A 54-year-old man presents to the hospital with a 3-day history of severe nausea, vomiting, and diarrhea. He has been unable to keep down substantial solids or liquids over the past few days and has become progressively weak. He also endorses subjective fevers and occasional abdominal pain. The patient’s medical history is significant for hypertension and chronic low back pain, for which he takes lisinopril and ibuprofen. He has a 4-year-old child that he picks up from daycare who has also had diarrhea. On examination, the patient is tachycardic with a blood pressure of 104/84 mmHg. He appears weak with dry mucus membranes. Routine laboratory values are drawn, which show a blood urea nitrogen (BUN) and creatinine of 40 mg/dL and 2.1 mg/dL, respectively. He denies any history of renal disease.
Of the following options, what would be most helpful in determining the etiology of this patient’s renal failure?
Fractional excretion of sodium (FENa). Acute kidney injury (AKI) was defined by the Acute Kidney Injury Network (AKIN) as an abrupt rise (within 48 hours) in serum creatinine by ≥0.3 mg/dL from baseline, a ≥50% increase in serum creatinine from baseline, or oliguria of <0.5 cc/kg/h for >6 hours. Once AKI is recognized, the next step in diagnosis is determining whether the etiology is prerenal, intrinsic renal, or postrenal (Figure below). These terms reflect the perceived sight of pathology; prerenal AKI is caused by decreased blood flow to the kidneys, intrinsic renal AKI is caused by direct damage to the kidney parenchyma (i.e., to the renal vasculature, tubules/interstitium, or glomeruli), and postrenal AKI is caused by an obstruction in the urinary tract leading away from the kidneys.
The patient in this question is hypovolemic (tachycardia, decreased pulse pressure, and dry mucus membranes) from acute gastroenteritis that he likely acquired from his child. In response to hypovolemia, the renal arterioles vasoconstrict, decreasing blood flow to the kidneys and decreasing the glomerular filtration rate (GFR). Prerenal AKI is a result of ischemia from poor perfusion; however, it can progress to acute tubular necrosis (ATN), which is a form of intrinsic renal AKI. Besides hypovolemia, his daily NSAID may also be contributing to the AKI since NSAIDs cause renal vasoconstriction. The combination of an NSAID and an ACE inhibitor can worsen a more mild renal failure. One of the best tests for differentiating between prerenal AKI and ATN is the FENa. In prerenal AKI, sodium is reabsorbed in an attempt to maintain circulating blood volume, and therefore there will be little sodium in the urine. (B) Although this is often reflected by the urine sodium, this value is affected by renal water handling and urine output. FENa is a better test, since it only measures the fraction of sodium excretion and is not affected by urine output. In general, low FENa values indicate prerenal AKI and high values indicate intrinsic renal AKI (tubular damage leads to salt wasting). The FENa will be <1% in prerenal AKI and >2% in ATN. (Note: FENa should not be used in the setting of diuretics, but the fractional excretion of urea may be used instead.)
(A) A urine dipstick is a helpful screening tool for things like proteinuria or infection, but it will not help to differentiate between prerenal and intrinsic renal AKI. (D) A renal ultrasound is helpful in excluding postrenal AKI, which is not suspected in this case (sudden urinary tract obstruction is unlikely given the patient’s history of vomiting and diarrhea). (E) The diagnosis of prerenal AKI versus ATN cannot be made by history alone.
A 68-year-old woman is brought into the Emergency Department because of severe difficulty breathing. She complains that for the past few days she has had a progressive fever and productive cough. She was diagnosed a few weeks ago with idiopathic focal segmental glomerulosclerosis (FSGS), and her other medical problems include hypertension and gastroesophageal reflux disease (GERD). Her vitals show a temperature of 38.3°C, blood pressure of 104/74 mmHg, heart rate of 98 beats per minute, respiratory rate of 22 breaths per minute, and oxygen saturation of 93% on room air. Her laboratory values are shown below.
An arterial blood gas shows a pH of 7.29 and a PaCO2 of 32 mmHg.
Which of the following is the likely cause of this patient’s acid/base status?
Lactic acidosis. This patient has sepsis (meets 3/4 systemic inflammatory response syndrome criteria with the likely infectious source being pneumonia) and has an anion gap metabolic acidosis (explained later). The recent diagnosis of nephrotic syndrome put her at an increased risk of infection because of immunoglobulin loss in the urine. In addition, patients with nephrotic syndrome are also at risk for thrombosis, protein malnutrition, and hypovolemia. Generally speaking, acid/base problems on the shelf examination will consist of a primary disturbance with a compensatory process (Table below); there will likely be no mixed acid/base problems. (Note: a major exception to this is salicylate overdose, in which there will initially be a primary anion gap metabolic acidosis with a primary respiratory alkalosis.) The first step in any acid–base problem is determining if there is an anion gap using the equation: Na+ − (Cl− + HCO3 − ). If so, then there is at least one type of metabolic acidosis (one can determine if there is another metabolic acidosis by checking the delta–delta, but this is probably beyond the scope of the examination). Next, check the pH, bicarbonate, and PaCO2 to determine the primary acid/base disorder. This will open up a list of potential differential diagnoses, only one of which will fit the findings in the vignette. An important part of this question is recognizing the anion gap metabolic acidosis. The initial calculated anion gap is 10 (normal range 6 to 12); however, this needs to be corrected for the low albumin. For every drop in albumin by 1, the expected anion gap drops by 2.5. The corrected anion gap is therefore 15, so there is an anion gap metabolic acidosis. Because this patient is septic, she likely has lactic acidosis. (She likely has a mixed acid/base picture with a primary respiratory alkalosis as a result of hypoxemia from pneumonia, but this is not important for the question.) (A, D) Both renal tubular acidosis and excessive IV saline administration will cause a nonanion gap metabolic acidosis. (B) Hyperaldosteronism will cause a metabolic alkalosis.
A 43-year-old Caucasian man comes to the physician because of fatigue and body swelling that has developed over the last few weeks. He has no significant medical history, and takes no medications. He does not smoke or drink alcohol, and exercises 3 times weekly. He is afebrile with a blood pressure of 128/86 mmHg, heart rate of 88 beats per minute, and respiratory rate of 16 breaths per minute. On physical examination, there is noticeable periorbital edema with diffuse edema of the extremities. His laboratory values are shown below.
Which of the following is also likely to be present in this patient?
Hypercholesterolemia. This patient has three characteristics of nephrotic syndrome: proteinuria, hypoalbuminemia, and generalized edema. Nephrotic range proteinuria must be confirmed with a 24-hour urine sample and is defined as >3.5 g/d. Another important characteristic of nephrotic syndrome is hyperlipidemia. In response to the reduction in plasma oncotic pressure due to the loss of albumin and other plasma proteins in the urine, the liver increases synthesis of lipoproteins resulting in hypercholesterolemia. In addition, there is impaired liver metabolism that often results in hypertriglyceridemia. Finally, lipiduria may also be present and is manifested as urine fatty casts with a “Maltese cross” appearance. (A) FSGS is the most common glomerulopathy in the setting of HIV infection. However, this patient does not have apparent risk factors for HIV infection and he better fits the epidemiologic profile of membranous nephropathy (middle-aged Caucasian). FSGS is seen more commonly in African American and Hispanic patients. (C) This patient has characteristics of nephrotic syndrome and therefore heart failure is not the correct diagnosis. (D) Though there is some overlap of nephrotic and nephritic syndromes, as well as the causes of each, hematuria is typically a feature of nephritic syndrome. There are typically few or no cells in the urine of nephrotic patients.
A 58-year-old man with congestive heart failure (CHF), hypertension, and dyslipidemia presents to his physician with low back pain. He complains that he was lifting a heavy box 1 week ago and felt sudden pain in his lower back. He denies any incontinence, lower-extremity weakness, or paresthesia. He has been taking acetaminophen and naproxen around the clock with little effect. His chronic medications include aspirin, carvedilol, furosemide, losartan, simvastatin, and niacin. There is some tenderness to palpation of the paraspinal muscles along the lower back, but the rest of the musculoskeletal and neurologic examinations are normal. Laboratory values are significant for a potassium of 5.2 mEq/L, a BUN of 42 mg/dL, and a creatinine of 1.9 mg/ dL (baseline 1.2 mg/dL). A urinalysis is unremarkable except for few hyaline casts.
Which of the following best represents the physiologic changes in the kidney that led to this patient’s acute kidney injury? (Note: GFR is glomerular filtration rate, IGP is intraglomerular pressure, AAT is afferent arteriole tension, and EAT is efferent arteriole tension.)
Decreased GFR, Decreased IGP, Increased AAT, Decreased EAT. This patient has prerenal AKI as indicated by the abrupt rise in creatinine, the BUN to creatinine ratio >20, and a bland urinalysis with few hyaline casts (nonspecific, but can be found in prerenal AKI). It is important to recognize risk factors for AKI, and this patient has a few. He has a baseline decrease in effective circulating volume due to heart failure, which causes two important results. The first is an increase in sympathetic activity and therefore an increase in systemic vascular resistance. An increase in norepinephrine causes afferent arteriole vasoconstriction, decreasing the GFR. The second important result of decreased effective circulating volume is activation of the renin–angiotensin–aldosterone system (RAAS, Figure below) by the kidneys in response to decreased blood flow. Angiotensin II causes efferent arteriole vasoconstriction, increasing the GFR. Overall, the net effect of decreased effective circulating volume is a decrease in GFR, which will continue to decline as activation of the RAAS leads to salt and water retention that worsens the patient’s already reduced cardiac function. However, the patient is on appropriate medications to counteract some of these harmful responses: diuretics, a β-blocker, and an angiotensin receptor blocker (ARB).
Another important consideration in this case is the patient’s use of both an ARB and an NSAID. ARBs will block the effect of angiotensin II on the efferent arteriole, thus causing relaxation of the efferent arteriole (decreasing IGP and GFR). The kidneys produce prostaglandins (primarily prostaglandins E2 and I2) that cause afferent arteriole vasodilation to preserve renal blood flow, and prostaglandin synthesis is elevated in situations of decreased effective circulating volume. By blocking the cyclooxygenase (COX) enzymes, NSAIDs inhibit the production of these prostaglandins, which leads to afferent arteriole vasoconstriction (decreasing GFR). It is important to remember that the combination of ACE inhibitors or ARBs with NSAIDs can lead to prerenal AKI or ischemia-induced ATN. (Note: Ang-I is angiotensin I, Ang-II is angiotensin II, CO is cardiac output, and MAP is mean arterial pressure.)
A 68-year-old man presents to the hospital with nausea, vomiting, muscle weakness, and palpitations. He has a history of ischemic cardiomyopathy and takes lisinopril, carvedilol, simvastatin, and aspirin. He recently started taking spironolactone due to an increase in heart failure symptoms. There are no recent changes in his diet, and he denies any chest pain or shortness of breath. His screening chemistry panel is shown below.
Which of the following treatments is LEAST beneficial in the acute setting?
: Sodium polystyrene sulfonate. This patient presents with symptoms and laboratory confirmation of hyperkalemia, which is likely caused by the recent addition of spironolactone to his medication regimen. Spironolactone inhibits aldosterone’s actions on the distal convoluted tubule of the nephron, which normally upregulates apical sodium channels and increases the activity of the sodium–potassium ATPase. The potential consequence is a rise in serum potassium concentration. ACE inhibitors have the effect of reducing the production of aldosterone, and therefore have a similar effect.
Sodium polystyrene sulfonate (kayexalate) is a cation exchange resin that increases potassium excretion in the GI tract and effectively removes potassium from the body; however, it takes hours to work and is the least beneficial in the acute setting. (B) The most rapid acting treatment of hyperkalemia is calcium gluconate, which acts within minutes to transiently stabilize cardiac membranes in order to prevent the fatal arrhythmogenic complications of hyperkalemia. (A) Insulin is used for its effect of increasing the activity of the sodium–potassium ATPase, driving potassium into cells. It should be given with sugar to prevent hypoglycemia. It is important to note that both calcium and insulin are important in the acute treatment but do not reduce total body potassium; they are “temporizing” measures. Sodium polystyrene sulfonate, furosemide, and hemodialysis are the only options that will reduce total body potassium. (D) Furosemide is a loop diuretic that causes potassium excretion in the urine, and takes roughly 30 minutes to work. Other options for the treatment of hyperkalemia include β2 agonists (e.g., albuterol) and bicarbonate.
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