Chronic kidney disease
Chronic kidney disease is abnormal kidney structure or function present for more than 3 months, staged by the Kidney Disease: Improving Global Outcomes (KDIGO) system using estimated glomerular filtration rate and albuminuria, and managed with blood pressure control, renin-angiotensin blockade, an SGLT2 inhibitor, and correction of its metabolic complications.
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What this article covers
- Overview
Chronic structural or functional kidney damage present for more than 3 months: chronic kidney disease (CKD) is defined as abnormal kidney structure or function persisting for more than 3 months…
- Epidemiology
Roughly 15% of US adults, rising with age: highest prevalence is in adults age 60 and older; overall prevalence has been stable across recent decades.
- Risk factors
Diabetes mellitus: the leading cause worldwide, via diabetic glomerulosclerosis.
- Pathophysiology
Chronic injury to glomeruli, tubulointerstitium, or vasculature: glomerular damage manifests as albuminuria, tubulointerstitial damage as impaired concentrating ability and low-grade tubular proteinuria.
- Clinical features
Typically asymptomatic until advanced stages (G4-G5): most CKD is detected on routine labs (elevated creatinine, abnormal urinalysis).
- Differential diagnosis
Acute kidney injury: creatinine rises over hours to days rather than months, with normal-sized, non-echogenic kidneys and often reversibility once the precipitant is treated.
- Diagnosis
CKD is diagnosed by an eGFR less than 60 mL/min/1.73 m^2 confirmed at least 3 months after the initial finding, or by persistent proteinuria/albuminuria regardless of eGFR, and is staged by the KDIGO…
- Management
First, treat blood pressure to a target below 130/80 mm Hg.
- Complications
Cardiovascular disease: the leading cause of death in CKD, 4-5 times more likely than progression to ESKD in stage G3-G4 disease.
- Prognosis
Most patients die of cardiovascular disease before reaching kidney failure: stages G4-G5 affect fewer than 1% of the general population.
- Prevention
Screen adults with diabetes, hypertension, or a family history of kidney disease with serum creatinine (for eGFR) and a urine albumin-creatinine ratio; routine screening of average-risk adults is not established.
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Related articles
- Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Diabetic kidney disease
Diabetic kidney disease is the leading cause of chronic kidney disease and end-stage kidney disease worldwide, driven by chronic hyperglycemia acting through advanced glycation end products on the glomerulus. It is diagnosed clinically from progressive albuminuria and falling eGFR in a patient with long-standing diabetes and other microvascular disease, and treatment centers on RAS blockade, SGLT2 inhibition, and glycemic and blood pressure control.
- Chronic kidney disease mineral and bone disorders
Chronic kidney disease-mineral and bone disorder (CKD-MBD) is the syndrome of disturbed calcium, phosphorus, PTH, vitamin D, and FGF-23 homeostasis, abnormal bone mineralization (renal osteodystrophy), and vascular calcification that develops as kidney function declines. Management centers on serial phosphorus/calcium/PTH monitoring, dietary phosphorus restriction plus phosphate binders (noncalcium-based preferred) to normalize phosphorus, avoiding hypercalcemia and unnecessary calcitriol before dialysis, and calcimimetics or activated vitamin D for uncontrolled secondary hyperparathyroidism on dialysis, reserving parathyroidectomy for tertiary disease.
- Anemia of chronic disease
Anemia of chronic disease, also called anemia of inflammation, is a normocytic normochromic anemia driven by hepcidin-mediated iron sequestration and cytokine blunting of erythropoiesis in patients with chronic infection, autoimmune disease, malignancy, or kidney disease. The iron-study pattern of low serum iron, low total iron-binding capacity, and normal-to-high ferritin distinguishes it from iron deficiency, and management centers on treating the underlying disease rather than iron supplementation.
- Metabolic acidosis
Metabolic acidosis is a primary fall in serum bicarbonate that is first confirmed with an arterial or venous blood gas, then classified by the serum anion gap into an increased anion gap process (unmeasured organic anion, most often lactate) or a normal anion gap process (bicarbonate loss from the gut or kidney). The urine anion gap and clinical context localize the cause, and management targets the underlying disease, reserving intravenous sodium bicarbonate for severe acidemia (pH less than 7.1-7.2) or specific indications such as chronic kidney disease and renal tubular acidosis.
- Renal replacement therapy
Renal replacement therapy (RRT), intermittent hemodialysis (IHD), continuous renal replacement therapy (CRRT), prolonged intermittent renal replacement therapy (PIRRT), or peritoneal dialysis (PD), substitutes for lost kidney function when acute kidney injury or end-stage kidney disease causes refractory acidosis, hyperkalemia, volume overload, or uremia. Modality is chosen mainly by hemodynamic stability: CRRT or PIRRT for the unstable patient, IHD for rapid clearance of severe hyperkalemia or a dialyzable toxin.