Which ONE of the following statements is TRUE regarding clinical features that are MOST consistent with the associated underlying cause of acute renal failure (ARF)?
Answer: C: ARF itself is usually asymptomatic until severe uraemia has developed. More commonly, patients will present with symptoms of the underlying cause. Papillary necrosis results from ischaemia of the renal medullary pyramids and papillae. This is usually associated with diabetes mellitus, analgesic use, pyelonephritis and urinary obstruction. Presenting symptoms in the acute form include fever and chills, flank or abdominal pain and haematuria. It may also manifest as episodes of pyelonephritis and hydronephrosis, and mimics nephrolithiasis. Acute renal artery occlusion is usually marked by flank pain, whereas gradual stenosis is asymptomatic. Fever, arthralgia and rash are common with acute interstitial nephritis. The presence of fever usually suggests an autoimmmune or infectious cause.
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Regarding the causes of ARF, which ONE of the following statements is TRUE?
Answer: C: Prerenal causes are responsible for 70% of community-acquired and 20% of hospital-acquired ARF, whereas intrinsic causes are responsible for 20% of community-acquired and 70% of hospital-acquired ARF. The incidence of postrenal causes is 10% and is similar in both community and hospital-acquired ARF. Up to 90% of community-acquired cases have a potentially reversible cause as volume depletion is responsible for the majority of communityacquired ARF.
Intrinsic renal failure is subdivided into four categories: tubular, glomerular, interstitial and smallvessel disease. Ischaemic ARF, typically acute tubular necrosis (ATN), is the most common cause of intrinsic renal failure. Acute interstitial nephritis is usually due to a drug reaction but may also be caused by autoimmune disease, infection or infiltrative disease.
Which ONE of the following statements is TRUE regarding mortality associated with ARF?
Answer: B: The mortality for ARF has not improved over many decades in spite of the introduction of dialysis, primarily because affected patients are now older and have more comorbid conditions. Infection is the most common cause of death associated with ARF, accounting for 75% of deaths.
Cardiorespiratory complications are the second most common cause of death. Surprisingly, patients aged over 80 years with ARF have mortality rates similar to those of young adults. ARF in children has a different set of causes and mortality rates average 25%.
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Medications may precipitate renal failure. Which ONE of the following statements is TRUE?
Answer: D: NSAIDs, ACE-I and angiotensin-receptor blockers (ARBs) usually cause a gradual and asymptomatic decrease in glomerular filtration rate (GFR) but can cause acute kidney injury.
ACE inhibitors may precipitate renal failure, most likely due to impairment of renal autoregulation. Renal autoregulation and maintenance of GFR mainly depends on a combination of preglomerular arteriolar vasodilatation, mediated by prostaglandins, and postglomerular arteriolar vasoconstriction, mediated by angiotensin II. Reduced angiotensin II levels may cause efferent arteriolar vasodilation and subsequently decrease GFR. This is particularly relevant in patients with bilateral renal artery stenosis and renal hypoperfusion (caused by volume depletion or decreased ‘effective’ circulating volume as in oedematous states) because maintenance of GFR is dependant on postglomerular arterial vasoconstriction. ACE inhibitors may cause hyperkalaemia but through a different mechanism than renal impairment as described above. Suppression of angiotensin II leads to a decrease in aldosterone levels. Aldosterone is responsible for increasing the excretion of potassium; therefore, ACE inhibitors ultimately can cause retention of potassium.
Similarly, NSAIDs (both selective and nonselective cyclooxygenase inhibitors) interfere with prostaglandin synthesis and can cause preglomerular arteriolar vasoconstriction with diminished renal flow and GFR. Patients with diminished renal perfusion due to underlying volume depletion, congestive heart failure, chronic renal failure and cirrhosis are particularly vulnerable to this effect. Renal vasodilator prostaglandins are critical in maintaining glomerular perfusion in these patients in which elevated circulating levels of renin and ANSWERS ANSWERS 199 angiotensin II act to diminish renal blood flow and GFR. NSAIDs do not usually impair renal function in healthy persons.
Angiotensin-receptor blockers can also precipitate renal failure, most likely due to a similar mechanism as mentioned above.
Regarding investigations performed in renal failure, which ONE of the following is TRUE?
Answer: A: There is a misconception that traditional serum markers of myocardial damage (CK and troponin) are unreliable in dialysis patients presenting with chest pain. These markers are, however, not significantly elevated in ESRD patients who undergo regular dialysis and are specific markers of myocardial ischaemia in such patients.
Uraemia is a clinical syndrome and no single symptom, sign or laboratory result reflects all aspects of uraemia. Both serum urea and creatinine levels are inaccurate markers of the clinical syndrome of uraemia, although there seems to be a correlation between the symptoms of uraemia and a low GFR. Serum and urine chemistry panels have some utility in distinguishing between prerenal and renal causes. FENa (UNa/PNa ÷ Ucr/Pcr) is commonly used to identify prerenal causes but has limitations that should be recognised. A FENa <1% is suggestive of prerenal causes of ARF, as is a urea to creatinine ratio >20:1.
Microscopic urine analysis is helpful in determining the underlying cause of renal failure. The urinary sediment of patients with pre- and postrenal failure is usually ‘bland’ and may contain hyaline casts. Intrinsic causes of ARF typically have ‘active’ urinary sediment with granular casts typical of tubular injury and red cell casts associated with glomerulonephritis.
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