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Chronic Kidney Disease (CKD)

Summary Table

Category	Key Features
Risk Factors	Diabetes mellitus, hypertension, age >60, family history of kidney disease, cardiovascular disease, obesity, recurrent AKI, chronic NSAID use, autoimmune disease, nephrolithiasis
Etiology	Diabetic nephropathy (#1), hypertensive nephrosclerosis (#2), glomerulonephritis, polycystic kidney disease, obstructive uropathy, chronic interstitial nephritis
Patient Presentation	Often asymptomatic in early stages; later: fatigue, edema, foamy urine, nocturia, pruritus, anorexia, nausea, dyspnea on exertion
Classic Physical Exam	Hypertension, peripheral edema, pallor (anemia), uremic frost (advanced), asterixis, pericardial friction rub (uremic pericarditis), Kussmaul respiration (acidosis)
Key Diagnostic Results	eGFR <60 mL/min/1.73m² for ≥3 months OR albuminuria (ACR ≥30 mg/g); small echogenic kidneys on ultrasound; normocytic anemia, hyperphosphatemia, hypocalcemia, elevated PTH, metabolic acidosis with high anion gap
Management	ACE inhibitor or ARB, SGLT2 inhibitor, BP target <120/80, finerenone (if diabetic), statin, dietary sodium and protein restriction, treat complications (anemia, mineral bone disease, acidosis, hyperkalemia), prepare for renal replacement therapy at G5
Keywords	"Bilateral small echogenic kidneys", "broad waxy casts", "anemia + bone pain + itching", "long-standing diabetes with proteinuria", "asterixis and pericardial rub", "albumin-to-creatinine ratio elevated for >3 months"

1. Pathophysiology

Chronic kidney disease is defined by structural or functional kidney abnormalities lasting longer than 3 months. The two diagnostic anchors are a sustained eGFR below 60 mL/min/1.73m² and markers of kidney damage such as albuminuria, hematuria, electrolyte abnormalities, or imaging abnormalities. The 3-month duration is what separates CKD from acute kidney injury, and exam vignettes will signal chronicity through prior labs, longstanding comorbidities, or imaging showing shrunken kidneys.

The dominant mechanism is progressive nephron loss triggered by an initial insult (hyperglycemia, sustained hypertension, immune-mediated glomerular injury, obstruction). Once a critical mass of nephrons is lost, the surviving nephrons undergo adaptive hyperfiltration, raising single-nephron GFR through afferent arteriolar dilation and efferent arteriolar constriction (driven by angiotensin II). This adaptation is initially helpful but causes glomerular hypertension, podocyte injury, proteinuria, and eventual glomerulosclerosis, perpetuating a self-amplifying cycle. This is why ACE inhibitors and ARBs (which dilate the efferent arteriole) and SGLT2 inhibitors (which restore tubuloglomerular feedback by increasing distal sodium delivery) slow progression independent of their glucose or BP effects.

The clinical syndrome reflects the kidney's lost regulatory functions. Excretory failure produces uremia, hyperkalemia, volume overload, and metabolic acidosis (failure to excrete the daily acid load and regenerate bicarbonate). Endocrine failure produces normocytic normochromic anemia (decreased erythropoietin from peritubular fibroblasts) and CKD mineral bone disease. The latter follows a stereotyped sequence: phosphate retention, decreased 1-alpha hydroxylation of vitamin D, hypocalcemia, and secondary hyperparathyroidism that drives osteitis fibrosa cystica. FGF-23 elevation is the earliest detectable abnormality, rising before phosphate or PTH change.

Cardiovascular complications dominate mortality. Patients with CKD are far more likely to die from cardiovascular disease than to reach dialysis. The mechanism combines accelerated atherosclerosis, vascular calcification (from disordered mineral metabolism), uremia-related cardiomyopathy, and chronic volume overload.

2. Classification and Clinical Manifestations

CKD Staging (KDIGO)

GFR Category	eGFR (mL/min/1.73m²)	Description
G1	≥90	Normal or high (CKD only if damage markers present)
G2	60 to 89	Mildly decreased (CKD only if damage markers present)
G3a	45 to 59	Mildly to moderately decreased
G3b	30 to 44	Moderately to severely decreased
G4	15 to 29	Severely decreased
G5	<15	Kidney failure

Albuminuria Categories

Category	ACR (mg/g)	Description
A1	<30	Normal to mildly increased
A2	30 to 300	Moderately increased
A3	>300	Severely increased (includes nephrotic range >2200 mg/g)

Clinical Manifestations by Stage

System	Manifestation	Stage Typically Appears
General	Fatigue, malaise	G3b onward
Cardiovascular	Hypertension, LVH, accelerated atherosclerosis, pericarditis	Hypertension early; pericarditis G5
Hematologic	Normocytic normochromic anemia, platelet dysfunction (uremic bleeding)	G3b to G4
Bone and mineral	Hyperphosphatemia, hypocalcemia, secondary hyperparathyroidism, osteitis fibrosa cystica, vascular calcification	G3a onward (FGF-23 earliest)
Acid-base and electrolytes	High anion gap metabolic acidosis, hyperkalemia	G3b to G4
Volume	Edema, pulmonary congestion	G4 to G5
Neurologic	Encephalopathy, asterixis, peripheral neuropathy, restless legs	G5 (uremia)
Dermatologic	Pruritus, uremic frost, calciphylaxis	G4 to G5
Gastrointestinal	Anorexia, nausea, metallic taste, uremic fetor	G5
Endocrine	Sexual dysfunction, infertility, insulin half-life prolongation (paradoxical hypoglycemia in diabetics)	G4 to G5

3. Diagnostic Workup

Test	Purpose	Finding
Serum creatinine + eGFR	Best initial test for kidney function	eGFR <60 mL/min/1.73m²
Urine albumin-to-creatinine ratio (ACR)	Best initial test for kidney damage	ACR ≥30 mg/g
Urinalysis with microscopy	Identify damage type	Broad waxy casts (chronicity), dysmorphic RBCs and RBC casts (glomerular), WBC casts (interstitial)
Renal ultrasound	Confirm chronicity, exclude obstruction	Bilaterally small echogenic kidneys (<9 cm); enlarged in diabetic nephropathy, amyloidosis, HIV nephropathy, polycystic kidney disease
Basic metabolic panel	Identify complications	Hyperkalemia, hyperphosphatemia, low bicarbonate
Calcium, phosphate, PTH, 25-OH vitamin D	Assess CKD mineral bone disease	Low Ca, high PO4, elevated PTH
CBC with iron studies	Assess anemia	Normocytic normochromic; check ferritin and TSAT before ESA
Lipid panel	Cardiovascular risk	Often dyslipidemia
Kidney biopsy	Most accurate for etiology when cause is unclear	Histologic diagnosis

The workup begins with documenting chronicity by the 3-month rule. Two confirmed measurements separated by at least 3 months are needed; a single low eGFR in an acutely ill patient is AKI, not CKD. The best initial functional test is the serum creatinine with calculated eGFR using the CKD-EPI 2021 equation (which removed the race coefficient). The best initial damage test is a spot urine ACR, preferred over a 24-hour collection because of convenience and accuracy. Together, these two values place the patient on the KDIGO heat map (G stage by A stage), which determines prognosis and follow-up frequency.

The next step is identifying chronicity with imaging. Renal ultrasound is ordered in nearly every CKD evaluation. Classic findings are bilaterally small (<9 cm) echogenic kidneys with cortical thinning. Note the high-yield exceptions where kidneys are large despite advanced disease: diabetic nephropathy (early), amyloidosis, HIV-associated nephropathy, and polycystic kidney disease. Ultrasound also rules out obstruction (hydronephrosis), which is reversible.

To determine etiology, the urinalysis is read like a forensic clue. Broad waxy casts indicate chronic tubular dilation and confirm chronicity. Dysmorphic red cells and red cell casts point to glomerulonephritis. Heavy proteinuria with lipiduria and oval fat bodies suggests nephrotic syndrome. In a patient with longstanding diabetes, retinopathy, and gradual proteinuria, the diagnosis is clinical and biopsy is unnecessary. Kidney biopsy is the most accurate test and is reserved for unclear etiology, suspected glomerulonephritis with active urine sediment, rapid decline in function, or significant proteinuria without an obvious cause.

Finally, every patient with G3a or worse needs a complications screen: hemoglobin, calcium, phosphate, PTH, 25-OH vitamin D, bicarbonate, and potassium. This is the testable triad of "what to order at the first CKD visit."

4. Management and Treatment

Intervention	Indication	Target / Dose
ACE inhibitor or ARB	Albuminuria (ACR ≥30) or hypertension in CKD	Titrate to maximum tolerated dose; accept up to 30% creatinine rise
SGLT2 inhibitor	CKD with eGFR ≥20 (with or without diabetes)	Dapagliflozin 10 mg daily; empagliflozin 10 mg daily
Finerenone	CKD with type 2 diabetes and albuminuria	10 to 20 mg daily based on eGFR and potassium
GLP-1 receptor agonist	Type 2 diabetes with CKD	Semaglutide standard dosing
Blood pressure control	All CKD	<120/80 mmHg per KDIGO 2021
Statin	Adults ≥50 with CKD; younger with risk factors	Moderate to high intensity
Sodium bicarbonate	Serum HCO3 <22 mmol/L	0.5 to 1 mEq/kg/day to keep HCO3 22 to 26
Iron + ESA	Hb <10 g/dL after iron repletion	Target Hb 10 to 11.5 (do not exceed 11.5)
Phosphate binder	Persistent hyperphosphatemia despite diet	Non-calcium binder preferred (sevelamer, lanthanum)
Vitamin D analog	Elevated PTH after correcting Ca/P/25-OH D	Calcitriol or paricalcitol
Dietary modification	All CKD	Sodium <2 g/day; protein 0.6 to 0.8 g/kg/day (non-dialysis)
Renal replacement therapy	G5 with uremic complications	Hemodialysis, peritoneal dialysis, or transplant

Management has two parallel tracks: slowing progression and treating complications.

The progression-slowing pillars are now considered the "four pillars" of cardio-renal protection. ACE inhibitors or ARBs remain the foundation for any patient with albuminuria or hypertension; they reduce intraglomerular pressure by dilating the efferent arteriole. Expect a creatinine rise up to 30% within 2 to 4 weeks, which is acceptable and reflects hemodynamic effect, not injury. Stop only if rise exceeds 30%, hyperkalemia is refractory, or the patient becomes pregnant. SGLT2 inhibitors are now first-line addition regardless of diabetes status; landmark trials (DAPA-CKD, EMPA-KIDNEY) showed reduction in progression even in non-diabetic CKD, and current indications start at eGFR 20 mL/min/1.73m². Finerenone, a non-steroidal mineralocorticoid receptor antagonist, adds further protection in patients with type 2 diabetes and albuminuria, with less hyperkalemia and gynecomastia than spironolactone. GLP-1 agonists complete the quartet for diabetic CKD. Aggressive blood pressure control (target <120/80 mmHg measured by standardized technique per KDIGO 2021) and statin therapy round out the regimen.

Complication management runs in parallel. Anemia of CKD is treated only after iron deficiency is corrected (target ferritin >100 and TSAT >20%). Once iron-replete, an erythropoiesis-stimulating agent is started when Hb is below 10 g/dL, with a target ceiling of 11.5 g/dL. Exceeding this ceiling increases stroke and thrombosis risk, a classic exam trap. Mineral bone disease is managed by sequencing: first restrict dietary phosphate, then add a phosphate binder taken with meals (non-calcium binders like sevelamer or lanthanum are preferred to limit vascular calcification), then correct vitamin D deficiency, and finally use an active vitamin D analog or calcimimetic (cinacalcet) for persistent hyperparathyroidism. Metabolic acidosis is treated with oral sodium bicarbonate when serum bicarbonate falls below 22 mmol/L; correcting acidosis itself slows CKD progression. Hyperkalemia is managed with dietary potassium restriction and newer binders (patiromer, sodium zirconium cyclosilicate), which often allow continuation of RAAS blockade.

Renal replacement therapy is initiated based on symptoms rather than a fixed eGFR threshold (in Indonesia it is suggested for all G5 patients). The mnemonic for absolute indications (urgent dialysis) is AEIOU: refractory Acidosis, refractory Electrolyte abnormalities (hyperkalemia), Intoxications (dialyzable toxins), refractory volume Overload (pulmonary edema), and Uremic complications (pericarditis, encephalopathy, bleeding). For non-urgent initiation, modality choice is shared decision-making between hemodialysis, peritoneal dialysis, and preemptive transplant. Vascular access planning (arteriovenous fistula creation) should occur 6 months before anticipated dialysis, ideally at G4. Kidney transplantation offers the best survival and quality of life, and preemptive transplant before dialysis is the optimal pathway.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It's Similar	Key Discriminator
Acute Kidney Injury (AKI)	Both show elevated creatinine and decreased GFR	AKI is <3 months; normal-sized kidneys on ultrasound; absence of anemia or mineral bone abnormalities; reversible course
Acute on chronic kidney disease	Patient has known CKD with sudden worsening	Look for triggering event (NSAIDs, contrast, sepsis, obstruction); creatinine returns toward baseline after correction
Pre-renal azotemia	Elevated creatinine and BUN	BUN:Cr ratio >20:1; FENa <1%; responds to volume; no chronicity markers
Obstructive uropathy	Elevated creatinine, can be chronic	Hydronephrosis on ultrasound; reversible with relief of obstruction; consider in elderly males with prostatic disease
Nephrotic syndrome	Edema and proteinuria	ACR usually >2200 mg/g, hypoalbuminemia, hyperlipidemia, lipiduria; CKD has lesser proteinuria unless diabetic
Heart failure	Edema, fatigue, dyspnea	BNP elevated; echocardiogram abnormal; kidney function preserved unless cardiorenal syndrome
Anemia of chronic disease	Normocytic anemia	Normal or elevated ferritin without iron deficiency, normal kidney function; CKD anemia tied to eGFR
Multiple myeloma	Elevated creatinine, anemia, bone pain in older adult	M-spike on SPEP, hypercalcemia (not hypocalcemia), lytic lesions, Bence Jones proteins; dipstick may miss light chains
Renal artery stenosis	Resistant hypertension, kidney dysfunction	Asymmetric kidney size, abdominal bruit, sudden creatinine rise after starting ACEi, flash pulmonary edema

6. Traps and High-Yield Pearls

The most common pitfall is mistaking AKI for CKD (or vice versa) when only a single creatinine value is given. The exam will tuck the discriminator into the history (longstanding diabetes, prior labs from years ago) or imaging (small echogenic kidneys, anemia, hyperparathyroidism). Always look for the chronicity package: small kidneys, normocytic anemia, and abnormal calcium-phosphate-PTH. If any of these are present, the picture is chronic. The reverse trap is the diabetic patient with enlarged kidneys despite advanced CKD; here the size will mislead a student into excluding chronic kidney disease, but diabetic nephropathy preserves or increases kidney size for years.

A second common error is starting an erythropoiesis-stimulating agent before checking iron studies, or pushing the hemoglobin target too high. Iron repletion comes first. Hemoglobin must stay at or below 11.5 g/dL; aiming for normal hemoglobin causes strokes and clotted access.

A third trap is mismanaging the predictable creatinine bump after starting an ACE inhibitor or ARB. A rise up to 30% is expected and reflects efferent arteriolar dilation. Stopping the drug at this point loses the long-term protective benefit. Stop the agent only when the rise exceeds 30%, when potassium climbs uncontrollably, or when bilateral renal artery stenosis is suspected (look for flash pulmonary edema, asymmetric kidneys, or an abdominal bruit).

A fourth trap is the timing of vascular access. Vignettes will describe a G4 patient and ask the next best step. The answer is referral to vascular surgery for arteriovenous fistula creation, not waiting for dialysis to become urgent. Catheter dialysis carries far higher infection and mortality risk than a matured fistula.

The final pearl concerns mineral bone disease sequencing. The earliest abnormality is elevated FGF-23, followed by phosphate retention, followed by hypocalcemia, and finally elevated PTH. When asked the first laboratory abnormality of CKD mineral bone disease, the answer is FGF-23 elevation, not hyperphosphatemia.

The core competencies tested across CKD vignettes are: separating acute from chronic kidney injury using duration and chronicity markers, applying the staging matrix to guide management, sequencing the four cardio-renal protective therapies, recognizing absolute indications for dialysis through the AEIOU framework, and avoiding the predictable management errors around RAAS blockade, ESA dosing, and access planning.Chronic Kidney Disease (CKD).

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