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Clinical Findings
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A Symptoms and Signs
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Peripheral edema is a hallmark of the nephrotic syndrome, occurring when the serum albumin concentration is less than 3 g/dL Edema is most likely due to sodium retention (from renal disease) rather than arterial underfilling from low plasma oncotic pressure Initially this presents in the dependent areas of the body such as the lower extremities; however, such edema can become generalized Patients can experience dyspnea due to pulmonary edema, pleural effusions, and diaphragmatic compromise with ascites Complaints of abdominal fullness may also be present in patients with ascites Patients may show symptoms and signs of infection more frequently than the general population owing to loss of immunoglobulins and certain complement moieties in the urine
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B Laboratory Findings
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1 Urinalysis Proteinuria occurs as a result of an alteration of the negative charge in the GBM The screening test for proteinuria is the urinary dipstick analysis; however, this test indicates albumin only The addition of sulfosalicylic acid to the urine sediment allows abnormal paraproteins to be detected Urine dipstick testing can detect as little as 15 mg/dL of protein, but the results must be interpreted along with the urine specific gravity Trace protein seen on highly concentrated specimens may be insignificant, while trace protein on dilute specimens may indicate true renal disease Microscopically, the urinary sediment has relatively few cellular elements or casts However, if marked hyperlipidemia is present, patients can have oval fat bodies in the urine These
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Table 22 10 Classification and findings in glomerulonephritis: Nephrotic syndromes
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Etiology Minimal change disease (nil disease; lipoid nephrosis) Focal and segmental glomerulosclerosis Membranous nephropathy Associated with allergy, Hodgkin s disease, NSAIDs Associated with heroin abuse, HIV infection, reflux nephropathy, obesity Associated with non-Hodgkin s lymphoma, carcinoma (gastrointestinal, renal, bronchogenic, thyroid), gold therapy, penicillamine, lupus erythematosus Type I associated with upper respiratory infection Histopathology Light: Normal (with or without mesangial proliferation) Immunofluorescence: No immunoglobulins Electron microscopy: Fusion foot processes Light: Focal segmental sclerosis Immunofluorescence: IgM and C3 in sclerotic segments Electron microscopy: Fusion foot processes Light: Thickened GBM and spikes Immunofluorescence: Granular IgG and C3 along capillary loops Electron microscopy: Dense deposits in subepithelial area Light: Increased mesangial cells and matrix with splitting of GBM Immunofluorescence: Granular C3, C1q, C4 with IgG and IgM Electron microscopy: Dense deposits in subendothelium Light: Same as type I Immunofluorescence: C3 only Electron microscopy: Dense material in GBM Pathogenesis Unknown
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Unknown
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In situ immune complex formation
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Membranoproliferative glomerulonephropathy
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Unknown
Type II
Unknown
NSAIDs, nonsteroidal anti-inflammatory drugs; GBM, glomerular basement membrane
Kidney Disease
mellitus often does not need to be biopsied, since nephrotic range proteinuria in these diseases represents irreversible damage, although bone marrow transplant with high-dose chemotherapy can be considered in some patients with amyloid The role of biopsy for other systemic renal diseases is debated However, it can be useful for prognosis and treatment An occasional unexpected diagnosis is made, such as membranous nephropathy due to lupus erythematosus without serologic evidence of that illness
CMDT 2008
NEPHROTIC DISEASE IN PRIMARY RENAL DISORDERS MINIMAL CHANGE DISEASE
Minimal change disease is most commonly seen in children but is occasionally present in adults In patients over 40 years with primary nephrotic syndrome, the incidence of minimal change disease is 20 25%, with equal distribution between men and women In younger patients, there is a male predominance Minimal change disease can be idiopathic but also occurs following viral upper respiratory infections, in association with tumors such as Hodgkin s disease, with drugs (gold and lithium), and with hypersensitivity reactions (especially to NSAIDs and bee stings)
Management of Nephrotic Syndrome
A Protein Loss
The daily total dietary protein intake should replace the daily urinary protein losses so as to avoid negative nitrogen balance Protein malnutrition often occurs with urinary protein losses greater than 10 g/d In the past, protein restriction was suggested for patients with renal insufficiency because experimental animal models had demonstrated a decrease in glomerulosclerosis among those animals fed low-protein diets The largest human trial to date (the MDRD Study) did not show a significant benefit, but two recent meta-analyses have shown a mild renal benefit For this reason, the KDOQI recommends protein restriction to 06 g/kg/d in patients with a GFR less than 25 mL/min prior to starting dialysis
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