Acute kidney injury

16.1 Acute kidney injury



Barry Wilkins




Essentials



1 Acute kidney injury (AKI, or acute renal failure) is acute reduction in glomerular filtration rate.

2 A high or rising plasma creatinine is the hallmark, but this does not necessarily distinguish it from chronic renal failure.

3 A normal plasma creatinine does not exclude AKI.

4 The commonest causes of AKI presenting to the ED are haemolytic uraemic syndrome and post-streptococcal glomerulonephritis.

5 Not all AKI is oliguric or anuric.

6 Most cases of oliguria are not AKI.

7 Most cases of elevated plasma urea are not AKI.

8 The most important treatment areas are circulating volume, potassium, and blood pressure.

9 Hyperkalaemia in acute kidney injury is not necessarily caused by potassium retention, especially when of short duration, but by potassium redistribution from cells.

10 Posterior urethral valves should be suspected in male infants with unexplained acute kidney injury.

11 Do not continue diuretics if two IV doses of furosemide of 1 mg kg–1, then 5 mg kg–1 (over 1 hour) produce no urine.


Introduction


Acute kidney injury (AKI), or acute renal failure (ARF), means any acute reduction in glomerular filtration rate (GFR), i.e. in the excretory function of the kidneys, with oliguria (<0.5 mL kg–1 hr–1 in children or <1 mL kg–1 hr–1 in infants) or anuria, and a rise in plasma creatinine. Occasionally it is non-oliguric. It may evolve over hours (e.g. hypoxic–ischaemic cause) or days (e.g. glomerulonephritis). AKI caused by acquired renal disease presenting to the emergency department (ED) is rare. However, it is common in hospitalised critically ill children, where it is associated with significant mortality. AKI caused by shock states may be preventable by attending to circulating volume.


Classically, AKI has been divided into three broad categories, but pathophysiological processes overlap, and the first and second groups can lead to the third when severe or prolonged.


Prerenal. Hypovolaemia, hypotension and low cardiac output reduce renal blood flow and cause elevation of plasma urea and a mild reduction in GFR and elevation in creatinine. This is not true renal failure, but a normal physiological adaptation to reduced renal blood flow, which responds to rehydration or other treatment of the cause.

Postrenal. Obstruction in the renal tract anywhere from the pelvicalyceal system to the urethra may lead to AKI or chronic renal failure (CRF). Crystalopathy (obstructing the tubules) is usually regarded as a ‘renal’ cause.

Renal. Primary disease in the glomerulus, which may be intrinsic (e.g. glomerulonephritis (GN)) or imposed (e.g. hypoxia, ischaemia, toxins).


Causes


See Table 16.1.1.












Table 16.1.1 Causes of AKI

1. Reduced renal blood flow
• Severe shock from hypovolaemia or myocardial failure

• Rarely, the following may cause acute tubular necrosis (ATN) or cortical necrosis, and are more common in children with pre-existing cardiac, renal or liver failure:
image Severe gastroenteritis

image Nephrotic syndromea

image Burns

image Diuretic use

image Haemorrhage

image Salt-wasting tubulopathies

image Hypoaldosteronism

• Cardiogenic shock

• Pericardial tamponade

• Coarctation of the aorta or renal artery stenosis

• Septic shock

• Anaphylactic shock

• Systemic inflammatory response syndromes (e.g. severe trauma, pancreatitis)

• Hepatorenal syndrome (rare)

• Malignant hypertension

• Arterial or venous thrombosis

• Disseminated intravascular coagulation (DIC)

• Drugs (e.g. angiotensin-converting enzyme (ACE) inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), tacrolimus, ciclosporin)

2. Intrinsic renal disease
• Haemolytic uraemic syndrome (HUS)b

• Thrombotic thrombocytopenic purpura (TTP)

• Acute proliferative glomerulonephritis (GN), including post-streptococcal and other post-infectiousc glomerulonephritis

• Acute tubular necrosis (ATN) caused by hypoxia plus ischaemia

• Systemic lupus erythematosus (SLE) or vasculitis

• IgA nephropathy

• Wegener’s granulomatosis

• Anti-glomerular basement membrane (anti-GBM) disease

• Pyelonephritis

• Toxins (e.g. petrol, carbon tetrachloride, heavy metals)

• Drugs (e.g. aminoglycosides, vancomycin, cisplatin, tacrolimus, ciclosporin, ACE inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), amphotericin B)

• Acute tubulointerstitial nephritis (TIN); drugs (e.g. furosemide, NSAIDs, penicillin, rifampicin, thiazides, allopurinol), immune-mediated diseases (e.g. IgA nephropathy, SLE) and infections (bacterial including Yersinia, viral, fungal, rickettsial) are causes

• HIV nephropathy

• Snake or arachnid envenomation

• Renal trauma

• Myoglobinuria from crush injury or rhabdomyolysis

• Haemoglobinuria (acute intravascular haemolysis, e.g. in G6PD deficiency)

• Sickle cell disease

• Leukaemic infiltration

• Shunt nephritis (ventriculoperitoneal shunt infection)

• Radiographic contrast agents (rare in children)

• Renal dysplasia, hypoplasia, and agenesis in neonates (chronic but acute presentation)

3. Urinary tract obstruction
• Posterior urethral valves (chronic but acute presentation)

• Urethral stricture

• Ureterocele

• Pelvic or retroperitoneal tumours

• Neurogenic bladder

• Retroperitoneal fibrosis (rare)

• Stones, sludge (metabolic disease), pus, fungal ball, sloughed renal papilla, clots, proteinaceous material or crystals (uric acid, calcium oxalate, aciclovir, methotrexate, purines, sulphonamides) in the ureters or renal tubules

4. Acute presentation of end-stage renal failure

a Sometimes nephrotic syndrome caused by mesangiocapillary GN may present with features similar to acute post-streptococcal GN.


b In developed countries HUS and post-streptococcal GN are the commonest causes presenting to the ED, whereas in tropical countries ‘prerenal’ causes predominate outside the hospital environment.


c Various infectious agents can produce nephritis similar to that of post-streptococcal GN (e.g. Mycoplasma, Leptospira, atypical Mycobacterium, Varicella, cytomegalovirus, Epstein–Barr virus, Toxoplasma, Rickettsia, hepatitis B and C).


There are many causes of oliguria other than AKI. Beware of urine retention or a blocked bladder catheter before assuming true oliguria (Table 16.1.2).


There are many causes of polyuria other than AKI (Table 16.1.3).

There are many causes of oedema other than AKI (Table 16.1.4).

There are many causes of elevated plasma urea (PUrea) other than AKI (Table 16.1.5).





Table 16.1.2 Causes of oliguria

• AKI

• Hypovolaemia

• Dehydration

• Low cardiac output

• Intrarenal vasoconstricting drugs when renal impairment is mild

• Syndrome of inappropriate antidiuretic hormone secretion (SIADH)





Table 16.1.3 Causes of polyuria

• AKI

• CRF

• Diuretics

• Osmotic diuresis, e.g. diabetic ketoacidosis

• Obstruction of the urinary tract

• Nephrogenic diabetes insipidus (DI)

• Nephrocalcinosis

• Interstitial nephritis

• Renal tubular disorders, e.g. Bartter’s syndrome

• Hypoaldosteronism, e.g. Addison’s disease, congenital adrenal hyperplasia

• Cerebral salt wasting

• Sickle cell disease

• Psychogenic polydipsia





Table 16.1.4 Causes of water retention and oedema

• AKI

• CRF

• Nephrotic syndrome (also has hypovolaemia and oliguria)

• Chronic liver disease

• Other causes of hypoproteinaemia (e.g. protein-losing enteropathy)

• Inappropriate ADH secretion or administration (oedema rare)

• Congestive heart failure (congenital or acquired structural heart disease, tachyarrythmias, pericardial effusion)

• Excess sodium and water intake





Table 16.1.5 Causes of uraemia

• AKI

• Increased dietary protein load

• Catabolic states with fever, e.g. sepsis, rhabdomyolysis

• Gastrointestinal or internal haemorrhage

• Hypovolaemia, dehydration, low cardiac output (increased reabsorption by the renal tubules)


Pathophysiology



Physiology


The kidney has three principal areas of function:


Excretion of waste products of metabolism (e.g. urea and non-volatile acid) and excess ingested elements (e.g. potassium). This is effected by glomerular filtration, measured by the GFR.

Regulation of the volume and mineral composition of body fluids. This is effected by tubular function, by absorption of >90% of filtered water, >99% of filtered sodium and 100% of glucose.

Endocrine functions, e.g. erythropoietin, renin.

Normal GFR is around 1 mL kg–1 min–1 in newborn infants, rising to 2 mL kg–1 min–1 in adults, but there is wide variation between and within individuals, reflected in wide variations in plasma creatinine (PCr) in normal children. Measurement of GFR is unhelpful in the acute situation. Creatinine clearance approximates to GFR. Plasma creatinine reflects GFR because creatinine production is remarkably constant, both within and between individuals, and is related to muscle mass. It is around 100 μmol kg–1 day–1 in infants, rising to around 200 μmol kg–1 day–1 in adults. There is a little absorption from, or secretion into, the tubule and this is abolished by Histamine-2 (H2) receptor antagonists. In AKI with complete cessation of glomerular function, plasma creatinine (PCr) increases by up to 150 μmol L–1 day–1 in infants and 300 μmol L–1 day–1 in adults. In less severe AKI, PCr rises by >50 μmol L–1 day–1. In stable renal function, GFR can be estimated by the formula: 70/PCr mL kg–1 min–1 in infants or 140/PCr mL kg–1 min–1 in adults, but this is an approximation. The formula does not hold true if GFR is changing.


Although there are published tables of PCr and GFR according to age, gender and size, the variability and different PCr assays in use preclude their being of much use in interpreting isolated creatinine results. A normal plasma creatinine does not exclude AKI. Generally any creatinine >100 μmol L–1 is abnormal, but in infants > 50 should raise a suspicion of impaired GFR, in a 5-year-old >70, in a 10-year-old >80, and in a 15-year-old >100. More important is the rate of increase of plasma creatinine in AKI, which takes 12–24 hours to become evident.


Renal blood flow (RBF) is normally very high (one quarter of cardiac output) in order to effect glomerular filtration. It is auto regulated over a wide perfusion pressure range. Normally 20% of the renal plasma flow is filtered. Up to 50% of urea is reabsorbed, more in oliguric states; hence plasma urea may reflect dehydration more than GFR. The high metabolic rate (for tubular reabsorption) and high endothelial mass (greater than any other organ by weight) make the kidney vulnerable to hypoxia and ischaemia.

Related posts:

Syncope Abdominal and pelvic trauma Paediatric advanced life support (PALS, APLS) Pertussis Infective endocarditis Default ThumbnailAvailing web-based resources

Stay updated, free articles. Join our Telegram channel
Tags:
Sep 7, 2016 | Posted by in EMERGENCY MEDICINE | Comments Off on Acute kidney injury

Full access? Get Clinical Tree
Get Clinical Tree app for offline access