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Chronic Kidney Disease (CKD)

Basics

  • CKD: kidney damage or GFR <60 mL/min/1.73 mΒ² lasting β‰₯3 months.
  • KDIGO GFR Categories (mL/min/1.73 mΒ²):
  • G1: β‰₯90 (normal/increased)
  • G2: 60–89 (mild decrease)
  • G3a: 45–59 (mild-moderate decrease)
  • G3b: 30–44 (moderate-severe decrease)
  • G4: 15–29 (severe decrease)
  • G5: <15 (kidney failure/dialysis)
  • Albuminuria Categories:
  • A1: <30 mg/g (normal to mildly increased)
  • A2: 30–300 mg/g (moderately increased)
  • A3: >300 mg/g (severely increased)

Epidemiology

  • African Americans 3.6Γ— more likely to develop CKD.
  • ESRD incidence higher in males (1.6Γ—).
  • Annual incidence ~1700 per million population.
  • Overall CKD prevalence ~14.8%; ESRD prevalence 1,752 per million.
  • Prevalence increases with age; peaks after 70 years.

Etiology & Pathophysiology

  • Progressive nephron loss β†’ declining GFR, doubling serum creatinine when GFR halves.
  • Hyperkalemia develops when GFR <20–25 mL/min/1.73 mΒ².
  • Anemia from decreased erythropoietin.
  • Types:
  • Renal parenchymal/glomerular (nephritic, nephrotic, proliferative)
  • Vascular (HTN, vasculitis, thrombotic microangiopathies)
  • Interstitial tubular (infection, toxins, obstruction)
  • Postrenal (obstruction e.g., BPH, neoplasm)
  • Genetic causes: Alport, Fabry, sickle cell anemia, SLE, polycystic kidney disease.
  • Polymorphisms in podocyte myosin IIA gene increase risk in African Americans.

Risk Factors

  • Diabetes mellitus (types 1 and 2) – most common
  • Age >60 years
  • Low socioeconomic status
  • Obesity, smoking, drug use
  • Chronic infections (Hep B/C, HIV)
  • Cardiovascular disease (HTN, renal artery stenosis)
  • Nephrotoxic drugs (NSAIDs, lithium, aminoglycosides, etc.)
  • Congenital anomalies, obstructive uropathy

Prevention

  • USPSTF: insufficient evidence to recommend screening asymptomatic adults.

Diagnosis

History

  • Usually asymptomatic in stages 1–3.
  • Possible symptoms: oliguria, nocturia, polyuria, bone disease, edema, hypertension, fatigue, pruritus, nausea, anorexia, sexual dysfunction.

Physical Exam

  • Assess volume status: pallor, BP/orthostatic changes, edema, JVD, weight.
  • Skin: sallow complexion, uremic frost, ammonia odor.
  • Cardiovascular: murmurs, bruits, pericarditis, pleural effusions.
  • Neurologic: asterixis, confusion, seizures, peripheral neuropathy.
  • Prostate exam if indicated.

Diagnostic Tests

  • Estimated GFR by MDRD or CKD-EPI; Cockcroft-Gault for drug dosing.
  • Urinalysis: casts, proteinuria, electrolytes.
  • Renal ultrasound: first imaging to evaluate cysts, masses, hydronephrosis, kidney size.
  • Blood: anemia (normocytic normochromic), elevated BUN/Cr, hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, elevated PTH, low vitamin D, hypoalbuminemia.
  • Serology: ANA, dsDNA, ANCA, complements, anti-GBM, hepatitis B/C, HIV.
  • Serum/urine immunoelectrophoresis.
  • ECG for arrhythmias due to electrolyte imbalances.
  • Renal biopsy if indicated (hematuria, proteinuria, progressive disease).

Lab Alerts

  • Drugs affecting serum Cr: cimetidine, trimethoprim, cefoxitin, flucytosine.
  • Calcium channel blockers and RAAS inhibitors reduce proteinuria.

Treatment

Blood Pressure

  • Target SBP 120 mm Hg (CKD G1–G3).
  • Use ACE inhibitors or ARBs in diabetic and nondiabetic CKD with albuminuria >30 mg/day.
  • Avoid combined ACEI, ARB, DRI therapy.
  • Discontinue RAAS blockers during pregnancy.

Mineral Bone Disease

  • Monitor and treat hyperphosphatemia, hypocalcemia, vitamin D deficiency.
  • Use phosphate binders (sevelamer, lanthanum) in CKD stages 3–5.
  • Reserve calcimimetics for ESRD patients on dialysis.

Anemia

  • Iron supplementation Β± erythropoiesis-stimulating agents (ESA).
  • ESA if Hb 9–10 g/dL; goal Hb 10–11 g/dL (not >11.5 g/dL).

Hyperlipidemia

  • Statins targeting LDL <70 mg/dL.

Glycemic Control

  • HbA1c goal 6.5–8.0%; monitor glucose logs in advanced CKD.
  • Review/discontinue metformin if GFR <30.
  • SGLT2 inhibitors for CKD patients with/without diabetes (if GFR >30).

Metabolic Acidosis

  • Sodium bicarbonate if serum bicarb <22 mEq/L.

Pain Management

  • Avoid NSAIDs.
  • Use acetaminophen first-line.
  • Opioids (oxycodone, fentanyl, methadone) cautiously with dose adjustment.

Other

  • Avoid herbal supplements that increase K+ or phosphorus or interfere with drug metabolism.

Referral

  • Nephrology:
  • Urgent: GFR 15–29
  • Nonurgent: GFR 30–59 with comorbidities
  • Immediate: GFR <15
  • Rapid eGFR decline, heavy proteinuria, management of complications
  • Urology for hematuria, masses, nephrolithiasis, hydronephrosis.
  • Support services: dietitian, PT/OT, social work.

Additional Therapies

  • Aspirin for secondary CVD prevention.
  • Multidisciplinary care to optimize nutrition, pain, mobility, access.

Admission Considerations

  • Contrast imaging if eGFR >30; volume expansion before iodinated contrast.
  • Hold metformin before iodinated contrast; resume after 48 hours.

Follow-Up

  • Monitor BP, serum creatinine, potassium 2–4 weeks after RAAS initiation.
  • Monitor Hb annually or biannually depending on CKD stage.
  • Monitor calcium, phosphate, PTH starting CKD stage G3.
  • Annual eGFR and vitamin B12 in metformin users >4 years.
  • Monitor pregnant CKD patients closely.

Diet

  • Sodium restriction <2 g/day.
  • Limit potassium and phosphorus as indicated.
  • Protein restriction in CKD 3–5: 0.6 g/kg/day (nondiabetic), 0.8 g/kg/day (diabetic).
  • Mediterranean diet preferred.
  • Fluid restriction based on volume status.

Prognosis

  • CKD progresses with declining GFR.
  • Rapid progression: >5 mL/min/1.73 mΒ² GFR decline/year.

Complications

  • Hypertension, anemia, hyperparathyroidism, renal osteodystrophy.
  • Sleep disturbances, infections, malnutrition.
  • Electrolyte imbalances, platelet dysfunction, gout, sexual dysfunction.

Clinical Pearls:

  • ACE inhibitors and ARBs are first-line antihypertensives in CKD with albuminuria.
  • Nephrology referral thresholds based on GFR and proteinuria.
  • Dietary sodium restriction and protein limitation reduce progression.
  • Multidisciplinary management improves outcomes.