Acute Kidney Failure Flashcards
How can ARF be classified?
Prerenal
Intrinsic renal disease
Post renal.
How does Prerenal ARF occur?
Through a reduction in renal blood flow.
Leads to under perfusion of otherwise normal kidneys.
Usually a result of: •Fall in systemic blood pressure •Dehydration •Blood loss •Septicaemia •Reduced cardiac output.
Prolonged Prerenal failure could progress to intrinsic renal failure.
Rarer causes of under perfusion are acute vascular syndromes (renal vein thrombosis, renal artery dissection or atheroembolic disease).
How does postrenal ARF occur?
Caused by obstruction of the urinary tract leading to increased intratubular pressure and a fall in glomerular filtration rate.
How does intrinsic renal failure occur?
Refers to injury within the kidney itself.
Commonest cause= ATN (usually as a result of prolonged hypotension or nephrotoxins)
Can also be caused by acute interstitial nephritis, acute glomerulonephritis and intratubular obstruction.
—in intratubular obstruction the tubules can be blocked by crystals (urate nephropathy) or protein (myoglobin in rhabdomyolysis and casts in myeloma)
Describe the incidence of acute renal failure.
A population-based study estimates an incidence of 1800 per million.
What would a patient suffering acute renal failure describe in their history?
Malaise, anorexia, nausea, vomiting, pruritus, drowsiness, convulsions, coma (caused by uraemia).
Symptoms of the cause or complications usually dominate
The clinical signs and sequel are reflect the functional area that is deranged, eg a history of bladder outlet disruption (hesitancy, nocturnal, poor flow…) would indicate post renal ARF.
What would be found on examination of a patient with acute kidney failure?
Oedema, signs of the cause and complications.
Eg. Patient could be septic, hypovolaemic, have fluid overload, an elevated respiratory rate due to metabolic acidosis…
What investigations would you perform for a patient with acute kidney failure?
Serum urea and creatinine ⬆️ and serum potassium frequently ⬆️.
ABG - may show metabolic acidosis.
Creatine kinase is ⬆️ in rhabdomyolysis and WCC and CRP ⬆️ in sepsis.
Eosinophilia may occur in acute interstitial nephritis.
Immunological tests may show presence of anti-neutrophil antibodies (ANCA) or anti glomerular basement membrane (GBM) antibodies.
Compliment may be reduced in glomerulonephritis.
ECG may shoe features of hyperkalaemia
Chest radiograph mah show pulmonary oedema or haemorrhage.
USS of renal tract necessary to exclude obstruction.
Urine biochemistry can help to distinguish prerenal from renal failure.
If the cause of ARF is not apparent, renal biopsy is required.
How would you manage a patient with acute renal failure?
Patients should be assessed for fluid balance.
•Hypovolaemia should be corrected aggressively with I.v fluids of blood transfusion.
•Central venous catheter often used to guide fluid replacement.
•Accurate charting of fluid intake and output is essential.
•If hypotension persists after rehydration, inotropic support may be required to achieve adequate blood supply.
Hyperkalaemia should be treated promptly - it can cause life threatening cardiac arrhythmias and sudden death.
•Intravenous calcium (gluconate or chloride) stabilises the myocardium and reduces risk of arrhythmias.
•Infusion of insulin and dextrose increases potassium uptake by cells and temporarily lowers serum levels.
•Nebulised beta-adrenergic agonists (eg. Salbutamol) also lower serum potassium levels.
•These efforts buy time for elimination of potassium from the gut using calcium resonium resin.
If a patient remains anuric or Oliguric despite adequate fluid replacement and adequate blood pressure they are likely to require dialysis.
An attempt should be made to correct the underlying cause of ARF where possible.
•If evidence of obstruction - remove immediately either via urinary catheter or nephrostomy.
•Any nephrotoxic drugs suspected of causing interstitial nephritis should be discontinued.
•AIN may respond to oral steroids
•Vascular is should be treated with immunosuppression.
•Intratubular obstruction should be treated with I.v fluids to maintain a high urinary output where possible.
What complications could a patient with acute renal failure face?
Common and life-threatening: •Hyperkalaemia, •sepsis, •metabolic acidosis, •pulmonary oedema, •hypertension.
Less common: •Gastric ulceration, •bleeding (platelet dysfunction), •muscle wasting (hypercatabolic state), •uraemic pericarditis, •uraemic encephalopathy, •acute cortical necrosis.
What would you expect the prognosis to be for a patient with ARF?
ATN has biphasic recovery starting with oliguria then leading to polyuria (resulting from regeneration of the tubular cells).
Prognosis depends on the number of other organs involved, e.g. heart, lung.
Many of those with ATN recover.
Acute cortical necrosis may cause hypertension and chronic renal failure.
According to F&B:
•Overall mortality from ARF is 50-80%
•Outcome is worse for older patients and those in multi organ failure.
•In ATN 90% of patients who survive will recover some degree of renal function.
Define acute kidney failure.
Impairment of renal function over days or weeks, which often results in ⬆️ plasma urea/creatinine and oliguria (
