Acute Kidney Injury (AKI) / Acute Renal Failure

Related Subjects: |Metabolic acidosis |Lactic acidosis |Acute Kidney Injury (AKI) / Acute Renal Failure |Renal/Kidney Physiology |Chronic Kidney Disease (CKD) |Anaemia in Chronic Kidney Disease |Analgesic Nephropathy |Medullary Sponge kidney |IgA Nephropathy (Berger's disease) |HIV associated nephropathy (HIVAN) |Balkan endemic nephropathy (BEN) | Acute Rhabdomyolysis |Autosomal Dominant Polycystic kidney disease

Investigate for acute kidney injury, by measuring serum creatinine and comparing with baseline and testing urine to look for acute nephritis. In most cases management is supportive until kidney function returns. Some cases need intervention e.g. stenting, catheter.

About

• AKI has replace the terminology of Acute Renal Failure
• There is a sudden and rapid reduction in renal function
• EGFR is not an accurate assessment of renal function in an AKI
• There is a rise in urea and creatinine
• There is a fall in the GFR
• There may be oliguria and anuria

Definition of AKI #1

• Acute kidney injury (AKI) can be defined as a decrease of the glomerular filtration rate (GFR) that appears acutely, is maintained for some time, causes an accumulation of waste products from metabolism and uraemic toxins, and conditions a mishandling of body fluids and a loss of the ability to maintain homeostasis of electrolytes and acid-base balance

Definition of AKI (KDIGO)

• Stage 1: Serum Creatinine 1.5–1.9 times baseline OR a rise in serum creatinine of 26 micromol/litre or greater within 48 hours or < 0.5 ml/kg/hr for 6-12 hours
• Stage 2: Serum Creatinine x 2-2.9 baseline or < 0.5 ml/kg/hr for 6-12 hours
• Stage 3: Serum Creatinine x 3 baseline or Initiation of RRT or Anuria for > 12 hours

Renal functions

• Impaired control of Water and electrolytes
• Impaired excretion of drugs and other metabolites
• Impaired acid base control - need to excrete acid load
• Impaired BP control, Impaired EPO synthesis, Vit D hydroxylation

Risk Assessment > 2 of below is patient at risk

• CKD eGFR < 60 ml/min
• Aged > 65
• Comorbidities IHD, CCF, DM
• Setting: Sepsis, Perioperative
• Hypovolaemia, SBP < 110 mmHg, Deteriorating NEWS
• Taking NSAIDS, COX2, ACEI, ARB
• Taking Aminoglycoside, IV Radiocontrast

Causes

Prerenal vs Renal disease

• In prerenal disease there is increased activation of RAA system and ADH release which causes increased urinary Na retention and more concentrated urine. In intrinsic renal disease this functionality such as concentrating urine is impaired.
• Urinary Specific gravity Prerenal > 1.02 and Intrinsic renal disease < 1.01
• Urinary Osmolality Prerenal > 500 and Intrinsic renal disease < 350 mOsm/kg
• Urinary Na Prerenal < 20 and Intrinsic renal disease >40 mmol/l

Clinical

• Malaise, lethargy, Delirium possible. Nausea vomiting and generalised anorexia
• There may be oliguria or polyuria with impaired renal concentrating
• Neurological findings such as delirium, drowsiness and even seizures and coma are seen. Hiccoughs. A peripheral neuropathy suggests chronic renal failure.
• Skin pigmentation, pallor and itch is common with evident scratch marks. Impaired platelet function and bruising is seen.
• Pulmonary oedema may result from fluid overload and there may be a pericardial rub due to uraemic pericarditis. A pericardial effusion may be found on echo or CXR. Tamponade is an emergency
• Anaemia is more a sign of Chronic renal failure

Urinalysis

• Perform urine dipstick testing for blood, protein, leukocytes, nitrites and glucose in all people as soon as AKI detected.
• Consider acute nephritis and referral to the nephrology team if AKI with no obvious cause and has urine dipstick results showing haematuria and proteinuria, without UTI or trauma due to catheterisation

Investigations

• U&E: High Urea/Creatinine. High Potassium
• Blood gases - Metabolic acidosis High [H+]
• Blood glucose - may be high
• Urine - shows blood, protein and red cell casts on microscopy
• Blood count and film - Anaemia not typical with ARF - look for an alternative cause
• Complement levels
• Renal USS - normal size is typical in ARF (small in CKD)
• Renal biopsy shows a Crescentic type picture in RPGN
• Elevated ESR - myeloma, infection
• Elevated CRP - may be elevated if infection/vasculitis/autoimmune
• Plasma protein electrophoresis and urine for Bence -Jones ( Always do both when looking for Multiple myeloma)
• ANCA (MPO and PR3) suggests Wegener's Granulomatosis
• Anti-GBM suggests Goodpasture's syndrome and Autoantibody screen ANA dsDNA
• Complement C3 and C4 (low)
• HIV tests where risk factors

Selected tests

Management - Liaise closely with renal physicians and urologists. Basics of Management by cause

• NEWS scores, Fluid balance charts, Maintenance fluids, Review medications, Avoid NSAIDs. Daily U&Es
• Pre-renal: Ensure adequate hydration and circulatory support. May need pressors and even IABP.
• Renal: Determine cause, involve nephrology, immunosuppression for vasculitis
• Post renal: Remove any obstruction. Get USS.

AKI management

• Monitor BP, Rate, Skin turgor, Daily U&E, weights and other clinical assessments of volume should be done.
• Fluid management: If volume assessment and history suggests volume depletion then start with 1L of 0.9% saline over 2-4 hours and reassess urine output and status. A more aggressive approach may be used in younger patients with normal cardiac function.
• If unsure and concerned about overload then small challenges with 250 mol of fluid aliquots and then a reassessment of urine output and fluid balance is reasonable. Once the fluid balance has been attained. Never prescribe more than 24 hrs of fluid at a time. Balanced salt solutions may be preferred to N-saline.
• Once hydrated if there is still oliguria then a diuretic stimulus with IV Furosemide 100-120 mg IV may be given slowly IV over 10-20 minutes. A failure to respond suggests that things have progressed beyond simple prerenal failure and we may be dealing with acute tubular necrosis. Frusemide 80 mg IV may be used for fluid overload.
• Once euvolemic then simply input should be output + 500 ml per day. Frequent assessment of BP, Rate, Skin turgor, Daily weights and other clinical assessments of volume should be done.
• Targets: SBP > 100 mmHg and Urine output > 0.5 ml/kg/day. Once euvolemic then simply input should be output + 500 ml per day. A catheter placed in the bladder will relieve any possible prostatic or urethral lesion.
• Drugs review: Stop all nephrotoxic drugs (Vancomycin/Gentamicin)and BP lowering drugs e.g. NSAIDS, Diuretics, ACEI, ARB, Lithium, Metformin, IV contrast and review all other drugs for safety of dosing in AKI in the BNF. Avoid giving Contrast for radiological procedures
• Urine dip: Think about a diagnosis of acute nephritis and referral to the nephrology team when an adult, child or young person with no obvious cause of acute kidney injury has urine dipstick results showing haematuria and proteinuria, without urinary tract infection or trauma due to catheterisation
• Nephritis: Where Rapidly progressive GN is suspected then quick card testing for ANA, cANCA and Anti GBM should be done and rapid transfer to renal team to consider immunosuppressant.
• Acidosis: Consider 1.26% Sodium bicarbonate
• Hyperkalaemia: is always a risk and needs actively managed with IV Calcium Gluconate, Insulin and Dextrose, Salbutamol (Albuterol), Calcium Resonium, IV Hydration. See Hyperkalaemia
• Imaging: An ultrasound scan should be done as a matter of urgency in all with anuric or oliguria to exclude a post renal obstructive lesion. USS may show hydronephrosis and a dilated urinary system. A catheter placed in the bladder will relieve any possible prostatic or urethral lesion. If a per urethral catheter cannot be placed due to an enlarged prostate or urethral stricture then a suprapubic catheter is needed. The finding of a dilated ureter and hydronephrosis will require percutaneous nephrostomy. Once post renal causes are treated there may be a marked diuresis which needs compensated for in the fluid management plan.
• Nutrition: Normal enteral nutrition should be maintained as much as possible.
• Catheter: If severe AKI Patients require catheterisation to measure urine output and to exclude bladder outlet obstruction as a cause. Milder cases where obstruction not the case a catheter can be avoided.

Indications for RRT and phone a nephrologist

• Refractory hyperkalaemia
• Pulmonary oedema
• Severe acidosis pH < 7.2
• Encephalopathy
• Bleeding due to uraemia
• Uraemic Pericarditis.

Haemofiltration

• The patient will need either ITU for haemofiltration or Renal Unit transfer.
• Haemofiltration is most commonly used acutely.
• Be sure to talk to your Intensivists and Renal Physicians early before this situation arises if at all possible.

References

• Acute kidney injury: prevention, detection and management NICE guideline Published: 18 December 2019