Renal · Chronic Kidney Disease
The facts most likely to be tested
The diagnosis of Chronic Kidney Disease (CKD) requires evidence of kidney damage or a glomerular filtration rate (GFR) < 60 mL/min/1.73m² for at least three months.
Diabetes mellitus and hypertension are the two most common etiologies of CKD in the United States.
Renal osteodystrophy results from secondary hyperparathyroidism due to phosphate retention, hypocalcemia, and decreased calcitriol production.
Normocytic, normochromic anemia in CKD is primarily caused by erythropoietin deficiency and is treated with erythropoiesis-stimulating agents (ESAs) only after correcting iron deficiency.
ACE inhibitors or ARBs are the first-line antihypertensive agents for patients with CKD and proteinuria due to their renoprotective effects.
Uremic pericarditis is a life-threatening complication of advanced CKD that serves as an absolute indication for urgent hemodialysis.
Hyperphosphatemia in CKD is managed with dietary phosphate restriction and oral phosphate binders such as sevelamer or calcium acetate.
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A 62-year-old male with a 15-year history of type 2 diabetes and hypertension presents for a routine follow-up. Laboratory studies reveal a serum creatinine of 2.4 mg/dL, a GFR of 32 mL/min/1.73m², and a hemoglobin of 9.8 g/dL. His parathyroid hormone (PTH) is elevated, and his serum phosphate is 5.8 mg/dL. He reports no chest pain, but complains of generalized pruritus and fatigue.
Which of the following is the most appropriate next step in the management of this patient's bone mineral metabolism?
Initiate oral phosphate binders
The patient has CKD stage 4 with hyperphosphatemia; managing phosphate levels is critical to prevent secondary hyperparathyroidism and renal osteodystrophy, as described in the seventh bet.
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High yield triage
Etiology / Epidemiology
Diabetes mellitus and hypertension are the leading causes. CKD is defined as kidney damage or GFR <60 mL/min/1.73m² for >3 months.
Clinical Manifestations
Often asymptomatic until advanced. Look for uremic frost, pericarditis, and anemia of chronic disease.
Diagnosis
Estimated GFR (eGFR) is the gold standard. Albumin-to-creatinine ratio (ACR) is required to stage proteinuria.
Treatment
ACE inhibitors or ARBs are first-line for proteinuria. Avoid NSAIDs to prevent further nephron loss.
Prognosis
High risk of cardiovascular disease. Monitor potassium and phosphate levels to prevent fatal arrhythmias.
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Epidemiology & Etiology
The most common causes are diabetes mellitus (type 2 > type 1) and hypertension. Other etiologies include polycystic kidney disease, glomerulonephritis, and chronic obstruction. Prevalence increases significantly with age and African American descent.
Pertinent Anatomy
The functional unit is the nephron. Progressive loss of nephrons leads to compensatory hyperfiltration in remaining units, eventually causing glomerulosclerosis and interstitial fibrosis.
Pathophysiology
Initial injury leads to a reduction in functional nephron mass. The remaining nephrons undergo compensatory hypertrophy and hyperfiltration, which paradoxically accelerates damage via glomerular hypertension. This cycle culminates in end-stage renal disease (ESRD) when the kidney can no longer maintain homeostasis.
Clinical Manifestations
Patients present with uremic syndrome including nausea, fatigue, and pruritus. Physical exam may reveal hypertension, uremic frost, and friction rub if pericarditis develops. Hyperkalemia and pulmonary edema are life-threatening emergencies.
Diagnosis
The gold standard is the eGFR calculated via the CKD-EPI equation. Diagnosis requires persistent GFR <60 or evidence of kidney damage (e.g., albuminuria >30 mg/g) for >3 months. Renal ultrasound is indicated to assess kidney size; small, echogenic kidneys suggest chronic disease.
Treatment
Initiate ACE inhibitors or ARBs for patients with albuminuria to provide renoprotection. NSAIDs are strictly contraindicated due to afferent arteriole vasoconstriction. Manage complications with phosphate binders, erythropoietin-stimulating agents for anemia, and calcium/vitamin D supplementation.
Prognosis
CKD is a major independent risk factor for cardiovascular mortality. Patients require regular monitoring of potassium, phosphorus, and parathyroid hormone (PTH). Progression to ESRD necessitates renal replacement therapy (dialysis or transplant).
Differential Diagnosis
Acute Kidney Injury: rapid rise in creatinine over hours/days
Nephrotic Syndrome: massive proteinuria >3.5g/day with edema
Renal Artery Stenosis: hypertension with flash pulmonary edema
Multiple Myeloma: elevated protein gap and bone pain
Polycystic Kidney Disease: palpable flank masses and family history