A 63-year-old Native American male, with a 6-year history of DM, hypertension, and hyperlipidemia, comes to your office as a new patient for a routine examination. He has been experiencing frequent lower back pain and headaches for which he is taking ibuprofen daily for the past 5 weeks. Moreover, he is complaining of mild fatigue. In addition, he is taking aspirin, atorvastatin, verapamil, and glipizide. His physical examination shows a blood pressure of 165/80 and heart rate of 90 bpm. In general, he was not in any distress. His funduscopic examination reveals no signs of diabetic retinopathy. Cardiac examination reveals a regular rate and rhythm with an S4 gallop. His lungs are clear and abdominal examination is unremarkable without any bruit auscultated. He also has 2+ lower extremity pitting edema. Rectal examination reveals brown stool, negative for occult blood. His laboratory results are as follows:Which additional of the following would best help in the determination of the etiology of this patient's nephrotic syndrome?
Answer(s): B
This patient's presentation and laboratory data are consistent with nephrotic syndrome. Nephrotic syndrome is typically associated with proteinuria of greater than 3.5 g/day, hypoalbuminemia, edema, and hyperlipidemia. Abnormalities commonly seen in nephrotic syndrome include hypocalcemia (due to vitamin D deficiency), low thyroxine levels (due to loss of thyroxine-binding globulin [TBG]), and microcytic, hypochromic anemia (due to transferring loss). Hypocomplementemia may be found in some forms of nephrotic syndrome, but this is not a typical finding. Hematuria is one of the components found in nephritic syndrome.This patient has history, physical, and laboratory findings that suggest possible multiple myeloma. For example, his history is pertinent for lower back pain and headaches. Moreover, Bence-Jones protein is not usually detected by urine dipstick but will be detected during a 24-hour urine collection. This would explain why there is relatively little urine protein detected on dipstick but over 5 g on the 24-hour urine. Lastly, multiple myeloma should be considered in an older patient with unexplained anemia. Given these findings, a serum and urine protein electrophoresis would be the best test to order next. A kidney biopsy would usually be diagnostic, but is unnecessary if the electrophoresis is positive. Complement levels and anti- GBM titer would not be of any use at the present time. Checking glycosylated Hgb will inform you of the adequacy of glucose control, but will be of little use with regard to the workup of the nephrotic syndrome. This patient has a low anion gap due to the presence of unmeasured cations in the blood. In this case, they arise from circulating immunoglobulins. The fractional excretion of sodium and urea can be helpful in differentiating prerenal causes from other etiologies of acute renal failure. A split 24-hour urine for protein is helpful in determining the presence of orthostatic proteinuria. Initiation of ACE inhibitors or angiotensin receptor blockers is the best option in patients with diabetic nephropathy, as these medications have been shown to slow the progression of kidney disease. The other medications listed may be used adjunctively, with an ACE inhibitor or angiotensin receptor blocker, if adequate blood pressure control could not be achieved with monotherapy. HIV-associated nephropathy is typically associated with a collapsing glomerulopathy, a variant of focal segmental glomerulosclerosis. Membranous nephropathy is associated with a number of other infections, including syphilis, hepatitis B, and hepatitis C virus. Membranoproliferative glomerulonephritis has also been associated with hepatitis C virus.
A 63-year-old Native American male, with a 6-year history of DM, hypertension, and hyperlipidemia, comes to your office as a new patient for a routine examination. He has been experiencing frequent lower back pain and headaches for which he is taking ibuprofen daily for the past 5 weeks. Moreover, he is complaining of mild fatigue. In addition, he is taking aspirin, atorvastatin, verapamil, and glipizide. His physical examination shows a blood pressure of 165/80 and heart rate of 90 bpm. In general, he was not in any distress. His funduscopic examination reveals no signs of diabetic retinopathy. Cardiac examination reveals a regular rate and rhythm with an S4 gallop. His lungs are clear and abdominal examination is unremarkable without any bruit auscultated. He also has 2+ lower extremity pitting edema. Rectal examination reveals brown stool, negative for occult blood. His laboratory results are as follows:Which of the following antihypertensive medications would be best implemented in patients with diabetic nephropathy?
Answer(s): A
A 63-year-old Native American male, with a 6-year history of DM, hypertension, and hyperlipidemia, comes to your office as a new patient for a routine examination. He has been experiencing frequent lower back pain and headaches for which he is taking ibuprofen daily for the past 5 weeks. Moreover, he is complaining of mild fatigue. In addition, he is taking aspirin, atorvastatin, verapamil, and glipizide. His physical examination shows a blood pressure of 165/80 and heart rate of 90 bpm. In general, he was not in any distress. His funduscopic examination reveals no signs of diabetic retinopathy. Cardiac examination reveals a regular rate and rhythm with an S4 gallop. His lungs are clear and abdominal examination is unremarkable without any bruit auscultated. He also has 2+ lower extremity pitting edema. Rectal examination reveals brown stool, negative for occult blood. His laboratory results are as follows:Which of the following microscopic findings on kidney biopsy is most usually associated with HIV infection?
Apatient you see routinely in the clinic has elevated liver function tests. ALT is 89, AST is 75, and the total bilirubin and alkaline phosphatase are normal. The patient has no past history of hepatitis, taking medications, or excessive drinking. You order hepatitis serologies. The results are as follows: Positive:HBsAg and anti-HBc. Negative: anti-HBs, anti-HBc IgM, anti-HAV, and anti-HCVWhat is your interpretation?
Answer(s): D
This patient has chronic hepatitis B. The different serologic studies for hepatitis B are shown in two figures below. The patient does not have acute hepatitis B because the IgM antibody to hepatitis B core is negative, and the total antibody to hepatitis B core is positive. Antibody to hepatitis B core occurs prior to the development of antibody to hepatitis B surface. IgM is found in acute infections; primarily IgG is seen in chronic infections.The presence of antibody to hepatitis B core with a positive hepatitis B surface antigen is indicative of chronic infection. Delta hepatitis infection requires the hepatitis B surface antigen. Delta hepatitis can occur concurrently with acute hepatitis B infection or later in the setting of chronic hepatitis B infection. There is no test for hepatitis C antigen. This is not a presentation of acute hepatitis A, which usually has very high transaminases. The antibody to hepatitis A virus occurs after 1 month and is associated with high transaminases Hepatitis Avaccine is indicated for patients with chronic liver disease. If this patient had hepatitis C, then hepatitis B vaccine would alsobe indicated. Hepatitis B vaccine is essentially hepatitis B surface antigen that causes the production of hepatitis B surface antibody. Since this patient has hepatitis B surface antigen already, choice C would be incorrect. Verifying the diagnosis with a qualitative hepatitis B viral load is not necessary. A quantitative hepatitis B viral load might be useful to evaluate for potential antiviral therapy. The only reason hepatitis Awould be recommended for the patient's spouse would be if the patient had acute hepatitis A. Investigating for other causes of hepatitis is not necessary as the diagnosis of chronic hepatitis B is already established.If the patient was found to be HBeAg positive, he would be considered highly infectious for the spread of hepatitis B. Hepatitis Be antigen is the DNA polymerase that shows active replication of the hepatitis B virion. These patients are 100 times more infectious than those lacking the hepatitis Be antigen. The window period is a situation where a patient is just recovering from hepatitis B. Hepatitis Bs antigen is negative and the antibody to hepatitis Bs has not been developed. The diagnosis is made by antibody to hepatitis B core. This is seen in Figure 1-6. Any patient who is hepatitis B surface antigen positive is at risk for delta hepatitis. This patient would be at risk for delta hepatitis by virtue of having a positive hepatitis B surface antigen. There is no level of transaminases, even normal transaminases, which would preclude antiviral therapy. The level of viral production indicated by the hepatitis B quantitative viral load, along with an assessment of the underlying liver pathology, is the best indication of need for treatment. As mentioned earlier, the antibody to hepatitis B would show the patient is less infectious and likely have a lower viral load.
Apatient you see routinely in the clinic has elevated liver function tests. ALT is 89, AST is 75, and the total bilirubin and alkaline phosphatase are normal. The patient has no past history of hepatitis, taking medications, or excessive drinking. You order hepatitis serologies. The results are as follows: Positive:HBsAg and anti-HBc. Negative: anti-HBs, anti-HBc IgM, anti-HAV, and anti-HCV What is the most appropriate next step for this patient?
This patient has chronic hepatitis B. The different serologic studies for hepatitis B are shown in two figures below. The patient does not have acute hepatitis B because the IgM antibody to hepatitis B core is negative, and the total antibody to hepatitis B core is positive. Antibody to hepatitis B core occurs prior to the development of antibody to hepatitis B surface. IgM is found in acute infections; primarily IgG is seen in chronic infections.The presence of antibody tohepatitis B core with a positive hepatitis B surface antigen is indicative of chronic infection. Delta hepatitis infection requires the hepatitis B surface antigen. Delta hepatitis can occur concurrently with acute hepatitis B infection or later in the setting of chronic hepatitis B infection. There is no test for hepatitis C antigen. This is not a presentation of acute hepatitis A, which usually has very high transaminases. The antibody to hepatitis A virus occurs after 1 month and is associated with high transaminases Hepatitis Avaccine is indicated for patients with chronic liver disease. If this patient had hepatitis C, then hepatitis B vaccine would alsobe indicated. Hepatitis B vaccine is essentially hepatitis B surface antigen that causes the production of hepatitis B surface antibody. Since this patient has hepatitis B surface antigen already, choice C would be incorrect. Verifying the diagnosis with a qualitative hepatitis B viral load is not necessary. A quantitative hepatitis B viral load might be useful to evaluate for potential antiviral therapy. The only reason hepatitis Awould be recommended for the patient's spouse would be if the patient had acute hepatitis A. Investigating for other causes of hepatitis is not necessary as the diagnosis of chronic hepatitis B is already established.If the patient was found to be HBeAg positive, he would be considered highly infectious for the spread of hepatitis B. Hepatitis Be antigen is the DNA polymerase that shows active replication of the hepatitis B virion. These patients are 100 times more infectious than those lacking the hepatitis Be antigen. The window period is a situation where a patient is just recovering from hepatitis B. Hepatitis Bs antigen is negative and the antibody to hepatitis Bs has not been developed. The diagnosis is made by antibody to hepatitis B core. This is seen in Figure 1-6. Any patient who is hepatitis B surface antigen positive is at risk for delta hepatitis. This patient would be at risk for delta hepatitis by virtue of having a positive hepatitis B surface antigen. There is no level of transaminases, even normal transaminases, which would preclude antiviral therapy. The level of viral production indicated by the hepatitis B quantitative viral load, along with an assessment of the underlying liver pathology, is the best indication of need for treatment. As mentioned earlier, the antibody to hepatitis B would show the patient is less infectious and likely have a lower viral load.
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