Acute Kidney Injury (AKI)

This is a term which describes a rapid deterioration in renal function, which leads to increased serum urea and creatinine combined with a low urine output.

It is very common, occurring in 50% of patients in intensive care units.

There are many different definitions of AKI but the widely used KDIGO criteria are:

Rise in creatinine > 26 uM within 48 hours

Rise in creatinine > 1.5 Å~ baseline value within 1 week

Urine output < 0.5 ml/kg/h for more than 6 consecutive hours

Causes

These can be divided into 3 categories: pre-renal, renal and post-renal:

Pre-renal

This describes a pathology upstream to the kidneys.

It results in reduced kidney perfusion, which leads to renal dysfunction.

Less blood flow decreases the GFR, causing poor excretion of urea and creatinine.

However, the kidney tubules still function and can reabsorb sodium to preserve volume. They are also able to reabsorb urea and concentrate the urine.

Triggers: Hypovolaemia (secondary dehydration, diarrhoea), poor perfusion (due to sepsis), renal artery stenosis 

Renal

This describes causes which cause intrinsic damage to the glomeruli, tubules, or kidney interstitium.

This gives the opposite picture where the kidneys themselves are unable to reabsorb sodium and urea, and so are not able to concentrate the urine.

Triggers: Acute tubular necrosis, glomerulonephritis, rhabdomyolysis

Post-renal

This includes causes which occur after the renal pelvis.

It is most commonly due to obstruction downstream of the kidney, e.g., renal stone.

Initially the blockage increases tubule pressure which helps push the urea back into the bloodstream. Therefore, this ends up mimicking a pre-renal cause.

Later, the raised pressure damages the tubular cells themselves.

This reduces their ability to reabsorb urea and sodium, mimicking a renal cause.

Symptoms

Can be asymptomatic

Reduced urine output

Pulmonary and peripheral oedema

Arrhythmias (due to hyperkalaemia)

Pericarditis or encephalopathy (due to high urea levels)

Key tests

Blood tests – raised urea, creatinine, and potassium

Urinalysis and culture – should be done to test for an infection

Imaging – patients with an AKI should get an ultrasound within 24 hours.

Management

For all causes, this involves treatment of the underlying etiology, as well as steps to manage the life-threatening complications such as acidosis and hyperkalaemia.

i) For hypovolemia: IV fluids, e.g., 500 mL crystalloid (0.9% saline) bolus

ii) For acidosis – can give bicarbonate, but the acidosis also improves as AKI resolves

iii) Hyperkalaemia – necessary to treat if K+ is high or if there are ECG changes

30 mL of 10% calcium gluconate (cardioprotective measure)

IV insulin/dextrose infusion – this stimulates intracellular shift of K+

Nebulised salbutamol

Selective potassium binders, e.g., sodium zirconium cyclosilicate

If patients have refractory hyperkalaemia, are uraemic or cannot manage their fluid balance (e.g., pulmonary oedema), they may require renal replacement therapy, such as hemofiltration or dialysis.

One of the most important parts of the management of any patient with an AKI is to stop drugs that may exacerbate the kidney injury (nephrotoxic), or those which have increased rick of toxicity since they are renally cleared.

Chronic Kidney Disease (CKD)

This is used to describe a chronic decrease in renal function, primarily characterized by a low GFR.

Causes

Diabetes

Hypertension

Glomerulonephritis

Nephrotoxic drugs

Genetic disorders, e.g., polycystic kidney disease, Alport syndrome

Symptoms

These can be remembered by the acronym H2 ONOUR

Hypertension – low GFR leads to excessive reabsorption of Na+, increasing ABP

Hypocalcaemia – due to less renal production of 1,25-DHCC and hyperphosphataemia

Oliguria – low urine output, leading to hyperkalaemia with a metabolic acidosis

Normocytic anemia – damage to kidney leads to decreased erythropoietin

Oedema – due to loss of ultrafiltration which leads to fluid overload in the body

Uremia – renal failure leads to a buildup of urea in the blood causing nausea, anorexia,

encephalopathy, pericarditis, and pruritus

Renal osteodystrophy – a form of metabolic bone disease characterised by bone

mineralisation deficiency, associated with secondary hyperparathyroidism

Grading

It is graded by 3 measures:

GFR – scale from G1 (> 90 mL/min) to G5 (< 15 mL/min) showing filtration rate

Albuminuria – scale of A1 to A3, used as a marker of kidney damage

Underlying disease – glomerular, vascular, cystic (indicates the type of pathology)

Management

This involves managing the complications of CKD

Hypertension – managed with antihypertensives e.g., ACE-i/ARBs

Hyperglycaemia – target HbA1C of 53 mM, using anti-diabetic drugs

Anaemia – treat initially with iron replacement, and then with erythropoietin stimulating agent aiming for Hb of 100–120 g/L

Hypocalcaemia – vitamin D supplements

Hyperphosphatasemia – phosphate binders e.g., sevelamer

Cardiovascular disease – statin (for all CKD stage 4) and antiplatelet therapy for patients at risk of atherosclerosis

Patients with end-stage renal failure will require dialysis – peritoneal or haemodialysis.

The definitive curative treatment for patients with CKD is a kidney transplant.