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Flashcards in Renal - AKI Deck (22):

What is AKI?

Acute Kidney Injury arises when there is an acute fall in glomerular filtration rate (GFR) and substances that are normally excreted by the kidneys accumulate in the blood. It can be caused by inadequate renal perfusion (pre renal), intrinsic renal disease (renal) and urinary tract obstruction (post renal). Pre-renal is the most common, accounting for 50-65% of cases. A large majority can regain normal renal function.


What are the risk factors for AKI?

Other organ failure/ chronic disease - e.g. heart failure, liver failure, DM
History of AKI
Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACEi, ARBs, diuretics)
Use of iodinated contrast agent in the last 7 days
Aged 65 years and over


What criteria can be used to define AKI?

i) rise in serum creatinine of 26 um/L or greater within 48 hours
ii) 50% or greater rise in serum creatinine over the last 7 days
iii) fall in urine output to less than 0.5ml/kg/ hour for more than 6 hours in an adult


What is the pathophysiology of pre-renal AKI?

Inadequate cardiac function, circulatory volume depletion and obstruction of the renal arterial supply to the kidneys can all impair renal perfusion. The resulting renal ischemia can cause acute tubular necrosis (ATN).


What is post-renal AKI?

Obstruction to urine outflow causes back pressure which inhibits filtration. The subsequent swelling compresses blood vessels causing ischemia. AKI arises only if both kidneys are obstructed or if there is only one functioning kidney and that kidney is obstructed. The cause of the obstruction can be within the urinary tract (such as a stone), within the wall of the tract (such as a tumour or stricture) or outside the wall (such as compression by a mass or fibrotic process).


What intrinsic renal diseases cause AKI?

Intrinsic renal causes of acute kidney injury are glomerular diseases, tubulointerstitial disease and drugs or toxins. The main glomerular causes of acute kidney injury are acute or rapidly progressive glomerulonephritis, Goodpasture's syndrome, vasculitis, and proliferative glomerulonephritis associated with multi-system disease or infection.


What tubular toxins can cause renal AKI?

Tubular injury can result from ischemia or from toxic effects of exogenous compounds such as drugs, heavy metals and contrast media, or endogenous compounds such as haemoglobin or myoglobin. Exercise, trauma or other causes of muscle damage cause rhabdomyolysis with myoglobin release. Haemolysis destroys red blood cells. Haemolytic uraemic syndrome consists of haemolysis plus AKI and can follow infection with E.coli O157:H7. Both haemolgobin and myoglobin are filtered by the glomerulus and are toxic to tubular cells. Acute hypercalcaemia can cause AKI not only by renal vasoconstriction but also by calcium phosphate precipitation in the tubules. In myeloma, light chain precipitation in the tubules can cause cast nephropathy and AKI. Crystals forming in the tubules can cause tubular injury and obstruction (e.g. gout, aciclovir, or indinavir crystals)


What drugs are associated with renal AKI?

ANY drug has the potential to cause allergic tubulointerstitial nephritis, especially NSAIDs and antibiotics. Other drugs include:
- cephalosporins - tubular toxin
- amphotericin B - vasoconstriction, membrane damage
- aciclovir/ indinavir - precipitation in tubules
- ciclosporin/ tacrolimus - indirect vascoconstriction
- radiocontrast - vasoconstriction

NSAIDs inhibit prostaglandin synthesis leading to vasoconstriction, which reduces renal blood flow. If there is volume depletion, the vasoconstrictive drive may be very strong causing a serious fall in GFR. Risk factors for NSAID induced kidney injury are volume depletion, diuretic use, pre-existing renal impairment, and an oedema state (congestive heart failure, liver cirrhosis, or nephrotic syndrome). ATII causes vasoconstriction of the efferent arteriole which helps maintain GFR. ACEi block this causing a large fall in GFR (decr. efferent arteriolar tone ---> decr. GFR)


What is acute tubular necrosis?

Most acute kidney injury results from ATN. This usually arises when there is renal hypoperfusion, with renal ischaemia in combination with other factors such as sepsis or circulating tubular toxins or nephrotoxic drugs. ATN is associated with tubular cell death and shedding into the tubular lumen, resulting in tubular blockage. This raises the tubular pressure which eventually stops further glomerular filtration. Swollen tubules also compress the nearby vasa recta, which further reduces perfusion.


What features in the history of AKI should be elicited?

Check for pre existing renal impairment, hypertension or diabetes mellitus, which all predispose to renal ischaemia. Frank haematuria followed by oligouria suggests glomerulonephritis; haemoptysis suggests Goodpasture's syndrome; a recent sore throat or skin infection suggests post infectious glomerulonephritis. In men, urinary frequency, nocturia, and a poor stream with hesitancy and dribbling suggest post renal obstruction resulting from prostate disease. Muscle pain and swelling after exercise suggest rhabdomyolysis. Recent gastroenteritis can indicate E.coli associated haemolytic uraemic syndrome.

PMH may reveal multisystem disease associated with glomerulonephritis, vascular disease (renal artery stenosis), malignancy (hypercalcaemia) or chronic infection. DHx should include possible self poisoning and analgesic use.


What examination features are important in a patient with AKI?

Assess the fluid volume status.
Look for signs of multisystem disease, of cholesterol emboli and of i.v. drug use. Muscle swelling or tenderness suggest rhabdomyolysis. The eyes may have hypertensive, diabetic or other diagnostic changes. Examine all bedsores, and surgical and traumatic wounds for sepsis.
Pulse, JVP and BP (lying and standing if necessary), and cardiac examination may indicate volume depletion, cardiac lesions or pericarditis. Examine the chest for pulmonary oedema and evidence of infection or bleeding. Upper airway disease or sinusitis suggests Wegener's. Polycystic kidneys may be palpable and a large palpable bladder suggests obstruction. Rectal examination may demonstrate prostate or pelvic disease.


What investigations should be performed in cases of AKI?

1) Biochemistry - hyperkalaemia and severe acidosis can cause cardiac arrest. In rhabdomyolysis, creatinine kinase is released from muscles and plasma levels are high

2) Haematology - anaemia can result from blood loss, suppressed erythropoiesis, low EPO levels or haemolysis. A high eosinophil count suggests acute interstitial nephritis. HUS causes haemolysis with anaemia, damaged RBCs and a low platelet count.

3) Urinalysis - should be performed in all cases. Heavy proteinuria suggests glomerulonephritis or myeloma. Haematuria indicates renal or post-renal disease, but can be caused by urinary catheterisation. Myoglobin in the urine suggests rhabdomyolysis, and haemoglobin in the urine suggests haemolysis. Granular tubular casts may occur in acute tubular necrosis. Red cell casts are diagnostic of glomerular disease. Eosinophils in the urine suggest interstitial nephritis.


What imaging is needed in cases of AKI?

USS is mandatory in AKI to exclude obstruction and to determine the size of the kidneys. Small kidneys indicate chronic kidney disease. Angiography or Doppler can evaluate renal perfusion.


When should immunology be requested in patients with AKI?

If the patient is haemodynamically stable and USS shows no evidence of obstruction, the next step is to investigate immunology for renal causes of AKI (principally glomerular diseases). Complement levels are low in SLE and post infectious glomerulonephritis. Antiglomerular basement membrane antibodies suggest Goodpasture's syndrome and ANCA antibodies suggest small vessel vasculitis. Antinuclear antibodies or anti-dsDNA suggest vasculitis secondary to SLE. Myeloma can be indicated by the presence of antibody free light chains (Bence Jones proteins) in the urine or a monoclonal band in plasma.


What are the clinical features of pre-renal AKI?

Patients with pre-renal AKI are typically hypotensive and tachycardic with signs of hypovolaemia including postural hypotension. Septic patients may have peripheral vasodilatation and yet have relative underfilling of the arterial tree and renal vasoconstriction leading to AKI with ATN. Check for trauma and burns. Hyperkalaemia is common. Dilutional hyponatraemia occurs if the patient has continued to drink freely despite oliguria or has received inappropriate i.v. dextrose. Metabolic acidosis develops unless prevented by loss of hydrogen ions through vomiting or aspiration of gastric contents.


What biochemical features can be used to distinguish pre renal from renal AKI?

1) Urine volume:
- Pre renal = LOW
- Intrinsic = HIGH (paradoxically these patients undergo a diuresis)

2) Plasma Na+:
- Pre-renal = HIGH
- Intrinsic = LOW

3) Urine Na+:
- Pre-renal = <15 (because of RAAS activation secondary to hypovolaemia)
- Intrinsic = >40

4) Serum elevation of urea vs creatinine
- Pre-renal = urea >>> creatinine
- Intrinsic = urea = creatinine


How should electrolytes be managed in AKI?

Plasma electrolytes should be measured daily. Potassium intake should be restricted and diuretics or renal replacement therapy are used to prevent hyperkalaemia.

Calcium gluconate (stabilises cardiac membrane) is given if the potassium reaches 6mmol/L. A combined insulin/ dextrose infusion or nebulised salbutamol can be used to shift the potassium from the extracellular to the intracellular compartment. However, the only way to remove the excess potassium is by calcium resonium, loop diuretics (if there is any renal function left) or dialysis.


How is the metabolic acidosis managed in AKI?

Acid inhibits metabolic processes. Severe acidosis with inadequate renal function must be treated with renal replacement therapy. Restoration of blood volume will correct acidosis by restoring kidney function. Severe acidosis can be treated with sodium bicarbonate if volume status allows.


How is volume regulated in patients with AKI?

Regularly assess the body fluid volume. When necessary (in very unwell patients) measure the central venous pressure with an internal jugular or subclavian venous catheter. Monitor the fluid intake and output. Urinary catheterisation provides accurate urine volumes, but is an infection risk. Daily insensible losses vary with a minimum of 500ml and around 500ml extra per degree of fever. Daily weighing of patients can guide volume replacement. Volume replacement should match known and insensible losses. BE CAREFUL fluid cures in pre-renal AKI, but kills in intrinsic AKI as patients develop fluid overload.


What general measures are important in AKI management?

Much of the management of AKI is supportive. Correct hypoxia with oxygen and if necessary, ventilation. Cardiac output should be maintained with inotropes. Haemoglobin should be kept at above 10g/dL to maintain tissue oxygenation. Patients are often hypercatabolic and must be fed nasogastrically or parenterally if they cannot eat. Hypertension should be controlled by adjusting fluid balance and antihypertensives if necessary.


What drugs should be stopped as part of AKI management?

Should be stopped in AKI as may exacerbate renal function:
- aminoglycosides
- ACEi
- Diuretics
- ARBs

Usually safe to continue:
- paracetamol
- warfarin
- statins
- aspirin (at a cardioprotective dose of 75mg)
- clopidogrel
- beta blockers

May have to be stopped as AKI can increase risk of toxicity (but doesn't usually worsen AKI itself):
- metformin
- digoxin
- lithium


When should a percutaneous renal biopsy be considered in patients with AKI?

Essential if an intrinsic lesion (e.g. vasculitis, other acute GTN, interstitial nephritis) is suspected, or if no ischeamic, septic or systemic inflammatory cause is apparaent, especially if there is no sign of improvement in renal function or if the oliguric phase is delayed.

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