Renal/Urology · PANCE / PANRE

Chronic Kidney Disease (CKD)

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Persistent decline in GFR or kidney damage for ≥3 months, staged by eGFR and albuminuria.

Also known as: CKD, chronic renal insufficiency, chronic renal failure

Overview

Abnormalities of kidney structure or function present for >3 months with implications for health. Defined by eGFR <60 mL/min/1.73 m² OR markers of kidney damage (albuminuria ≥30 mg/g, urine sediment abnormalities, electrolyte/structural abnormalities, biopsy findings, or kidney transplant) lasting ≥3 months.

Epidemiology

Affects ~14% of US adults. Diabetes and hypertension cause >70% of cases. Black, Hispanic, and Native American populations have higher incidence and progression rates.

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Question 1RenalMedium
A 60-year-old male with diabetes mellitus, hypertension, and chronic kidney disease (CKD) stage 3 (eGFR 42) has a creatinine of 1.8 and is starting an ACE inhibitor (ACEi). Creatinine rises to 2.1 (17% increase) over 2 weeks. Potassium is 4.8. He is otherwise well. Which of the following is the most appropriate next step?
  • ADiscontinue the ACE inhibitor
  • BSwitch the ACE inhibitor to amlodipine
  • CHalve the ACE inhibitor dose
  • DContinue the ACE inhibitor and monitor
Reveal answer & full explanation
Correct answer: D — Continue the ACE inhibitor and monitor
  • ADiscontinue the ACE inhibitor
  • BSwitch the ACE inhibitor to amlodipine
  • CHalve the ACE inhibitor dose
  • DContinue the ACE inhibitor and monitor✓

Why Continue the ACE inhibitor and monitor is correct

  • ACE inhibitor (ACEi) and angiotensin receptor blocker (ARB) dilate the efferent arteriole, reducing glomerular hydraulic pressure and GFR acutely — this is the mechanism of long-term renoprotection (reduces hyperfiltration)
  • A creatinine rise of up to 30-35% from baseline is expected and acceptable
  • This patient has a 17% rise — within the acceptable range; continue ACEi if the creatinine rise plateaus below 30-35%
  • Potassium of 4.8 is normal and does not warrant stopping the ACEi

Why the others are wrong

  • A) Discontinue the ACE inhibitor — discontinuation is only warranted if creatinine rises above 30-35%, bilateral renal artery stenosis (RAS) is suspected, or hyperkalemia exceeds 5.5; none of those apply here
  • B) Switch the ACE inhibitor to amlodipine — switching abandons proven renoprotection for a 17% rise that is well within the acceptable threshold
  • C) Halve the ACE inhibitor dose — dose reduction is not indicated for an acceptable creatinine rise and would reduce the renoprotective benefit

Additional high-yield points

  • Stop ACEi/ARB if: creatinine rise above 30-35%, bilateral RAS suspected (bilateral RAS causes a dramatic GFR drop), or hyperkalemia above 5.5
  • Renoprotection evidence: ACEi/ARBs reduce proteinuria, slow chronic kidney disease (CKD) progression, and reduce end-stage renal disease (ESRD) risk in diabetes mellitus (DM) — renal benefits vastly outweigh the acceptable acute GFR decline
Question 2RenalMedium
A 50-year-old man with stage 3b chronic kidney disease (eGFR 38 mL/min/1.73 m2) and hypertension is started on lisinopril for proteinuria. Two weeks later his potassium has risen from 4.2 to 5.4 mEq/L and his serum creatinine from 1.7 to 2.0 mg/dL (an 18% increase). His blood pressure is 128/80 mm Hg and he is asymptomatic. Which of the following is the most appropriate management?
  • AContinue lisinopril
  • BDiscontinue lisinopril
  • CAdd furosemide
  • DIncrease the lisinopril dose
Reveal answer & full explanation
Correct answer: A — Continue lisinopril
  • AContinue lisinopril✓
  • BDiscontinue lisinopril
  • CAdd furosemide
  • DIncrease the lisinopril dose

Why Continue lisinopril is correct

  • This patient illustrates the expected hemodynamic response to ACE inhibition in chronic kidney disease: a creatinine rise up to 30% and a potassium up to 5.5 mEq/L are acceptable and do not warrant stopping the drug
  • His creatinine rose only 18% (from 1.7 to 2.0 mg/dL) and his potassium is 5.4 mEq/L — both within tolerable thresholds
  • He remains asymptomatic with controlled blood pressure (128/80 mm Hg)
  • Continue lisinopril with dietary potassium restriction, recheck labs in 2-3 weeks, and add a potassium binder if potassium exceeds 5.5; renoprotective and cardiovascular benefits are preserved

Why the others are wrong

  • Discontinue lisinopril — reserved for refractory hyperkalemia above 5.5, a creatinine rise greater than 30% (suggesting bilateral renal artery stenosis or AKI), or symptomatic hypotension — none present (premature closure)
  • Add furosemide — can worsen volume depletion and precipitate acute kidney injury in this euvolemic, normotensive patient (right-concept-wrong-patient)
  • Increase the lisinopril dose — premature before electrolytes and renal function stabilize; uptitration could push potassium into a dangerous range (anchoring on benefit)
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Risk factors

  • Diabetes mellitus (leading cause)
  • Hypertension (second leading cause)
  • Glomerulonephritis, polycystic kidney disease, recurrent AKI
  • Age >60, family history, obesity, smoking, nephrotoxin exposure
  • APOL1 high-risk genotype (African ancestry)

Pathophysiology

Progressive nephron loss triggers compensatory hyperfiltration in surviving glomeruli → glomerular hypertension, sclerosis, and tubulointerstitial fibrosis. Activation of the renin-angiotensin-aldosterone system, oxidative stress, and inflammatory cytokines accelerate decline. Loss of functional mass impairs erythropoietin production, vitamin D activation, acid-base homeostasis, and phosphate excretion.

Clinical presentation

Symptoms

  • Often asymptomatic until advanced (stage 4-5)
  • Fatigue, weakness, anorexia, weight loss
  • Pruritus, restless legs, muscle cramps
  • Foamy urine (albuminuria), nocturia, peripheral edema
  • Late: dyspnea, nausea, confusion, bleeding

Signs / physical exam

  • Hypertension (cause and consequence)
  • Pallor (anemia of CKD), volume overload (edema, elevated JVP, crackles)
  • Uremic features: sallow skin, asterixis, pericardial rub
  • Diabetic retinopathy, peripheral neuropathy supportive of diabetic etiology

Classic findings

Small echogenic kidneys on ultrasound (except in diabetes, amyloid, HIV-associated nephropathy, and PKD where kidneys may be normal or enlarged).

Differential diagnosis

  • Acute kidney injury — Abrupt onset (<3 months), often reversible; baseline labs critical to distinguish — small echogenic kidneys favor CKD
  • Diabetic nephropathy — Long-standing diabetes, retinopathy, gradual albuminuria progression; biopsy shows Kimmelstiel-Wilson nodules
  • Hypertensive nephrosclerosis — Long-standing HTN, minimal proteinuria, small bilateral kidneys, no active sediment
  • Glomerulonephritis (chronic) — Persistent proteinuria, hematuria, active sediment; biopsy diagnostic
  • Polycystic kidney disease — Family history, enlarged kidneys with cysts on imaging, extrarenal cysts
  • Obstructive uropathy — Hydronephrosis on US, history of stones, BPH, or pelvic malignancy
  • Multiple myeloma / monoclonal gammopathy — Anemia disproportionate to CKD stage, hypercalcemia, bone pain; SPEP/UPEP with free light chains

Diagnostic workup

Diagnostic criteria

CKD requires kidney damage OR eGFR <60 for ≥3 months. Staged G1-G5 by eGFR (G1 ≥90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 <15) and A1-A3 by UACR (A1 <30, A2 30-300, A3 >300 mg/g).

Labs

  • Serum creatinine with eGFR (CKD-EPI 2021 race-free equation)
  • Urine albumin-to-creatinine ratio (UACR) on spot sample — preferred over dipstick
  • Urinalysis with microscopy
  • BMP (K, HCO3, Ca, phosphate), CBC (anemia), albumin
  • Stage 3-5: PTH, 25-OH vitamin D, iron studies, lipid panel

Imaging

  • Renal ultrasound — assess size, echogenicity, cysts, obstruction

Diagnostic algorithm

StageeGFR (mL/min/1.73 m²)DescriptionAction
G1≥90Normal GFR with kidney damageTreat comorbidities, slow progression
G260-89Mild GFR decrease with damageEstimate progression
G3a45-59Mild-moderate decreaseEvaluate and treat complications
G3b30-44Moderate-severe decreaseEvaluate and treat complications
G415-29Severe GFR decreasePrepare for RRT, transplant referral
G5<15Kidney failureRRT if uremia present
KDIGO CKD staging by eGFR. Combine with albuminuria categories A1-A3 for full risk stratification.

Treatment

First-line

  • BP target <120/80 (KDIGO 2021); use validated office BP measurement
  • ACEi (lisinopril, ramipril, enalapril) or ARB (losartan, valsartan, irbesartan) — first-line for albuminuria or diabetes; reduces progression
  • SGLT2 inhibitor — dapagliflozin, empagliflozin, canagliflozin — for diabetic or non-diabetic CKD with eGFR ≥20 and UACR ≥200 (proven mortality and renal benefit)
  • Nonsteroidal MRA — finerenone — for type 2 diabetes with albuminuric CKD on maximal ACEi/ARB
  • Glycemic control: A1c 6.5-8% individualized; metformin safe down to eGFR 30
  • Statin therapy — atorvastatin, rosuvastatin — for all adults ≥50 with CKD or any age with diabetes/CVD

Second-line / adjunct

  • Anemia: iron repletion first; ESA (epoetin alfa, darbepoetin) when Hb <10 with caution to avoid >11.5
  • Mineral-bone disease: phosphate binders (sevelamer, lanthanum, calcium acetate), active vitamin D (calcitriol, paricalcitol), calcimimetics (cinacalcet, etelcalcetide)
  • Metabolic acidosis: sodium bicarbonate when HCO3 <22 (slows progression)
  • Hyperkalemia: dietary restriction, loop diuretic, potassium binder — patiromer, sodium zirconium cyclosilicate
  • Prepare for RRT at eGFR ~20: education, vascular access (AV fistula 6+ months in advance), transplant referral

Complications

  • Cardiovascular disease (leading cause of death in CKD)
  • Anemia (decreased EPO production)
  • CKD-mineral bone disease: hyperphosphatemia, low calcitriol, secondary hyperparathyroidism, renal osteodystrophy
  • Metabolic acidosis, hyperkalemia, hypocalcemia
  • Uremic complications: pericarditis, encephalopathy, platelet dysfunction
  • Progression to ESRD requiring dialysis or transplant

PANCE pearls

  • The 2021 CKD-EPI equation removed the race coefficient and is now the standard eGFR calculation in the US.
  • ACEi/ARB may cause an initial 30% Cr rise — this is acceptable and does not require discontinuation if K stable.
  • SGLT2 inhibitors are now first-line for CKD with proteinuria regardless of diabetes status (DAPA-CKD, EMPA-KIDNEY).
  • Avoid NSAIDs, gadolinium (eGFR <30), and excessive iodinated contrast in CKD.
  • Refer to nephrology at eGFR <30, rapid decline >5 mL/min/year, persistent UACR >300, or refractory complications.

References

  • KDIGO 2024 — KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease (Kidney Int 2024)
  • KDIGO 2021 BP — KDIGO 2021 Clinical Practice Guideline for the Management of Blood Pressure in CKD
  • DAPA-CKD — Dapagliflozin in Patients with Chronic Kidney Disease (Heerspink et al., NEJM 2020)
  • EMPA-KIDNEY — Empagliflozin in Patients with Chronic Kidney Disease (NEJM 2023)

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Commonly confused with

vs Acute Kidney Injury

Related Renal/Urology diagnoses

Acute Kidney Injury (AKI)End-Stage Renal Disease and DialysisNephrotic SyndromeNephritic SyndromeIgA NephropathyAcute Tubular Necrosis (ATN)Acute Interstitial Nephritis (AIN)Post-Streptococcal Glomerulonephritis (PSGN)Autosomal Dominant Polycystic Kidney Disease (ADPKD)Urolithiasis (Kidney Stones)Acute Cystitis (Uncomplicated UTI)Acute PyelonephritisRenal Cell Carcinoma (RCC)Bladder Cancer

Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.