Chronic Kidney Disease for the ABIM
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Chronic Kidney Disease (CKD) for the ABIM Exam
Definition
- Chronic Kidney Disease (CKD): Progressive and irreversible decline in kidney function lasting for at least 3 months, defined by decreased glomerular filtration rate (GFR) or markers of kidney damage such as proteinuria, hematuria, or structural abnormalities.
- Diagnosis Criteria:
- GFR <60 mL/min/1.73 m² for ≥3 months, with or without evidence of kidney damage, or
- Evidence of kidney damage for ≥3 months, such as albuminuria (albumin-to-creatinine ratio ≥30 mg/g), hematuria, or imaging abnormalities.
Staging (KDIGO Classification)
- Stage 1: GFR ≥90 mL/min/1.73 m² with evidence of kidney damage.
- Stage 2: GFR 60–89 mL/min/1.73 m² with evidence of kidney damage.
- Stage 3:
- 3a: GFR 45–59 mL/min/1.73 m².
- 3b: GFR 30–44 mL/min/1.73 m².
- Stage 4: GFR 15–29 mL/min/1.73 m².
- Stage 5: GFR <15 mL/min/1.73 m² (end-stage renal disease requiring dialysis or transplantation).
Etiology
- Diabetes Mellitus (DM): The most common cause of CKD in developed countries. Hyperglycemia leads to glomerular hyperfiltration, glomerulosclerosis, and nephron loss over time.
- Hypertension: Chronic hypertension causes nephrosclerosis, which progressively reduces renal blood flow and leads to glomerular ischemia and scarring.
- Glomerulonephritis: Inflammatory diseases of the glomeruli, such as IgA nephropathy, lupus nephritis, or post-infectious glomerulonephritis, can result in CKD due to permanent scarring.
- Polycystic Kidney Disease (PKD): A genetic disorder that causes multiple renal cysts, leading to progressive kidney enlargement, compression of normal parenchyma, and eventual renal failure.
- Other Causes:
- Obstructive uropathy (e.g., due to kidney stones, prostatic hypertrophy).
- Chronic use of nephrotoxic drugs (e.g., NSAIDs, certain antibiotics).
- Chronic pyelonephritis or recurrent urinary tract infections.
Pathophysiology
- Hyperfiltration Injury: Initial injury to nephrons (e.g., from DM or HTN) leads to compensatory hyperfiltration in remaining nephrons, causing further damage and loss of nephrons.
- Glomerulosclerosis and Fibrosis: Progressive damage leads to glomerulosclerosis, tubular atrophy, and interstitial fibrosis, which result in worsening kidney function.
- Electrolyte and Acid-Base Imbalances: As GFR declines, the kidneys lose their ability to excrete waste products and maintain electrolyte balance, leading to azotemia, hyperkalemia, metabolic acidosis, and other imbalances.
- Uremia: Advanced CKD leads to the accumulation of uremic toxins, causing systemic symptoms like anorexia, nausea, pruritus, pericarditis, and encephalopathy.
Clinical Presentation
- Early Stages (Stages 1–3):
- Often asymptomatic or non-specific symptoms such as fatigue, weakness, or hypertension.
- Proteinuria may be the first sign, particularly in diabetic patients.
- Edema due to impaired sodium and water excretion.
- Late Stages (Stages 4–5):
- Symptoms related to uremia: nausea, vomiting, anorexia, pruritus, muscle cramps, sleep disturbances, and confusion.
- Volume overload: dyspnea, pulmonary edema, peripheral edema, and ascites.
- Hypertension: Due to sodium retention and activation of the renin-angiotensin-aldosterone system (RAAS).
- Anemia: Due to reduced erythropoietin production by the failing kidneys.
- Bone Disease: Secondary hyperparathyroidism, renal osteodystrophy, and bone pain resulting from altered calcium-phosphorus metabolism.
Diagnostic Evaluation
- Laboratory Tests:
- Serum Creatinine and GFR: Used to assess kidney function and stage CKD.
- Urine Studies:
- Proteinuria: Measured via urine albumin-to-creatinine ratio (UACR); proteinuria >30 mg/g suggests kidney damage.
- Urinalysis: May show hematuria, casts, or evidence of infection.
- Electrolytes: Hyperkalemia, hyperphosphatemia, and hypocalcemia are common in advanced CKD.
- Complete Blood Count (CBC): May show anemia due to decreased erythropoietin production.
- Imaging:
- Renal Ultrasound: Often shows small, shrunken kidneys in advanced CKD.
- CT/MRI: May be used to assess structural abnormalities or detect polycystic kidney disease.
Management
- Control Underlying Causes:
- Diabetes Management: Tight glycemic control with a goal HbA1c of <7%.
- Hypertension Management: Use of ACE inhibitors or ARBs to reduce proteinuria and slow progression of CKD. Target blood pressure <130/80 mmHg.
- Dietary Management:
- Protein Restriction: Reducing dietary protein intake (0.8 g/kg/day) to slow the accumulation of nitrogenous wastes.
- Salt Restriction: Reducing sodium intake to manage volume overload and hypertension.
- Phosphorus Restriction: To prevent hyperphosphatemia and secondary hyperparathyroidism.
- Management of Complications:
- Anemia: Erythropoiesis-stimulating agents (ESAs) and iron supplementation.
- Hyperkalemia: Dietary potassium restriction, loop diuretics, and potassium-binding agents (e.g., sodium polystyrene sulfonate).
- Metabolic Acidosis: Sodium bicarbonate supplementation to maintain serum bicarbonate ≥22 mEq/L.
- Bone Disease: Phosphate binders (e.g., calcium carbonate), vitamin D analogs, and management of secondary hyperparathyroidism with calcimimetics or parathyroidectomy in severe cases.
- End-Stage Renal Disease (ESRD):
- Dialysis: Initiated when patients develop uremic symptoms or intractable complications (e.g., hyperkalemia, fluid overload) despite medical management.
- Hemodialysis: Typically performed three times per week.
- Peritoneal Dialysis: An alternative method where dialysis fluid is exchanged through the peritoneal cavity.
- Kidney Transplantation: The definitive treatment for ESRD, offering the best long-term survival and quality of life.
Prognosis
- The progression of CKD can be slowed but not reversed. Early detection and aggressive management of underlying causes (e.g., hypertension, diabetes) are key to delaying progression.
- CKD patients are at significantly increased risk of cardiovascular events and mortality, especially as GFR declines.
- ESRD requires dialysis or transplantation, both of which carry significant morbidity and mortality risks.
Complications
- Cardiovascular Disease: CKD is a major risk factor for cardiovascular disease, including heart failure, ischemic heart disease, and arrhythmias. Most CKD patients die from cardiovascular causes before reaching ESRD.
- Fluid Overload: Can lead to heart failure, pulmonary edema, and hypertension.
- Electrolyte Imbalances: Hyperkalemia and metabolic acidosis can cause life-threatening complications such as arrhythmias.
- Bone and Mineral Disease: CKD disrupts calcium and phosphorus metabolism, leading to renal osteodystrophy, bone pain, fractures, and vascular calcification.
- Anemia: CKD-associated anemia contributes to fatigue, reduced exercise capacity, and increased cardiovascular risk.
Key Points
- CKD is a progressive and irreversible decline in kidney function lasting ≥3 months, diagnosed by reduced GFR or markers of kidney damage (e.g., albuminuria).
- Common causes include diabetes, hypertension, glomerulonephritis, and polycystic kidney disease.
- Management focuses on controlling underlying conditions (e.g., blood pressure and blood glucose), dietary modifications, and managing complications such as anemia, hyperkalemia, and metabolic acidosis.
- ESRD requires renal replacement therapy (dialysis or transplantation).
- Cardiovascular disease is the leading cause of death in CKD patients, and early intervention is critical to reducing risk.