Urinary loss of protein results in hypoalbuminemia and decreased plasma oncotic pressure. As a result, plasma water translocates out of the intravascular space into the interstitial space and results in a decrease in intravascular volume and edema.Oncotic pressure, or colloid osmotic pressure, is a form of osmotic pressure exerted by proteins, notably albumin, in a blood vessel's plasma (blood/liquid) that usually tends to pull water into the circulatory system.* Minimal change disease causes abrupt onset of edema and heavy proteinuria, mostly in children. Renal function is typically normal. Diagnosis is based on clinical findings or renal biopsy. Prognosis is excellent. Treatment is with corticosteroids or, in patients who do not respond, cyclophosphamide or cyclosporine.Minimal change disease (MCD) is the most common cause of nephrotic syndrome in children 4 to 8 yr (80 to 90% of childhood nephrotic syndrome), but it also occurs in adults (10 to 20% of adult nephrotic syndrome—see Overview of Nephrotic Syndrome). The cause is almost always unknown, although rare cases may occur secondary to drug use (especially NSAIDs) and hematologic cancers (especially Hodgkin lymphoma).MCD causes nephrotic syndrome, usually without hypertension or azotemia; microscopic hematuria occurs in about 20% of patients, mainly adults. Azotemia can occur in secondary cases and in patients > 60 yr. Albumin is lost in the urine of patients with MCD more so than larger serum proteins probably because MCD causes changes in the charge barrier that affect albumin selectively.DiagnosisRenal biopsy in adults with idiopathic nephrotic syndromeIn children, the following:Sudden onset of unexplained nephrotic-range proteinuria that is mainly albuminNormal renal functionNon-nephritic urine sedimentRenal biopsy in atypical casesRenal biopsy is required in atypical cases and in adults. Electron microscopy demonstrates edema with diffuse swelling (effacement) of foot processes of the epithelial podocytes. Complement and Ig deposits are absent on immunofluorescence. Although effacement is not observed in the absence of proteinuria, heavy proteinuria may occur with normal foot processes.TreatmentCorticosteroidsSometimes cyclophosphamide or cyclosporineSpontaneous remissions occur in 40% of cases, but most patients are given corticosteroids. About 80 to 90% of patients respond to initial corticosteroid therapy (eg, prednisone 60 mg/m2 po once/day for 4 to 6 wk in children and 1 to 1.5 mg/kg po once/day for 6 to 8 wk in adults), but 40 to 60% of responders relapse. Patients who respond (ie, have cessation of proteinuria or a diuresis if edema is present) should continue prednisone for another 2 wk and change to a maintenance regimen to minimize toxicity (2 to 3 mg/kg on alternate days for 4 to 6 wk in children and for 8 to 12 wk in adults, tapering during the next 4 mo). More prolonged initial therapy and slower tapering of prednisone lower relapse rates. Nonresponsiveness may be due to underlying focal sclerosis that was missed on biopsy due to sampling error.In corticosteroid nonresponders (< 5% of children and > 10% of adults), frequent relapsers, and corticosteroid-dependent patients, prolonged remission may be achieved with an oral cytotoxic drug (usually cyclophosphamide 2 to 3 mg/kg once/day for 12 wk or chlorambucil 0.15 mg/kg once/day for 8 wk). However, these drugs may suppress gonadal function (most serious in prepubertal adolescents), cause hemorrhagic cystitis, have mutagenic potential, and suppress bone marrow and lymphocyte function. Dosage should be monitored with frequent CBCs, and hemorrhagic cystitis should be sought by urinalysis. Adults, particularly if older or hypertensive, are more prone to adverse effects from these cytotoxic drugs. Another alternative is cyclosporine 3 mg/kg po bid, adjusted to obtain a whole-blood trough concentration of 50 to 150 μg/L (40 to 125 nmol/L).Key Points• MCD accounts for most cases of nephrotic syndrome in children and is usually idiopathic.• Suspect MCD in children who have sudden onset of nephrotic range proteinuria with normal renal function and a non-nephritic urine sediment.• Confirm the diagnosis by renal biopsy in adults and atypical childhood cases.• Treatment with corticosteroids is usually sufficient.CLINICAL VIGNETTESA 20-year-old male with a history of nephrotic syndrome is seen in clinic after a renal biopsy. He presented a week ago with anasarca, and foamy urine without hematuria. His blood pressure is 100/60 mm Hg. Examination reveals periorbital edema, with clear lungs, a normal cardiac examination and 4+ edema and anasarca. His 24 -hour urine contains 8 grams of protein and his serum creatinine. is 0.8 mg/dL. His urinalysis shows 4+ protein, but no red cells or casts. His renal biopsy is read as minimal change disease. Which of the following is the most appropriate next step in management?A. Intravenous pulse cyclophosphamide B. Oral prednisone C. Observation D. Oral FK506 (Prograft) E. Renal transplant B. Minimal change disease is a cause of nephrotic syndrome. Although it is more common in children, it can still be seen in adults. These patients will usually have a paucity of hematuria or azotemia. Most patients will have a good response to oral steroids, which are considered to be the initial treatment of choice.Intravenous pulse cyclophosphamide (choice A) is the drug of choice for proliferative lupus nephritis. It may occasionally be used for other glomerular diseases that fail steroid therapy. Observation (choice C) would not be a reasonable choice in a patient with a treatable cause of nephrotic syndrome.FK506 (choice D) is an anti-rejection medication used to treat patients with organ transplants. It is only rarely used as a drug to treat glomerular diseases. Renal transplant (choice E) is of value for patients with advanced renal failure. This is not the case in this patient.A 3-year-old child develops severe generalized edema following a viral infection. On the basis of clinical chemistry tests, a renal biopsy is performed, with normal light microscopic findings. Which of the following abnormal laboratory values might be expected in this individual?A. Decreased alpha globulin levels B. Decreased fibrinogenC. Increased serum calcium levelsD. Low serum albumin levelsE. Red blood cell casts in the urineThe correct answer is D. This child has minimal change disease, which is the major cause (over 90% of cases) of nephrotic syndrome in children aged 2 to 6 years. The most prominent clinical chemistry finding in these patients is massive proteinuria. The urinary protein in minimal change disease, in contrast to other causes of nephrotic syndrome, is often composed predominantly of albumin. Many other clinical chemistry changes may also be seen, including decreased serum albumin levels, hyperlipidemia, increased serum levels of alpha2- and beta-globulins, decreased IgG, and increased fibrinogen. Minimal change disease characteristically shows normal or near normal appearance of the glomeruli by light microscopy and extensive fusion of foot processes of the glomerular podocytes by electron microscopy. A point not always recognized by beginners is that the podocyte alterations may represent a reaction to, rather than a cause of, the proteinuria (e.g., an attempt to "seal the holes" in the glomerulus), since varying degrees of foot process fusion (together with more specific features) may sometimes be seen in other glomerular diseases associated with the nephrotic syndrome. Alpha-globulin levels (choice A) would be increased, rather than decreased, in minimal change disease. Fibrinogen levels are increased, rather than decreased (choice B). Serum calcium levels (choice C) are typically decreased in the nephrotic syndrome, possibly due to renal loss of vitamin D binding protein. Red blood cell casts in the urine (choice E) are indicative of glomerulonephritis, rather than the nephrotic syndrome.
Geriatrics clinical case for USMLE, MRCP PACES, and board review
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Exciting News! Third Year Rotation Sites!!!
We have just received our rotation sites for next year and I couldn't be more excited!!
...apartment, but since we are moving all over, sites in the smaller towns
usually provide housing - which is SO nice! For example, in some of the
hospitals they have a room set aside for med students (like a hotel room).
Others just own an apartment and let you live there for free or for a small
fee. Others may have housing with the actual physician or someone at the
hospital. Our med school doesn't ban us from jobs. Actually, John and I
both work at school and as TAs so we make a small income.
Thanks!! We can't wait! We apply for loans each year. Usually each school
has a budget and you decide how much you want to take out in loans. For
example, if one year's tuition is $40,000 they may offer a total of $60,000
to help pay for rent, food, medical bills, clothes, phone bills, internet,
etc. So, if you were to take out the maximum you would have $20,000 to live
off of for that year. For third year, many students are in the same city
they are now, so they just pay rent for their same...
yay so happy for you!! Just curious, does the school pay for where you guys
stay? Does medical school give you any money during the year since most
medical schools dont allow their students to have jobs?
For sure! I would love to do a video on that, I want it to be helpful so it
may take some time and lots of thought. I will definitely work on it, but
it may not be ready for a while! :)