A 28-year-old IV drug user presents to the hospital with shortness of breath. The murmur of tricuspid regurgitation is heard on cardiac auscultation, and a chest x-ray shows multiple opacities in both lungs. An echocardiogram confirms endocarditis, and the patient is started on empiric vancomycin and gentamicin while blood cultures are pending. Two days later, the following results are seen on her laboratory tests.
Which of the following should be done next?
Stop gentamicin. This patient developed ATN, most likely as a consequence of using an aminoglycoside antibiotic. Pigmented granular casts (“muddy brown casts”) on urinalysis are highly suggestive of ATN (Table below), which can be caused by ischemia (progression of prerenal AKI) or toxins (medications, contrast, hemoglobin/myoglobin, crystals, and proteins such as light chains in multiple myeloma). Besides aminoglycosides, other important medications that can cause ATN include cisplatin, amphotericin, foscarnet, tenofovir, and contrast agents. Certain medications can also cause ATN by causing crystal formation; these include acyclovir, indinavir, and methotrexate. Treatment of ATN is largely supportive, and the first step of management is to remove the offending agent (in this case, gentamicin). (D) Vancomycin can be continued, which will cover MSSA and MRSA since S. aureus is the most common cause of endocarditis in IV drug users. Antibiotic therapy can be tailored to the blood culture results once they are available. (Note: There is some controversy about vancomycin causing AKI, but certainly gentamicin would be the first medication to stop.)
(A) IV fluids would be the correct answer if this patient’s ATN were a result of advanced prerenal disease from hypovolemia; however, it is more likely to be toxin-induced ATN. (B) This patient does not meet any indications for dialysis (Question 13) from the information provided. (E) Septic emboli can travel from left-sided vegetations (mitral or aortic valves) and cause renal failure; however, this patient has right-sided disease (hence the septic emboli to the lungs).
Differential Diagnosis of Renal Disease Based on Urinalysis:
A 76-year-old man is hospitalized for pneumonia and was started on empiric antibiotics. He developed a rash in response to the antibiotics, and the symptoms were somewhat relieved with diphenhydramine. Several days after this, the patient developed oliguria. His laboratory values are shown below.
A urinalysis is unremarkable. A renal ultrasound shows bilateral dilation of the renal pelvis and calyces.
Which of the following is the most likely anatomic site of obstruction in this patient?
Bladder. The abrupt onset of oliguria with a rise in creatinine indicates AKI, and the renal ultrasound showing hydronephrosis limits the differential diagnosis to postrenal AKI (obstructive nephropathy). An important historical clue given in the vignette is the administration of diphenhydramine, which is an antihistamine that also has anticholinergic properties. Elderly patients are often very sensitive to anticholinergics, and can experience adverse reactions such as confusion and urinary retention. Urinary retention results from the failure of the detrusor muscle to cause bladder contraction, since it contracts via cholinergic stimulation. Patients with BPH, which is a common diagnosis in older men, may also experience postrenal AKI with anticholinergics. This patient should have a urethral or suprapubic catheter placed to decompress the bladder and urinary tract.
(A, C, E) An obstruction in the renal arteries, tubules, or veins would cause renal injury but would not cause an obstruction in the urinary tract leading to hydronephrosis. (B) The ureters and ureteropelvic junction are common places for kidney stones to become lodged; however, it is important to know that AKI from ureteral obstruction occurs only if the obstruction is bilateral. This is due to the fact that obstruction of one ureter decreases the filtration rate of that kidney, but the other kidney will increase its GFR to compensate. It would be unlikely for two kidney stones to become lodged at the same time in this patient. Besides BPH and anticholinergic medications, other important causes of obstructive nephropathy include retroperitoneal fibrosis, neurogenic bladder (e.g., spinal cord injury), and malignancy (e.g., prostate cancer, abdominal cancer compressing the urinary tract, etc.).
A 63-year-old man complains of persistent abdominal pain for several weeks. In addition, he endorses an unintentional weight loss of 10 kg over the past few months. His medical history is significant for hypertension and diabetes. He has a 45 pack-year smoking history and drinks alcohol moderately. His hemoglobin is found to be 18.8 g/dL, and his urinalysis shows 23 RBCs per high power field. A CT scan is performed and shows a large mass within the left kidney.
Besides erythrocytosis, what is another potential complication of this disease?
Hypercalcemia. Renal cell carcinoma (RCC) is the most common malignancy affecting the kidneys. The “classic triad” of RCC is flank pain, abdominal mass, and hematuria; however, these three symptoms/signs are rarely seen together in the same patient. The diagnosis is suggested by the patient’s risk factors (age, hypertension, smoking), laboratory findings (erythrocytosis, hematuria), and CT scan showing a renal mass. Anemia is actually much more common in RCC than erythrocytosis, but erythrocytosis is a potential paraneoplastic syndrome (when EPO is secreted and functional; the majority of tumors will secrete nonfunctional EPO, which is why anemia is more common). Other important paraneoplastic syndromes associated with RCC include hypercalcemia from parathyroid hormone-related protein (PTHrP) secretion, thrombocytosis, secondary amyloidosis, polymyalgia rheumatica, and liver disease (Stauffer syndrome).
(A) Limbic encephalitis is an autoimmune process affecting the medial temporal lobes or limbic structures that presents with confusion, memory impairment, and/or seizures, and it may be paraneoplastic or nonparaneoplastic. In cases of paraneoplastic limbic encephalitis, it is most commonly associated with small cell lung cancer (SCLC), testicular and thymic tumors, breast cancer, and Hodgkin lymphoma. (B) Muscle weakness and double vision suggests a neuromuscular disorder such as myasthenia gravis, which is most commonly associated with thymic tumors. (D) Hyponatremia caused by the syndrome of inappropriate ADH (SIADH) is associated with SCLC, other extrapulmonary small cell cancers, and head and neck cancers.
A 28-year-old man presents to his physician with complaints of fatigue and muscle cramps that have developed slowly over the past few months. In addition, he says that he often needs to get up in the middle of the night to urinate. He has no significant past medical history or family history, does not take any medications or supplements, eats a regular diet, and does not smoke, drink alcohol, or use illicit drugs. He denies any recent illnesses, vomiting, or diarrhea. His temperature is 36.8°C, blood pressure is 102/68 mmHg, heart rate is 82 beats per minute, and respiratory rate is 10 breaths per minute. His laboratory values and urine studies are shown below.
Arterial blood gas
Urine studies show high levels of potassium and chloride, and low levels of calcium.
Which of the following conditions would produce similar findings to this patient’s disease?
Chronic chlorthalidone use. This patient has Gitelman syndrome, a rare autosomal recessive disease caused by a defect in the thiazide-sensitive sodium–chloride cotransporter in the nephron. The effect is similar to the chronic use of a thiazide diuretic, and often presents in early adulthood with hypokalemia, metabolic alkalosis, hypomagnesemia, and a low blood pressure. (D) Bartter syndrome is a similar genetic disease but mimics the chronic use of a loop diuretic such as furosemide, bumetanide, or ethacrynic acid. Thus, urine calcium levels can help to differentiate between Bartter and Gitelman syndromes. Treatment of both Bartter and Gitelman syndromes is with a potassium-sparing diuretic (e.g., spironolactone, amiloride) that will help correct the hypokalemia, hypomagnesemia, and metabolic alkalosis. Though the reader may not have been familiar with the diagnosis, they are expected to know that thiazide diuretics can cause all of the same findings.
(A) Chronic diarrhea will produce hypokalemia with a metabolic acidosis due to GI loss of potassium and bicarbonate. Surreptitious vomiting and diuretic abuse, on the other hand, present similarly to Bartter and Gitelman syndromes. Surreptitious vomiting will have a low urine chloride (<20 mEq/L). (B) Both Bartter and Gitelman syndromes produce a hyper-renin–hyperaldosterone state in response to chronic volume contraction; however, primary hyperaldosteronism from an adrenal tumor will present with hypertension and low renin.
A 53-year-old man with a history of diabetes and diabetic nephropathy is undergoing workup for a suspected diagnosis of coronary artery disease. His exercise stress test results place him in the high risk category, and he elects to undergo further workup with coronary angiography. The procedure was uneventful, and 2 days later he has laboratory tests drawn that are significant for a creatinine of 1.9 mg/dL (baseline 1.3 mg/dL). The serum leukocyte count, as well as the differential, is normal. A urinalysis shows pigmented granular casts with no RBCs or white blood cells (WBCs), and a FENa is calculated at 0.85%. The patient denies any flank pain or dysuria, and his vitals, physical examination, and urine output are normal.
Which of the following is the most likely diagnosis?
Reaction to a contrast agent. Patients with a history of CKD (especially diabetic CKD) are at an increased risk of contrast-induced nephropathy. The onset is typically 24 to 48 hours after the contrast agent is administered, and patients will usually have a mildly increased creatinine without oliguria. Contrast agents are thought to produce ATN as a result of direct toxic effects as well as renal vasoconstriction. Most cases are reversible. Pretreating at-risk patients can reduce the risk of this complication; options include IV fluids (± bicarbonate) and N-acetylcysteine.
(B) Atheroembolic events are a potential complication of angiography, and should be considered in the differential diagnosis. However, the absence of eosinophilia and other embolic phenomena (e.g., ischemia of several toes) makes this diagnosis less likely. (C) Although a FENa <1% is typical of prerenal AKI and a FENa >2% is typical of ATN, contrast-induced nephropathy typically produces a FENa <1%. (D) The absence of other cells or casts (especially WBCs) on urinalysis makes acute interstitial nephritis (AIN) very unlikely. In addition, AIN would most likely produce a FENa >2%. (E) The pigmented granular casts on urinalysis confirm ATN, but ischemia- or toxin-induced ATN would have a FENa >2%, so this is not the best answer choice.
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