What are the definitions, risk factors, clinical features, and management strategies for chronic kidney disease compared to acute kidney injury?

Chronic Kidney Disease vs Acute Kidney Injury

Acute kidney injury (AKI) is an abrupt decrease in kidney function occurring over less than 7 days, requiring immediate interventions like nephrotoxin cessation and volume optimization, while chronic kidney disease (CKD) is persistent kidney dysfunction lasting beyond 3 months, requiring long-term strategies focused on slowing progression through blood pressure control, proteinuria reduction, and cardiovascular risk management. 1

Definitions and Temporal Framework

AKI is defined by:

• Serum creatinine increase ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, OR 1, 2
• Serum creatinine increase to ≥1.5 times baseline within 7 days, OR 1, 2
• Urine output <0.5 mL/kg/h for 6 hours 1, 2
• Duration: less than 7 days from onset 1, 3

CKD is defined by:

• Structural or functional kidney abnormalities persisting >3 months, OR 1
• eGFR <60 mL/min/1.73 m² for >3 months with or without kidney damage 1
• Persistent albuminuria (ACR ≥30 mg/g) for >3 months 1

The critical temporal distinction: Kidney dysfunction lasting 7-90 days is classified as Acute Kidney Disease (AKD), which bridges AKI and CKD and represents the highest-risk period for progression. 1, 3

Risk Factors

AKI risk factors include:

• Pre-existing CKD (dramatically increases AKI risk) 1, 4
• Diabetes mellitus 1
• Nephrotoxic medications (NSAIDs, aminoglycosides, contrast agents) 1, 3
• Volume depletion or hypotension 3, 4
• Medications altering renal hemodynamics (diuretics, ACE inhibitors, ARBs) 1

CKD risk factors include:

• Diabetes and hypertension (most common causes in developed countries) 1, 5
• Cardiovascular disease 1, 6
• Family history of kidney failure 1, 6
• Advanced age (prevalence highest in older adults) 7, 8
• Atherosclerosis and cumulative vascular disease 8

Clinical Features

AKI presents with:

• Rapid rise in serum creatinine over hours to days 1, 2
• Oliguria or anuria (though not always present) 1, 2
• Volume overload or depletion depending on etiology 3, 4
• Often symptomatic with acute illness 1
• Small creatinine increases (≥0.3 mg/dL) independently associated with fourfold increase in hospital mortality 2

CKD presents with:

• Asymptomatic in early stages, detected on routine screening 1, 6
• Gradual, progressive loss of kidney function over months to years 1, 5
• Less than 5% of patients with early CKD report awareness of their disease 5
• Complications emerge when eGFR falls below 60 mL/min/1.73 m² (hyperkalemia, metabolic acidosis, anemia, bone disease) 1, 5

Diagnostic Approach

For suspected AKI:

• Establish baseline creatinine from prior records (superior to imputed baselines) 2
• Do NOT assume chronicity based on single abnormal eGFR or ACR, as this could represent recent AKI 1
• Monitor serum creatinine and urine output closely (multiple times daily in acute phase) 3, 4
• Identify precipitating cause urgently (prerenal, intrinsic, postrenal) 3, 4
• Consider kidney biopsy for unresolving AKI when etiology remains unclear 1, 4

For suspected CKD:

• Confirm chronicity by repeating tests beyond 3 months OR reviewing past measurements OR imaging showing reduced kidney size/cortical thinning 1
• Use both creatinine-based eGFR (eGFRcr) and urine albumin measurement (ACR) for detection 1
• Stage using CGA classification: Cause, GFR category (G1-G5), Albuminuria category (A1-A3) 1
• Establish cause using clinical context, family history, medications, imaging, and consider kidney biopsy when clinically appropriate 1

Critical pitfall: Relying solely on serum creatinine without urine output criteria may miss AKI cases; failure to establish accurate baseline creatinine leads to misclassification. 2

Management Strategies

AKI Management (Immediate, Hours Matter)

Immediate interventions:

• Discontinue ALL nephrotoxic agents immediately (NSAIDs, aminoglycosides, vancomycin, contrast agents) 3, 4
• Ensure adequate volume status and perfusion pressure to restore renal blood flow 3, 4
• Adjust ALL medication doses immediately based on current eGFR, not baseline—this is high-priority and cannot wait 4

Monitoring during acute phase:

• Monitor serum creatinine and urine output multiple times daily 3, 4
• Track daily fluid balance (positive fluid balance predicts poor outcomes) 4
• Monitor electrolytes, acid-base status closely 4

Renal replacement therapy considerations:

• Do not delay RRT when clear indications present (severe oliguria, refractory hyperkalemia, metabolic acidosis, uremic complications) 4
• Mortality increases with delayed initiation in appropriate clinical contexts 4

Nutritional support in AKI:

• Provide 20-30 kcal/kg/day total energy intake, preferably enterally 1, 4
• Protein: 0.8-1.0 g/kg/day for noncatabolic AKI patients not requiring dialysis 4
• Increase to 1.0-1.5 g/kg/day if requiring RRT 4

CKD Management (Long-term, Months to Years)

Slowing disease progression (prioritize early stages):

• Blood pressure control: Target <130/80 mmHg using ACE inhibitors or ARBs for patients with hypertension and proteinuria 1, 3, 5
• Avoid dual RAAS blockade (increases hyperkalemia and AKI risk) 3
• Reduce proteinuria using ACE inhibitors or ARBs 1, 5
• Glycemic control in diabetic patients 9, 5

Lifestyle modifications:

• Dietary changes (sodium restriction, protein modification based on stage) 9, 5
• Physical activity 9
• Smoking cessation 9

Monitoring frequency:

• Annual monitoring of both eGFR and albuminuria to detect progression, superimposed AKI, and assess complications 1
• When eGFR <60 mL/min/1.73 m², screen for complications: anemia, metabolic bone disease, electrolyte abnormalities, metabolic acidosis 1, 5

Nephrology referral criteria:

• eGFR <30 mL/min/1.73 m² 5
• Albuminuria ≥300 mg per 24 hours 5
• Rapid decline in eGFR 5
• Poorly controlled blood pressure despite multiple agents 8
• Suspected inherited renal disease 8

Medication management:

• Avoid nephrotoxins (NSAIDs, certain antibiotics) 5
• Adjust drug dosing for all renally eliminated medications based on current eGFR 5
• Cardiovascular risk reduction with statins 5

AKI Superimposed on CKD (Highest Risk Phenotype)

This represents the most dangerous scenario:

• Patients with AKD on CKD have 47% mortality vs 19% for CKD alone 2
• Odds ratio of 16.8 for incident CKD progression 2
• Adjusted hazard ratio of 2.51 for mortality compared to those without AKD 2

Management approach:

• Apply ALL immediate AKI interventions listed above 4
• Continue nephrotoxin avoidance throughout entire AKD period (7-90 days) 4
• Arrange nephrology consultation during AKD period (reduces mortality, cardiovascular events, and sepsis) 4
• Nephrology follow-up within 3 months post-discharge is mandatory 4

Common Pitfalls and How to Avoid Them

In AKI:

• Do NOT wait until AKI stage 2 to adjust medication doses—adjust immediately upon diagnosis 4
• Do NOT continue nephrotoxic medications during recovery phase 4
• Do NOT aggressively fluid resuscitate in established AKI with volume overload 4
• Do NOT fail to arrange nephrology follow-up—even after apparent recovery, long-term kidney failure risk remains elevated 2, 4

In CKD:

• Do NOT assume elderly patients with low eGFR have progressive kidney failure—many have stable, age-related decline 8
• Do NOT use urine output criteria in cirrhotic patients with ascites—they are frequently oliguric yet may maintain normal GFR 2
• Do NOT rely on imputed baseline eGFR of 75 mL/min/1.73 m² in populations with high CKD prevalence—this overestimates AKI incidence 2
• Do NOT initiate CKD treatment without confirming chronicity (repeat tests beyond 3 months OR review past measurements) 1

Critical distinction: If kidney dysfunction persists 7-90 days, classify as AKD and investigate whether antecedent AKI occurred; if >90 days, classify as CKD with history of AKD. 1, 2