A 21-year-old college student presents to the Emergency Department with severe epigastric abdominal pain that radiates to her back. She is nauseous but has not vomited, and denies any diarrhea. She is admitted and her laboratory values show an elevated serum amylase and lipase.
Which of the following electrolyte abnormalities is associated with this disease?
Hypocalcemia. The first step is making the diagnosis of acute pancreatitis, which in her case is likely from alcohol. Acute pancreatitis can cause hypocalcemia due to extravascular binding of calcium to free fatty acids, which surround the pancreas as a result of pancreatic autodigestion by lipase. The other electrolyte abnormalities are not as strongly associated with acute pancreatitis as hypocalcemia. Note: One important teaching point for the interpretation of serum calcium is that the total calcium level represents both the ionized form (the physiologically active form) as well as the 45% that is bound to serum proteins (primarily albumin). Therefore, patients with low albumin will have a low total calcium but a normal ionized calcium level and will likely not have any symptoms. On the other hand, alkalosis will increase the binding affinity of albumin for calcium, causing a low ionized calcium but a normal total calcium. Bottom line: Do not be tricked by a “low” total calcium level in the setting of low albumin; you must correct for the low albumin.
A 52-year-old man presents for a routine physical examination. He has not been to a primary care physician since he was a teenager, and now he wants a colonoscopy since his friend was recently diagnosed with colon cancer. He denies any medical history and takes no medications. He is found to be hypertensive during his clinic appointment (164/98 mmHg), and the diagnosis of hypertension is later confirmed with the use of outpatient blood pressure monitoring. On examination, a bruit is heard over the left carotid artery, an S4 is heard on cardiac auscultation, and he has weak lower-extremity pulses. He has baseline laboratory tests drawn, is started on lisinopril, and is instructed to follow up for repeat laboratory work 1 week later. At the follow-up appointment, his blood pressure is 172/102 mmHg and the following laboratory results are seen.
What should be done next in the management of this patient?
Stop lisinopril. This patient has an abrupt rise in creatinine after 1 week of taking an ACE inhibitor, indicating that this medication may have caused acute renal failure. One potential side effect of ACE inhibitors and ARBs is a reduction in GFR, which occurs within several days after starting therapy. Although it is rare for these medications to cause AKI, patients with the following conditions are at risk: chronic kidney disease (CKD), polycystic kidney disease, heart failure, hypertensive nephrosclerosis, and bilateral renal artery stenosis.
This patient has hypertension with physical examination findings that suggest chronic hypertension (S4) and peripheral arterial disease (carotid bruit, weak peripheral pulses). In addition, he has hypokalemia at baseline. One condition that should be considered is bilateral renal artery stenosis from atherosclerosis. Because patients with this condition have poor kidney perfusion at baseline, they are in a high renin, high aldosterone state (potentially causing hypokalemia) with dilation of the afferent arteriole and vasoconstriction of the efferent arteriole to maintain GFR. ACE inhibitors cause relaxation of the efferent arteriole through a reduction in angiotensin II, further decreasing GFR and potentially causing ischemic AKI. Other clues to the diagnosis of renal artery stenosis are a renal bruit on examination and episodes of flash pulmonary edema. Bilateral renal artery stenosis can also be caused by fibromuscular dysplasia, which is less common and typically occurs in young women.
(A) The first step in the treatment of AKI is to remove the offending agent, so treating his hypertension and ignoring his AKI is not the right answer. (B) The patient is prediabetic and should be encouraged to change his diet and lifestyle before pursuing pharmacotherapy. (D) It is not appropriate to continue therapy with an agent that precipitated AKI.
A 38-year-old woman presents to her physician with fatigue and edema. She is an IV drug abuser and has been diagnosed with chronic hepatitis C infection. A urinalysis shows 1+ protein, 1+ blood, and red blood cell (RBC) casts. The rest of her laboratory values are shown below.
Laboratory testing 2 weeks ago showed a normal creatinine (0.8 mg/dL). A renal biopsy is performed which shows glomerular crescent formation. Antinuclear antibody, antinuclear cytoplasmic antibody, and antiglomerular basement membrane (GBM) antibody testing is negative.
Which of the following is the most likely diagnosis?
Membranoproliferative glomerulonephritis. This patient has a rapidly progressive glomerulonephritis (RPGN) indicated by three things: the rapid decrease in GFR over a short period of time, RBC casts on urinalysis that suggests a glomerulonephritis, and crescent formation on renal biopsy. (A) The most common causes of RPGN are antineutrophil cytoplasmic antibody (ANCA)-positive vasculitides (e.g., granulomatosis with polyangiitis); however, testing for ANCA was negative in this case. (E) Goodpasture syndrome can also cause RPGN, but was ruled out with negative anti-GBM antibodies. Therefore, the cause of this patient’s RPGN is likely immunecomplex mediated, and the next step in diagnosis is looking at serum complement levels. (D) This patient had low complement levels, ruling out causes of RPGN with normal complement levels such as IgA nephropathy and Henoch– Schönlein purpura. (B) SLE can cause RPGN with low complement levels; however, antinuclear antibody (ANA) is a sensitive test and therefore rules this out. Membranoproliferative glomerulonephritis may or may not be associated with cryoglobulins and has a variety of causes, including infections (e.g., HIV, hepatitis C, hepatitis B), collagen vascular diseases (e.g., SLE, rheumatoid arthritis), and monoclonal gammopathies (e.g., multiple myeloma). This patient has chronic hepatitis C infection and this is likely the cause. Below is a helpful overview of the various causes of glomerulonephritis (Figure below).
A 69-year-old man presents to the physician for fatigue and bone pain. His workup shows that he is anemic with the presence of an M-protein in the serum and urine, and he is diagnosed with multiple myeloma. Some of his other laboratory values are shown below.
An arterial blood gas shows that he has a pH of 7.3 and a PaCO2 of 35 mmHg. He has urine studies performed, which are significant for glucosuria, a urine pH of 7.8 after bicarbonate infusion, and a fractional excretion of bicarbonate of 25%.
Which of the following best represents the acid/base abnormality in this patient?
Nonanion gap metabolic acidosis with a compensatory respiratory alkalosis. This question is a good reminder to read the question and skim the answer choices first before going on to read the vignette. In this case, the diagnosis of multiple myeloma and proximal (type 2) renal tubular acidosis (presenting with the Fanconi syndrome, which is a syndrome of proximal tubule dysfunction with a decrease in the reabsorption of bicarbonate, phosphate, amino acids, and glucose) are not important for answering the question, which happens often on the shelf examination. (A, C) From the laboratory values, the calculated anion gap is 10, ruling out an anion gap metabolic acidosis. The pH, bicarbonate, and PaCO2 are all low, indicating a metabolic acidosis. To compensate, patients will increase their ventilation to decrease the amount of CO2 in the blood, producing a compensatory respiratory alkalosis. To determine if the respiratory compensation is appropriate, Winter formula can be used: PaCO2 = (1.5 × HCO3) + 8 ± 2. (D) In the case above, the PaCO2 should be 30 to 36 mmHg, which fits with the actual value of 35 mmHg confirming that the compensation is appropriate. If the patient were overcompensating (e.g., PaCO2 28 mmHg), then a primary respiratory alkalosis would be present; if undercompensating (e.g., PaCO2 38 mmHg), then a primary respiratory acidosis would be present.
Briefly, monoclonal gammopathies are the most common cause of acquired type 2 renal tubular acidosis, which is caused by an inability of the proximal convoluted tubule to reabsorb important compounds (e.g., bicarbonate, glucose, phosphate, etc.). Patients will excrete bicarbonate in the urine, leading to a moderate nonanion gap metabolic acidosis. The diagnosis is confirmed by an inappropriately elevated urine pH in response to a bicarbonate infusion as well as an increased fractional excretion of bicarbonate >15%. Distal (type 1) renal tubular acidosis is caused by a failure to reabsorb bicarbonate in the distal convoluted tubule, leading to severe acidosis with a urine pH consistently >5.3. Type 4 renal tubular acidosis is a result of hypoaldosteronism and will produce a mild acidosis.
A patient with end-stage renal disease caused by diabetic nephropathy is scheduled to start dialysis due to fluid overload and electrolyte abnormalities.
Which of the following best represents the likely changes seen in her laboratory results? (Note: Hb is hemoglobin, PTH is parathyroid hormone, TG is triglycerides.)
Increased K+ , Increased POـــ4, Decreased Ca2+ , Decreased Hb, Increased PTH, Increased TG. It is important to recognize and understand the changes that take place in chronic renal failure. Consider some of the important regulatory mechanisms of the kidneys (e.g., salt and water balance, RAAS, waste product secretion, role in vitamin D activation, role in erythropoiesis, etc.), and consider what the changes would be if they failed to work properly. Failure of the RAAS and other mechanisms of salt and water balance lead to fluid overload, hyponatremia, hyperkalemia, and hyperphosphatemia. Hypocalcemia is due to several factors: a loss in the active form of vitamin D (leading to decreased GI absorption and renal reabsorption), high serum phosphate levels, and metabolic acidosis (failure to excrete daily acid load). As a response, serum PTH will be elevated (secondary hyperparathyroidism, which may lead to tertiary hyperparathyroidism with time); consistently elevated PTH will increase burn turnover and produce osteodystrophy. Other changes include anemia due to loss of erythropoietin (EPO) secretion by the kidneys, dyslipidemia (commonly hypertriglyceridemia), and hypertension. Uremia refers to the clinical syndrome that accompanies the elevation in BUN and creatinine and includes nausea, vomiting, anorexia, encephalopathy, pericarditis, and bleeding from platelet dysfunction.
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