Renal-AKI and CKD Flashcards
AKI and AoCKD
What is the definition of Acute Kidney Injury (AKI)?
AKI is a sudden decline in kidney function characterized by an increase in serum creatinine, a decrease in urine output, or both, occurring over hours to days
What are the causes of prerenal AKI?
Prerenal AKI is caused by decreased renal perfusion, including:
Hypovolemia (e.g., hemorrhage, dehydration, vomiting, diarrhea)
Low cardiac output (e.g., heart failure, cardiogenic shock)
Systemic vasodilation (e.g., sepsis, anaphylaxis)
Renal vasoconstriction (e.g., NSAIDs, ACE inhibitors, hepatorenal syndrome)
How does prerenal AKI present clinically?
Oliguria (low urine output)
Signs of volume depletion (e.g., dry mucous membranes, hypotension, tachycardia)
BUN:Creatinine ratio > 20:1
Low FeNa (<1%) and high urine osmolality (>500 mOsm/kg)
What are the causes of intrinsic AKI?
Intrinsic AKI is caused by direct kidney damage, including:
Acute tubular necrosis (ATN) (ischemia, nephrotoxins like aminoglycosides, contrast)
Glomerulonephritis (e.g., post-streptococcal, lupus nephritis)
Acute interstitial nephritis (AIN) (drugs like NSAIDs, PPIs, infections)
Vascular causes (thrombotic microangiopathy, malignant hypertension)
How does intrinsic AKI present clinically?
Variable urine output
BUN:Creatinine ratio ~10-15:1
ATN: Muddy brown casts in urine, FeNa >2%
AIN: Eosinophilia, WBC casts, recent drug exposure
Glomerulonephritis: Hematuria, RBC casts, proteinuria
What are the causes of postrenal AKI?
Postrenal AKI results from urinary tract obstruction, including:
Prostate hypertrophy or cancer
Kidney stones (urolithiasis)
Ureteral obstruction (e.g., malignancy, fibrosis)
Neurogenic bladder (e.g., spinal cord injury)
How does postrenal AKI present clinically?
Fluctuating urine output (oliguria or anuria)
Suprapubic pain or distended bladder
Hydronephrosis on ultrasound
BUN:Creatinine ratio ~10-15:1
What are the key diagnostic tests for AKI?
- Serum creatinine & BUN (to assess kidney function)
- Urinalysis (casts, protein, WBCs, RBCs)
- Urine sodium & FeNa (distinguish prerenal vs intrinsic)
- Renal ultrasound (hydronephrosis for postrenal causes)
- Serological tests (autoimmune markers for glomerulonephritis)
How is AKI managed?
- Prerenal AKI: Restore volume (IV fluids), treat underlying cause
- Intrinsic AKI: Stop nephrotoxins, manage underlying disease (e.g., steroids for AIN)
- Postrenal AKI: Relieve obstruction (e.g., catheterization, surgery)
Dialysis if severe (AEIOU: Acidosis, Electrolytes, Intoxication, Overload, Uremia)
What are the major causes of CKD?
- Diabetes mellitus (most common cause)
- Hypertension
- Glomerulonephritis (e.g., IgA nephropathy, lupus nephritis)
- Polycystic kidney disease (PKD)
- Chronic infections (e.g., HIV, hepatitis B/C)
- Obstructive nephropathy (e.g., kidney stones, BPH)
What are the pathophysiological mechanisms of CKD?
- Nephron loss → Remaining nephrons compensate, leading to hyperfiltration
- Glomerular hypertension → Further nephron damage
- Fibrosis & scarring → Progressive loss of kidney function
What are the clinical features of CKD?
Early stages: Often asymptomatic
Late stages:
Fatigue, weakness
Edema (peripheral, pulmonary)
Hypertension
Anemia (↓ erythropoietin)
Uremic symptoms (pruritus, nausea, metallic taste)
What are the complications of CKD?
Cardiovascular disease (leading cause of death)
A WET BED-
Anemia
Water
Electrolytes
Toxin
BP
Erythropoietin
D (vitamin)
What are the diagnostic tests for CKD?
one of the following for >3months
- Serum creatinine & GFR (assess kidney function)
- albumin-to-creatinine ratio (UACR->=30mg/g)
- Electrolytes (hyperkalemia, metabolic acidosis)
- Renal ultrasound (small, shrunken kidneys in CKD)
- Urine sediment abnormalities
What are the treatment goals for CKD?
Kidney protection:
1. Control blood pressure (target <130/80 mmHg)
2. ACE inhibitors/ARBs (protect kidneys)
3. Manage diabetes
4. Dietary modifications (↓ sodium, protein, phosphorus, potassium)
5. Use of SGLT2-I
6. Lifestyle - smoking cessation, weight loss and exercise (HbA1c target ~7%)
Symptom management:
1. Correct electrolyte imbalances
2. Treat anemia (EPO-stimulating agents, iron supplements)
When is dialysis indicated in CKD?
Dialysis is needed in End-Stage Renal Disease (ESRD) or when symptoms appear. Indications:
AEIOU criteria (despite medical therapy):
Acidosis (severe metabolic acidosis)
Electrolyte imbalance (severe hyperkalemia)
Intoxications (e.g., lithium, methanol)
Overload (fluid overload unresponsive to diuretics)
Uremia (encephalopathy, pericarditis)
- Urea >100 mg/dL
- S K >6 mmol/L
- S HCO3 <12 mmol/L or
- pH <7.15
- PaO2/FiO2 <200
- CXR with APO
(despite medical therapy)
How would you stage AKI?
Stage 1: SCr increase >=26.5mmol/L or 1.5-1.9x baseline SCr. UOP<0.5ml/kg/hour for 6-12hours
Stage 2: 2-2.9x SCr. UOP<0.5ml/kg/hr for >=12hours
Stage 3: SCr>=3x SCr or increase SCr to >=354mml/L or HD initiation. UOP<0.3ml/kg/hour >=24hours or anuria >=12hours
What are the causes of intrinsic AKI?
Acute tubular injury
(eg. prolonged pre-renal AKI, rhabdomyolysis, hemoglobinuria, nephrotoxins)
Tubulointerstitial injury
GN, Myeloma, vasculitis (Lupus, ANCA associated)
What is the formula to calculate frusemide quantity for stress test
IV Furosemide 1 mg/kg or
1.5 mg/kg if history of
furosemide in past 7 days
What is considered Frusemide Stress test responsive
UO >200 mL in 2 hours
Functional staging of CKD based on GFR
G1 >=90
G2 60-89
G3a 45-59
G3b 30-44
G4 15-29
G5 <15
Albuminuria categories in CKD
A1 AER<30mg/24hrs, ACR<30mg/g
A2 AER 30-300mg/24hrs, ACR 30-300mg/g
A3 AER>300mg/24hrs, ACR >300mg/g
What medicine to avoid if critically sick or unable to maintain adequate hydration?
– S - sulfonylureas
– A - ACE-inhibitors
– D - diuretics
– M -metformin
– A - ARB
– N - NSAIDs / Cox-2 inhibitors
– S – SGLT-2 inhibitor
For renal patients, how do you work up anemia?
- Hb
- If Hb low, Fe study (transferrin sat and ferritin)
Absolute iron deficiency when TSAT <=20%, Ferritin <=100ng/ml (CKD/PD) or <=200ng/ml (HD)
Functional iron deficiency when TSAT <=20%, ferritin much higher (as high as 800ng/ml)
