Step 2 CK · Internal Medicine · Nephrology

Chronic Kidney Disease

Name: Chronic Kidney Disease
Creator: Veli Bakalov, MD

Stage it, treat the complications, slow the decline

Nephrology·Chronic Kidney Disease & Renal Replacement·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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CKD = GFR <60 or kidney damage (albuminuria) for ≥3 months; diabetes is the leading cause, then hypertension, then glomerulonephritis.
GFR stages: G1 ≥90, G2 60–89, G3a 45–59, G3b 30–44, G4 15–29, G5 <15; albuminuria A1 <30, A2 30–300, A3 >300 mg/g.
ACEi or ARB is first-line for diabetic or albuminuric CKD; accept a creatinine rise up to ~30%, and never combine an ACEi with an ARB.
SGLT2 inhibitors slow CKD even without diabetes (DAPA-CKD, EMPA-KIDNEY); finerenone adds benefit in albuminuric diabetic CKD; target BP <130/80.
CKD anemia is low-EPO normocytic: ESA plus iron to hemoglobin ~10–11.5 g/dL; normalizing raises stroke and cardiovascular events.
CKD-MBD: high phosphate + low calcitriol → hypocalcemia → secondary hyperparathyroidism; phosphate restriction and non-calcium binders first, then active vitamin D and cinacalcet.
Treat metabolic acidosis with oral bicarbonate to HCO3 ≥22 (slows progression); manage hyperkalemia with diet, diuretics, and binders rather than reflexively stopping ACEi/ARB.
Diabetic nephropathy: Kimmelstiel-Wilson nodules; screen yearly with urine albumin-to-creatinine ratio and eGFR.
Start dialysis for uremic symptoms (pericarditis, encephalopathy, neuropathy) or refractory overload, K, or acidosis, not at a set GFR; AV fistula placed early; transplant is best.

Definition and staging

Three months makes it chronic. CKD is a GFR under 60 mL/min/1.73 m² or markers of kidney damage (albuminuria, abnormal sediment, imaging, or biopsy) persisting at least 3 months. Diabetes is the leading cause, followed by hypertension, then glomerulonephritis. Cardiovascular disease, not kidney failure, is the most common cause of death.

KDIGO GFR categories

Category	eGFR (mL/min/1.73 m²)	Description
G1	≥90	Normal GFR, counts only with kidney damage
G2	60–89	Mildly decreased, counts only with kidney damage
G3a / G3b	45–59 / 30–44	Moderate; complications begin to appear
G4	15–29	Severe; nephrology care and planning for dialysis or transplant
G5	<15	Kidney failure (ESRD)

Example: an eGFR of 40 is G3b.

Albuminuria. Stage the urine albumin-to-creatinine ratio as A1 (<30 mg/g, normal), A2 (30–300 mg/g, moderately increased; the old "microalbuminuria"), or A3 (>300 mg/g, severely increased). Albuminuria independently predicts progression and cardiovascular risk, and lower GFR combined with higher albuminuria multiplies both risks.

Slowing progression

Drugs that change the trajectory

Therapy	How it helps	Key points
ACE inhibitor or ARB	Dilates the efferent arteriole, lowering intraglomerular pressure and proteinuria	First-line in diabetic and albuminuric CKD; a creatinine rise up to ~30% is expected; never combine the two
SGLT2 inhibitor (dapagliflozin, empagliflozin)	Cuts renal and cardiovascular events	Works in diabetic and nondiabetic CKD (DAPA-CKD, EMPA-KIDNEY); add to ACEi/ARB
Finerenone	Nonsteroidal mineralocorticoid receptor antagonist	Extra benefit in diabetic CKD with albuminuria; watch potassium
Oral sodium bicarbonate	Corrects metabolic acidosis	Keep HCO₃⁻ ≥22 mEq/L; slows progression and limits muscle and bone catabolism

ACEi/ARB creatinine rule. Hold the drug only for a rise greater than about 30% or for hyperkalemia; the expected small bump reflects lower intraglomerular pressure, not injury.

Blood pressure and glucose. Target BP is generally under 130/80 mmHg, with an ACE inhibitor or ARB preferred when albuminuria is present. Tight blood pressure and glycemic control together slow the loss of GFR.

Protect what is left. Avoid NSAIDs and other nephrotoxins, dose renally cleared drugs for eGFR, stop metformin below an eGFR of 30, and avoid gadolinium in advanced CKD because of nephrogenic systemic fibrosis. Refer to nephrology once eGFR falls below 30.

Complications

Managing the predictable complications

Complication	Mechanism	Management
Anemia	Low erythropoietin; normocytic, normochromic	Exclude iron deficiency; ESA plus iron to hemoglobin ~10–11.5 g/dL
Mineral bone disease	Phosphate retention and low 1α-hydroxylation → low calcitriol → hypocalcemia → secondary hyperparathyroidism	Phosphate restriction and binders first, then active vitamin D and cinacalcet
Hyperkalemia	Impaired K excretion, worsened by oliguria, ACEi/ARB, low aldosterone	Dietary K restriction, loop or thiazide diuretic, binders (patiromer, sodium zirconium cyclosilicate), correct acidosis
Metabolic acidosis	Impaired acid excretion: normal gap early, high gap as GFR falls	Oral sodium bicarbonate to HCO₃⁻ ≥22

Do not normalize hemoglobin with ESAs: targets of 13 or more raised stroke, thrombosis, and cardiovascular events in trials (TREAT, CHOIR, CREATE).

Mineral bone disease in detail. FGF23 rises early to push phosphate out and further suppresses calcitriol. The result is renal osteodystrophy, from high-turnover osteitis fibrosa cystica to low-turnover adynamic bone when PTH is oversuppressed. Prefer non-calcium binders (sevelamer, lanthanum) and avoid aluminum binders, which cause dementia and osteomalacia. Control phosphate first; parathyroidectomy is reserved for refractory disease.

Potassium and ACE inhibitors. Do not automatically stop a beneficial ACEi or ARB for mild hyperkalemia; restrict dietary potassium and add a diuretic or binder first.

Diabetic nephropathy

The leading cause of ESRD. Early hyperfiltration gives way to progressive albuminuria and falling GFR. Pathology shows mesangial expansion, GBM thickening, and nodular glomerulosclerosis (Kimmelstiel-Wilson nodules). Kidneys are typically normal-sized or large despite advanced disease, and diabetic retinopathy usually coexists.

Screening and treatment. Screen yearly with a spot urine albumin-to-creatinine ratio and eGFR, starting at diagnosis in type 2 diabetes and 5 years after diagnosis in type 1. Treat with an ACE inhibitor or ARB, an SGLT2 inhibitor, and glycemic and BP control, adding finerenone for persistent albuminuria.

Dialysis and transplant

Symptoms, not a number. Start dialysis for uremic symptoms (encephalopathy with asterixis, pericarditis, neuropathy) or for volume overload, hyperkalemia, or acidosis refractory to medical therapy. Starting early at a fixed GFR showed no benefit (IDEAL).

Plan ahead. An arteriovenous fistula is the preferred long-term hemodialysis access; create it well before dialysis is needed so it can mature, and protect the arm veins from venipuncture and PICC lines. Kidney transplant offers the best survival and quality of life, ideally preemptively; waiting time can accrue once eGFR is 20 or below.