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A Symptoms and Signs
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Patients can exhibit the manifestations of nephrotic syndrome They are more susceptible to infection, especially with gram-positive organisms, have a tendency toward thromboembolic events, develop severe hyperlipidemia, and experience protein malnutrition Minimal change disease can rarely cause acute renal failure due to tubular changes and interstitial edema
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B Edema
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Dietary salt restriction is essential for managing edema; most patients also require diuretic therapy Commonly used diuretics include thiazide and loop diuretics Both are highly protein bound With hypoalbuminemia, diuretic delivery to the kidney is reduced, and patients often require large doses The combination of loop and thiazide diuretics can potentiate the diuretic effect This may be needed for patients with refractory fluid retention associated with pleural effusions and ascites
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B Histologic Findings
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Glomeruli show no changes on light microscopy or immunofluorescence On electron microscopy, there is a characteristic fusion of epithelial foot processes A subgroup of patients also shows mesangial cell proliferation These people have more hematuria and hypertension and respond poorly to corticosteroid treatment
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C Hyperlipidemia
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Hypercholesterolemia and hypertriglyceridemia occur as outlined above Dietary management in patients with nephrotic syndrome is of little value; however, dietary modification and exercise should be advocated Aggressive pharmacologic treatment should be pursued This is discussed in 27
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Treatment
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Treatment is with prednisone, 1 mg/kg/d In children, the response is excellent, but about 10% of patients become corticosteroid resistant after 4 6 weeks Adults often require longer therapy It can take up to 16 weeks to achieve a response to corticosteroids Treatment should be continued for several weeks after complete remission of proteinuria A significant number of patients will relapse and require further corticosteroid treatment Patients with frequent relapses and corticosteroid resistance may need cyclophosphamide or chlorambucil to induce subsequent remissions Progression to ESRD is rare Complications most often arise from prolonged corticosteroid use
Fogo AB Minimal change disease and focal segmental glomerulosclerosis Nephrol Dial Transplant 2001;16 Suppl 6:74 6 [PMID: 11568250]
D Hypercoagulable State
Patients with serum albumin less than 2 g/dL can become hypercoagulable Nephrotic patients have urinary losses of antithrombin III, protein C, and protein S and increased platelet activation Patients are prone to renal vein thrombosis and other venous thromboemboli, particularly with membranous glomerulopathy Anticoagulation therapy is warranted for at least 3 6 months in patients with evidence of thrombosis Patients with renal vein thrombosis and recurrent thromboemboli require indefinite anticoagulation
DeSanto NG et al Nephrotic edema Semin Nephrol 2001 May; 21(3):262 8 [PMID: 11320491] Schwarz A New aspects of the treatment of nephrotic syndrome J Am Soc Nephrol 2001 Feb;12 Suppl 17:S44 7[PMID: 11251031]
MEMBRANOUS NEPHROPATHY
Membranous nephropathy is the most common cause of primary nephrotic syndrome in adults It is an immunemediated disease characterized by immune complex deposition in the subepithelial portion of glomerular capillary walls
CMDT 2008
The antigens in primary disease are not known Secondary disease is associated with infections, such as hepatitis B, endocarditis, and syphilis; autoimmune disease, such as systemic lupus erythematosus, mixed connective tissue disease, and thyroiditis; carcinoma; and certain drugs, such as gold, penicillamine, and captopril Membranous nephropathy occurs most commonly in adults in their fifth and sixth decades and almost always after age 30 years
FOCAL SEGMENTAL GLOMERULAR SCLEROSIS
This lesion can present as idiopathic disease or secondary to such conditions as heroin use, morbid obesity, and HIV infection Clinically, patients show evidence of nephrotic syndrome, but they also have more nephritic features than membranous nephropathy or minimal change disease Eighty percent of patients have microscopic hematuria at presentation, and many are hypertensive Decreased renal function is present in 25 50% at time of diagnosis Patients with focal segmental glomerular sclerosis and nephrotic syndrome typically progress to ESRD in 6 8 years Diagnosis requires renal biopsy Light microscopy shows the lesions of focal segmental glomerular sclerosis It is thought that these lesions occur first in the juxtamedullary glomeruli and are then seen in the superficial renal cortex IgM and C3 are seen in the sclerotic lesions on immunofluorescence Electron microscopy shows fusion of epithelial foot processes as seen in minimal change disease (Table 22 10) Treatment is controversial, though supportive care for nephrotic patients is indicated Longer courses of corticosteroids are now being used because a higher percentage of patients enter remission High-dose oral prednisone (1 15 mg/kg/d) for 2 3 months followed by a slow taper can induce remission in over half of patients Most patients achieve remission within 5 9 months Other cytotoxic drug therapy can be considered but is disappointing (< 20% remission in most series)
Chun MJ et al Focal segmental glomerulosclerosis in nephrotic adults: presentation, prognosis, and response to therapy of the histologic variants J Am Soc Nephrol 2004 Aug;15(8): 2169 77 [PMID: 15284302]
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