A 36-year-old African American man presents to the Emergency Department with new onset body swelling. He has a history of HIV and is taking antiretrovirals and trimethoprim–sulfamethoxazole for prophylaxis. His last CD4 count was 125 cells/mm3 . His temperature is 38.2°C, blood pressure is 168/98 mmHg, heart rate is 94 beats per minute, and respiratory rate is 24 breaths per minute. Laboratory workup reveals a creatinine of 1.8 mg/dL, and a urine dipstick shows 4+ protein.
What is most likely to be seen on renal biopsy under light microscopy?
Collapsed and sclerotic glomeruli surrounded by normal glomeruli. FSGS is one of the most common causes of nephrotic syndrome, and it is the most common cause in both black patients and in HIV patients. The diagnosis can be made with a renal biopsy that shows focal (only affecting some glomeruli) and segmental (only affecting part of a glomerulus) sclerosis. In HIV, the most common histologic variant is the collapsing form of FSGS. It is important to recognize that FSGS is a common cause of the nephrotic syndrome, especially in black patients and HIV patients. (A) Minimal change disease will show normal appearing glomeruli under light microscopy and epithelial foot process fusion under electron microscopy. (B) This pathologic finding is seen with membranous nephropathy. (C) This finding is seen in Alport syndrome, which is caused by a mutation in type IV collagen.
A 19-year-old college student develops fever, headache, and nuchal rigidity. Cerebrospinal fluid (CSF) cultures grow Neisseria meningitidis. She receives appropriate treatment, and her close contacts are given prophylactic antibiotic treatment. Her mother, who took this prophylactic treatment, developed a fever and maculopapular rash afterward. She is brought to the Emergency Department, and her laboratory values are shown below.
Which of the following represents the likely antibiotic and complication that the mother experienced?
Rifampin, Acute interstitial nephritis. There are several recommended prophylactic drugs for close contacts of a patient with bacterial meningitis from N. meningitidis: rifampin, ciprofloxacin, and ceftriaxone. (D) Trimethoprim–sulfamethoxazole is therefore not a correct option. The next step is identifying the complication that the mother experienced. She developed an abrupt rise in creatinine (AKI) with a rash; her urine studies showed WBCs and eosinophils. Taken together, the correct diagnosis is AIN, which is a type of intrinsic renal AKI. Though it is rare to see all of these symptoms together, drug-induced AIN may produce fever, rash, arthralgias, and/or eosinophilia/eosinophiluria. It is characterized by inflammatory cell infiltrates in the renal interstitium, and the most common cause is an allergic reaction to medications. There are many antibiotics that can cause this, and all of the ones listed above can cause it. Methicillin is not used as an antibiotic anymore, but it has a very high incidence of AIN. Other etiologic medications include NSAIDs, PPIs, cimetidine, diuretics, and allopurinol.
Besides medications, other causes of AIN include infections (e.g., Legionella, cytomegalovirus, tuberculosis; pyelonephritis can cause both an acute and chronic AIN) and systemic conditions (e.g., sarcoidosis, SLE, Sjögren syndrome, IgG4-related disease, lymphoma, leukemia, and others). Withdrawal of the offending agent is the first step in managing AIN; if the patient fails to respond, renal biopsy may aid in the diagnosis and assess the extent of damage, and corticosteroids may be beneficial. The only answer choice that includes AIN is B, and rifampin is an appropriate prophylactic treatment for close contacts. (Of note, rifampin is also the prophylactic treatment of choice for close contacts of invasive H. influenzae type B infection.) (A) Urine eosinophils and rash may be seen in cholesterol emboli syndrome, but ceftriaxone does not cause this. (C) ATN would most likely show muddy brown casts on urinalysis. (E) Meningococcemia occurs with or without concurrent meningitis and often presents with a petechial rash (not maculopapular) and systemic toxicity. WBC casts and eosinophiluria suggest the diagnosis of AIN, not meningococcemia.
A 49-year-old woman is hospitalized for pneumonia. She is managed appropriately and laboratory values are drawn. She has no past medical history, and a complete blood count and chemistry panel from 1 year ago were normal. Her laboratory values from this hospitalization are shown below.
What is the most likely cause of this patient’s renal disease?
Acute tubular necrosis. This question tests the reader’s knowledge of the most common cause of intrinsic renal AKI. Because the details in the vignette are quite limited, many of the answers could be the true diagnosis. However, on the shelf examination there are often similar questions that require the reader to “play the odds” and pick the most common cause. In this case, it is important to know that prerenal causes and ATN make up the majority of AKI cases in hospitalized patients. The FENa >2% indicates that this is intrinsic renal disease, and therefore the correct answer is ATN. (A, C) Pyelonephritis is a cause of AIN; however, AIN is not the most common cause of intrinsic renal AKI. AIN might have been selected since the patient likely took antibiotics for pneumonia; however, many antibiotics cause ATN as well. (B) Prerenal AKI from renal ischemia would be the correct answer if the FENa was <1%. (D) Cholesterol emboli syndrome usually occurs after catheterization procedures involving the aorta and would be suggested by a rash and urine eosinophils. (Goodpasture syndrome) presents with hemoptysis and/or hematuria, causing a nephritic syndrome. (Urinary tract obstruction) Postrenal AKI is not as common as prerenal AKI or ATN, and can be ruled out with a renal ultrasound. (Fibromuscular dysplasia) Fibromuscular dysplasia is most common in middle-aged women and is a cause of secondary hypertension. It may cause renal failure, but is not the most likely answer.
A 48-year-old woman presents to your clinic complaining of excessive urination and constant hunger and thirst. She has no other complaints and no past medical history. Her family history is significant for hypertension, type 2 diabetes mellitus, and hyperlipidemia. She does not smoke but lives a sedentary lifestyle. On examination, she is afebrile with a blood pressure of 134/88 mmHg, heart rate of 84 beats per minute, and respiratory rate of 14 breaths per minute. The rest of her examination is normal. The patient is scheduled for a return visit to have fasting laboratory tests drawn. At her return visit, her blood pressure is 138/86 mmHg. Her fasting glucose is 156 mg/dL, and urine albumin-to-creatinine ratio is 200 mg/g.
What is the next step in management for this patient?
Start an ACE inhibitor now. This patient is presenting with a new diagnosis of diabetes mellitus and is normotensive; however, she has moderate albuminuria. Although there is debate over whether ACE inhibitors (or ARBs) should be used as primary prevention for diabetic nephropathy, there is good data to support starting an ACE inhibitor with at least moderate albuminuria (early diabetic nephropathy). It can be started whether or not the patient is hypertensive. The reason ACE inhibitors are thought to be renoprotective comes from their role in reducing intraglomerular pressure. Early in the course of diabetes, there is hyperfiltration and intraglomerular hypertension that damages the nephrons. ACE inhibitors and ARBs prevent angiotensin II from causing vasoconstriction of the efferent arterioles. The effect is relaxation of the efferent arteriole and a reduction in the intraglomerular pressure, which decreases proteinuria (which is itself toxic to the tubules) and delays the onset of diabetic nephropathy. The bottom line for the shelf examination is that ACE inhibitors and ARBs are renoprotective in diabetes, and should be taken in nearly all diabetic patients with hypertension, nephropathy, and/or cardiovascular disease, whether or not they are hypertensive.
(A) Encouraging diet and lifestyle modifications is always a right answer, but is not always the best answer. In this case, it would be inappropriate to counsel the patient without starting an ACE inhibitor. (B) The patient is stable and can be managed as an outpatient. If the patient had diabetic ketoacidosis or hyperosmolar hyperglycemic state, then she should be managed as an inpatient. (D) The Eighth Joint National Committee (JNC 8) recommended a blood pressure target of <140/90 mmHg in all diabetic patients, and so an antihypertensive agent without renoprotective effects (e.g., hydrochlorothiazide) should not be started. (Note: remember that the shelf examination is not always up to date and might recommend a blood pressure goal of <130 to 135/80 to 85 mmHg.)
A 28-year-old woman with Crohn disease presents to the Emergency Department with back pain that started last night. She describes a colicky pain that is located on the right side of her back and shoots down to her groin. The pain is also associated with nausea and vomiting. Her temperature is 37.3°C, blood pressure is 128/84 mmHg, heart rate is 98 beats per minute, and respiratory rate is 18 breaths per minute. The patient appears uncomfortable and has some right flank pain on palpation. A pelvic examination is performed and shows no cervical discharge or cervical motion tenderness. Her laboratory values show a normal hemoglobin and leukocyte count, a urine pregnancy test is negative, and a urine dipstick shows 2+ blood but is negative for nitrites or leukocyte esterase.
What is the most likely diagnosis?
Nephrolithiasis. This patient is presenting with the typical symptoms of a kidney stone. Patients with Crohn disease are at risk of developing calcium oxalate stones due to increased absorption of oxalate in the GI tract (and therefore increased oxaluria), which has two causes. First, malabsorption of bile salts and GI tract inflammation increase mucosal permeability. Second, fatty acids (also a result of malabsorption) bind intestinal calcium, and so less calcium is available to bind and trap intestinal oxalate. This causes an increase in free oxalate that can be absorbed, eventually making it back to the kidneys to be excreted.
Calcium stones are the most common type of kidney stones, and patients with these stones are encouraged to increase their dietary intake of calcium (in order to decrease oxalate absorption in the GI tract). Thiazide diuretics may also be beneficial since they increase calcium reabsorption and therefore decrease urine calcium. Ammonium magnesium phosphate (struvite) stones are caused by urinary tract infections with urease-positive organisms (e.g., Proteus, Klebsiella) and can form staghorn calculi. Uric acid stones are associated with hyperuricemia (e.g., leukemia, gout). Cystine stones are seen in the genetic disease cystinuria and are treated by alkalinizing the urine with acetazolamide.
(A) Pyelonephritis would also produce flank pain, but unlike nephrolithiasis it would also produce fever, leukocytosis, and a urine dipstick showing infection (e.g., positive nitrites, positive leukocyte esterase). (C) Appendicitis is important to consider in any young patient with abdominal pain; however, it would be unusual for appendicitis to cause hematuria. (D) Ectopic pregnancies can mimic the pain of a kidney stone; however, this diagnosis is unlikely given the negative pregnancy test.
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