • •Add an SGLT2 inhibitor (dapagliflozin 10 mg, empagliflozin 10 mg, or canagliflozin 100 mg daily) for CKD with eGFR ≥20-25 mL/min/1.73 m² and UACR ≥200 mg/g, irrespective of diabetes status. DAPA-CKD reported a 39% reduction in the primary composite (≥50% eGFR decline, ESKD, or renal/CV death; NNT 19). An early eGFR dip >10% is benign and predicts slower long-term decline. Continue until eGFR <20 mL/min/1.73 m² or dialysis initiation.
  • •Add finerenone 10-20 mg daily (10 mg if eGFR ≥60, 20 mg if eGFR <60) for CKD with type 2 diabetes and albuminuria (UACR ≥30 mg/g, eGFR ≥25). In FIDELIO-DKD the kidney composite was reduced by 18% (HR 0.82); in FIGARO-DKD the CV composite was reduced by 13% (HR 0.87). Hyperkalemia >5.5 mmol/L occurs in 21.4% vs 9.2% but rarely leads to discontinuation (2.3% vs 0.9%). Consider combining with an SGLT2i for additive albuminuria reduction (CONFIDENCE trial: 29% greater UACR reduction vs finerenone alone).
  • •Consider semaglutide 1.0 mg subcutaneously weekly for CKD with type 2 diabetes and albuminuria. The FLOW trial showed a 24% reduction in major kidney disease events (HR 0.76) and a 20% reduction in all-cause mortality. Tirzepatide is emerging as an alternative with similar renal benefits. GLP-1 RA benefits appear additive to SGLT2i.
  • •Target systolic BP <120 mmHg in patients with CKD and hypertension based on SPRINT (HR 0.72 for all-cause death). Achieve with RAASi plus calcium channel blockers or thiazide-like diuretics as needed. Dietary sodium restriction to <2 g/day is essential.
  • •Manage hyperkalemia to preserve RAASi and nsMRA therapy: use sodium zirconium cyclosilicate 5 g PO TID for 48 hours then 5 mg once daily, or patiromer 4.2 g BID (titrate to max 8.4 g BID). SGLT2i also reduce hyperkalemia risk (HR 0.74 vs DPP-4i). Do not discontinue RAASi for mild hyperkalemia, this increases mortality (HR 1.47).
  • •Correct metabolic acidosis (serum bicarbonate <22 mmol/L) with oral sodium bicarbonate 0.5-1.0 mEq/kg/day (e.g., 650 mg tabs, 1-3 tabs TID). A meta-analysis of 14 RCTs showed improved eGFR slope and reduced hospitalizations (OR 0.37). Avoid overcorrection; monitor for volume overload and hypertension.
  • •Treat anemia of CKD when Hb <10 g/dL with erythropoiesis-stimulating agents (target Hb 10-12 g/dL) plus intravenous iron to maintain ferritin 400-600 μg/L. Consider roxadustat 70 mg thrice weekly as an oral alternative, it raised Hb by 1.75 g/dL and reduced transfusion risk by 63%.
  • •Manage CKD-mineral bone disease: restrict dietary phosphate (to <800-1000 mg/day), use phosphate binders (calcium acetate, sevelamer, or lanthanum) when serum phosphate is elevated. Use active vitamin D analogs (calcitriol or paricalcitol) and calcimimetics (cinacalcet) to control secondary hyperparathyroidism. Target PTH 2-9 times the upper limit of normal.
  • •Recommend a plant-dominant, low-sodium diet (increased vegetables, fruits, legumes, whole grains), regular exercise (≥150 minutes/week of moderate activity), smoking cessation, and avoidance of nephrotoxins (NSAIDs, aminoglycosides, aristolochic acid, high-dose PPIs). Weight management is important in obesity.
  • •For disease-specific therapy: in IgA nephropathy, add SGLT2i and consider sparsentan 200-400 mg daily or nefecon 16 mg daily for high-risk patients. In ADPKD, start tolvaptan when eGFR >25 and rapid progression is documented. In lupus nephritis or ANCA vasculitis, use immunosuppression (cyclophosphamide, rituximab, mycophenolate) per KDIGO guidelines.
  • •Refer to nephrology when eGFR <30 mL/min/1.73 m², persistent UACR >300 mg/g, rapidly progressive disease, diagnostic uncertainty, or complications requiring specialist management (resistant hypertension, refractory hyperkalemia, severe anemia, CKD-MBD).
  • •Prepare for renal replacement therapy when eGFR declines to 15-20 mL/min/1.73 m² with symptoms, not based on a fixed eGFR threshold (IDEAL trial). Discuss modalities: hemodialysis, peritoneal dialysis, and preemptive kidney transplantation. Create a KDOQI Life-Plan for vascular access, AVF is preferred but individualize based on maturation probability.
  • •What NOT to do: avoid NSAIDs in any stage of CKD; do not discontinue RAASi for hyperkalemia without trying potassium binders first; do not target Hb >12 g/dL with ESAs (increases stroke risk); do not initiate statin therapy de novo in dialysis-dependent CKD; do not use race in eGFR equations.
  • •For hyperkalemia emergencies: first give calcium gluconate 1 g IV over 2-5 minutes for cardiac protection if K+ >6.5 or ECG changes, then regular insulin 10 units IV plus D50W 25 g IV, plus albuterol 10-20 mg nebulized. For sustained removal: SZC or patiromer. Escalate to emergent hemodialysis if K+ >6.5 mmol/L despite medical therapy (AEIOU criteria).

Board Review — High Yield

  • •KDIGO CGA staging - Classify every CKD patient by cause, GFR (G1-G5), and albuminuria (A1-A3); the combination predicts risk of progression and mortality.
  • •Albuminuria (UACR ≥30 mg/g) - An independent, log-linear predictor of cardiovascular and all-cause mortality with no threshold; as important as eGFR for risk stratification.
  • •SGLT2 inhibitors - Reduce kidney disease progression by 37% and cardiovascular death in CKD regardless of diabetes; continue until eGFR <20 or dialysis.
  • •Finerenone (nonsteroidal MRA) - Reduces CKD progression and CV events in T2DM with albuminuria; additive albuminuria reduction when combined with SGLT2i.
  • •Hyperkalemia management - Do NOT stop RAASi/nsMRA for hyperkalemia; instead use potassium binders (SZC or patiromer) to maintain cardiorenal protection.
  • •Cystatin C confirmatory testing - Order in patients with eGFRcr 45-59 and no albuminuria; up to 17% will reclassify as having no CKD.
  • •AKI-to-CKD transition - Even mild AKI (stage 1, <3 days) increases future CKD risk (HR 8.8); mandates structured follow-up including eGFR and UACR.
  • •Metabolic acidosis correction - Serum bicarbonate <22 mmol/L accelerates progression; treat with oral sodium bicarbonate to preserve eGFR and reduce hospitalizations.
  • •Anemia target - Treat when Hb <10 g/dL, target 10-12 g/dL; higher targets increase stroke risk without CV benefit.
  • •Remission paradigm - Aim for eGFR slope <1 mL/min/1.73 m²/yr or normalized albuminuria with preserved eGFR; increasingly achievable with early quadruple therapy.

Deep Dive — Evidence Details

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