Acute Kidney Injury

Acute Kidney Injury Definition Acute rise in serum urea over baseline levels Oliguria Usually present but not always less than 400 ml/day or persistently less than 30 ml/hour Causes Pre-Renal Intra-renal Post-Renal Nephrotoxin drugs NSAIDs Ureters ACEi Stones sepsis ARBs Esp. if bilateral dehydration Antibiotics Tumours haemorrhage E.g. aminoglycosides cardiac failure Chemotherapy Mural or extramural renal artery stenosis E.g. cisplatin liver failure Parenchymal disease causing hepatorenal syndrome Glomerulonephritis drugs NSAIDs, ACEIs and ARBs (due to efferent arteriole dilation) any intra-operative damage to the renal arteries e.g. accident graft occlusion, endovascular emboli or proximal aortic clamp applied for too long Rhabdomyolysis Blocked catheter Haemolytic uraemic syndrome Urethral Multiple myeloma Most common Thrombolytic micro angiopathies KDIGO and RIFLE criteria Used to define AKI Any of the following: At least 50% rise in Cr from baseline within the last 7 days Increase in serum Cr by at least 26.5 micromol/l within 48 hours Oliguria Clinical Features Bladder Acute urinary Acute interstitial nephritis retention Acute tubular necrosis Urine output of less than 0.5mls/kg/hr for more than 6 hours Abdominal cancers Prostate enlargement BPH or malignancy Renal stones History Physical Examination Oliguria or anuria Signs of hypovolaemia Dry mucus membranes Hard to diagnose because of: Reduced skin turgor Usually asymptomatic Tachycardia Non-specific features: Hypotension Nausea Signs of volume overload Fatigue Hypertension Confusion Pulmonary oedema Can be mistaken as a symptom of the underlying cause Peripheral oedema Elevated JVP Urinary symptoms should be asked about Features of uraemia Frequency Ecchymosis Urgency Incomplete emptying Due to platelet dysfunction and uraemic encephalopathy E.g. asterixis, confusion, seizures Features of post-renal obstruction Palpable or tender AKI Severity Classification Stage Values I 1.5 to 1.9 times the baseline II 2 to 2.9 times the baseline III More than 3 times the baseline Investigations Labs U&E Creatinine BUN Calcium phosphate K+ Na+ FBC Anaemia Leukocytopenia Thrombocytopenia LFTs VBG -> assess for acidaemia Urine studies Urine analysis Proteinuria Albuminuria Haemoglobinuria WBC Glucose Urine volume measurement Urine microscope and sediments Crystals Casts Urine osmolarity and specific gravity Dehydration Urinary eosinophil count Imaging PVR: can be done rabidly at bedside using a bladder scan U/S KUB Kidney size Hydronephrosis Postrenal obstruction Renal lesions CT urogram Investigate for urinary tract bleeding CT non-contrast Radio-opaque and non-radio opaque caliculi Ureteric obstruction CT triphasic kidney Dedicated cross sectional imaging for renal lesions Usually to clarify masses seen on U/S Renal biopsy Considered when suspecting AKI or a rapidly progressive glomerulonephritis Not done when ATN is clinical suspected Lab differentiation of pre-renal AKI, intra-renal AKI and post-renal AKI Pre-renal AKI Intra-renal AKI Post-renal AKI Concentration urine Low urine Na+ (fraction excretion of Na+), water and urea Increase Sr Na+, urea and creatinine Increased serum nitrogen -> azotaemia Elevated BUN High specific gravity Increased urinary Na+, water and urea Decreased BUN Increased serum creatinine Decreased serum Na+ and water Decreased urinary Na+, water and urea Increased serum urea and creatinine-> azotaemia Muddy brown glandular casts and renal tubular cells on urine sediment Hyaline casts on urine sediment Management General management Nephrotoxic drug withdrawal Medication dose adjustment Fluid resus Urinary catherisation For measuring UO Relieves urinary obstruction Targeted management Diuretics Relieves volume overloaded patients Esp. if there is pulmonary oedema Immunosuppression with glucocorticoids for AIN or PRGN to slow progression t irreversible injury Relief of obstruction Indwelling catheter, nephrostomy tubes or ureteric stent insertion Depends based on site and cause of obstruction Renal replacement therapy For severe causes A life sustaining treatment that takes over the job of failing kidneys removing wastes, excess fluid and balancing electrolytes Indications: Acidosis Electrolyte abnormalities Ingested toxins Fluid overload Uraemia Methods Dialysis Peritoneal dialysis Hemofiltration Kidney transplant Complications Electrolyte imbalance Hyperkalaemia -> arrythmias Metabolic acidosis Fluid overload Pulmonary oedema -> SOB Abdominal ascites -> abdominal compartment syndrome Periorbital oedema Uremic syndromes Multiorgan dysfunction Choric kidney disease Increased fracture risk Deceased drug excretion e.g. heparin -> increases bleeding risk i.e. increased risk of the drug adverse effects Criteria for Admission KDIGO stage II and III Rapidly rising creatinine in 48 hours with ongoing rise Worsening kidney function Oliguria Urine output of less than 0.5 ml/kg/hr for more than 6 hours Anuria for 12 or more hours Presence of life-threatening complications Hyperkalaemia Metabolic acidosis Pulmonary oedema and fluid overload Uraemic complications: Encephalopathy Pericarditis Severe nausea/vomit or bleeding Underlying cause such as: Sepsis Rhabdomyolysis Drug induced Post renal AKI requiring catheterisation or urology input Glomerulonephritis Vasculitis