One-liner#

CKD management requires accurate staging (eGFR + albuminuria), identifying and treating reversible causes, slowing progression (BP control, ACE-I/ARB, SGLT2i), avoiding nephrotoxins, and preparing for renal replacement therapy when eGFR approaches 15-20.

Quick nav#

• Definition and epidemiology
• Pathophysiology
• Clinical presentation
• Diagnostic workup
• Treatment
• Patient education
• Prognosis and monitoring
• Special populations
• When to refer
• Smartphrase snippets
• Related pages

Definition and epidemiology#

Diagnostic criteria#

CKD is defined as (KDIGO 2012):

• Abnormalities of kidney structure or function present for >3 months
• With implications for health

Requires one of the following for ≥3 months:

• eGFR <60 mL/min/1.73m² (with or without markers of kidney damage)
• Markers of kidney damage (with or without decreased eGFR):
  • Albuminuria (UACR ≥30 mg/g)
  • Urine sediment abnormalities (hematuria, RBC casts)
  • Electrolyte abnormalities due to tubular disorders
  • Structural abnormalities on imaging
  • History of kidney transplantation

CKD Staging by eGFR (GFR categories):

Albuminuria categories:

Complete staging requires both GFR category AND albuminuria category (e.g., “CKD G3bA2”)

Epidemiology#

CKD affects approximately 15% of US adults (37 million people). Only 10% of those with CKD are aware of their diagnosis. Leading causes: diabetes (44%), hypertension (29%), glomerulonephritis (7%). Risk factors include diabetes, hypertension, cardiovascular disease, obesity, age >60, family history of kidney disease, Black or Hispanic ethnicity, and history of AKI. CKD is a major risk factor for cardiovascular disease—patients with CKD are more likely to die from CVD than progress to ESKD.

Pathophysiology#

Mechanism (clinical understanding)#

Nephron loss and hyperfiltration: Regardless of initial cause, CKD involves progressive nephron loss. Remaining nephrons compensate by hyperfiltrating, which initially maintains GFR but causes further glomerular damage over time. This explains why CKD often progresses even after the initial insult is removed.

Key pathways of progression:

• Glomerular hypertension: Increased pressure damages glomeruli; ACE-I/ARB reduce this pressure
• Proteinuria: Filtered protein is directly toxic to tubular cells; reducing proteinuria slows progression
• RAAS activation: Angiotensin II causes vasoconstriction, fibrosis, and inflammation
• Inflammation and fibrosis: Common final pathway leading to scarring and nephron loss

Metabolic consequences of CKD:

• Decreased erythropoietin: Anemia (typically normocytic, normochromic)
• Decreased 1,25-vitamin D activation: Hypocalcemia, secondary hyperparathyroidism, bone disease
• Decreased phosphorus excretion: Hyperphosphatemia, vascular calcification
• Decreased acid excretion: Metabolic acidosis
• Decreased potassium excretion: Hyperkalemia (especially with ACE-I/ARB)
• Decreased sodium/water excretion: Volume overload, hypertension

Why SGLT2 inhibitors work: SGLT2 inhibitors reduce glomerular hyperfiltration by restoring tubuloglomerular feedback. They also reduce inflammation, fibrosis, and have direct cardioprotective effects. Benefits are independent of diabetes status.

How to explain to patients#

Your kidneys are filters that clean your blood and remove waste through your urine. When you have chronic kidney disease, these filters are damaged and do not work as well as they should.

Think of your kidneys like a coffee filter. When the filter is damaged, it cannot do its job properly. Waste builds up in your blood, and important things like protein leak through into your urine.

The good news is that we can slow down kidney disease with medications and lifestyle changes. The most important things are controlling your blood pressure, taking your kidney-protecting medications, and avoiding things that can hurt your kidneys further.

Your kidneys also do other important jobs like making hormones for red blood cells and keeping your bones healthy. As kidney disease progresses, we may need to treat these problems too.

Clinical presentation#

Characteristic symptoms#

Early CKD (stages 1-3a): Usually asymptomatic

• Detected on routine labs (elevated creatinine, abnormal UA)
• May have symptoms of underlying cause (diabetes, hypertension)

Moderate CKD (stages 3b-4):

• Fatigue (anemia, uremia)
• Nocturia (loss of concentrating ability)
• Edema (sodium retention)
• Foamy urine (proteinuria)
• Decreased appetite
• Difficulty concentrating

Advanced CKD (stage 5/uremia):

• Severe fatigue, weakness
• Nausea, vomiting, anorexia
• Metallic taste, uremic fetor (ammonia breath)
• Pruritus (uremic itch)
• Restless legs
• Sleep disturbances
• Cognitive impairment
• Pericarditis (late finding—indication for urgent dialysis)
• Bleeding tendency (platelet dysfunction)

Physical exam findings#

Vital signs:

• Hypertension (present in 80-85% of CKD patients)
• May have orthostatic hypotension if volume depleted

Volume status:

• Edema (peripheral, periorbital)
• Elevated JVP
• Pulmonary crackles (volume overload)

Skin:

• Pallor (anemia)
• Uremic frost (rare; late finding—crystallized urea on skin)
• Excoriations (pruritus)
• Easy bruising

Cardiovascular:

• S3 or S4 gallop
• Pericardial friction rub (uremic pericarditis—emergency)

Neurologic:

• Asterixis (uremic encephalopathy)
• Peripheral neuropathy
• Restless legs

Red flags#

• Rapid decline in eGFR (>5 mL/min/year or >25% decline in 3 months): evaluate for reversible causes
• New or worsening proteinuria: may indicate active glomerular disease
• Hematuria with RBC casts: suggests glomerulonephritis
• Pericardial friction rub: uremic pericarditis—urgent dialysis indication
• Severe hyperkalemia (K >6.5 or ECG changes): medical emergency
• Severe metabolic acidosis (HCO3 <12): may need urgent dialysis
• Uremic encephalopathy (confusion, asterixis): urgent dialysis indication
• Pulmonary edema refractory to diuretics: may need urgent dialysis

Diagnostic workup#

Initial evaluation#

Confirm CKD (requires abnormality present for >3 months):

• Serum creatinine and eGFR: Use CKD-EPI equation (most accurate); repeat in 3 months if new finding
• Urine albumin-to-creatinine ratio (UACR): Spot urine; repeat to confirm if elevated
• Urinalysis with microscopy: Hematuria, proteinuria, casts

Identify cause:

• History: Diabetes, hypertension, NSAIDs, family history of kidney disease, prior AKI
• Renal ultrasound: Kidney size (small = chronic), asymmetry, obstruction, cysts, masses
• Diabetes workup: A1c if not known diabetic
• Serologies if glomerulonephritis suspected: ANA, C3/C4, ANCA, anti-GBM, hepatitis B/C, HIV

Assess complications:

• CBC: Anemia (typically develops when eGFR <45)
• BMP: Potassium, bicarbonate, calcium
• Phosphorus: Elevated in CKD stages 4-5
• PTH: Secondary hyperparathyroidism (check when eGFR <45)
• 25-OH vitamin D: Deficiency common; treat if low
• Iron studies: Ferritin, TSAT (iron deficiency common with anemia)

Confirmatory testing#

Renal ultrasound (order for all new CKD diagnoses):

• Normal kidney size: 9-12 cm
• Small kidneys (<9 cm): chronic, irreversible damage
• Asymmetric kidneys: consider renal artery stenosis, reflux nephropathy
• Hydronephrosis: obstruction
• Cysts: polycystic kidney disease if multiple bilateral
• Increased echogenicity: chronic parenchymal disease

When to consider kidney biopsy (nephrology decision):

• Unexplained CKD (no diabetes, hypertension, or other clear cause)
• Nephrotic-range proteinuria (>3.5 g/day)
• Active urine sediment (RBC casts, dysmorphic RBCs)
• Rapidly progressive decline
• Suspected glomerulonephritis

Specialized testing (nephrology-directed):

• SPEP/UPEP: if multiple myeloma suspected
• Complement levels (C3, C4): glomerulonephritis workup
• ANCA, anti-GBM: vasculitis workup
• Hepatitis B/C, HIV: associated glomerular diseases

When to refer for specialist workup#

• eGFR <30 (stage 4-5): nephrology co-management
• Rapidly declining eGFR (>5 mL/min/year)
• Significant proteinuria (UACR >300 mg/g or protein/creatinine ratio >500 mg/g)
• Active urine sediment (RBC casts, dysmorphic RBCs)
• Unexplained CKD (no clear cause)
• Difficult-to-control hypertension or hyperkalemia
• Suspected glomerulonephritis or systemic disease
• Hereditary kidney disease (e.g., ADPKD)
• Recurrent nephrolithiasis

What NOT to order#

• Routine kidney biopsy: This is a nephrology decision based on specific indications
• 24-hour urine collection for protein: Spot UACR is sufficient for most purposes
• Cystatin C routinely: Use if eGFR accuracy is questioned (extremes of muscle mass)
• Renal artery imaging without clinical suspicion: Not routine for CKD workup
• Repeat imaging if prior ultrasound showed chronic changes: Unlikely to change management

Treatment#

Goals of therapy#

Primary goals:

• Slow CKD progression: Target <3-5 mL/min/year decline in eGFR
• Reduce cardiovascular risk: CKD patients die more often from CVD than ESKD
• Manage complications: Anemia, bone disease, acidosis, hyperkalemia
• Prepare for renal replacement therapy: When eGFR approaches 15-20

BP targets (KDIGO 2021):

• Target SBP <120 mmHg if tolerated (based on SPRINT)
• Individualize in elderly, orthostatic hypotension, or high fall risk

Proteinuria targets:

• Reduce UACR by ≥30% from baseline
• Lower is better; proteinuria reduction correlates with slower progression

Non-pharmacologic management#

Pharmacologic management#

RAAS blockade (cornerstone of CKD management):

SGLT2 inhibitors (add to ACE-I/ARB for additional protection):

Diuretics (for volume management):

Potassium management:

Anemia management (typically nephrology-directed in advanced CKD):

Bone and mineral management:

Metabolic acidosis:

Patient counseling points#

For ACE-I/ARB:

• “This medication protects your kidneys by reducing pressure inside them. It’s one of the most important medications for slowing kidney disease.”
• “We’ll check your blood tests 1-2 weeks after starting. A small rise in creatinine is expected and okay—it means the medicine is working.”
• “Call if you develop swelling of your lips or tongue, or a severe dry cough.”

For SGLT2 inhibitors:

• “This medication provides extra protection for your kidneys and heart, even if you don’t have diabetes.”
• “You may urinate more at first. Drink enough fluids to avoid dehydration.”
• “Watch for signs of urinary or genital yeast infections—itching, burning, or discharge. These are treatable.”
• “If you feel very sick, especially with nausea and vomiting, stop the medication and call us.”

For dietary changes:

• “Limiting salt is one of the most important things you can do. Most salt comes from processed and restaurant foods.”
• “You don’t need to severely restrict protein unless your kidney disease is very advanced. Aim for moderate portions.”
• “If your potassium is high, we’ll give you a list of high-potassium foods to limit.”

Monitoring and follow-up#

Monitoring frequency by CKD stage:

What to monitor:

Patient education#

What is this condition?#

Chronic kidney disease means your kidneys are not working as well as they should. Your kidneys filter waste from your blood and remove it in your urine. When they are damaged, waste can build up in your body.

Kidney disease is measured in stages from 1 to 5. Stage 1 is mild damage with normal filtering. Stage 5 means the kidneys are barely working and you may need dialysis or a transplant.

The most common causes are diabetes and high blood pressure. These conditions damage the tiny blood vessels in your kidneys over time.

The good news is that kidney disease often progresses slowly, and there is a lot we can do to slow it down or even stop it from getting worse.

What you can do#

Take your blood pressure and kidney-protecting medications every day. These are the most important treatments for slowing kidney disease.

Limit salt in your diet. Aim for less than 2000 mg of sodium per day. Avoid processed foods, canned soups, and fast food. Read nutrition labels.

Avoid medications that can hurt your kidneys. Do not take ibuprofen (Advil, Motrin) or naproxen (Aleve) unless your doctor says it is okay. Acetaminophen (Tylenol) is usually safe.

Stay hydrated, but do not overdo it. Drink when you are thirsty. If you have swelling, you may need to limit fluids.

If you have diabetes, keep your blood sugar well controlled. High blood sugar damages your kidneys.

Do not smoke. Smoking makes kidney disease worse and increases your risk of heart disease.

When to seek care#

Call your doctor if you have new or worsening swelling in your legs, feet, or face.

Call your doctor if you have significant decrease in how much you urinate.

Call your doctor if you have nausea, vomiting, or loss of appetite that does not go away.

Call your doctor if you feel very tired, weak, or confused.

Go to the emergency room if you have chest pain, severe shortness of breath, or cannot urinate at all.

Questions to ask your doctor#

What stage is my kidney disease? How fast is it progressing?

What caused my kidney disease? Can we treat the cause?

What medications should I avoid?

Should I see a kidney specialist (nephrologist)?

What are my options if my kidneys fail? When should we start planning for dialysis or transplant?

Prognosis and monitoring#

Expected course#

Progression rates:

• Average eGFR decline: 1-2 mL/min/year in general population
• With diabetes or proteinuria: 3-5 mL/min/year without treatment
• With optimal treatment (ACE-I/ARB + SGLT2i + BP control): can slow to <2 mL/min/year

Risk of progression to ESKD:

• Depends on eGFR, proteinuria, and underlying cause
• KFRE (Kidney Failure Risk Equation) predicts 2- and 5-year risk of ESKD
• Higher proteinuria = faster progression

Cardiovascular risk:

• CKD is a coronary artery disease equivalent
• Patients with CKD G3-5 have 2-3x higher CV mortality than general population
• Most CKD patients die from CVD before reaching ESKD

Factors predicting faster progression:

• Higher proteinuria (strongest predictor)
• Lower baseline eGFR
• Uncontrolled hypertension
• Diabetes with poor glycemic control
• Smoking
• Recurrent AKI episodes
• African American race

Monitoring parameters#

Complications to watch for#

Cardiovascular:

• Accelerated atherosclerosis
• Heart failure (volume overload, uremic cardiomyopathy)
• Arrhythmias (hyperkalemia)
• Pericarditis (uremia—dialysis indication)

Hematologic:

• Anemia (decreased erythropoietin)
• Bleeding tendency (platelet dysfunction)

Bone and mineral:

• Secondary hyperparathyroidism
• Renal osteodystrophy
• Vascular calcification

Metabolic:

• Hyperkalemia
• Metabolic acidosis
• Hyperphosphatemia
• Hypocalcemia

Neurologic:

• Uremic encephalopathy
• Peripheral neuropathy
• Restless legs syndrome

Other:

• Malnutrition (uremic anorexia)
• Pruritus
• Increased infection risk

Special populations#

Elderly/geriatric#

Diagnosis considerations:

• eGFR naturally declines with age (~1 mL/min/year after age 40)
• Isolated low eGFR (G3a) without proteinuria in elderly may represent normal aging
• Cystatin C-based eGFR may be more accurate (less affected by muscle mass)

Treatment considerations:

• Benefits of ACE-I/ARB and SGLT2i still apply in elderly
• Start at lower doses; titrate more slowly
• Higher risk of hyperkalemia—monitor more frequently
• Higher risk of AKI with volume depletion—counsel on sick day rules
• BP targets may be less aggressive if orthostatic hypotension or falls

Beers criteria considerations:

• NSAIDs: avoid in CKD (nephrotoxic, worsen hypertension)
• Metformin: adjust dose or avoid based on eGFR
• Many medications require dose adjustment—review all prescriptions

Dialysis decisions:

• Consider goals of care and life expectancy
• Conservative management (no dialysis) is a valid option for frail elderly
• Discuss advance directives early

Chronic kidney disease#

This section addresses medication adjustments for patients with CKD who have other conditions. Since this IS the CKD problem page, the medication adjustments throughout this document already account for renal function.

Common medications requiring adjustment in CKD:

Contrast dye considerations:

• Risk of contrast-induced AKI increases with lower eGFR
• Hold metformin before and 48 hours after contrast
• Ensure adequate hydration
• Use lowest effective contrast volume
• Avoid repeat contrast within 48-72 hours

Other populations#

Diabetes:

• Diabetes is the leading cause of CKD
• Tight glycemic control (A1c <7%) slows progression in early CKD
• Less aggressive A1c targets (7.5-8%) in advanced CKD (hypoglycemia risk)
• SGLT2 inhibitors: dual benefit for diabetes and CKD
• GLP-1 agonists: cardiovascular and possible renal benefits

Heart failure:

• CKD and HF commonly coexist (cardiorenal syndrome)
• SGLT2 inhibitors benefit both conditions
• ACE-I/ARB: use for both; accept Cr rise up to 30%
• Diuretics: may need higher doses; monitor for over-diuresis
• Coordinate care between cardiology and nephrology

Polypharmacy:

• Review all medications for renal dosing
• Avoid nephrotoxins (NSAIDs, aminoglycosides, certain herbals)
• Drug interactions: ACE-I + K supplements + K-sparing diuretics = hyperkalemia
• Simplify regimens when possible
• Medication reconciliation at every visit

When to refer#

Specialist referral criteria#

Nephrology referral indications:

Urgency levels#

Smartphrase snippets#

CKD, stable: CKD stage [G3a/G3b/G4] (eGFR [X]) due to [diabetes/HTN/unknown], stable. On lisinopril [dose] and dapagliflozin 10 mg with BP at goal. Continue current regimen; recheck BMP and UACR in [3-6] months.

CKD, starting SGLT2i: CKD stage [X] with proteinuria. Adding dapagliflozin 10 mg daily for renal and cardiovascular protection. Counseled on volume depletion and sick day rules; recheck BMP in 2-4 weeks.

CKD, nephrology referral: CKD stage 4 (eGFR [X]) with [indication]. Referring to nephrology for co-management and RRT planning. Patient counseled on importance of follow-up.

CKD, medication adjustment: CKD stage [X] (eGFR [X]). Reviewed medications for renal dosing and [adjusted/held] [medication]. Counseled to avoid NSAIDs; recheck BMP in [timeframe].

Related pages#

• Edema (complaint) — CKD causes edema through sodium retention
• Hypertensive Urgency (complaint) — CKD is both cause and consequence of hypertension
• Hematuria (complaint) — hematuria workup may reveal CKD
• Flank Pain (complaint) — obstructive uropathy can cause CKD
• Hypertension (problem) — HTN causes CKD; CKD worsens HTN; shared management
• Heart Failure (problem) — cardiorenal syndrome; SGLT2i benefits both
• Type 2 Diabetes (problem) — diabetes is leading cause of CKD; shared medications
• Benign Prostatic Hyperplasia (problem) — obstructive uropathy from BPH can cause CKD