Nephrotic syndrome, treatment

Hypotonic hyponatremia with an increase in ECF is also known as dilutional hyponatremia. In this scenario, patients have an excess of total body sodium and TBW however, the excess in TBW is greater than the excess in total body sodium. Common causes include CHF, hepatic cirrhosis, and nephrotic syndrome. Treatment includes sodium and fluid restriction in conjunction with treatment of the underlying disorder—for example, salt and water restrictions are used in the setting of CHF along with loop diuretics, angiotensin-converting enzyme inhibitors, and spironolactone.15... 

Unlabeled Uses Treatment of edema associated with CHF, liver cirrhosis, and nephrotic syndrome treatment of hypertension reduces lithium-induced polyuria, slows pulmonary function reduction in cystic fibrosis... 

Loop diuretics are the drugs of choice for the treatment of edematous patients with congestive heart failure, cirrhosis of the liver, and nephrotic syndrome. Excretion of Na is helpful only to the extent that some of the... 

Loop diuretics are used in the treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. These drug s are particularly useful when a greater diuretic effect is desired. Furosemide is the drug of choice when a rapid diuresis is needed or if the patient has renal insufficiency. Furosemide and torsemide are also used to treat hypertension. Ethacrynic acid is also used for the short-term management of ascites caused by a malignancy, idiopathic edema, or lymphedema. 

Amiloride (Midamor) is used in the treatment of CHF and hypertension and is often used with a thiazide diuretic. Spironolactone and triamterene are also used in tiie treatment of hypertension and edema caused by CHF, cirrhosis, and the nephrotic syndrome Amiloride, spironolactone, and triamterene are also available with hydrochlorothiazide, a thiazide diuretic that enhances tiie antihypertensive and diuretic effects of the drug combination while still conserving potassium. 

Clofibrate causes a necrotizing myopathy, particularly in patients with renal failure, nephrotic syndrome or hypothyroidism. The myopathy is painful and myokymia of unknown origin is sometimes present. The mechanism of damage is not known, but p-chlorophenol is a major metabolite of clofibrate and p-chlorophe-nol is a particularly potent uncoupler of cellular oxidative phosphorylation and disrupts the fluidity of lipid membranes. Muscle damage is repaired rapidly on the cessation of treatment. 

Adults (CHF, hepatic cirrhosis, nephrotic syndrome) - Initially, 100 mg/day (range, 25 to 200 mg/day). When given as the sole diuretic agent, continue for 5 days at the initial dosage level, then adjust to the optimal level. If after 5 days an adequate diuretic response has not occurred, add a second diuretic, which acts more proximally in the renal tubule. Because of the additive effect of spironolactone with such diuretics, an enhanced diuresis usually begins on the first day of combined treatment combined therapy is indicated when more rapid diuresis is desired. Spironolactone dosage should remain unchanged when other diuretic therapy is added. 

Hodson EM, Willis NS, Craig JC. Non-corticosteroid treatment for nephrotic syndrome in children. Cochrane Database Syst Rev 2008. 

This syndrome is characterized by proteinuria >3.5 g/day, hypoalbuminuria <3 g/dl, hyperlip-idaemia with an elevation of serum cholesterol, edema and oval fat bodies and fatty casts in the urinary sediment. A variety of disorders may produce nephrotic syndrome but, in the majority of cases, no cause is found. It is appropriate to define the selection of studies from the history and physical examination. Tests to order are antinuclear antibody, rheumatoid factor, cryoglobulins, serum complement, HBsAg VDRL serology (syphilis), protein electrophoresis of the serum and urine and HIV. If the cause is unclear a renal biopsy is done to define the glomerular lesion as treatment may on the underlying glomerular lesion. 

Hypercholesterolaemia and hypertriglyceridaemia commonly occur in patients with severe proteinuria. It may be associated with a higher incidence of cardiovascular disease. Dietary treatment is of limited value if the underlying cause of the nephrotic syndrome is not successfully controlled. Statins should be considered to lower the serum cholesterol. 

Schieppati A, Perna A, Zamora J, Giuhano GA, Braun N, Remuzzi G. Immunosuppressive treatment for idiopathic membranous nephropathy in adults with nephrotic syndrome. Cochrane Database Syst Rev 2004. 

Nephrotic syndrome is characterized by proteinuria and edema due to some form of glomerulonephritis. The resulting fall in plasma protein concentration decreases vascular volume, which leads to diminished renal blood flow. This in turn causes secondary aldosteronism characterized by Na and water retention and K+ depletion. Rigid control of dietary Na is essential. Therapy of the nephrotic syndrome using a thiazide (possibly with a K -sparing diuretic) to control the secondary aldosteronism, is a useful initial approach to treatment Since nephrotic edema is frequently more difficult to control than cardiac edema, it may be necessary to switch to a loop diuretic (and spironolactone) to obtain adequate diuresis. 

The first point is that treatment with steroids is generally palliative rather than curative, and only in a very few diseases, such as leukemia and nephrotic syndrome, do corticosteroids alter prognosis. One must also consider which is worse, the disease to be treated or possible induced hypercortisolism. The patient s age can be an important factor, since such adverse effects as hypertension are more apt to occur in old and infirm individuals, especially in those with underlying cardiovascular disease. Glucocorticoids should be used with caution during pregnancy. If steroids are to be employed, prednisone or prednisolone should be used, since they cross the placenta poorly. 

Unlabeled Uses Treatment of biliary cirrhosis, chronic acfive hepatitis, glomerulonephritis, inflammatory bowel disease, inflammatory myopathy, multiple sclerosis, myasthenia gravis, nephrotic syndrome, pemphigoid, pemphigus, polymyositis, systemic lupus erythematosus... 

The nephrotic syndrome, characterized clinically by proteinuria, is a rare and idiosyncratic reaction to lithium. As with other uncommon adverse effects, the issue of causation versus coincidence must be considered. Treatment includes cessation of the drug and, when necessary, corticosteroids such as prednisone ( 322). 

The main clinical uses of immunosuppressive drugs are suppression of organ and tissue rejection after transplant surgery and the treatment of diseases with an autoimmune component. Thses include renal diseases, e.g. glomerulonephritis, some nephrotic syndromes, connective tissue diseases, such as systemic lupus erythematosus rheumatoid arthritis, and systemic vasculitis. 

Cyclosporin is usually given orally, although absorption is often unpredictable. The intravenous route is usually restricted to patients who cannot take the drug orally, because of the risk of anaphylactic reactions. Other uses of cyclosporin include psoriasis and severe, active rheumatoid arthritis when these do not respond to conventional treatment, and steroid-resistant nephrotic syndrome. 

A 6-year-old girl, who had taken prednisone for 2.5 years for nephrotic syndrome with seven relapses in 3 years, developed symptoms of benign intracranial hypertension after oral glucocorticoid dosage reduction over 10 months from 30 mg/day to 2.5 mg/every other day (46). Laboratory studies and head CT scan were normal, but there was bilateral papilledema and the cerebrospinal fluid pressure was increased. She was given prednisone 1 mg/kg/day initially, with acetazola-mide, and 25 ml of cerebrospinal fluid was removed. All her symptoms resolved and treatment was gradually withdrawn. She developed no further visual failure. 

The author proposed that raised arterial pressure, which is an adverse effect of high dose glucocorticoid treatment, and low oncotic pressure due to a low protein plasma concentration in a patient with nephrotic syndrome, could have increased trans-synovial fluid flow at a lower arterial pressure than normal. 

Withdrawal symptoms disappear if the glucocorticoid is resumed, but as a rule they will in any case vanish spontaneously within a few days. More serious consequences can ensue, however, in certain types of cases and if adrenal cortical atrophy is severe. In patients treated with corticoids for the nephrotic syndrome and apparently cured, the syndrome is particularly likely to relapse on withdrawal of therapy if the adrenal cortex is atrophic (SEDA-3,305). In some cases, acute adrenocortical insufficiency after glucocorticoid treatment has actually proved fatal. It is advisable to withdraw long-term glucocorticoid therapy gradually so that the cortex has sufficient opportunity to recover. Table 5 lists methods of... 

Sumboonnanonda A, Vongjirad A, Suntornpoch V, Petrarat S. Adrenal function after prednisolone treatment in childhood nephrotic syndrome. J Med Assoc Thai 1994 77(3) 126-9. 

Bridgman JF, Rosen SM, Thorp JM. Complications during clofibrate treatment of nephrotic-syndrome hyperlipopro-teinaemia. Lancet 1972 2(7776) 506-9. 

Nephrotic syndrome. Thiazide or loop diuretics are used in the treatment of this kidney disorder that causes increased protein in the urine. 

The concomitant administration of ibuprofen antagonizes the irreversible platelet inhibition induced by aspirin. Thus, treatment with ibuprofen in patients with increased cardiovascular risk may limit the cardioprotective effects of aspirin. Rare hematologic effects include agranulocytosis and aplastic anemia. Effects on the kidney (as with all NSAIDs) include acute renal failure, interstitial nephritis, and nephrotic syndrome, but these occur very rarely. Finally, hepatitis has been reported. 

Persistent nephrotic syndrome is a life-threatening disease (mainly due to the risk of thromboembolic and infectious complications) and clearly confers a high risk of progression into end-stage renal failure, which is related to the degree of proteinuria (Jl). The therapeutic goal is therefore the remission of nephrotic syndrome, or at least reduction of proteinuria. In patients with persistent nephrotic syndrome, symptomatic treatment (or prevention) of hyperlipidemia, hypercoagulability, and sodium and water retention is also warranted. 

This volume continues our objective of expanding the intellectual horizon of clinical chemistry. Included are chapters on Clinical Applications of Cytokine Assays Diagnosis and Treatment of Acute Pancreatitis Mitochondrial Mutations and Mitochondrial Diseases Pathobiochemistry of Nephrotic Syndrome Total Antioxidant Capacity Autoantibodies to dsDNA, Ro/SSA, and LaSSB in Systemic Lupus Erythematosis and Lymphoid Malignancies and Immunosuppressive Analysis. The meld of analytical, anatomical, subcellular, and molecular sciences represented by these subjects will continue to evolve and expand. Clinical chemistry is a vibrant and vital profession. Future volumes, their editors, and their contributors will undoubtedly be an important part of the practice and science of clinical chemistry. 

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