Makindo Medical Notes

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 (AKI) by measuring serum creatinine, 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 or catheterization.

About

• AKI has replaced 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) is a decrease in the glomerular filtration rate (GFR) that appears acutely, persists for some time, and causes an accumulation of metabolic waste products and uraemic toxins. This leads to mishandling of body fluids and a loss of the ability to maintain electrolyte and acid-base homeostasis.

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, and Vitamin D hydroxylation.

Risk Assessment: > 2 of below indicates the patient is 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 inhibitors, ACEI, ARBs.
• Taking aminoglycosides, IV radiocontrast.

Causes

Prerenal vs. Renal Disease

• In prerenal disease, there is increased activation of the RAA system and ADH release, causing increased urinary Na retention and more concentrated urine. Intrinsic renal disease impairs this function.
• Urinary Specific Gravity: Prerenal > 1.02, intrinsic renal disease < 1.01.
• Urinary Osmolality: Prerenal > 500, intrinsic renal disease < 350 mOsm/kg.
• Urinary Na: Prerenal < 20, intrinsic renal disease > 40 mmol/L.

Clinical Presentation

• Malaise, lethargy, possible delirium. Nausea, vomiting, and generalised anorexia.
• Possible oliguria or polyuria with impaired renal concentrating ability.
• Neurological symptoms such as delirium, drowsiness, seizures, and coma. Hiccoughs. Peripheral neuropathy suggests chronic renal failure.
• Skin pigmentation, pallor, and pruritus; bruising may be present.
• Pulmonary oedema due to fluid overload; pericardial rub from uraemic pericarditis. Tamponade is an emergency.
• Anaemia is more indicative of chronic renal failure.

Urinalysis

• Perform urine dipstick testing for blood, protein, leukocytes, nitrites, and glucose as soon as AKI is detected.
• Consider acute nephritis and referral to nephrology if AKI presents without an obvious cause and urine dipstick shows haematuria and proteinuria without UTI or trauma.

Investigations

• U&E: High urea/creatinine, high potassium.
• Blood gases: Metabolic acidosis (high [H⁺]).
• Blood glucose: May be elevated.
• Urine analysis: Shows blood, protein, and red cell casts on microscopy.
• Blood count and film: Anaemia not typical with ARF; look for alternative causes.
• Complement levels.
• Renal USS: Typically normal-sized kidneys in ARF (small in CKD).
• Renal biopsy: Crescentic pattern in RPGN.
• ESR: Elevated in myeloma or infection.
• CRP: Elevated if infection, vasculitis, or autoimmune.
• Plasma protein electrophoresis and urine for Bence-Jones proteins (especially for multiple myeloma).
• ANCA (MPO and PR3): Suggests Wegener’s Granulomatosis.
• Anti-GBM: Suggests Goodpasture's syndrome.
• Autoantibody screen (ANA, dsDNA).
• Complement C3 and C4 (low levels).
• HIV tests as needed.

Selected Tests

Management – Liaise Closely with Renal Physicians and Urologists

• NEWS scores, fluid balance charts, maintenance fluids, review medications, avoid NSAIDs, daily U&Es.
• Prerenal: Ensure adequate hydration and circulatory support. May need pressors and even IABP.
• Renal: Determine cause, involve nephrology, consider immunosuppression for vasculitis.
• Postrenal: Remove any obstruction. Get USS.

AKI Management

• Monitor BP, rate, skin turgor, daily U&E, weights, and other clinical volume assessments.
• Fluid management: If volume depleted, start with 1L of 0.9% saline over 2-4 hours and reassess. Use smaller aliquots in uncertain cases.
• If euvolemic but oliguric, attempt diuretic stimulation with IV furosemide (100-120 mg). A lack of response may indicate ATN.
• Set input to output + 500 ml per day once euvolemic.
• Drugs review: Stop nephrotoxic drugs, BP-lowering drugs, and NSAIDs. Avoid contrast.
• For suspected nephritis, consult nephrology and consider ANA, cANCA, Anti-GBM testing.
• Acidosis: Consider 1.26% sodium bicarbonate.
• Hyperkalaemia: Manage with IV calcium gluconate, insulin and dextrose, salbutamol, and IV hydration.
• Imaging: Obtain ultrasound urgently to rule out postrenal causes.
• Nutrition: Maintain normal enteral nutrition if possible.
• Catheterize in severe AKI for monitoring and to rule out bladder outlet obstruction.

Indications for RRT – Consult a Nephrologist

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

Haemofiltration

• Indicated for acute situations, usually requiring ITU or renal unit transfer.
• Discuss with intensivists and renal physicians as early as possible if haemofiltration is anticipated.

References

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