ACUTE RENAL FAILURE
Acute renal failure is a comorbidity that can be encountered in the long case setting. It can also be incidentally encountered when an electrolyte profile with renal function indices is given to the candidate by an examiner during the discussion. In such situations it is important that the candidate correctly interpret the results and take charge of the discussion.
Case vignette
An 81-year-old man is admitted after an episode of syncope. On arrival in hospital his pulse rate is 30 bpm and blood pressure is 80/50 mmHg. He has a background history of paroxysmal atrial fibrillation, which has been managed with digoxin, and hypertension, managed with enalapril. He has been recently commenced on a non-steroidal antiinflammatory drug for painful arthritis of the knees. Investigations reveal his creatinine level to be 247 μmol/L and urea 26 mmol/L. His serum potassium level is 6.5 mmol/L. ECG reveals sinus bradycardia with tall tented T waves.
Approach to the patient
History
Ask about:
• the patient’s family history suggestive of any hereditary renal disease
• a past history of renal conditions
• whether the patient has taken any potentially renal-toxic drugs such as allopurinol, NSAIDs etc
• whether the patient has been recently commenced on or subjected to a dose increment of an agent such as a diuretic or an ACE inhibitor
• whether the patient has had recent vascular catheterisation procedures and/or radiocontrast exposure. Catheterisation can lead to cholesterol embolisation, which can cause acute renal damage. Radiocontrast material can be nephrotoxic.
• recent falls and prolonged immobilisation—these can lead to rhabdomyolysis, which in turn leads to acute renal failure due to myoglobin toxicity. It is important to rule this out in debilitated patients.
Remember: dehydration and hypovolaemia are the most common causes of acute renal failure, and assessment of the patient’s state of hydration is of primary importance in this setting.
In order of frequency, the most common causes of acute renal failure are:
Examination
1. Check the patient’s fluid status by examining the oral mucosa and checking skin turgur.
2. Check blood pressure and pulse.
3. Assess the JVP, look for peripheral oedema, and auscultate the lung fields for crepitations, looking for evidence of cardiac failure.
4. Look for rashes of vasculitis and evidence of connective tissue disease.
5. Examine the temperature chart for fevers, which would suggest sepsis.
6. Examine for wasting, hard mass lesions and lymphadenopathy, which would indicate malignancy.
7. Listen to the abdomen for a renal bruit, which may suggest renal artery stenosis.
8. In the anuric patient it is important to catheterise the bladder to exclude urethral obstruction and, if already catheterised, to flush the catheter to relieve any catheter obstruction.
9. Ask for the results of the urine analysis and the per rectum and per vagina examinations, looking for any pelvic mass lesions.
10. It is also important to request the results of microscopic examination of a fresh urine sample, looking for red cells, red cell casts and changes in the red cell morphology.
Causes of acute renal failure
• Impaired renal perfusion—shock, dehydration, severe left ventricular failure, renal artery obstruction
• Renal vein thrombosis
• Acute glomerular nephritis
• Acute vasculitis
• Acute tubular necrosis—ischaemic/toxic
• Exogenous renal toxins—drugs/ionic contrast agents
• Rhabdomyolysis
• Multiple myeloma
• Crystal-induced—e.g. urate, oxalate, pyrophosphate
• Haemolytic uraemic syndrome
• Thrombotic thrombocytopenic purpura
• Outflow tract obstruction—ureteric, bladder-related or urethral
Common causes of acute renal failure according to anatomy of location
1. Prerenal causes—severe congestive cardiac failure, hypovolaemia, dehydration, bilateral renal artery stenosis
2. Intrinsic renal causes—acute glomerulonephritis, tubulointerstitial nephritis, drug toxicity, fat embolism, cholesterol emboli, hepatorenal syndrome, haemolytic-uraemic syndrome, acute tubular necrosis.
3. Postrenal causes—renal outflow tract obstruction due to calculi, blood clots, trauma and retroperitoneal fibrosis.
Remember: both kidneys need to be affected to cause acute renal failure, unless only one kidney, anatomically or functionally, is present.
Investigations
In addition to serum biochemistry, the following investigations would be helpful:
1. Full blood count—looking for anaemia (may suggest chronicity), leucocytosis (may suggest sepsis or inflammation) and thrombocytopenia (possibly lupus nephritis).
2. Erythrocyte sedimentation rate—if elevated, can suggest multiple myeloma, connective tissue disease or vasculitis.
3. Urine analysis and midstream urine—for microscopy, culture and sensitivities. The presence of red cell casts and dysmorphic red cells in the phase-contrast microscopy would suggest glomerulonephritis; hyaline casts are non-specific; white blood cell casts suggest tubulointerstitial disease.
4. Urinary electrolytes and creatinine—the following findings, if present, would suggest a prerenal cause for the renal failure:
6. Renal arterial Doppler study—looking for evidence of renal artery stenosis. The renal vascular resistive index should also be checked. This gives an assessment of the renal microvascular resistance and hence intrarenal vascular disease.
7. According to the clinical indication, the following tests can also be requested: serum electrophoresis, immunoelectrophoresis, antinuclear antibody test (ANA), extractable nuclear antibody tests (ENA), antineutrophil cytoplasmic antibody tests (ANCAs), serum complement levels, streptococcal serology (antistreptolysin-O test (ASOT) and anti-DNAseB), hepatitis B serology and hepatitis C RNA assay, HIV serology and blood cultures if the patient is febrile.
8. If the kidney size is normal and the diagnosis is still uncertain, a renal biopsy is indicated.
Management
Fundamental steps in management are as follows:
1. Stop all non-essential renal-toxic drugs (e.g. NSAIDs, ACE inhibitors, ARBs, gentamicin, amphotericin B, allopurinol) that would have potentially contributed to the current pathology. Decrease the dose of all renally excreted drugs.
2. Restore plasma volume and maintain a strict fluid balance, to avoid dehydration or volume overload. The daily fluid intake can be maintained at a volume equivalent to the previous day’s losses + 500 mL. Correct electrolyte imbalances, particularly hyperkalaemia. Monitor the patient’s body weight together with the fluid input and output on a daily basis.
3. Good nursing care is essential to prevent pressure sores and ensure hygiene.
4. Treat other acute medical conditions such as sepsis, vasculitis and thromboembolism.
5. Monitor renal function and electrolyte status regularly, to assess the need for renal replacement therapy.
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