Management of Acute Renal Failure in the Elderly Patient

Abstract

Numerous anatomical and functional changes occurring in the aging kidney lead to reduced glomerular filtration rate, lower renal blood flow and impaired renal autoregulation. The elderly are especially vulnerable to the development of renal dysfunction and in this population acute renal failure (ARF) is a common problem. ARF is often iatrogenic and multifactorial; common iatrogenic combinations include pre-existing renal dysfunction and exposure to nephrotoxins such as radiocontrast agents or aminoglycosides, use of NSAIDs in patients with congestive cardiac failure and use of ACE inhibitors and diuretics in patients with underlying atherosclerotic renal artery stenosis. The aetiology of ARF is classically grouped into three categories: prerenal, intrinsic and postrenal. Prerenal ARF is the second most common cause of ARF in the elderly, accounting for nearly one-third of all hospitalized cases. Common causes can be grouped into true volume depletion (e.g. decreased fluid intake), decreased effective blood volume (e.g. systemic vasodilation) and haemodynamic (e.g. renal artery stenosis, NSAID use). Acute tubular necrosis (ATN) is the most common cause of intrinsic ARF and is responsible for over 50% of ARF in hospitalized patients, and up to 76% of cases in patients in intensive care units. ATN usually occurs after an acute ischaemic or toxic event. The pathogenesis of ATN involves an interplay of processes that include endothelial injury, microvascular flow disruption, tubular hypoxia, dysfunction and apoptosis, tubular obstruction and trans-tubular back-leak. Vasculitis causing ARF should not be missed as this condition is potentially life threatening. The likelihood of a postrenal cause for ARF increases with age. Benign prostatic hypertrophy, prostatic carcinoma and pelvic malignancies are all important causes. Early identification of ARF secondary to obstruction with renal imaging is essential, and complete or partial renal recovery usually ensues following relief of the obstruction.A comprehensive medical and drug history and physical examination are all invaluable. Particular attention should be paid to the fluid status of the patient (skin turgor, jugular venous pressure, lying and standing blood pressure, urine output). Urinalysis should be performed to detect evidence of proteinuria and haematuria, which will aid diagnosis. Fractional excretion of sodium and urine osmolality may be measured but the widespread use of diuretics in the elderly gives rise to unreliable results. Renal imaging, usually ultrasound scanning, is routinely performed for assessment of renal size and to exclude urinary obstruction. In some cases, renal biopsy is necessary to provide specific diagnostic information. The general principles of managing ARF include treatment of life-threatening features such as shock, respiratory failure, hyperkalaemia, pulmonary oedema, metabolic acidosis and sepsis; stopping and avoiding administration of nephrotoxins; optimization of haemodynamic and fluid status; adjustment of drug dosage appropria...

Risk factors and outcomes of acute kidney injury after intracoronary stent implantation

“…The increased incidence of AKI in the elderly is thought to be multifactorial, and it is attributable in part to anatomic and physiologic changes in the aging kidney, to an increased burden of comorbidities (hypertension, diabetes mellitus) affecting kidney function, to more frequent exposure to medications and interventions that alter renal hemodynamics or are nephrotoxic, and to alterations in drug metabolism and clearance associated with aging. [9,10] Taken together, the loss of renal functional reserve in the elderly is considered an increased risk for the development of AKI. [11] T h e p r e s e n c e o f b a s e l i n e p r o t e i n u r i a i s a n independent risk factor for AKI.…”

Toward the optimal clinical use of the fraction excretion of solutes in oliguric azotemia

“…[30][31][32][33][34][35][36]101 Surprisingly, while use of diuretics are well known to make the FeNa unreliable, [35][36][37][38] other drugs, such as amphotericin, that are known to cause proximal tubular damage may not. 39 Rarely liver disease can result in prerenal azotemia with an elevated FeNa because of sodium bicarbonate wasting from alkalosis 30 or alternatively because of loss of urea production that is necessary for water reabsorption and urine concentration. 101 Similarly bicarbonate conservation in acute (but not chronic) respiratory acidosis may cause a false depression through sodium bicarbonate conservation and generation 31 while metabolic acidosis has also been associated with an elevated FeNa regardless of volume 32,33 perhaps through hypercalcemia and hypomagnesemia may also interfere with tubular ability to conserve sodium even in the presence of hypovolemia.…”

“…Unfortunately, there are many other clinical situations where drugs 12,13 or diseases 112 interfere with glomerular or tubular function 37,38 which can result in an altered renal handling of sodium 108,113, that makes the FeNa less reliable which has led some to avoid the use of the FeNa. 39 Many causes may not appear obvious, unless the clinician maintains a clear understanding of renal physiology. Severe metabolic alkalosis from vomiting can result in bicarbonate concentrations that exceed the tubular threshold resulting in sodium and bicarbonate wasting that occurs even while chloride conservation remains intact, that will falsely elevate the FeNa, 31 and if the clinician is unaware of renal physiology he will be led to incorrect diagnoses.…”

“…32 Chronic metabolic acidosis may also result in sodium wasting, 33,34 presumably because of a different mechanism where acidosis may disrupt active transport. Surprisingly, while use of diuretics are well known to make the FeNa unreliable, [36][37][38][39] other drugs, such as amphotericin, that are known to cause proximal tubular damage may not.…”

Early identification of acute hypoxia based on brain NADH fluorescence and cerebral blood flow

“…Hypoxia is a common pathological phenomenon, accompanying with many diseases, such as neurologic complications, 1 ischemic heart disease, 2 acute renal failure, 3 intestinal ischemia, 4 pulmonary disease, 5 carbon monoxide poisoning, 6 traumatic brain injury, 7 perinatal asphyxia, 8 sudden cardiac death, 9 etc. Severe hypoxia often leads to death.…”