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Acute kidney injury (Diagnosis (Physical Exam. (Skin – new rashes:
Livedo…
Acute kidney injury
Diagnosis
Physical Exam.
- Skin – new rashes:
Livedo reticularis–atheroemboli, SLE, cryoglobulins.
Petechiae–HSP.
Malar rash–SLE.
- Eye:
Papilledema–malignant HTN.
Roth’sspots–endocarditis.
- CV:
Rub–suggestive of uremic pericarditis, lupus.
Gallop – suggesting CHF.
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3 tests
- Fluid/volume assessment PRE
- Urinalysis RENAL
- Ultrasound POST
urinalysis
- Unremarkable in pre and post renal causes
- Differentiates ATN vs. AIN. vs. AGN
• Muddy brown casts in ATN
• WBC casts in AIN
• RBC casts in AGN
- Hansel stain for Eosinophils
- Blood urea nitrogen and serum creatinine
- CBC, peripheral smear, and serology
- Urinalysis, Urine electrolytes, U/S kidneys
- Serology: ANA,ANCA, Anti DNA, HBV, HCV, Anti GBM, cryoglobulin, CK, urinary Myoglobulin
Urinary Indices
- FENa (Fractional excretion of Na+) = (UNa x PCr / PNa x UCr) x 100
- FENa < 1% (Pre-renal state)
May be low in selected intrinsic cause: Contrast nephropathy, Acute GN, Myoglobin induced ATN
- FENa > 1% (intrinsic cause of ARF)
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Causes
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Renal (25% to 40%)
Glomerular
- Anti–glomerular basement membrane (GBM) disease (Goodpasture syndrome)
- Anti–neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-associated GN) (Wegener granulomatosis, Churg-Strauss syndrome, microscopic polyangiitis)
- Immune complex GN (lupus, postinfectious, cryoglobulinemia, primary membranoproliferative glomerulonephritis)
Tubular (ATN)
- Ischemic
- Totoxic
– Heme pigment (rhabdomyolysis, intravascular hemolysis)
– Crystals (tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir, methotrexate)
– Drugs (aminoglycosides, lithium, amphotericin B, pentamidine, cisplatin, ifosfamide, radiocontrast agents)
Interstitial
- Drugs (penicillins, cephalosporins, NSAIDs, proton-pump inhibitors, allopurinol, rifampin, indinavir, mesalamine, sulfonamides)
- Infection (pyelonephritis, viral nephritides)
- Systemic disease (Sjogren syndrome, sarcoid, lupus, lymphoma, leukemia, tubulonephritis, uveitis
- Laboratory findings:
Oliguria—always, BUN/Cr Ratio <20:1, Urine Osmolality <350 mOsm, Urine Sodium >40mEq/L.
- Important to attempt to categorize broadly into one of 3 groups:
sepsis/hypovolemia 70% (PRE-RENAL)
drug related, acute GN, toxic 20% (RENAL)
obstruction 10% (POST-RENAL)
Management
- Maintain renal perfusion
- Correct metabolic derangements
- Provide adequate nutrition
- Role of diuretics
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- In the absence of uremic symptoms, start hemodialysis if BUN is around 100 mg/dL
- No additional benefit seen with earlier HD initiation nor more intensive HD prescription
Acute tubular necrosis
- most common cause of Renal AKI
Causes
- most often from renal ischaemia but can also be caused by toxins
- Haemorrhage, Burns, Diarrhoea and vomiting, fluid loss from fistulae, Pancreatitis, Diuretics, Congestive cardiac failure, Endotoxic shock, Snake bite, Myoglobinaemia, Haemoglobinaemia, Hepatorenal syndrome, Abruptio placentae, Pre-eclampsia and eclampsia
Pathogenesis
- Intrarenal microvascular vasoconstriction
- Tubular cell injury
- Tubular cellular recovery
- Glomerular contraction
- ‘Back leak’ of filtrate
- Obstruction of the tubule
Complications
- hyperkalemia: can occur rapidly and cause serious arrhythmias
- metabolic acidosis, decreased Ca2+, increased PO43-, hypoalbuminemia
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risk factors
- Most people have > 1 risk factor
- Age, Drugs (ACEi, diuretics, NSAIDS)
- Chronic kidney disease, Hypovolemia/Sepsis
- Diabetes
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Complications
- Hyperkalemia: due to low execration of K+
- Metabolic acidosis: due to low execration of H2
- Hypocalcemia, Uremia, Infection
- A rapid decline in renal function over a period of hours to days, resulting in
the failure of the kidney to excrete nitrogenous waste products and
to maintain fluid and electrolyte homeostasis
- Increase in SCr by ≥0.3 mg/dL (≥26.5 μmol/L) within 48 hours; or
- Increase in SCr to ≥1.5 times baseline, which is known or presumed to have occurred within the prior 7 days; or
- Urine volume <0.5 mL/kg/h for 6 hours.
- Mortality is high:
up to 75–90% in patients with sepsis infection
35–45% in those without
