What are the current guidelines for managing acute kidney injury and chronic kidney disease, including workup, treatment of underlying causes, volume and electrolyte management, anemia, blood pressure control, dietary recommendations, and indications for renal replacement therapy?

Renal Failure Management Guidelines

Acute Kidney Injury (AKI) Management

Definition and Diagnosis

AKI is diagnosed when serum creatinine rises ≥0.3 mg/dL within 48 hours, increases ≥50% from baseline within 7 days, or urine output falls below 0.5 mL/kg/hour for 6 consecutive hours. 1, 2, 3

• Stage AKI using KDIGO criteria: Stage 1 (1.5-1.9× baseline or ≥0.3 mg/dL rise), Stage 2 (2.0-2.9× baseline), Stage 3 (≥3.0× baseline or creatinine ≥4.0 mg/dL or need for renal replacement therapy) 1, 3
• Perform urinalysis with microscopy to identify casts: muddy-brown casts suggest acute tubular necrosis, red-cell casts indicate glomerulonephritis, white-cell casts point to interstitial nephritis 3
• Calculate fractional excretion of sodium (FENa): <1% favors prerenal azotemia, >2% suggests intrinsic renal injury 3, 4
• Obtain renal ultrasound in most patients, particularly older men, to exclude obstruction 4

Immediate Management Steps

Discontinue all nephrotoxic medications immediately upon AKI diagnosis, including NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, and contrast media. 2, 3, 5

• Hold beta-blockers when AKI is diagnosed to prevent further kidney injury 2
• Review all medications including over-the-counter drugs that may contribute to kidney injury 2
• Avoid the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs, which significantly increases AKI risk 2
• Each additional nephrotoxic drug increases odds of developing AKI by 53% 2

Fluid and Hemodynamic Management

Use isotonic crystalloids (preferably lactated Ringer's solution) rather than colloids for initial volume expansion in hypovolemic patients. 2, 3, 5

• Target mean arterial pressure of at least 65 mmHg to ensure adequate renal perfusion 2, 3, 5
• Use vasopressor therapy if fluid resuscitation fails to restore adequate blood pressure; prefer norepinephrine over dopamine as first-line vasopressor 2
• Avoid dopamine to prevent or treat AKI 2
• Avoid hydroxyethyl starch-containing fluids as they are associated with harm and increased risk of worsening AKI 2, 5
• Monitor for fluid overload using urine output, vital signs, and when indicated, echocardiography or central venous pressure 2

Monitoring and Reassessment

For persistent AKI (continuing beyond 48 hours), reassess the underlying etiology and perform precise measurement of kidney function. 1, 2

• Monitor serum creatinine and electrolytes every 12-24 hours during acute management 5
• Re-evaluate hemodynamic and volume status, adequacy of kidney perfusion, and identify complications such as fluid overload, acidosis, and hyperkalemia 1, 2
• Timed urine creatinine clearance is the best available estimate of kidney function for patients with persistent AKI in steady state 1
• Equations to estimate GFR in chronic kidney disease are not accurate for assessment of renal function in persistent AKI 1
• Consider nephrology consultation if the etiology of AKI is unclear or subspecialist care is needed 1, 2

Special Populations: Cirrhosis with AKI

In cirrhotic patients with AKI and doubling of serum creatinine, administer intravenous albumin 1 g/kg/day (maximum 100 g/day) for two consecutive days. 2, 3, 5

• Immediately discontinue diuretics and beta-blockers upon AKI diagnosis in cirrhotic patients 2, 3
• Use ICA-AKI criteria (creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% from baseline) without a fixed 1.5 mg/dL threshold, as baseline creatinine underestimates true GFR in cirrhosis due to reduced muscle mass 3
• Perform rigorous search for infection including diagnostic paracentesis to evaluate for spontaneous bacterial peritonitis 3
• Start broad-spectrum antibiotics when infection is strongly suspected 3
• For hepatorenal syndrome (HRS-AKI), when creatinine remains elevated despite initial management, add vasoactive agents (terlipressin, norepinephrine, or midodrine plus octreotide) along with albumin 2, 3

Indications for Renal Replacement Therapy (RRT)

Individualize timing of RRT based on overall clinical condition rather than specific creatinine or BUN thresholds. 2, 3

Absolute indications for immediate RRT include:

• Refractory hyperkalemia unresponsive to medical therapy 2, 3

• Severe volume overload causing pulmonary edema or respiratory compromise 2, 3

• Intractable metabolic acidosis (e.g., pH <7.1) 2, 3

• Uremic complications such as encephalopathy, pericarditis, or bleeding 2, 3

• Do not delay RRT when absolute indications are present, as postponement is associated with increased mortality 2

• Reassess the need for ongoing RRT daily rather than adhering to a fixed schedule 2, 3

• Avoid subclavian catheters if possible to preserve future vascular access 1

Management of Complications

Manage metabolic acidosis with sodium bicarbonate in selected cases. 2

• Correct electrolyte abnormalities, particularly hyperkalemia, which may require urgent intervention 3
• Monitor serum potassium, phosphorus, and magnesium, as these may be altered during AKI 5

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Chronic Kidney Disease (CKD) Management

Definition and Classification

CKD is defined by persistence of kidney disease for >90 days, characterized by decreased GFR (<60 mL/min/1.73 m²) or markers of kidney damage (albuminuria, structural abnormalities). 1

• Stage CKD by GFR: Stage 1 (GFR ≥90 with kidney damage), Stage 2 (GFR 60-89 with damage), Stage 3 (GFR 30-59), Stage 4 (GFR 15-29), Stage 5 (GFR <15 or dialysis) 1
• Use cause-specific classification combined with GFR and albuminuria levels (CGA classification) 1
• Assess all persons during routine health encounters to determine risk for developing CKD based on clinical and sociodemographic factors 1

Pharmacological Treatment for CKD with Type 2 Diabetes

In adults with type 2 diabetes and CKD, initiate an SGLT2 inhibitor to reduce kidney disease progression and cardiovascular events. 1

• Add a nonsteroidal mineralocorticoid receptor antagonist (MRA) to a RAS inhibitor and SGLT2 inhibitor for treatment of type 2 diabetes and CKD 1
• To mitigate hyperkalemia risk with nonsteroidal MRA, select people with consistently normal serum potassium (≤4.8 mmol/L) and monitor regularly 1
• Initiate finerenone 10 mg daily if eGFR 25-59 mL/min/1.73 m², or 20 mg daily if eGFR ≥60 mL/min/1.73 m² 1
• Hold finerenone if potassium >5.5 mmol/L; consider reinitiation when potassium ≤5.0 mmol/L 1
• Monitor potassium at 1 month after initiation and then every 4 months 1
• For patients not achieving glycemic targets despite metformin and SGLT2 inhibitor, add a long-acting GLP-1 receptor agonist with documented cardiovascular benefits 1

Blood Pressure and Cardiovascular Management

Control hypertension carefully in all CKD patients, as it is both a cause and complication of chronic kidney disease. 1

• Implement interventions to slow progression of kidney disease and reduce cardiovascular disease risk beginning in Stage 1 and Stage 2 1

Metabolic Complications

Consider pharmacological treatment with or without dietary intervention to prevent development of acidosis when serum bicarbonate falls below 18 mmol/L in adults. 1

• Monitor treatment for metabolic acidosis to ensure serum bicarbonate does not exceed the upper limit of normal and does not adversely affect blood pressure, serum potassium, or fluid status 1

Hyperkalemia Management

Be aware of variability in potassium laboratory measurements and factors influencing potassium measurement including diurnal and seasonal variation, plasma versus serum samples, and medication effects. 1

• Implement an individualized approach in CKD G3-G5 with emergent hyperkalemia that includes dietary and pharmacologic interventions 1
• Provide advice to limit intake of foods rich in bioavailable potassium (especially processed foods) for CKD G3-G5 patients with history of hyperkalemia 1

Hyperuricemia and Gout

Offer uric acid-lowering intervention to CKD patients with symptomatic hyperuricemia. 1

• Consider initiating uric acid-lowering therapy after the first episode of gout, particularly when there is no avoidable precipitant or serum uric acid >9 mg/dL (535 µmol/L) 1
• Prescribe xanthine oxidase inhibitors in preference to uricosuric agents in CKD with symptomatic hyperuricemia 1
• For symptomatic treatment of acute gout in CKD, low-dose colchicine or intra-articular/oral glucocorticoids are preferable to NSAIDs 1

Anemia Management

Evaluation and treatment of anemia should be undertaken during Stage 3, as prevalence rises when GFR declines below 60 mL/min/1.73 m². 1

Preparation for Renal Replacement Therapy

Preparation for kidney replacement therapy should begin during Stage 4 (GFR 15-29 mL/min/1.73 m²), well before the stage of kidney failure. 1

• Initiation of dialysis and transplantation is triggered by onset of uremic symptoms 1
• Preparations should begin when GFR declines below 15 mL/min/1.73 m² (Stage 5) 1

Nephrology Referral

Refer patients to a nephrologist for consultation and comanagement when GFR falls below 30 mL/min/1.73 m². 1

• Consider referral if the primary physician cannot adequately evaluate and treat the patient 1
• Late referral is associated with increased mortality after initiation of dialysis 1

Monitoring and Follow-up

Monitor kidney function closely in all patients with or at risk for kidney disease. 1, 3

• Perform laboratory evaluation including serum creatinine, urinalysis, and assessment for proteinuria/albuminuria 1
• Schedule close post-discharge clinical evaluation for patients with moderate to severe AKI, as even one episode increases risk of cardiovascular disease, chronic kidney disease, and death 3, 6

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Acute Kidney Disease (AKD)

Definition and Continuum

AKD describes acute or subacute kidney damage and/or loss of function lasting between 7 and 90 days after an AKI initiating event. 1

• Persistent AKI is characterized by continuance of AKI by serum creatinine or urine output criteria beyond 48 hours from AKI onset 1
• Complete reversal of AKI within 48 hours characterizes rapid reversal of AKI 1
• A minimum of 48 hours is necessary to separate two distinct AKI episodes 1
• AKI and AKD form a continuum; persistent AKI frequently becomes AKD when criteria for AKI Stage 1 or greater persist ≥7 days 1
• After 3 months, most patients without resolution of AKD will meet criteria for CKD and be described as having CKD with a history of AKD 1

Management Considerations for AKD

Initial management of persistent AKI/AKD should include reassessment of the underlying etiology and precise measurement of kidney function. 1

• Continue nephrotoxin avoidance during the recovery phase of AKD to prevent re-injury 2
• Educate patients to avoid taking NSAIDs or new medications without consulting their healthcare provider 2
• Check for changes in drug dosing requirements (high relevance in AKD) 1
• Consider kidney biopsy for unresolving AKI/AKD when etiology remains unclear 1