Chronic Kidney Disease

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Basics

Chronic kidney disease (CKD) is defined as structural or functional abnormalities of the kidney, as determined by either pathologic abnormalities or markers of damage (abnormalities in blood or urine tests, histology, imaging studies) or a glomerular filtration rate (GFR) <60 mL/min/1.73 m2. Findings present for ≥3 months. CKD is classified based on the cause, GFR category (G1 to G5), and albuminuria category (A1 to A3).

Description

  • Kidney Disease: Improving Global Outcomes (KDIGO) categories by GFR estimation (in mL/min/1.73 m2): G1: kidney damage with normal or increased GFR ≥90; G2: mild ↓ GFR 60 to 89; G3a: mild to moderate ↓ GFR 45 to 59; G3b: moderate to severe ↓ GFR 30 to 44; G4: severe ↓ GFR 15 to 29; G5: kidney failure: GFR <15 or dialysis
  • CKD per albumin-to-creatinine ratio (ACR) category: A1: normal to mildly increased: <30 mg/g or <3 mg/mmol; A2: moderately increased: 30 to 300 mg/g or 3 to 30 mg/mmol; A3: severely increased: >300 mg/g or >30 mg/mm

Epidemiology

  • African Americans are 3.6 times more likely to develop CKD than Caucasians.
  • Similar in both sexes; however, rate of end-stage renal disease (ESRD) is 1.6 times higher in males than females.

Incidence
Estimated annual incidence of 1,700/1 million population

Prevalence
Overall prevalence of CKD (stages 1 to 5) is 14.8%. Unadjusted prevalence and incidence rates of ESRD (stage 5) are 1,752 and 362.4/1 million, respectively. Numbers do not reflect the burden of earlier stages of CKD (stages 1 to 4), which are estimated to affect 13.1% of the population in the United States. Prevalence increases with age and peaks after 70.

Etiology and Pathophysiology

Progressive destruction of kidney nephrons; GFR will drop gradually, and plasma Cr values will approximately double, with 50% reduction in GFR and 75% loss of functioning nephrons mass. Hyperkalemia usually develops when GFR falls to <20 to 25 mL/min. Anemia develops from decreased renal synthesis of erythropoietin.

  • Renal parenchymal/glomerular
    • Nephritic: hematuria, red blood cell (RBC) casts, hypertension (HTN), variable proteinuria
      • Focal proliferative: IgA nephropathy, systemic lupus erythematosus (SLE), Henoch-Schönlein purpura, Alport syndrome, proliferative glomerulonephritis, crescentic glomerulonephritis
      • Diffuse proliferative: membranoproliferative glomerulonephritis, SLE, cryoglobulinemia, rapidly progressive glomerulonephritis (RPGN), Goodpasture syndrome
    • Nephrotic: proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, and edema
      • Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis
      • Amyloidosis, diabetic nephropathy
  • Vascular: HTN, thrombotic microangiopathies, vasculitis (Wegener), scleroderma, crush injury
  • Interstitial tubular: infections, obstruction, toxins, allergic interstitial nephritis, multiple myeloma, connective tissue disease, cystic disease, nephrolithiasis
  • Postrenal: obstruction (benign prostatic hyperplasia [BPH]), neoplasm, neurogenic bladder

Genetics

  • Alport syndrome, Fabry disease, sickle cell anemia, SLE, and autosomal dominant polycystic kidney disease can lead to CKD.
  • Polymorphisms in gene that encodes for podocyte nonmuscle myosin IIA are more common in African Americans than Caucasians and appear to increase risk for nondiabetic ESRD.

Risk Factors

Type 1 or 2 diabetes mellitus (DM) (most common), age > 60 years, low socioeconomic status, obesity, smoking, drug use, chronic infection (hepatitis B/C, HIV), CVD (HTN, renal artery stenosis, atherosclerosis), prior kidney transplant, BPH, autoimmune disease, vasculitis, connective tissue disease, nephrotoxic drugs (nonsteroidal anti-inflammatory drugs [NSAIDs], lithium, sulfonamide, aminoglycosides, vancomycin, PPIs, allopurinol, loop diuretics, chemotherapeutic agents), congenital anomalies, obstructive uropathy, renal aplasia/hypoplasia/dysplasia/reflux nephropathy)

General Prevention

The U.S. Preventive Services Task Force has concluded the evidence is insufficient to recommend screening asymptomatic adults for CKD (1)[C].

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Basics

Chronic kidney disease (CKD) is defined as structural or functional abnormalities of the kidney, as determined by either pathologic abnormalities or markers of damage (abnormalities in blood or urine tests, histology, imaging studies) or a glomerular filtration rate (GFR) <60 mL/min/1.73 m2. Findings present for ≥3 months. CKD is classified based on the cause, GFR category (G1 to G5), and albuminuria category (A1 to A3).

Description

  • Kidney Disease: Improving Global Outcomes (KDIGO) categories by GFR estimation (in mL/min/1.73 m2): G1: kidney damage with normal or increased GFR ≥90; G2: mild ↓ GFR 60 to 89; G3a: mild to moderate ↓ GFR 45 to 59; G3b: moderate to severe ↓ GFR 30 to 44; G4: severe ↓ GFR 15 to 29; G5: kidney failure: GFR <15 or dialysis
  • CKD per albumin-to-creatinine ratio (ACR) category: A1: normal to mildly increased: <30 mg/g or <3 mg/mmol; A2: moderately increased: 30 to 300 mg/g or 3 to 30 mg/mmol; A3: severely increased: >300 mg/g or >30 mg/mm

Epidemiology

  • African Americans are 3.6 times more likely to develop CKD than Caucasians.
  • Similar in both sexes; however, rate of end-stage renal disease (ESRD) is 1.6 times higher in males than females.

Incidence
Estimated annual incidence of 1,700/1 million population

Prevalence
Overall prevalence of CKD (stages 1 to 5) is 14.8%. Unadjusted prevalence and incidence rates of ESRD (stage 5) are 1,752 and 362.4/1 million, respectively. Numbers do not reflect the burden of earlier stages of CKD (stages 1 to 4), which are estimated to affect 13.1% of the population in the United States. Prevalence increases with age and peaks after 70.

Etiology and Pathophysiology

Progressive destruction of kidney nephrons; GFR will drop gradually, and plasma Cr values will approximately double, with 50% reduction in GFR and 75% loss of functioning nephrons mass. Hyperkalemia usually develops when GFR falls to <20 to 25 mL/min. Anemia develops from decreased renal synthesis of erythropoietin.

  • Renal parenchymal/glomerular
    • Nephritic: hematuria, red blood cell (RBC) casts, hypertension (HTN), variable proteinuria
      • Focal proliferative: IgA nephropathy, systemic lupus erythematosus (SLE), Henoch-Schönlein purpura, Alport syndrome, proliferative glomerulonephritis, crescentic glomerulonephritis
      • Diffuse proliferative: membranoproliferative glomerulonephritis, SLE, cryoglobulinemia, rapidly progressive glomerulonephritis (RPGN), Goodpasture syndrome
    • Nephrotic: proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, and edema
      • Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis
      • Amyloidosis, diabetic nephropathy
  • Vascular: HTN, thrombotic microangiopathies, vasculitis (Wegener), scleroderma, crush injury
  • Interstitial tubular: infections, obstruction, toxins, allergic interstitial nephritis, multiple myeloma, connective tissue disease, cystic disease, nephrolithiasis
  • Postrenal: obstruction (benign prostatic hyperplasia [BPH]), neoplasm, neurogenic bladder

Genetics

  • Alport syndrome, Fabry disease, sickle cell anemia, SLE, and autosomal dominant polycystic kidney disease can lead to CKD.
  • Polymorphisms in gene that encodes for podocyte nonmuscle myosin IIA are more common in African Americans than Caucasians and appear to increase risk for nondiabetic ESRD.

Risk Factors

Type 1 or 2 diabetes mellitus (DM) (most common), age > 60 years, low socioeconomic status, obesity, smoking, drug use, chronic infection (hepatitis B/C, HIV), CVD (HTN, renal artery stenosis, atherosclerosis), prior kidney transplant, BPH, autoimmune disease, vasculitis, connective tissue disease, nephrotoxic drugs (nonsteroidal anti-inflammatory drugs [NSAIDs], lithium, sulfonamide, aminoglycosides, vancomycin, PPIs, allopurinol, loop diuretics, chemotherapeutic agents), congenital anomalies, obstructive uropathy, renal aplasia/hypoplasia/dysplasia/reflux nephropathy)

General Prevention

The U.S. Preventive Services Task Force has concluded the evidence is insufficient to recommend screening asymptomatic adults for CKD (1)[C].

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