Acute Renal Failure: Multiple Causes and Multiple Complications

Sheldon Tobe, MD, FRCPC

Case
The patient is an 80-year-old man, weighing 60 kg. He has a long standing history of hypertension and a more recent history of type 2 diabetes mellitus. He is taking an ACE inhibitor for the treatment of hypertension and microalbuminuria. The patient presents to the local ER suffering from colicky flank pain of 1-day duration. Past medical history includes a remote episode of kidney stones and he says that the pain was similar. He has vomited twice that day and has not taken food or drink since the previous night. He complains that the ER is cold and the nursing notes indicate that he seems peripherally shut down, with hands that are cold and pale. His blood pressure is 110/74 supine and 100/70 standing. His heart rate is 90. A dipstick urinalysis reveals blood and trace protein. Microscopy of the urine reveals hemegranular casts. An IVP is arranged after a KUB suggests the presence of a kidney stone. Ketoprofen, a non-steroidal anti-inflammatory (NSAID) is administered for pain relief. The IVP is non-diagnostic and the patient is admitted for further investigation. The following morning, an urgent call from the lab tells you that the patient's potassium is 6.8 mmol/L, his bicarbonate 14, his urea 15 and his creatinine 200 µmol/L. His ER lab results showed that the urea was 10 mmol/L and the creatinine 120 µmol/L the night before. You are coming on service and find yourself responsible for his care. Results from an abdominal ultrasound taken 6 months earlier show smallish 9 cm kidneys, with thinning of the cortices. Creatinine at that time was 110µmol/L. What is your approach to this patient?

Definition
Clearly this patient has acute renal failure, which is defined as the sudden loss of kidney function leading to an increase in concentration of serum creatinine; a by-product of muscle metabolism that is usually excreted in the urine (creatinine rises 50-150 µmol/day). ARF may occur in up to 5% of patients admitted to hospital and 30% of patients admitted to intensive care.¹

Approach

Once the patient is medically stabilized and the ABC's (airway, breathing, circulation) have been dealt with, the cause of the ARF must be found. The classic approach is to define ARF as pre-renal, renal and post renal (Table 1). Pre-renal causes are the results of problems with perfusion of the kidneys and are responsible for 55% of the cases of ARF. Perfusion problems most often result from a loss of volume due to blood loss, GI losses, accumulation of ascites or overdiuresis. In this case, on presentation the patient appears to be peripherally shut down and is given a non-steroidal anti-inflammatory (NSAID) followed by a contrast dye. NSAIDs block the production of vasodilatory renal prostaglandins. Prostaglandins help to protect the renal circulation from systemic vasoactive hormones such as catecholamines and vasopressin, which rise to defend the circulation in settings of volume depletion. The loss of renal prostaglandins leads to a reduction in renal perfusion thereby decreasing GFR. Pre-renal ARF responds to the restoration of normal blood volume. Does this patient have pre-renal ARF alone or is there more to the story?

Renal causes account for 40% of the cases of ARF, and can be broken down according to the main components of the kidney: the glomeruli, the tubules and the interstitium (Table 1). Glomerulonephritis, a spectacular and greatly feared form of ARF, is relatively uncommon. It is usually accompanied